Category: Nutrition

Is your diet working against your thyroid gland? Find out which foods interfere with healthy thyroid function and how to minimize your risk.

Hypothyroidism 101

Thyroid hormone tells all of the cells in your body how busy they should be. Too much thyroid hormone (hypERthyroidism), and your body goes into overdrive; not enough thyroid hormone (hypOthyroidism), and your body slows down. The most common causes of hypothyroidism worldwide are dietary—protein malnutrition and iodine deficiency. This is because the two main ingredients needed to make thyroid hormone are tyrosine (an amino acid from dietary protein) and iodine (a naturally-occurring salt).

In the developed world, where protein is plentiful and many countries add iodine to salt and processed foods, we don’t typically need to worry about protein malnutrition or iodine deficiency. However, the rest of the world is not so lucky. More than 2 billion people around the world suffer from hypothyroidism due to iodine deficiency. 2 billion! We are told that the reason for this planetary epidemic is that iodine comes from the ocean, and that the soil of inland areas has had most of its iodine washed away over time by erosion:

“A teaspoon of iodine is all a person requires in a lifetime, but because iodine cannot be stored for long periods by the body, tiny amounts are needed regularly. In areas of endemic iodine deficiency, where soil and therefore crops and grazing animals do not provide sufficient dietary iodine to the populace, food fortification and supplementation have proven highly successful and sustainable interventions.” [Brahmbhatt 2001].

But the iodine erosion explanation does not make sense to me, and here’s why.

Iodine is an essential ingredient in thyroid hormone, and thyroid hormone is critical to the growth and development of the bodies and brains of all baby vertebrates (animals with backbones). Since they need iodine just as much as we do, and they do not have access to artificially iodized salt, how do they get their iodine? Do they have a secret stash somewhere that they’re not sharing with us? I assume they are getting enough iodine because if they weren’t, they would all be born brain-damaged runts, and many would be infertile if they survived to adulthood. To the best of my knowledge, wild inland animals are not herds of sterile, stupefied miniatures roaming the landscape in search of iodine . . . 

Iodine requirements

We are told that humans need an average of about 150 micrograms of iodine per day. Below is the iodine content of some familiar foods [in micrograms]:

Cod fish (3 ounces)	99
Shrimp (3 ounces)	35
Turkey (3 ounces)	34
Low-fat milk (1 cup)	56
Egg (1 large)	24
Prunes (5 whole)	13
Banana (1 whole)	3

When you look at this list, it is easy to imagine how it might be difficult to obtain 150 micrograms per day of iodine, depending on what you eat. This is why we are told we should use iodized salt, which contains 142 micrograms of added iodide per ½ teaspoon:

“More than 70 countries, including the United States and Canada, have salt iodization programs. As a result, approximately 70% of households worldwide use iodized salt, ranging from almost 90% of households in North and South America to less than 50% in Europe and the Eastern Mediterranean regions. In the United States, salt manufacturers have been adding iodine to table salt since the 1920s, although it is still a voluntary program.”1

I suspect that there is actually enough iodine in the environment to go around, and that we actually need less than 150 micrograms per day of iodine. From the above list, you can see that animal foods are much richer in iodine than plant foods—so how do herbivores (animals which eat a plant-based diet, such as rabbits and deer) get enough iodine? I suspect that there is something about the human diet which interferes with our ability to absorb, utilize, and/or retain iodine, and that this is why we appear to be iodine-deficient compared to other animals. So, what might the possible culprits be? Hmmm . . . 

Plant goitrogens

When in doubt, blame plants. Yes, plant foods, once again, are the usual suspects (to read more about why plants are untrustworthy when it comes to human health, see my vegetables page). Many plant foods contain naturally-occurring chemicals which disrupt normal thyroid function.

The main job of the thyroid gland is to combine the salt iodine with the amino acid tyrosine to make thyroid hormone. Whenever the thyroid gland has a hard time making enough thyroid hormone, it becomes stressed and grows bigger to try to do its job better, forming a “goiter” (enlarged thyroid). Substances that interfere with normal thyroid function are called “goitrogens” because they have the potential to cause goiter.

Goitrin

Goitrin is the most powerful plant goitrogen. Unlike most other goitrogens, this chemical can cause goiter even if there is plenty of iodine in the diet. Goitrin weakens the activity of the enzyme thyroid peroxidase, which is required to insert iodine into thyroid hormone.

Foods containing goitrin include seeds of cruciferous vegetables and rutabaga (aka swede, yellow turnip).

Thiocyanates

Thiocyanates are sulfur-containing compounds found in a variety of popular vegetables.

Thiocyanates make it harder for the thyroid gland to absorb iodine because they compete with iodine for entry into the gland. This effect can be minimized by supplementing the diet with iodine; the excess iodine can then crowd out the thiocyanate and win the competition.

Thiocyanates also weaken the activity of the enzyme thyroid peroxidase, required to insert iodine into thyroid hormone. This effect can be greatly reduced by iodine supplementation.

Foods that form thiocyanates:

• Bamboo shoots
• Cassava*
• Corn
• Flax
• Lima beans
• Sweet potato
• Cruciferous vegetables [for a complete list of crucifers, see my post: “Is Broccoli Good for You?“]

The foods listed above do not contain any thiocyanate when they are in their living, intact state, because thiocyanates do not form until the plant is cut, crushed, or chewed. For example, fresh broccoli contains a harmless substance called glucosinolate, which turns into a thiocyanate called sulforaphane when the vegetable is damaged (see my broccoli post for more information).

*Cassava bears special mention here. You may have heard of it because it is the starchy root vegetable from which tapioca is made, but cassava is also a popular staple food in many Third World countries, where it is eaten boiled, mashed, or ground into flour. Fresh cassava root contains a harmless substance called linamarin, which can turn into hydrocyanic acid (aka cyanide!) when the plant is damaged or eaten. Flaxseeds also contain linamarin. Cyanide is very toxic, so the human body converts it into thiocyanate (which, although it does interfere with thyroid function, is less toxic than cyanide and easier for the body to eliminate).

Thiocyanates easily cross the placenta and can cause thyroid dysfunction in newborns, especially if the infant is not getting enough iodine. Cooking, soaking, and fermentation can reduce cyanide and thiocyanate levels in these foods. For more information about cyanide in foods, read this UN FAO fact sheet.

Flavonoids

Flavonoids are a large family of related plant compounds—at least 3,000 different flavonoids have been discovered thus far—but we will concentrate on those that are especially risky when it comes to thyroid health.

Soy flavonoids (genistein, daidzein)

Soy flavonoids are perhaps better known as “soy isoflavones”, which we are usually told are good for us. Yet, “it is well described but little known that the soybean and goiter have long been associated in animals and humans.” [Doerge 2002]

Soy flavonoids reduce the activity of thyroid peroxidase, the enzyme required to insert iodine into thyroid hormone. There is strong clinical evidence demonstrating the anti-thyroid effects of soy products on infants, children, and adults.

“Infants fed soy formula are at higher risk for hypothyroidism and for later development of autoimmune thyroid diseases. In humans, goiter has been seen in infants fed soy formula; this is usually reversed by changing to cow milk or iodine-supplemented diets. After the 1960s, manufacturers reportedly began adding iodine to formulas to mitigate thyroid effects.” [Doerge 2002]

When a baby is born with hypothyroidism, thyroid hormone supplements are administered to correct the deficiency. Babies fed soy formula require 25% higher doses of thyroid hormone than babies fed soy-free formula. [Xiao 2008] For this reason, doctors recommend that children with hypothyroidism avoid soy products if at all possible.

In adults, the recommendations are stated more softly, perhaps because of the widespread belief that soy is good for us, or because some people prefer to eat soy instead of meat:

“Some evidence suggests that soy foods, by inhibiting absorption, may increase the dose of thyroid hormone required by hypothyroid patients. However, hypothyroid adults need not avoid soy foods. In addition, there remains a theoretical concern based on in vitro and animal data that in individuals with compromised thyroid function and/or whose iodine intake is marginal, soy foods may increase risk of developing clinical hypothyroidism. Therefore, it is important for soy food consumers to make sure their intake of iodine is adequate.” [Messina 2006]

Note that the recommendation for adults is to increase iodine intake rather than to decrease soy intake. But take a look at this interesting clinical study [Sathyaplan 2011]:

60 patients with borderline hypothyroidism were given either 2 mg of soy isoflavones (the amount found in the typical omnivore’s diet) or 16 mg of soy isoflavones (the amount found in the typical vegetarian’s diet). The “vegetarian” dose of soy isoflavones was 3 times more likely to cause patients to convert from borderline (“subclinical”) hypothyroidism to full-blown (“overt clinical”) hypothyroidism.

In my experience, most people are unaware of the connection between soy and thyroid problems. If a study like this had been about an ingredient in red meat, you can bet you’d see a giant headline in the New York Times trumpeting that red meat causes thyroid disease, and everyone would be talking about it . . . 

Cooking does not destroy the goitrogenic activity of soy isoflavones.

Millet flavonoids (apigenin, glucosylorientine, vitexin)

Millet is most familiar to us in the developed world as birdseed, but it is also a common staple grain eaten by people in developing countries, because it grows well in hot places with poor quality soil.

Millet flavonoids greatly reduce the activity of thyroid peroxidase, the enzyme that inserts iodine into thyroid hormone. (Apigenin is the most potent of the three listed above.) Millet flavonoids also (quite rudely) push thyroid hormone off of carrier proteins in the bloodstream.

In the Darfur Province of western Sudan, goiter in schoolchildren is closely linked to millet consumption:

“Goiter is more prevalent in rural villages of the Darfur Province in Sudan, where as much as 74% of dietary energy is derived from millet, than in an urban area, where millet provides only 37% of calories, even though the degree of iodine deficiency is similar in the two areas.” [Gaitan 1990]

Other foods containing apigenin include:

• Chamomile
• Citrus fruits
• Parsley
• Onions
• Wheat sprouts
• Red wine
• Beer

Just as with soy, cooking does not destroy millet flavonoids.

Quercetin and friends

Quercetin and its relatives work in two ways to interfere with thyroid hormone metabolism. 1. They reduce activity of thyroperoxidase, the enzyme required to insert iodine into thyroid hormone; and 2. they reduce activity of hepatic deiodinase, a liver enzyme required to activate thyroid hormone.

Quercetin is found in significant amounts in capers, cranberries, onions, tea, broccoli, red wine, black currants, apples, grapes, blueberries, gingko biloba, and apricots.

Kaempferol is found in significant amounts in tea, capers, grapefruit, and endive. Kaempferol is closely related to quercetin and even more easily absorbed.

Rutin is found in significant amounts in buckwheat, asparagus, citrus fruits, cranberries. Rutin is also a close relative of quercetin, but less well absorbed.

Boiling destroys up to 30% of the quercetin, kaempferol and rutin in food.

Can you eat too much iodine?

Yes. The safe upper limit of iodine intake is considered to be 1,100 micrograms (1.1 mg) per day. Since 1 teaspoon of iodized salt contains 284 micrograms of iodine, if you eat 4 teaspoons of iodized salt in a day, you have already exceeded the safe amount.

Strange as it may seem, hypothyroidism can be caused both by too much iodine and by too little iodine. Excess iodine interferes with the release of thyroid hormone into the bloodstream and can cause goiter and hypothyroidism.

“Excess iodine is generally well tolerated, but individuals with underlying thyroid disease or other risk factors may be susceptible to iodine-induced thyroid dysfunction following acute or chronic exposure. Sources of increased iodine exposure include the global public health efforts of iodine supplementation, the escalating use of iodinated contrast radiologic studies, amiodarone administration in vulnerable patients [amiodarone is a drug used to treat heart rhythm problems], excess seaweed consumption, and various miscellaneous sources.” [Leung 2012]

The foods most commonly associated with excess iodine are seaweed and iodized salt. A single gram (0.035 ounce) of seaweed can contain anywhere between 16 and 2,984 micrograms of iodine!

In addition to containing high amounts of iodine, seaweeds in the Laminaria family (kelp family) contain phloroglucinol and other polyhydroxyphenols, which are potent anti-thyroid compounds themselves.

Dietary recommendations for hypothyroidism

If you have hypothyroidism, or want to reduce your risk for hypothyroidism, you may want to consider the following strategies:

1. Eliminate the most potent goitrogens from your diet (soy, millet, and rutabaga).
2. Minimize or at least thoroughly cook all other goitrogenic foods listed in this article, such as cruciferous vegetables and sweet potatoes.
3. If you choose to include significant amounts of goitrogenic foods in your diet, be sure to consume 150 micrograms per day of iodine.
4. Be careful not to consume too much iodized salt or seaweed.

Hold on to your hat—this is going to be a wild ride . . . 

The hullabaloo over Dr. Hazen’s red meat study

A few days ago, a brand new study by Dr. Stanley Hazen’s group at the Cleveland Clinic was published,1 incriminating an unfamiliar ingredient within red meat as the cause of heart disease. The New York Times trumpeted:

“Culprit in heart disease goes beyond meat’s fat“

“The real culprit, they proposed, was a little-studied chemical that is burped out by bacteria in the intestines after people eat red meat. It is quickly converted by the liver into yet another little-studied chemical called TMAO that gets into the blood and increases the risk of heart disease.” [Gina Kolata, New York Times 4/7/13]

This article received a lot of attention, so I was asked by readers and friends to comment on it. This new study is actually a conglomeration of mouse experiments, human clinical studies, and human epidemiological studies, which the authors then weave together to make their case against red meat. Straightforward it is NOT. It is a many-headed beast, armed with tentacles and suckers; but is smart, elegant in many ways, and deserving of detailed scrutiny.

Much like a game of Twister, the authors stretch so far to try to connect the dots between their studies that their sophisticated theory ultimately collapses into a sad, lifeless heap. The bottom line is that there are no new reasons to fear red meat and no proof within this study (or any other study, for that matter) that red meat causes heart disease. But if you want to know how I came to this conclusion, trudge forth, gentle reader. And Godspeed.

The authors’ beliefs

(or why they conducted these studies in the first place)

The article opens this way (emphases mine):

“The high level of meat consumption in the developed world is linked to CVD (cardiovascular disease) risk, presumably owing to the large content of saturated fats and cholesterol in meat. However, a recent meta-analysis of prospective cohort studies showed no association between dietary saturated fat intake and CVD, prompting the suggestion that other environmental exposures linked to increased meat consumption are responsible.”2

If after more than 40 years of studying meat and heart disease, this is the strongest statement intelligent scientists can make condemning meat, then maybe, just maybe, the theory is weak . . . or heaven forbid, completely false.

Allow me to summarize the authors’ line of reasoning:

1. Red meat must cause heart disease somehow, because epidemiological studies (which have no power to demonstrate cause and effect) suggest that people who eat more red meat are at higher risk for heart disease. Epidemiological studies also suggest that vegetarians have lower rates of heart disease than omnivores
2. But a recent meta-analysis showed no connection between dietary saturated fat and heart disease, so fat is not the culprit after all . . .
3. We need to find a new villainous ingredient within red meat to blame for heart disease, because the possibility that red meat might NOT cause heart disease either hasn’t occurred to us, or sounds preposterous to us. [Perhaps they are not aware that some groups of people eating very high-meat diets, like the Inuit, had very low rates of heart disease. I will never understand how intelligent people can believe that an ancient food is causing a modern disease.]
4. Hey . . . red meat contains more L-carnitine than white meat, and plant foods are extremely low in carnitine, so maybe L-carnitine causes heart disease!
5. Oh . . . but wait . . . L-carnitine is a vital nutrient in our bodies. L-carnitine is used to transport fat into the mitochondria of our cells so it can be burned for energy. It is so essential that if we don’t eat enough of it, we go out of our way to make it from scratch. Since L-carnitine itself is innocent, we have to work extra super hard to connect it to heart disease. How can we can pin the tail on this red-meat-filled donkey?

But first, a map of the forest, so we won’t get disoriented in the trees.

Introducing carnitine

Carnis is the Latin word for meat. Because carnitine is vital to animal energy production, all animal foods contain carnitine, but red meat has a LOT more than other foods because dark muscle fibers rely most heavily on fat for energy:

Selected food sources of carnitine

Food	Milligrams (mg)
Beef steak, cooked, 4 oz	56-162
Ground beef, cooked, 4 oz	87-99
Milk, whole, 1 cup	8
Codfish, cooked, 4 oz	4-7
Chicken breast, cooked, 4 oz	3-5
Ice cream, ½ cup	3
Cheese, cheddar, 2 oz	2
Whole-wheat bread, 2 slices	0.2
Asparagus, cooked, ½ cup	0.1

Source: NIH: Carnitine fact sheet for health professionals

Carnitine in meat exists as “acetyl-L-carnitine esters”, not as free carnitine. All this means is that meaty carnitine has special little attachments that make it easier for the small intestine to absorb (i.e. more “bioavailable”) than free L-carnitine. If we eat meat, we absorb a large percentage of the natural form of carnitine it contains. Vegans and vegetarians absorb more carnitine (66-86%) than meat-eaters (54-72%), because the body needs carnitine and it’s easier to get it from food than to make it from scratch. By contrast, if we swallow a supplement containing free L-carnitine, we only absorb about 10 to 20% of it.

Carnitine that is not absorbed by the small intestine can make it all the way down to the colon, where some types of bacteria can break it down, releasing a by-product called “TMA” (trimethylamine). TMA is a gas that smells like rotten fish. TMA wafts into the bloodstream and makes its way to the liver, where special enzymes convert it into TMAO (trimethylamine oxide)—an odorless substance that is easily excreted in the urine. TMAO is the molecule that Dr. Hazen’s group thinks causes heart disease.

Why would our bodies contain an enzyme that would go out of its way to deliberately turn a rotten gas (TMA) into a substance that can kill us (TMAO)? I doubt it would. . . . While TMA itself does not seem to be toxic, it can combine with proteins to form potentially cancer-causing nitrosamines. This may be just one reason why the liver works to transform it into something the body can get rid of.

Hey, what about choline?

Carnitine is not the only nutrient that bacteria can turn into TMA. Another common food molecule—choline—can also be turned into TMA. Choline is found in all kinds of foods, not just in meat:

mg choline per 100g of food

Egg yolks	680
Egg whites	270
Liver	195-333
Toasted wheat germ	152
Meat/seafood	34-103
Nuts	29-72
Brussel sprouts/broccoli	40

Source: USDA choline data sheet

“The normal human diet contains approximately 500 mg of free choline/d and humans do not usually smell ‘fishy’ unless they are treated with large oral doses of choline. Supplementary choline is ingested in ‘health food’ preparations by many individuals, and choline supplements.”1

Something’s fishy

If TMAO is bad for us, we should also stop eating saltwater fish. We don’t even need bacteria to generate TMAO from fish—fish naturally contain TMAO; they use it to regulate their fluid balance so they won’t shrivel up in the salty waters of the sea:2

Flounder	400 mg/100 g
Alaskan pollack and cod	1000 mg/100 g

So, why pick on red meat, when TMAO can result from the digestion of other foods, such as egg whites, fish, wheat germ, nuts, and cruciferous vegetables?

The authors acknowledge that choline can form TMA and TMAO but do not mention that choline comes from plant foods as well as animal foods, and they do not mention fish TMAO at all. Either they did not do their homework, or their biases have blinded them to the facts. Such is human nature—believing is seeing.

Onward.

The authors’ arguments

(or how they think TMAO might cause heart attacks)

In order to draw the conclusion that red meat causes heart disease, you have to buy the following series of arguments. If you read only these 6 points, and you are someone who wants to believe that red meat is bad for you, I can see how you would come away feeling as if your beliefs are validated.

Point #1. People with heart disease tend to have higher TMAO levels3 .

Point #2. Vegans and vegetarians naturally have lower TMAO levels.

Point #3. Vegans and vegetarians produce less TMAO after consuming steak and L-carnitine than meat-eaters do.

Point #4. Vegans and vegetarians have different kinds of bacteria living in their colon than omnivores do, and this may explain why they produce less TMAO.

Point #5. L-carnitine supplements increase atherosclerosis in genetically-altered mice.

Point #6. TMAO interferes with “reverse cholesterol transport” (RCT) in genetically-altered mice, so it’s harder for their bodies to get rid of excess cholesterol.

and one giant leap for mankind . . . 

If you eat red meat, your body will fill up with cholesterol and you will have a heart attack.

Counterpoint #1

The observation that people with heart disease are more likely to have higher TMAO levels does not mean that TMAO causes heart attacks (and the authors do not claim that it does). It might or it might not. TMAO could simply be an innocent bystander—a red (meat) herring. We have no idea why people who have heart disease tend to have higher TMAO levels. Most importantly, researchers did not ask these people what they eat. Did they eat healthy whole foods diets or junky diets? How many of them were vegans? Vegetarians? Omnivores? Were the ones with the highest TMAO levels all omnivores? Were the ones with the lowest TMAO levels vegans? That would have been very interesting and helpful information.

Counterpoint #2

Not all vegans and vegetarians have lower TMAO levels compared to omnivores. From this figure, taken from Figure 2 of Hazen’s study, it looks like only a small percentage of them do.

The fact that there is so much overlap in TMAO levels between meat-eaters and non-meat-eaters suggests that there is something else about diet—something other than the presence or absence of meat—that is playing a significant role in TMAO levels. Dietary choline is the most logical and likely explanation, but may not be the only one.

Counterpoint #3

a. The form of carnitine found in red meat—acetyl-L-carnitine—was not used in the study; free L-carnitine supplements were used in the study instead. Because these supplements contain the form of carnitine that is hardest to absorb, the majority of it bypasses the small intestines and makes it down to the colon, where bacteria can turn it into the maximum amount of TMA (and TMAO) possible. This study does not tell us whether acetyl-L-carnitine—the form of carnitine found in red meat—raises TMAO levels. Even if TMAO turns out to be the scourge of the West, all you will have shown with this study is that people who want to avoid heart attacks should not take L-carnitine supplements with their steak.

b. NONE of the subjects was fed steak alone—they all received either L-carnitine supplements alone or in combination with steak. There is no proof anywhere in this paper that simply eating steak all by itself will raise anyone’s TMAO levels. In order to convince people that steak raises TMAO levels, you have to include a steak-only experiment. Any high school science student could tell you that.

Here’s an example of what the scientists did:

Experiment: Give one male vegan and one female omnivore each an 8-oz steak (which contains 180 mg of acetyl L-carnitine) plus a capsule containing 250 mg of free L-carnitine and watch what happens to their TMAO levels. [Poor vegan man . . . he really took one for the team. Give that man a year’s supply of tofu!]

Result: The vegan man produced virtually no TMAO after the steak + carnitine supplement whereas the meat-eating woman generated a TMAO spike in her bloodstream.

Given that studies have shown vegans absorb more carnitine than meat-eaters, isn’t it possible that the vegan man, whose body may have been pining for some long-overdue, prefabricated carnitine, absorbed much more carnitine than the omnivorous woman, so that much less of it made it to his colon to be turned into TMA? Isn’t it possible that the vegan man didn’t generate a TMAO spike because his liver for some reason couldn’t turn TMA into TMAO? In this case, he would have generated a TMA spike, but TMA was not measured. Chris Masterjohn wrote an excellent review of this study and proposes other interesting possibilities, including gender differences and vitamin deficiency issues. He also does a beautiful job of analyzing the omnivore vs vegan/vegetarian experiments.

Counterpoint #4

Yes, what we eat determines the types of bacteria in our colon, but we have no idea which mix of bacteria is healthiest for us, we have no idea which diet encourages the best mix of bacteria, and we have no idea whether any of this has anything to do with heart disease.

The researchers detailed the interesting differences in bacterial patterns they discovered between meat-eaters and non-meat-eaters. One type of intestinal bacteria called Prevotella was strongly associated with higher TMAO production. Four of the human volunteers were found to have bacterial colonies in their colons that were rich in Prevotella. Were all four of these individuals meat-eaters? No. Three of them were omnivores (5.9% of all omnivores in the study), and one was not (3.8% of all non-meat-eaters). To quote the authors, this suggested:

“more complexity in the human gut microbiome than anticipated. . . . Indeed, other studies have demonstrated variable results in associating human bacterial genera . . . including Prevotella, to omnivorous and vegetarian eating habits.”

Translation: Even if you are convinced that having Prevotella colonies setting up house in your innards is bad for you, eating a vegan/vegetarian diet will not guarantee you a low-Prevotella colon.

Counterpoint #5

• Yes, L-carnitine supplements caused an increase in atherosclerosis in genetically altered mice. However, L-carnitine is not red meat. It is not even the form of carnitine found in red meat (acetyl-L-carnitine).
• The dose of L-carnitine used in these mice was extremely high. According to Chris Masterjohn, it was the equivalent of a human eating 1000 sirloin steaks.
• For reasons I don’t understand, the mice used in these studies were genetically-altered so that they were missing a gene (apoE) required for normal cholesterol processing. These mice are popular with scientists who study heart disease because they are very good at developing atherosclerosis. It’s already a big stretch to apply information from mouse studies to human health, why widen the gap by using unnaturally defective mice? Absurd.

Counterpoint #6

Now here’s where the authors really jumped the shark. They fed their miscreant mice standard mouse chow supplemented with L-carnitine, choline, or TMAO itself. Then a trusty lab assistant was charged with the delightful task of measuring how much cholesterol the mice . . . um . . . released. Makes me nostalgic for the 7 years I spent as a lab tech . . . not. They found that mouse pellets from animals fed TMAO contained 30% less cholesterol than those fed unsupplemented chow. This is how they propose TMAO causes human heart disease. There is so much I could say about these studies, but the take-home message for your refrigerator magnet is this:

Just because the cage droppings of mutant mice deliberately fed TMAO contained less cholesterol than those who were not fed TMAO does not mean that a human who eats a steak is going to have a heart attack.

My BIGGEST BEEF with this study

Like most studies that try to connect red meat to human disease, this collection of studies does not control for refined carbohydrate intake. We do not know how healthy the diets of the human volunteers were before this study began. Were the vegans and vegetarians health-conscious types who avoided junk foods? What about the omnivores? What if it turned out that everyone who had a higher TMAO level (including the veg/vegans with higher TMAO) also happened to eat a lot more sugar and flour?

After all, if there is one clear culprit emerging from the piles of studies about diet and heart disease, it is refined carbohydrate—not saturated fat, not cholesterol, not red meat. So, in this day and age, in my humble opinion, if you are going to conduct a study of diet and heart disease, you simply must take refined carbohydrate into consideration in order to be taken seriously.

Let’s look at two clear examples in this study of how refined carbohydrate intake was completely ignored by the authors.

The authors measured TMAO levels in 2,595 people and concluded that there was a dose-dependent relationship between TMAO levels and cardiovascular disease (CVD) risk, after adjustment for “traditional CVD risk factors,” which were age, gender, diabetes, smoking, blood pressure, cholesterol levels, and medications. Notice the absence of refined carbohydrate intake, fasting blood glucose, hemoglobin A1C or any other related values.

But hope was kindled when, within a description of one of their mouse studies, I came across this promising line:

“Of note, the increase in atherosclerotic plaque burden with dietary L-carnitine occurred in the absence of proatherogenic changes in plasma lipid, lipoprotein, glucose, or insulin levels.”

Excellent, they acknowledged glucose and insulin as potential risk factors! Had they actually determined that carnitine caused atherosclerosis despite healthy glucose and insulin levels? The sentence above, which is found in the primary article, would lead you to believe this, but if you dig through the 40-page supplementary information, you unearth this telling table:

As you can see, the triglyceride, cholesterol, glucose and insulin levels of mice being fed normal chow are already pretty high (insulin levels at baseline convert to 16.3 microunits/ml). When carnitine is added, there is no statistically significant change in any of these levels (as indicated by P values greater than 0.05). The authors phrased their sentence carefully so that what they say is true—there were no proatherogenic (artery-clogging) changes in these profiles. They were already proatherogenic to begin with.

These mice, like most laboratory animals, are fed unbelievably junky diets. In this case, they were eating a “standard chow control diet”, called “Teklad 2018”:

Ingredients (in descending order of inclusion): Ground wheat, ground corn, wheat middlings, dehulled soybean meal, corn gluten meal, soybean oil, calcium carbonate, dicalcium phosphate, brewers dried yeast, iodized salt, L-lysine, DL-methionine, choline chloride, kaolin, magnesium oxide, vitamin E acetate, menadione sodium bisulfite complex (source of vitamin K activity), manganous oxide, ferrous sulfate, zinc oxide, niacin, calcium pantothenate, copper sulfate, pyridoxine hydrochloride, riboflavin, thiamin mononitrate, vitamin A acetate, calcium iodate, vitamin B12 supplement, folic acid, biotin, vitamin D3 supplement, cobalt carbonate.

This chow is comprised almost entirely of processed wheat, corn, and soy—nearly 100% refined carbohydrate, held together with soybean oil. This is not a diet that exists in nature. Poor little mice. No wonder manufacturers have to supplement this stuff with 18 vitamins and minerals. Look familiar? Is anyone reminded of the ingredient list on the side of your typical cereal box? Coat these mouse pellets with chocolate frosting or sprinkles and you’ve got yourself a yummy breakfast treat.

The authors provide evidence that vegans/vegetarians have a different mix of bacteria living in their colon than omnivores, and they do an excellent job of convincing us that you can’t generate TMAO without bacteria (humans do not possess this capability). Then, because they believe that red meat is bad for us, they try to connect red meat to bacterial metabolism of carnitine to TMAO. Now allow me to do the same thing with refined carbs. It took me about 3 minutes to find this reference:

“Phosphotransferase systems involved in microbial processing of carbohydrates also were found to be over expressed in the intestines of obese people, notably from Prevotellaceae”1

I am not saying that carbs increase Prevotella activity or that Prevotella causes heart attacks. All I’m saying is that refined carbohydrates may also play an important role in what kind of bacteria elbow their way to your colonic buffet table.

Guilt by association

Based on the thousands of scientific articles I have read about food and health, in combination with my personal experience, clinical experience, and common sense, I find nothing to suggest that red meat is bad for people, and plenty of evidence that red meat is good for people (see my meats page). Every article I’ve ever read that tries to blame meat for our health problems fails to to take refined carbohydrate into consideration. In my opinion, damning nutritious meat for your heart attack is like pouring sugar into your gas tank and then cursing the gasoline when your car breaks down.

If you want to scare me away from eating meat using mouse experiments, you are going to have to raise a slew of mice on a healthy whole foods vegetarian diet, prove to me that those mice show no signs of cardiovascular disease, then start feeding them one miniature sirloin steak for dinner every night until they all clutch their furry little chests, keel over, and die.

Has the fat lady sung?

As far as I can tell, the authors’ theory that red meat provides carnitine for bacteria to transform into TMA which our liver then converts to TMAO, which causes our macrophages to fill up with cholesterol, block our arteries, and cause heart attacks is just that: a theory—full of sound and fury, signifying nothing.

Read my critique of the World Health Organization’s 2015 proclamation that red and processed meats cause cancer: “WHO Says Meat Causes Cancer?“

Hold on to your hat—this is going to be a wild ride . . . 

The hullabaloo over Dr. Hazen’s red meat study

A few days ago, a brand new study by Dr. Stanley Hazen’s group at the Cleveland Clinic was published,1 incriminating an unfamiliar ingredient within red meat as the cause of heart disease. The New York Times trumpeted:

“Culprit in heart disease goes beyond meat’s fat“

“The real culprit, they proposed, was a little-studied chemical that is burped out by bacteria in the intestines after people eat red meat. It is quickly converted by the liver into yet another little-studied chemical called TMAO that gets into the blood and increases the risk of heart disease.” [Gina Kolata, New York Times 4/7/13]

This article received a lot of attention, so I was asked by readers and friends to comment on it. This new study is actually a conglomeration of mouse experiments, human clinical studies, and human epidemiological studies, which the authors then weave together to make their case against red meat. Straightforward it is NOT. It is a many-headed beast, armed with tentacles and suckers; but is smart, elegant in many ways, and deserving of detailed scrutiny.

Much like a game of Twister, the authors stretch so far to try to connect the dots between their studies that their sophisticated theory ultimately collapses into a sad, lifeless heap. The bottom line is that there are no new reasons to fear red meat and no proof within this study (or any other study, for that matter) that red meat causes heart disease. But if you want to know how I came to this conclusion, trudge forth, gentle reader. And Godspeed.

The authors’ beliefs

(or why they conducted these studies in the first place)

The article opens this way (emphases mine):

“The high level of meat consumption in the developed world is linked to CVD (cardiovascular disease) risk, presumably owing to the large content of saturated fats and cholesterol in meat. However, a recent meta-analysis of prospective cohort studies showed no association between dietary saturated fat intake and CVD, prompting the suggestion that other environmental exposures linked to increased meat consumption are responsible.”2

If after more than 40 years of studying meat and heart disease, this is the strongest statement intelligent scientists can make condemning meat, then maybe, just maybe, the theory is weak . . . or heaven forbid, completely false.

Allow me to summarize the authors’ line of reasoning:

1. Red meat must cause heart disease somehow, because epidemiological studies (which have no power to demonstrate cause and effect) suggest that people who eat more red meat are at higher risk for heart disease. Epidemiological studies also suggest that vegetarians have lower rates of heart disease than omnivores
2. But a recent meta-analysis showed no connection between dietary saturated fat and heart disease, so fat is not the culprit after all . . .
3. We need to find a new villainous ingredient within red meat to blame for heart disease, because the possibility that red meat might NOT cause heart disease either hasn’t occurred to us, or sounds preposterous to us. [Perhaps they are not aware that some groups of people eating very high-meat diets, like the Inuit, had very low rates of heart disease. I will never understand how intelligent people can believe that an ancient food is causing a modern disease.]
4. Hey . . . red meat contains more L-carnitine than white meat, and plant foods are extremely low in carnitine, so maybe L-carnitine causes heart disease!
5. Oh . . . but wait . . . L-carnitine is a vital nutrient in our bodies. L-carnitine is used to transport fat into the mitochondria of our cells so it can be burned for energy. It is so essential that if we don’t eat enough of it, we go out of our way to make it from scratch. Since L-carnitine itself is innocent, we have to work extra super hard to connect it to heart disease. How can we can pin the tail on this red-meat-filled donkey?

But first, a map of the forest, so we won’t get disoriented in the trees.

Introducing carnitine

Carnis is the Latin word for meat. Because carnitine is vital to animal energy production, all animal foods contain carnitine, but red meat has a LOT more than other foods because dark muscle fibers rely most heavily on fat for energy:

Selected food sources of carnitine

Food	Milligrams (mg)
Beef steak, cooked, 4 oz	56-162
Ground beef, cooked, 4 oz	87-99
Milk, whole, 1 cup	8
Codfish, cooked, 4 oz	4-7
Chicken breast, cooked, 4 oz	3-5
Ice cream, ½ cup	3
Cheese, cheddar, 2 oz	2
Whole-wheat bread, 2 slices	0.2
Asparagus, cooked, ½ cup	0.1

Source: NIH: Carnitine fact sheet for health professionals

Carnitine in meat exists as “acetyl-L-carnitine esters”, not as free carnitine. All this means is that meaty carnitine has special little attachments that make it easier for the small intestine to absorb (i.e. more “bioavailable”) than free L-carnitine. If we eat meat, we absorb a large percentage of the natural form of carnitine it contains. Vegans and vegetarians absorb more carnitine (66-86%) than meat-eaters (54-72%), because the body needs carnitine and it’s easier to get it from food than to make it from scratch. By contrast, if we swallow a supplement containing free L-carnitine, we only absorb about 10 to 20% of it.

Carnitine that is not absorbed by the small intestine can make it all the way down to the colon, where some types of bacteria can break it down, releasing a by-product called “TMA” (trimethylamine). TMA is a gas that smells like rotten fish. TMA wafts into the bloodstream and makes its way to the liver, where special enzymes convert it into TMAO (trimethylamine oxide)—an odorless substance that is easily excreted in the urine. TMAO is the molecule that Dr. Hazen’s group thinks causes heart disease.

Why would our bodies contain an enzyme that would go out of its way to deliberately turn a rotten gas (TMA) into a substance that can kill us (TMAO)? I doubt it would. . . . While TMA itself does not seem to be toxic, it can combine with proteins to form potentially cancer-causing nitrosamines. This may be just one reason why the liver works to transform it into something the body can get rid of.

Hey, what about choline?

Carnitine is not the only nutrient that bacteria can turn into TMA. Another common food molecule—choline—can also be turned into TMA. Choline is found in all kinds of foods, not just in meat:

mg choline per 100g of food

Egg yolks	680
Egg whites	270
Liver	195-333
Toasted wheat germ	152
Meat/seafood	34-103
Nuts	29-72
Brussel sprouts/broccoli	40

Source: USDA choline data sheet

“The normal human diet contains approximately 500 mg of free choline/d and humans do not usually smell ‘fishy’ unless they are treated with large oral doses of choline. Supplementary choline is ingested in ‘health food’ preparations by many individuals, and choline supplements.”1

Something’s fishy

If TMAO is bad for us, we should also stop eating saltwater fish. We don’t even need bacteria to generate TMAO from fish—fish naturally contain TMAO; they use it to regulate their fluid balance so they won’t shrivel up in the salty waters of the sea:2

Flounder	400 mg/100 g
Alaskan pollack and cod	1000 mg/100 g

So, why pick on red meat, when TMAO can result from the digestion of other foods, such as egg whites, fish, wheat germ, nuts, and cruciferous vegetables?

The authors acknowledge that choline can form TMA and TMAO but do not mention that choline comes from plant foods as well as animal foods, and they do not mention fish TMAO at all. Either they did not do their homework, or their biases have blinded them to the facts. Such is human nature—believing is seeing.

Onward.

The authors’ arguments

(or how they think TMAO might cause heart attacks)

In order to draw the conclusion that red meat causes heart disease, you have to buy the following series of arguments. If you read only these 6 points, and you are someone who wants to believe that red meat is bad for you, I can see how you would come away feeling as if your beliefs are validated.

Point #1. People with heart disease tend to have higher TMAO levels3 .

Point #2. Vegans and vegetarians naturally have lower TMAO levels.

Point #3. Vegans and vegetarians produce less TMAO after consuming steak and L-carnitine than meat-eaters do.

Point #4. Vegans and vegetarians have different kinds of bacteria living in their colon than omnivores do, and this may explain why they produce less TMAO.

Point #5. L-carnitine supplements increase atherosclerosis in genetically-altered mice.

Point #6. TMAO interferes with “reverse cholesterol transport” (RCT) in genetically-altered mice, so it’s harder for their bodies to get rid of excess cholesterol.

and one giant leap for mankind . . . 

If you eat red meat, your body will fill up with cholesterol and you will have a heart attack.

Counterpoint #1

The observation that people with heart disease are more likely to have higher TMAO levels does not mean that TMAO causes heart attacks (and the authors do not claim that it does). It might or it might not. TMAO could simply be an innocent bystander—a red (meat) herring. We have no idea why people who have heart disease tend to have higher TMAO levels. Most importantly, researchers did not ask these people what they eat. Did they eat healthy whole foods diets or junky diets? How many of them were vegans? Vegetarians? Omnivores? Were the ones with the highest TMAO levels all omnivores? Were the ones with the lowest TMAO levels vegans? That would have been very interesting and helpful information.

Counterpoint #2

Not all vegans and vegetarians have lower TMAO levels compared to omnivores. From this figure, taken from Figure 2 of Hazen’s study, it looks like only a small percentage of them do.

The fact that there is so much overlap in TMAO levels between meat-eaters and non-meat-eaters suggests that there is something else about diet—something other than the presence or absence of meat—that is playing a significant role in TMAO levels. Dietary choline is the most logical and likely explanation, but may not be the only one.

Counterpoint #3

a. The form of carnitine found in red meat—acetyl-L-carnitine—was not used in the study; free L-carnitine supplements were used in the study instead. Because these supplements contain the form of carnitine that is hardest to absorb, the majority of it bypasses the small intestines and makes it down to the colon, where bacteria can turn it into the maximum amount of TMA (and TMAO) possible. This study does not tell us whether acetyl-L-carnitine—the form of carnitine found in red meat—raises TMAO levels. Even if TMAO turns out to be the scourge of the West, all you will have shown with this study is that people who want to avoid heart attacks should not take L-carnitine supplements with their steak.

b. NONE of the subjects was fed steak alone—they all received either L-carnitine supplements alone or in combination with steak. There is no proof anywhere in this paper that simply eating steak all by itself will raise anyone’s TMAO levels. In order to convince people that steak raises TMAO levels, you have to include a steak-only experiment. Any high school science student could tell you that.

Here’s an example of what the scientists did:

Experiment: Give one male vegan and one female omnivore each an 8-oz steak (which contains 180 mg of acetyl L-carnitine) plus a capsule containing 250 mg of free L-carnitine and watch what happens to their TMAO levels. [Poor vegan man . . . he really took one for the team. Give that man a year’s supply of tofu!]

Result: The vegan man produced virtually no TMAO after the steak + carnitine supplement whereas the meat-eating woman generated a TMAO spike in her bloodstream.

Given that studies have shown vegans absorb more carnitine than meat-eaters, isn’t it possible that the vegan man, whose body may have been pining for some long-overdue, prefabricated carnitine, absorbed much more carnitine than the omnivorous woman, so that much less of it made it to his colon to be turned into TMA? Isn’t it possible that the vegan man didn’t generate a TMAO spike because his liver for some reason couldn’t turn TMA into TMAO? In this case, he would have generated a TMA spike, but TMA was not measured. Chris Masterjohn wrote an excellent review of this study and proposes other interesting possibilities, including gender differences and vitamin deficiency issues. He also does a beautiful job of analyzing the omnivore vs vegan/vegetarian experiments.

Counterpoint #4

Yes, what we eat determines the types of bacteria in our colon, but we have no idea which mix of bacteria is healthiest for us, we have no idea which diet encourages the best mix of bacteria, and we have no idea whether any of this has anything to do with heart disease.

The researchers detailed the interesting differences in bacterial patterns they discovered between meat-eaters and non-meat-eaters. One type of intestinal bacteria called Prevotella was strongly associated with higher TMAO production. Four of the human volunteers were found to have bacterial colonies in their colons that were rich in Prevotella. Were all four of these individuals meat-eaters? No. Three of them were omnivores (5.9% of all omnivores in the study), and one was not (3.8% of all non-meat-eaters). To quote the authors, this suggested:

“more complexity in the human gut microbiome than anticipated. . . . Indeed, other studies have demonstrated variable results in associating human bacterial genera . . . including Prevotella, to omnivorous and vegetarian eating habits.”

Translation: Even if you are convinced that having Prevotella colonies setting up house in your innards is bad for you, eating a vegan/vegetarian diet will not guarantee you a low-Prevotella colon.

Counterpoint #5

• Yes, L-carnitine supplements caused an increase in atherosclerosis in genetically altered mice. However, L-carnitine is not red meat. It is not even the form of carnitine found in red meat (acetyl-L-carnitine).
• The dose of L-carnitine used in these mice was extremely high. According to Chris Masterjohn, it was the equivalent of a human eating 1000 sirloin steaks.
• For reasons I don’t understand, the mice used in these studies were genetically-altered so that they were missing a gene (apoE) required for normal cholesterol processing. These mice are popular with scientists who study heart disease because they are very good at developing atherosclerosis. It’s already a big stretch to apply information from mouse studies to human health, why widen the gap by using unnaturally defective mice? Absurd.

Counterpoint #6

Now here’s where the authors really jumped the shark. They fed their miscreant mice standard mouse chow supplemented with L-carnitine, choline, or TMAO itself. Then a trusty lab assistant was charged with the delightful task of measuring how much cholesterol the mice . . . um . . . released. Makes me nostalgic for the 7 years I spent as a lab tech . . . not. They found that mouse pellets from animals fed TMAO contained 30% less cholesterol than those fed unsupplemented chow. This is how they propose TMAO causes human heart disease. There is so much I could say about these studies, but the take-home message for your refrigerator magnet is this:

Just because the cage droppings of mutant mice deliberately fed TMAO contained less cholesterol than those who were not fed TMAO does not mean that a human who eats a steak is going to have a heart attack.

My BIGGEST BEEF with this study

Like most studies that try to connect red meat to human disease, this collection of studies does not control for refined carbohydrate intake. We do not know how healthy the diets of the human volunteers were before this study began. Were the vegans and vegetarians health-conscious types who avoided junk foods? What about the omnivores? What if it turned out that everyone who had a higher TMAO level (including the veg/vegans with higher TMAO) also happened to eat a lot more sugar and flour?

After all, if there is one clear culprit emerging from the piles of studies about diet and heart disease, it is refined carbohydrate—not saturated fat, not cholesterol, not red meat. So, in this day and age, in my humble opinion, if you are going to conduct a study of diet and heart disease, you simply must take refined carbohydrate into consideration in order to be taken seriously.

Let’s look at two clear examples in this study of how refined carbohydrate intake was completely ignored by the authors.

The authors measured TMAO levels in 2,595 people and concluded that there was a dose-dependent relationship between TMAO levels and cardiovascular disease (CVD) risk, after adjustment for “traditional CVD risk factors,” which were age, gender, diabetes, smoking, blood pressure, cholesterol levels, and medications. Notice the absence of refined carbohydrate intake, fasting blood glucose, hemoglobin A1C or any other related values.

But hope was kindled when, within a description of one of their mouse studies, I came across this promising line:

“Of note, the increase in atherosclerotic plaque burden with dietary L-carnitine occurred in the absence of proatherogenic changes in plasma lipid, lipoprotein, glucose, or insulin levels.”

Excellent, they acknowledged glucose and insulin as potential risk factors! Had they actually determined that carnitine caused atherosclerosis despite healthy glucose and insulin levels? The sentence above, which is found in the primary article, would lead you to believe this, but if you dig through the 40-page supplementary information, you unearth this telling table:

As you can see, the triglyceride, cholesterol, glucose and insulin levels of mice being fed normal chow are already pretty high (insulin levels at baseline convert to 16.3 microunits/ml). When carnitine is added, there is no statistically significant change in any of these levels (as indicated by P values greater than 0.05). The authors phrased their sentence carefully so that what they say is true—there were no proatherogenic (artery-clogging) changes in these profiles. They were already proatherogenic to begin with.

These mice, like most laboratory animals, are fed unbelievably junky diets. In this case, they were eating a “standard chow control diet”, called “Teklad 2018”:

Ingredients (in descending order of inclusion): Ground wheat, ground corn, wheat middlings, dehulled soybean meal, corn gluten meal, soybean oil, calcium carbonate, dicalcium phosphate, brewers dried yeast, iodized salt, L-lysine, DL-methionine, choline chloride, kaolin, magnesium oxide, vitamin E acetate, menadione sodium bisulfite complex (source of vitamin K activity), manganous oxide, ferrous sulfate, zinc oxide, niacin, calcium pantothenate, copper sulfate, pyridoxine hydrochloride, riboflavin, thiamin mononitrate, vitamin A acetate, calcium iodate, vitamin B12 supplement, folic acid, biotin, vitamin D3 supplement, cobalt carbonate.

This chow is comprised almost entirely of processed wheat, corn, and soy—nearly 100% refined carbohydrate, held together with soybean oil. This is not a diet that exists in nature. Poor little mice. No wonder manufacturers have to supplement this stuff with 18 vitamins and minerals. Look familiar? Is anyone reminded of the ingredient list on the side of your typical cereal box? Coat these mouse pellets with chocolate frosting or sprinkles and you’ve got yourself a yummy breakfast treat.

The authors provide evidence that vegans/vegetarians have a different mix of bacteria living in their colon than omnivores, and they do an excellent job of convincing us that you can’t generate TMAO without bacteria (humans do not possess this capability). Then, because they believe that red meat is bad for us, they try to connect red meat to bacterial metabolism of carnitine to TMAO. Now allow me to do the same thing with refined carbs. It took me about 3 minutes to find this reference:

“Phosphotransferase systems involved in microbial processing of carbohydrates also were found to be over expressed in the intestines of obese people, notably from Prevotellaceae”1

I am not saying that carbs increase Prevotella activity or that Prevotella causes heart attacks. All I’m saying is that refined carbohydrates may also play an important role in what kind of bacteria elbow their way to your colonic buffet table.

Guilt by association

Based on the thousands of scientific articles I have read about food and health, in combination with my personal experience, clinical experience, and common sense, I find nothing to suggest that red meat is bad for people, and plenty of evidence that red meat is good for people (see my meats page). Every article I’ve ever read that tries to blame meat for our health problems fails to to take refined carbohydrate into consideration. In my opinion, damning nutritious meat for your heart attack is like pouring sugar into your gas tank and then cursing the gasoline when your car breaks down.

If you want to scare me away from eating meat using mouse experiments, you are going to have to raise a slew of mice on a healthy whole foods vegetarian diet, prove to me that those mice show no signs of cardiovascular disease, then start feeding them one miniature sirloin steak for dinner every night until they all clutch their furry little chests, keel over, and die.

Has the fat lady sung?

As far as I can tell, the authors’ theory that red meat provides carnitine for bacteria to transform into TMA which our liver then converts to TMAO, which causes our macrophages to fill up with cholesterol, block our arteries, and cause heart attacks is just that: a theory—full of sound and fury, signifying nothing.

Read my critique of the World Health Organization’s 2015 proclamation that red and processed meats cause cancer: “WHO Says Meat Causes Cancer?“

Hold on to your hat—this is going to be a wild ride . . . 

The hullabaloo over Dr. Hazen’s red meat study

A few days ago, a brand new study by Dr. Stanley Hazen’s group at the Cleveland Clinic was published,1 incriminating an unfamiliar ingredient within red meat as the cause of heart disease. The New York Times trumpeted:

“Culprit in heart disease goes beyond meat’s fat“

“The real culprit, they proposed, was a little-studied chemical that is burped out by bacteria in the intestines after people eat red meat. It is quickly converted by the liver into yet another little-studied chemical called TMAO that gets into the blood and increases the risk of heart disease.” [Gina Kolata, New York Times 4/7/13]

This article received a lot of attention, so I was asked by readers and friends to comment on it. This new study is actually a conglomeration of mouse experiments, human clinical studies, and human epidemiological studies, which the authors then weave together to make their case against red meat. Straightforward it is NOT. It is a many-headed beast, armed with tentacles and suckers; but is smart, elegant in many ways, and deserving of detailed scrutiny.

Much like a game of Twister, the authors stretch so far to try to connect the dots between their studies that their sophisticated theory ultimately collapses into a sad, lifeless heap. The bottom line is that there are no new reasons to fear red meat and no proof within this study (or any other study, for that matter) that red meat causes heart disease. But if you want to know how I came to this conclusion, trudge forth, gentle reader. And Godspeed.

The authors’ beliefs

(or why they conducted these studies in the first place)

The article opens this way (emphases mine):

“The high level of meat consumption in the developed world is linked to CVD (cardiovascular disease) risk, presumably owing to the large content of saturated fats and cholesterol in meat. However, a recent meta-analysis of prospective cohort studies showed no association between dietary saturated fat intake and CVD, prompting the suggestion that other environmental exposures linked to increased meat consumption are responsible.”2

If after more than 40 years of studying meat and heart disease, this is the strongest statement intelligent scientists can make condemning meat, then maybe, just maybe, the theory is weak . . . or heaven forbid, completely false.

Allow me to summarize the authors’ line of reasoning:

1. Red meat must cause heart disease somehow, because epidemiological studies (which have no power to demonstrate cause and effect) suggest that people who eat more red meat are at higher risk for heart disease. Epidemiological studies also suggest that vegetarians have lower rates of heart disease than omnivores
2. But a recent meta-analysis showed no connection between dietary saturated fat and heart disease, so fat is not the culprit after all . . .
3. We need to find a new villainous ingredient within red meat to blame for heart disease, because the possibility that red meat might NOT cause heart disease either hasn’t occurred to us, or sounds preposterous to us. [Perhaps they are not aware that some groups of people eating very high-meat diets, like the Inuit, had very low rates of heart disease. I will never understand how intelligent people can believe that an ancient food is causing a modern disease.]
4. Hey . . . red meat contains more L-carnitine than white meat, and plant foods are extremely low in carnitine, so maybe L-carnitine causes heart disease!
5. Oh . . . but wait . . . L-carnitine is a vital nutrient in our bodies. L-carnitine is used to transport fat into the mitochondria of our cells so it can be burned for energy. It is so essential that if we don’t eat enough of it, we go out of our way to make it from scratch. Since L-carnitine itself is innocent, we have to work extra super hard to connect it to heart disease. How can we can pin the tail on this red-meat-filled donkey?

But first, a map of the forest, so we won’t get disoriented in the trees.

Introducing carnitine

Carnis is the Latin word for meat. Because carnitine is vital to animal energy production, all animal foods contain carnitine, but red meat has a LOT more than other foods because dark muscle fibers rely most heavily on fat for energy:

Selected food sources of carnitine

Food	Milligrams (mg)
Beef steak, cooked, 4 oz	56-162
Ground beef, cooked, 4 oz	87-99
Milk, whole, 1 cup	8
Codfish, cooked, 4 oz	4-7
Chicken breast, cooked, 4 oz	3-5
Ice cream, ½ cup	3
Cheese, cheddar, 2 oz	2
Whole-wheat bread, 2 slices	0.2
Asparagus, cooked, ½ cup	0.1

Source: NIH: Carnitine fact sheet for health professionals

Carnitine in meat exists as “acetyl-L-carnitine esters”, not as free carnitine. All this means is that meaty carnitine has special little attachments that make it easier for the small intestine to absorb (i.e. more “bioavailable”) than free L-carnitine. If we eat meat, we absorb a large percentage of the natural form of carnitine it contains. Vegans and vegetarians absorb more carnitine (66-86%) than meat-eaters (54-72%), because the body needs carnitine and it’s easier to get it from food than to make it from scratch. By contrast, if we swallow a supplement containing free L-carnitine, we only absorb about 10 to 20% of it.

Carnitine that is not absorbed by the small intestine can make it all the way down to the colon, where some types of bacteria can break it down, releasing a by-product called “TMA” (trimethylamine). TMA is a gas that smells like rotten fish. TMA wafts into the bloodstream and makes its way to the liver, where special enzymes convert it into TMAO (trimethylamine oxide)—an odorless substance that is easily excreted in the urine. TMAO is the molecule that Dr. Hazen’s group thinks causes heart disease.

Why would our bodies contain an enzyme that would go out of its way to deliberately turn a rotten gas (TMA) into a substance that can kill us (TMAO)? I doubt it would. . . . While TMA itself does not seem to be toxic, it can combine with proteins to form potentially cancer-causing nitrosamines. This may be just one reason why the liver works to transform it into something the body can get rid of.

Hey, what about choline?

Carnitine is not the only nutrient that bacteria can turn into TMA. Another common food molecule—choline—can also be turned into TMA. Choline is found in all kinds of foods, not just in meat:

mg choline per 100g of food

Egg yolks	680
Egg whites	270
Liver	195-333
Toasted wheat germ	152
Meat/seafood	34-103
Nuts	29-72
Brussel sprouts/broccoli	40

Source: USDA choline data sheet

“The normal human diet contains approximately 500 mg of free choline/d and humans do not usually smell ‘fishy’ unless they are treated with large oral doses of choline. Supplementary choline is ingested in ‘health food’ preparations by many individuals, and choline supplements.”1

Something’s fishy

If TMAO is bad for us, we should also stop eating saltwater fish. We don’t even need bacteria to generate TMAO from fish—fish naturally contain TMAO; they use it to regulate their fluid balance so they won’t shrivel up in the salty waters of the sea:2

Flounder	400 mg/100 g
Alaskan pollack and cod	1000 mg/100 g

So, why pick on red meat, when TMAO can result from the digestion of other foods, such as egg whites, fish, wheat germ, nuts, and cruciferous vegetables?

The authors acknowledge that choline can form TMA and TMAO but do not mention that choline comes from plant foods as well as animal foods, and they do not mention fish TMAO at all. Either they did not do their homework, or their biases have blinded them to the facts. Such is human nature—believing is seeing.

Onward.

The authors’ arguments

(or how they think TMAO might cause heart attacks)

In order to draw the conclusion that red meat causes heart disease, you have to buy the following series of arguments. If you read only these 6 points, and you are someone who wants to believe that red meat is bad for you, I can see how you would come away feeling as if your beliefs are validated.

Point #1. People with heart disease tend to have higher TMAO levels3 .

Point #2. Vegans and vegetarians naturally have lower TMAO levels.

Point #3. Vegans and vegetarians produce less TMAO after consuming steak and L-carnitine than meat-eaters do.

Point #4. Vegans and vegetarians have different kinds of bacteria living in their colon than omnivores do, and this may explain why they produce less TMAO.

Point #5. L-carnitine supplements increase atherosclerosis in genetically-altered mice.

Point #6. TMAO interferes with “reverse cholesterol transport” (RCT) in genetically-altered mice, so it’s harder for their bodies to get rid of excess cholesterol.

and one giant leap for mankind . . . 

If you eat red meat, your body will fill up with cholesterol and you will have a heart attack.

Counterpoint #1

The observation that people with heart disease are more likely to have higher TMAO levels does not mean that TMAO causes heart attacks (and the authors do not claim that it does). It might or it might not. TMAO could simply be an innocent bystander—a red (meat) herring. We have no idea why people who have heart disease tend to have higher TMAO levels. Most importantly, researchers did not ask these people what they eat. Did they eat healthy whole foods diets or junky diets? How many of them were vegans? Vegetarians? Omnivores? Were the ones with the highest TMAO levels all omnivores? Were the ones with the lowest TMAO levels vegans? That would have been very interesting and helpful information.

Counterpoint #2

Not all vegans and vegetarians have lower TMAO levels compared to omnivores. From this figure, taken from Figure 2 of Hazen’s study, it looks like only a small percentage of them do.

The fact that there is so much overlap in TMAO levels between meat-eaters and non-meat-eaters suggests that there is something else about diet—something other than the presence or absence of meat—that is playing a significant role in TMAO levels. Dietary choline is the most logical and likely explanation, but may not be the only one.

Counterpoint #3

a. The form of carnitine found in red meat—acetyl-L-carnitine—was not used in the study; free L-carnitine supplements were used in the study instead. Because these supplements contain the form of carnitine that is hardest to absorb, the majority of it bypasses the small intestines and makes it down to the colon, where bacteria can turn it into the maximum amount of TMA (and TMAO) possible. This study does not tell us whether acetyl-L-carnitine—the form of carnitine found in red meat—raises TMAO levels. Even if TMAO turns out to be the scourge of the West, all you will have shown with this study is that people who want to avoid heart attacks should not take L-carnitine supplements with their steak.

b. NONE of the subjects was fed steak alone—they all received either L-carnitine supplements alone or in combination with steak. There is no proof anywhere in this paper that simply eating steak all by itself will raise anyone’s TMAO levels. In order to convince people that steak raises TMAO levels, you have to include a steak-only experiment. Any high school science student could tell you that.

Here’s an example of what the scientists did:

Experiment: Give one male vegan and one female omnivore each an 8-oz steak (which contains 180 mg of acetyl L-carnitine) plus a capsule containing 250 mg of free L-carnitine and watch what happens to their TMAO levels. [Poor vegan man . . . he really took one for the team. Give that man a year’s supply of tofu!]

Result: The vegan man produced virtually no TMAO after the steak + carnitine supplement whereas the meat-eating woman generated a TMAO spike in her bloodstream.

Given that studies have shown vegans absorb more carnitine than meat-eaters, isn’t it possible that the vegan man, whose body may have been pining for some long-overdue, prefabricated carnitine, absorbed much more carnitine than the omnivorous woman, so that much less of it made it to his colon to be turned into TMA? Isn’t it possible that the vegan man didn’t generate a TMAO spike because his liver for some reason couldn’t turn TMA into TMAO? In this case, he would have generated a TMA spike, but TMA was not measured. Chris Masterjohn wrote an excellent review of this study and proposes other interesting possibilities, including gender differences and vitamin deficiency issues. He also does a beautiful job of analyzing the omnivore vs vegan/vegetarian experiments.

Counterpoint #4

Yes, what we eat determines the types of bacteria in our colon, but we have no idea which mix of bacteria is healthiest for us, we have no idea which diet encourages the best mix of bacteria, and we have no idea whether any of this has anything to do with heart disease.

The researchers detailed the interesting differences in bacterial patterns they discovered between meat-eaters and non-meat-eaters. One type of intestinal bacteria called Prevotella was strongly associated with higher TMAO production. Four of the human volunteers were found to have bacterial colonies in their colons that were rich in Prevotella. Were all four of these individuals meat-eaters? No. Three of them were omnivores (5.9% of all omnivores in the study), and one was not (3.8% of all non-meat-eaters). To quote the authors, this suggested:

“more complexity in the human gut microbiome than anticipated. . . . Indeed, other studies have demonstrated variable results in associating human bacterial genera . . . including Prevotella, to omnivorous and vegetarian eating habits.”

Translation: Even if you are convinced that having Prevotella colonies setting up house in your innards is bad for you, eating a vegan/vegetarian diet will not guarantee you a low-Prevotella colon.

Counterpoint #5

• Yes, L-carnitine supplements caused an increase in atherosclerosis in genetically altered mice. However, L-carnitine is not red meat. It is not even the form of carnitine found in red meat (acetyl-L-carnitine).
• The dose of L-carnitine used in these mice was extremely high. According to Chris Masterjohn, it was the equivalent of a human eating 1000 sirloin steaks.
• For reasons I don’t understand, the mice used in these studies were genetically-altered so that they were missing a gene (apoE) required for normal cholesterol processing. These mice are popular with scientists who study heart disease because they are very good at developing atherosclerosis. It’s already a big stretch to apply information from mouse studies to human health, why widen the gap by using unnaturally defective mice? Absurd.

Counterpoint #6

Now here’s where the authors really jumped the shark. They fed their miscreant mice standard mouse chow supplemented with L-carnitine, choline, or TMAO itself. Then a trusty lab assistant was charged with the delightful task of measuring how much cholesterol the mice . . . um . . . released. Makes me nostalgic for the 7 years I spent as a lab tech . . . not. They found that mouse pellets from animals fed TMAO contained 30% less cholesterol than those fed unsupplemented chow. This is how they propose TMAO causes human heart disease. There is so much I could say about these studies, but the take-home message for your refrigerator magnet is this:

Just because the cage droppings of mutant mice deliberately fed TMAO contained less cholesterol than those who were not fed TMAO does not mean that a human who eats a steak is going to have a heart attack.

My BIGGEST BEEF with this study

Like most studies that try to connect red meat to human disease, this collection of studies does not control for refined carbohydrate intake. We do not know how healthy the diets of the human volunteers were before this study began. Were the vegans and vegetarians health-conscious types who avoided junk foods? What about the omnivores? What if it turned out that everyone who had a higher TMAO level (including the veg/vegans with higher TMAO) also happened to eat a lot more sugar and flour?

After all, if there is one clear culprit emerging from the piles of studies about diet and heart disease, it is refined carbohydrate—not saturated fat, not cholesterol, not red meat. So, in this day and age, in my humble opinion, if you are going to conduct a study of diet and heart disease, you simply must take refined carbohydrate into consideration in order to be taken seriously.

Let’s look at two clear examples in this study of how refined carbohydrate intake was completely ignored by the authors.

The authors measured TMAO levels in 2,595 people and concluded that there was a dose-dependent relationship between TMAO levels and cardiovascular disease (CVD) risk, after adjustment for “traditional CVD risk factors,” which were age, gender, diabetes, smoking, blood pressure, cholesterol levels, and medications. Notice the absence of refined carbohydrate intake, fasting blood glucose, hemoglobin A1C or any other related values.

But hope was kindled when, within a description of one of their mouse studies, I came across this promising line:

“Of note, the increase in atherosclerotic plaque burden with dietary L-carnitine occurred in the absence of proatherogenic changes in plasma lipid, lipoprotein, glucose, or insulin levels.”

Excellent, they acknowledged glucose and insulin as potential risk factors! Had they actually determined that carnitine caused atherosclerosis despite healthy glucose and insulin levels? The sentence above, which is found in the primary article, would lead you to believe this, but if you dig through the 40-page supplementary information, you unearth this telling table:

As you can see, the triglyceride, cholesterol, glucose and insulin levels of mice being fed normal chow are already pretty high (insulin levels at baseline convert to 16.3 microunits/ml). When carnitine is added, there is no statistically significant change in any of these levels (as indicated by P values greater than 0.05). The authors phrased their sentence carefully so that what they say is true—there were no proatherogenic (artery-clogging) changes in these profiles. They were already proatherogenic to begin with.

These mice, like most laboratory animals, are fed unbelievably junky diets. In this case, they were eating a “standard chow control diet”, called “Teklad 2018”:

Ingredients (in descending order of inclusion): Ground wheat, ground corn, wheat middlings, dehulled soybean meal, corn gluten meal, soybean oil, calcium carbonate, dicalcium phosphate, brewers dried yeast, iodized salt, L-lysine, DL-methionine, choline chloride, kaolin, magnesium oxide, vitamin E acetate, menadione sodium bisulfite complex (source of vitamin K activity), manganous oxide, ferrous sulfate, zinc oxide, niacin, calcium pantothenate, copper sulfate, pyridoxine hydrochloride, riboflavin, thiamin mononitrate, vitamin A acetate, calcium iodate, vitamin B12 supplement, folic acid, biotin, vitamin D3 supplement, cobalt carbonate.

This chow is comprised almost entirely of processed wheat, corn, and soy—nearly 100% refined carbohydrate, held together with soybean oil. This is not a diet that exists in nature. Poor little mice. No wonder manufacturers have to supplement this stuff with 18 vitamins and minerals. Look familiar? Is anyone reminded of the ingredient list on the side of your typical cereal box? Coat these mouse pellets with chocolate frosting or sprinkles and you’ve got yourself a yummy breakfast treat.

The authors provide evidence that vegans/vegetarians have a different mix of bacteria living in their colon than omnivores, and they do an excellent job of convincing us that you can’t generate TMAO without bacteria (humans do not possess this capability). Then, because they believe that red meat is bad for us, they try to connect red meat to bacterial metabolism of carnitine to TMAO. Now allow me to do the same thing with refined carbs. It took me about 3 minutes to find this reference:

“Phosphotransferase systems involved in microbial processing of carbohydrates also were found to be over expressed in the intestines of obese people, notably from Prevotellaceae”1

I am not saying that carbs increase Prevotella activity or that Prevotella causes heart attacks. All I’m saying is that refined carbohydrates may also play an important role in what kind of bacteria elbow their way to your colonic buffet table.

Guilt by association

Based on the thousands of scientific articles I have read about food and health, in combination with my personal experience, clinical experience, and common sense, I find nothing to suggest that red meat is bad for people, and plenty of evidence that red meat is good for people (see my meats page). Every article I’ve ever read that tries to blame meat for our health problems fails to to take refined carbohydrate into consideration. In my opinion, damning nutritious meat for your heart attack is like pouring sugar into your gas tank and then cursing the gasoline when your car breaks down.

If you want to scare me away from eating meat using mouse experiments, you are going to have to raise a slew of mice on a healthy whole foods vegetarian diet, prove to me that those mice show no signs of cardiovascular disease, then start feeding them one miniature sirloin steak for dinner every night until they all clutch their furry little chests, keel over, and die.

Has the fat lady sung?

As far as I can tell, the authors’ theory that red meat provides carnitine for bacteria to transform into TMA which our liver then converts to TMAO, which causes our macrophages to fill up with cholesterol, block our arteries, and cause heart attacks is just that: a theory—full of sound and fury, signifying nothing.

Read my critique of the World Health Organization’s 2015 proclamation that red and processed meats cause cancer: “WHO Says Meat Causes Cancer?“

We are taught that meat is an unhealthy, artery-clogging, fattening, cholesterol-raising, heart-attack inducing, constipating, tumor-producing food that should be avoided like the plague, and that a plant-based diet is the holy grail of health.

To the best of my knowledge, the world has yet to produce a civilization which has eaten a vegan diet from childhood through death, whereas there are numerous examples throughout recorded history of people from a variety of cultural, ethnic and geographical backgrounds who have lived on mainly-meat diets for decades, lifetimes, generations. What exactly did these carnivorous cultures eat, and how healthy or unhealthy were they?

In my opinion, examples of real people eating mostly-meat diets for long periods of time gives us much more powerful information about meat and health than conventional scientific studies conducted over short periods of time in which one group of people eats a little more meat or a few extra servings of vegetables than another group of people.

Meet the meat mongers

• The Inuit of the Canadian Arctic thrived on fish, seal, walrus and whale meat.
• The Chukotka of the Russian Arctic lived on caribou meat, marine animals and fish.
• The Masai, Samburu, and Rendille warriors of East Africa survived on diets consisting primarily of milk and meat.
• The steppe nomads of Mongolia ate mostly meat and dairy products.
• The Sioux of South Dakota enjoyed a diet of buffalo meat.
• The Brazilian Gauchos nourished themselves with beef.

Dangerously unbalanced?

How many servings of fruits and vegetables did most Arctic peoples eat most days of the year? Zero. How much fiber is there in a seal, or a fish, or an Arctic bird? None whatsoever. Physician Samuel Hutton, who treated Eskimos in the Canadian province of Labrador at the turn of the 20^th century, wrote:

“I wonder are the Eskimos unique among the nations in their disregard of vegetable foods? I sometimes saw them getting young willow shoots and one or two other little bits of green, and eating them as a relish to their meat; but they make absolutely no attempt to till what soil there is, and they do not even make the most of the plants that grow. During the short weeks of summer the vegetation springs up in a perfectly marvelous manner. . . . Surely among this wild scramble of plant life there must be some things that are good to eat! I know that there are plenty of dandelion leaves, and I have tasted worse things in my time, but the people never touch them.”1

By all accounts, these people ate little to no plant foods for most of the year (summertime was an exception):

“But though gardening is entirely foreign to the Eskimo nature, they do not entirely scorn the good things of the earth . . . In most years the scrubby bushes that crawl upon the ground are loaded with succulent berries—a truly marvelous provision—and the people gather them not only by the handfuls and bucketfuls, but by barrelfuls.”2

Their diets were therefore extremely low in fiber most of the time, and very high in animal protein and animal fat. These traditional ways of eating would terrify the USDA, the American Heart Association, the American Cancer Society, not to mention the Harvard School of Public Health, which remains a staunchly anti-meat, anti-saturated fat, anti-cholesterol institution.

How in the world did these uninformed fringe types manage to get all their vitamins and minerals without the heaping helpings of colorful fruits, vegetables, and whole grains without which we are told we shall surely perish? Weren’t they cancer-riddled, heart-clenching, constipated, fat slobs who died young from scary deficiency diseases like rickets and scurvy?

Let’s look at the two groups of people for whom we have the most medical information available to see if we can begin to answer some of these very important questions. What follows is not meant to be a complete review; I wrote this article because I was excited to share some of the fascinating things I am learning as I research meat and human health.

A tale of two cities

Well, cities is a bit of a stretch . . . in fact neither of these groups of people were city folk, but that is where the similarities end. The only thing these people had in common was that they ate few if any plant foods.

You could not ask for two more different cultures than the Arctic “Eskimos” and the East African herdsmen:

• North Pole vs. Equator
• Asian vs. African
• Non-dairy vs. Dairy
• Surf vs. Turf

Arctic peoples studied were living in the northernmost “circumpolar” parts of Alaska, Canada, Russia and Greenland. The diets of most Arctic people began changing in the late 1800s as trade routes began providing access to European foods including sugar, flour, and dairy products, but prior to that their diet consisted primarily of animal protein and fat for most of the year.

East African herdsmen (Masai, Samburu and Rendille peoples) studied hailed from what are now Kenya and Tanzania, along the African equator. By tradition, males in these tribes ate only animal foods (meat and dairy products) from age 14 until at least age 28, when they completed their warrior years.

These unique groups of people were the subjects of intense medical investigation several decades ago, and there have been numerous scientific articles written about their diet and health.

Meat and heart disease

More than 40 years ago, the remote region of Point Hope, Alaska (where a mostly-meat diet was still being consumed due to its isolated location) was the subject of a research study published in 1972:

“The Point Hope inhabitants represent one of the few remnants of the Eskimo whale, sea, and walrus hunting cultures in the world . . . Average total daily caloric intake was approximately 3,000 kcal [calories] per person, ranging from 2,300 to 4,500 kcal. Approximately 50% of the calories were derived from fat and 30 to 35% from protein. Carbohydrate accounted for only 15 to 20% of their calories, largely in the form of glycogen [animal starch] from the meat they consumed. Grain products were scarce and although sucrose [table sugar] was not unknown, the average adult ingested less than 3 g/day, primarily for sweetening tea or coffee.”1

Researchers found that the incidence of heart disease among Point Hope residents was ten times lower than in the general Caucasian population of the United States. Not only that—their triglyceride levels (levels of fat in the bloodstream) averaged 85 mg/dL, whereas the average U.S. triglyceride levels at that time averaged over 100 mg/dL.

[To read more about why carbohydrates are not necessary in the diet and how carbohydrates cause the body to produce extra fat, please see my carbohydrates page]

Lest you think that these Alaskans were special—that their triglyceride levels were low because of genetic differences, or because they had become adapted over centuries to their meaty diet, and that it wasn’t fair to compare their triglyceride levels to those of mainland Americans—you may want to think twice.

A much more recent study conducted in remote areas of southwestern Alaska compared native people who reported eating the highest percentage of traditional animal foods to native people who reported eating the lowest percentage of traditional animal foods. Native Alaskans following a more traditional diet were eating much more animal protein and animal fat, yet had triglyceride levels on average 25 points lower than their more Westernized neighbors. 2

Even as recently as the 1980s, only 3.5% of all deaths in Greenland Eskimos were due to heart disease, despite a life span of more than 60 years.

Now, some Arctic peoples did have some cholesterol buildup in their arteries, but this was apparently mild and primarily seen in those who were eating a mixture of modern and traditional foods:

“The rarity of ischaemic heart disease has been repeatedly noted, with due allowance for the life-expectancy of Eskimos. Rabinowitch, discussing the contention of others that arteriosclerosis was rare in Eskimos, stated that this was not the case in those he examined in the eastern Arctic of Canada where contact with white man had altered the diet, but in the most northerly parts there was no evidence of arteriosclerosis; total cholesterol in serum was low. 18 necropsies by Gottman between 1956 and 1958, and by Arthaud between 1959 and 1968, on Alaskan Eskimos partly on European diets, showed that atherosclerosis was mild and not a major cause of death.”3

Meanwhile, back in Africa…

As for our pastoral African nomad friends, heart attacks were essentially unknown among Masai males, despite living well into their 60s. Researchers examined 600 living Masai men, more than half of whom were over 40 years old, and found that only one of them had ever had a heart attack. In fact, researchers went so far as to collect and examine the hearts of 50 Masai who had dropped dead, and found no evidence of a heart attack in a single one. Just as with Eskimos, they did find “fatty streaks” and some cholesterol deposits inside of their arteries, but not enough to cause any blockages.

It was estimated that these men obtained 66% of their daily calories from pure animal fat, eating about 300 grams of fat and 600 milligrams of cholesterol per day. Americans are advised to keep fat intake to 20 to 35% of calories and to keep cholesterol intake below 300 mg per day, therefore these men were eating twice as much cholesterol and 2 to 3 times as much fat as we are told to eat.

Meat and blood pressure

Once upon a time, there was a group of Inuit from Greenland who had been raised on a diet high in meat, fish, and animal fat, and very low in fruits, vegetables, and dairy products. In the 1980s and 1990s, some of them immigrated south to Denmark, and in the process, turned their diets upside-down. They started eating the way Danish people ate—adding lots more plant foods and dairy products to their menus, and eating fewer animal foods. This is the advice we are given by public health officials if we want to improve our health. So, did these transplanted Greenlanders become healthier? Researchers discovered that the Inuit who had moved to Denmark and changed their diets had blood pressures ten points higher than those who had stayed behind in Greenland. This was despite the fact that they weighed less, smoked less, drank less, and got the same amount of exercise as their Greenland brothers and sisters.

Unfortunately the researchers did not ask about junk food intake, so we don’t know if the Inuit were also eating more refined carbohydrates, salt, and chemicals after relocating to Denmark, although that would be a safe bet. My point is that simply eating less meat and eating more fruits and vegetables, which is what we are told we should do to be healthier, did not improve or protect their health–at least not when it came to blood pressure.

While back in the shadow of Mount Kilimanjaro . . .

Blood pressures among the Masai of East Africa averaged 120/80 in males ranging in age from 14 to over 55; only 1% of Masai men had high blood pressure. Among the Samburu, as well, blood pressures were excellent, averaging 112/76, with systolic (upper) blood pressure values tending to rise only a few points after the age of 60.

Meat and obesity

The problem of overweight and obesity did not exist among the Masai, Samburu, or Rendille people. The average Masai male measured approximately 5 feet 7 inches tall and weighed 134 pounds. The average Samburu man was equally as tall and weighed 126 pounds. The typical Rendille man weighed only 121 pounds. Weights within all of these groups of people remained stable throughout their lifetimes.

Out of Africa . . .

I just adore these passages written in 1936 by noted Canadian anthropologist Vilhjalmur Stefansson:

“Eskimos, when still on their native meats, are never corpulent—at least I have seen none. They may be well-fleshed. Some especially women, are notably heavier in middle age than when young. But they are not corpulent in our sense.

When you see Eskimos in their native garments you do get the impression of fat round faces on fat round bodies, but the roundness of face is a racial peculiarity and the rest of the effect is produced by loose and puffy garments. See them stripped and you do not find the abdominal protuberances and folds which are numerous at Coney Island beaches and so persuasive in arguments against nudism.

There is no racial immunity among Eskimos to corpulence. You prove that by how quickly they get fat and how fat they grow on European diets.”

I can relate…ich bin ein Eskimo…

Unanswered questions

If meat, saturated fat and cholesterol are supposed to cause heart disease, and if colorful, fiber-rich fruits and vegetables are supposed to protect us from heart disease, why didn’t these people, who were eating MUCH more meat and FAR less plant food than most of us ever will, suffer from heart disease and all of the health problems we associate with heart disease risk, such as high blood pressure, obesity, and high triglycerides?

This post was not designed to provide an airtight argument for meat and health, but I do hope that it has at least prompted those of you who remain skeptical about meat to rethink what you’ve been led to believe.

To read my detailed critique of the World Health Organization’s 2015 report claiming that red meat causes cancer, read my post “Who Says Meat Causes Cancer?“

If you’ve got a hankerin’ for more information about meat and health, take a look at my meats page.

What about cholesterol levels in carnivorous cultures? It turns out that cholesterol is the most complicated topic of all . . . as usual . . . but ask a silly question. . . . In the meantime, if you are worried that eating a high-cholesterol diet will raise your “bad” cholesterol, you may want to read my cholesterol page to see why you don’t need to worry about this.

Are you thinking of trying an all-meat diet?

Jessica Haggard recently (2019) published The Carnivore Cookbook. She has created many tasty recipes, and includes good tips for finding affordable meat and how best to use different cuts of meat. There is also an entire chapter on offal (organ meats). If you do try an all-meat diet, you should know that in order to get all of the nutrients you need to support your good health, it may be important to include organ meats in your diet. If not, you can be at risk for deficiency in retinol (vitamin A), folate, vitamin D3, vitamin K2, vitamin C, and the essential fatty acids EPA and DHA (although the fatty acids can also be found in fatty fish).

You may also want to check out my conversation with Tristan Haggard on his Primal Edge Health podcast about the benefits of eating meat for mental health. It is available both in audio and video format.

The dynamic duo Maria and Craig Emmerich also just released a brand new carnivore cookbook (2020) with over 100 tasty recipes that introduce creative ways to add flavor and variety to an all-meat diet. As with most of Maria’s cookbooks, they open this book with an in-depth introduction to the science behind carnivore diets, provide historical/anthropological context, and explain why some people might benefit from going plant-free. The book includes meal plans with grocery lists and tips for safely transitioning to the diet. I am a big fan of the Emmerichs’ other cookbooks and highly recommend this one for those interested in trying a  carnivore diet or are already enjoying the benefits of an all-meat diet.

We are taught that meat is an unhealthy, artery-clogging, fattening, cholesterol-raising, heart-attack inducing, constipating, tumor-producing food that should be avoided like the plague, and that a plant-based diet is the holy grail of health.

To the best of my knowledge, the world has yet to produce a civilization which has eaten a vegan diet from childhood through death, whereas there are numerous examples throughout recorded history of people from a variety of cultural, ethnic and geographical backgrounds who have lived on mainly-meat diets for decades, lifetimes, generations. What exactly did these carnivorous cultures eat, and how healthy or unhealthy were they?

In my opinion, examples of real people eating mostly-meat diets for long periods of time gives us much more powerful information about meat and health than conventional scientific studies conducted over short periods of time in which one group of people eats a little more meat or a few extra servings of vegetables than another group of people.

Meet the meat mongers

• The Inuit of the Canadian Arctic thrived on fish, seal, walrus and whale meat.
• The Chukotka of the Russian Arctic lived on caribou meat, marine animals and fish.
• The Masai, Samburu, and Rendille warriors of East Africa survived on diets consisting primarily of milk and meat.
• The steppe nomads of Mongolia ate mostly meat and dairy products.
• The Sioux of South Dakota enjoyed a diet of buffalo meat.
• The Brazilian Gauchos nourished themselves with beef.

Dangerously unbalanced?

How many servings of fruits and vegetables did most Arctic peoples eat most days of the year? Zero. How much fiber is there in a seal, or a fish, or an Arctic bird? None whatsoever. Physician Samuel Hutton, who treated Eskimos in the Canadian province of Labrador at the turn of the 20^th century, wrote:

“I wonder are the Eskimos unique among the nations in their disregard of vegetable foods? I sometimes saw them getting young willow shoots and one or two other little bits of green, and eating them as a relish to their meat; but they make absolutely no attempt to till what soil there is, and they do not even make the most of the plants that grow. During the short weeks of summer the vegetation springs up in a perfectly marvelous manner. . . . Surely among this wild scramble of plant life there must be some things that are good to eat! I know that there are plenty of dandelion leaves, and I have tasted worse things in my time, but the people never touch them.”1

By all accounts, these people ate little to no plant foods for most of the year (summertime was an exception):

“But though gardening is entirely foreign to the Eskimo nature, they do not entirely scorn the good things of the earth . . . In most years the scrubby bushes that crawl upon the ground are loaded with succulent berries—a truly marvelous provision—and the people gather them not only by the handfuls and bucketfuls, but by barrelfuls.”2

Their diets were therefore extremely low in fiber most of the time, and very high in animal protein and animal fat. These traditional ways of eating would terrify the USDA, the American Heart Association, the American Cancer Society, not to mention the Harvard School of Public Health, which remains a staunchly anti-meat, anti-saturated fat, anti-cholesterol institution.

How in the world did these uninformed fringe types manage to get all their vitamins and minerals without the heaping helpings of colorful fruits, vegetables, and whole grains without which we are told we shall surely perish? Weren’t they cancer-riddled, heart-clenching, constipated, fat slobs who died young from scary deficiency diseases like rickets and scurvy?

Let’s look at the two groups of people for whom we have the most medical information available to see if we can begin to answer some of these very important questions. What follows is not meant to be a complete review; I wrote this article because I was excited to share some of the fascinating things I am learning as I research meat and human health.

A tale of two cities

Well, cities is a bit of a stretch . . . in fact neither of these groups of people were city folk, but that is where the similarities end. The only thing these people had in common was that they ate few if any plant foods.

You could not ask for two more different cultures than the Arctic “Eskimos” and the East African herdsmen:

• North Pole vs. Equator
• Asian vs. African
• Non-dairy vs. Dairy
• Surf vs. Turf

Arctic peoples studied were living in the northernmost “circumpolar” parts of Alaska, Canada, Russia and Greenland. The diets of most Arctic people began changing in the late 1800s as trade routes began providing access to European foods including sugar, flour, and dairy products, but prior to that their diet consisted primarily of animal protein and fat for most of the year.

East African herdsmen (Masai, Samburu and Rendille peoples) studied hailed from what are now Kenya and Tanzania, along the African equator. By tradition, males in these tribes ate only animal foods (meat and dairy products) from age 14 until at least age 28, when they completed their warrior years.

These unique groups of people were the subjects of intense medical investigation several decades ago, and there have been numerous scientific articles written about their diet and health.

Meat and heart disease

More than 40 years ago, the remote region of Point Hope, Alaska (where a mostly-meat diet was still being consumed due to its isolated location) was the subject of a research study published in 1972:

“The Point Hope inhabitants represent one of the few remnants of the Eskimo whale, sea, and walrus hunting cultures in the world . . . Average total daily caloric intake was approximately 3,000 kcal [calories] per person, ranging from 2,300 to 4,500 kcal. Approximately 50% of the calories were derived from fat and 30 to 35% from protein. Carbohydrate accounted for only 15 to 20% of their calories, largely in the form of glycogen [animal starch] from the meat they consumed. Grain products were scarce and although sucrose [table sugar] was not unknown, the average adult ingested less than 3 g/day, primarily for sweetening tea or coffee.”1

Researchers found that the incidence of heart disease among Point Hope residents was ten times lower than in the general Caucasian population of the United States. Not only that—their triglyceride levels (levels of fat in the bloodstream) averaged 85 mg/dL, whereas the average U.S. triglyceride levels at that time averaged over 100 mg/dL.

[To read more about why carbohydrates are not necessary in the diet and how carbohydrates cause the body to produce extra fat, please see my carbohydrates page]

Lest you think that these Alaskans were special—that their triglyceride levels were low because of genetic differences, or because they had become adapted over centuries to their meaty diet, and that it wasn’t fair to compare their triglyceride levels to those of mainland Americans—you may want to think twice.

A much more recent study conducted in remote areas of southwestern Alaska compared native people who reported eating the highest percentage of traditional animal foods to native people who reported eating the lowest percentage of traditional animal foods. Native Alaskans following a more traditional diet were eating much more animal protein and animal fat, yet had triglyceride levels on average 25 points lower than their more Westernized neighbors. 2

Even as recently as the 1980s, only 3.5% of all deaths in Greenland Eskimos were due to heart disease, despite a life span of more than 60 years.

Now, some Arctic peoples did have some cholesterol buildup in their arteries, but this was apparently mild and primarily seen in those who were eating a mixture of modern and traditional foods:

“The rarity of ischaemic heart disease has been repeatedly noted, with due allowance for the life-expectancy of Eskimos. Rabinowitch, discussing the contention of others that arteriosclerosis was rare in Eskimos, stated that this was not the case in those he examined in the eastern Arctic of Canada where contact with white man had altered the diet, but in the most northerly parts there was no evidence of arteriosclerosis; total cholesterol in serum was low. 18 necropsies by Gottman between 1956 and 1958, and by Arthaud between 1959 and 1968, on Alaskan Eskimos partly on European diets, showed that atherosclerosis was mild and not a major cause of death.”3

Meanwhile, back in Africa…

As for our pastoral African nomad friends, heart attacks were essentially unknown among Masai males, despite living well into their 60s. Researchers examined 600 living Masai men, more than half of whom were over 40 years old, and found that only one of them had ever had a heart attack. In fact, researchers went so far as to collect and examine the hearts of 50 Masai who had dropped dead, and found no evidence of a heart attack in a single one. Just as with Eskimos, they did find “fatty streaks” and some cholesterol deposits inside of their arteries, but not enough to cause any blockages.

It was estimated that these men obtained 66% of their daily calories from pure animal fat, eating about 300 grams of fat and 600 milligrams of cholesterol per day. Americans are advised to keep fat intake to 20 to 35% of calories and to keep cholesterol intake below 300 mg per day, therefore these men were eating twice as much cholesterol and 2 to 3 times as much fat as we are told to eat.

Meat and blood pressure

Once upon a time, there was a group of Inuit from Greenland who had been raised on a diet high in meat, fish, and animal fat, and very low in fruits, vegetables, and dairy products. In the 1980s and 1990s, some of them immigrated south to Denmark, and in the process, turned their diets upside-down. They started eating the way Danish people ate—adding lots more plant foods and dairy products to their menus, and eating fewer animal foods. This is the advice we are given by public health officials if we want to improve our health. So, did these transplanted Greenlanders become healthier? Researchers discovered that the Inuit who had moved to Denmark and changed their diets had blood pressures ten points higher than those who had stayed behind in Greenland. This was despite the fact that they weighed less, smoked less, drank less, and got the same amount of exercise as their Greenland brothers and sisters.

Unfortunately the researchers did not ask about junk food intake, so we don’t know if the Inuit were also eating more refined carbohydrates, salt, and chemicals after relocating to Denmark, although that would be a safe bet. My point is that simply eating less meat and eating more fruits and vegetables, which is what we are told we should do to be healthier, did not improve or protect their health–at least not when it came to blood pressure.

While back in the shadow of Mount Kilimanjaro . . .

Blood pressures among the Masai of East Africa averaged 120/80 in males ranging in age from 14 to over 55; only 1% of Masai men had high blood pressure. Among the Samburu, as well, blood pressures were excellent, averaging 112/76, with systolic (upper) blood pressure values tending to rise only a few points after the age of 60.

Meat and obesity

The problem of overweight and obesity did not exist among the Masai, Samburu, or Rendille people. The average Masai male measured approximately 5 feet 7 inches tall and weighed 134 pounds. The average Samburu man was equally as tall and weighed 126 pounds. The typical Rendille man weighed only 121 pounds. Weights within all of these groups of people remained stable throughout their lifetimes.

Out of Africa . . .

I just adore these passages written in 1936 by noted Canadian anthropologist Vilhjalmur Stefansson:

“Eskimos, when still on their native meats, are never corpulent—at least I have seen none. They may be well-fleshed. Some especially women, are notably heavier in middle age than when young. But they are not corpulent in our sense.

When you see Eskimos in their native garments you do get the impression of fat round faces on fat round bodies, but the roundness of face is a racial peculiarity and the rest of the effect is produced by loose and puffy garments. See them stripped and you do not find the abdominal protuberances and folds which are numerous at Coney Island beaches and so persuasive in arguments against nudism.

There is no racial immunity among Eskimos to corpulence. You prove that by how quickly they get fat and how fat they grow on European diets.”

I can relate…ich bin ein Eskimo…

Unanswered questions

If meat, saturated fat and cholesterol are supposed to cause heart disease, and if colorful, fiber-rich fruits and vegetables are supposed to protect us from heart disease, why didn’t these people, who were eating MUCH more meat and FAR less plant food than most of us ever will, suffer from heart disease and all of the health problems we associate with heart disease risk, such as high blood pressure, obesity, and high triglycerides?

This post was not designed to provide an airtight argument for meat and health, but I do hope that it has at least prompted those of you who remain skeptical about meat to rethink what you’ve been led to believe.

To read my detailed critique of the World Health Organization’s 2015 report claiming that red meat causes cancer, read my post “Who Says Meat Causes Cancer?“

If you’ve got a hankerin’ for more information about meat and health, take a look at my meats page.

What about cholesterol levels in carnivorous cultures? It turns out that cholesterol is the most complicated topic of all . . . as usual . . . but ask a silly question. . . . In the meantime, if you are worried that eating a high-cholesterol diet will raise your “bad” cholesterol, you may want to read my cholesterol page to see why you don’t need to worry about this.

Are you thinking of trying an all-meat diet?

Jessica Haggard recently (2019) published The Carnivore Cookbook. She has created many tasty recipes, and includes good tips for finding affordable meat and how best to use different cuts of meat. There is also an entire chapter on offal (organ meats). If you do try an all-meat diet, you should know that in order to get all of the nutrients you need to support your good health, it may be important to include organ meats in your diet. If not, you can be at risk for deficiency in retinol (vitamin A), folate, vitamin D3, vitamin K2, vitamin C, and the essential fatty acids EPA and DHA (although the fatty acids can also be found in fatty fish).

You may also want to check out my conversation with Tristan Haggard on his Primal Edge Health podcast about the benefits of eating meat for mental health. It is available both in audio and video format.

The dynamic duo Maria and Craig Emmerich also just released a brand new carnivore cookbook (2020) with over 100 tasty recipes that introduce creative ways to add flavor and variety to an all-meat diet. As with most of Maria’s cookbooks, they open this book with an in-depth introduction to the science behind carnivore diets, provide historical/anthropological context, and explain why some people might benefit from going plant-free. The book includes meal plans with grocery lists and tips for safely transitioning to the diet. I am a big fan of the Emmerichs’ other cookbooks and highly recommend this one for those interested in trying a  carnivore diet or are already enjoying the benefits of an all-meat diet.

We are taught that meat is an unhealthy, artery-clogging, fattening, cholesterol-raising, heart-attack inducing, constipating, tumor-producing food that should be avoided like the plague, and that a plant-based diet is the holy grail of health.

To the best of my knowledge, the world has yet to produce a civilization which has eaten a vegan diet from childhood through death, whereas there are numerous examples throughout recorded history of people from a variety of cultural, ethnic and geographical backgrounds who have lived on mainly-meat diets for decades, lifetimes, generations. What exactly did these carnivorous cultures eat, and how healthy or unhealthy were they?

In my opinion, examples of real people eating mostly-meat diets for long periods of time gives us much more powerful information about meat and health than conventional scientific studies conducted over short periods of time in which one group of people eats a little more meat or a few extra servings of vegetables than another group of people.

Meet the meat mongers

• The Inuit of the Canadian Arctic thrived on fish, seal, walrus and whale meat.
• The Chukotka of the Russian Arctic lived on caribou meat, marine animals and fish.
• The Masai, Samburu, and Rendille warriors of East Africa survived on diets consisting primarily of milk and meat.
• The steppe nomads of Mongolia ate mostly meat and dairy products.
• The Sioux of South Dakota enjoyed a diet of buffalo meat.
• The Brazilian Gauchos nourished themselves with beef.

Dangerously unbalanced?

How many servings of fruits and vegetables did most Arctic peoples eat most days of the year? Zero. How much fiber is there in a seal, or a fish, or an Arctic bird? None whatsoever. Physician Samuel Hutton, who treated Eskimos in the Canadian province of Labrador at the turn of the 20^th century, wrote:

“I wonder are the Eskimos unique among the nations in their disregard of vegetable foods? I sometimes saw them getting young willow shoots and one or two other little bits of green, and eating them as a relish to their meat; but they make absolutely no attempt to till what soil there is, and they do not even make the most of the plants that grow. During the short weeks of summer the vegetation springs up in a perfectly marvelous manner. . . . Surely among this wild scramble of plant life there must be some things that are good to eat! I know that there are plenty of dandelion leaves, and I have tasted worse things in my time, but the people never touch them.”1

By all accounts, these people ate little to no plant foods for most of the year (summertime was an exception):

“But though gardening is entirely foreign to the Eskimo nature, they do not entirely scorn the good things of the earth . . . In most years the scrubby bushes that crawl upon the ground are loaded with succulent berries—a truly marvelous provision—and the people gather them not only by the handfuls and bucketfuls, but by barrelfuls.”2

Their diets were therefore extremely low in fiber most of the time, and very high in animal protein and animal fat. These traditional ways of eating would terrify the USDA, the American Heart Association, the American Cancer Society, not to mention the Harvard School of Public Health, which remains a staunchly anti-meat, anti-saturated fat, anti-cholesterol institution.

How in the world did these uninformed fringe types manage to get all their vitamins and minerals without the heaping helpings of colorful fruits, vegetables, and whole grains without which we are told we shall surely perish? Weren’t they cancer-riddled, heart-clenching, constipated, fat slobs who died young from scary deficiency diseases like rickets and scurvy?

Let’s look at the two groups of people for whom we have the most medical information available to see if we can begin to answer some of these very important questions. What follows is not meant to be a complete review; I wrote this article because I was excited to share some of the fascinating things I am learning as I research meat and human health.

A tale of two cities

Well, cities is a bit of a stretch . . . in fact neither of these groups of people were city folk, but that is where the similarities end. The only thing these people had in common was that they ate few if any plant foods.

You could not ask for two more different cultures than the Arctic “Eskimos” and the East African herdsmen:

• North Pole vs. Equator
• Asian vs. African
• Non-dairy vs. Dairy
• Surf vs. Turf

Arctic peoples studied were living in the northernmost “circumpolar” parts of Alaska, Canada, Russia and Greenland. The diets of most Arctic people began changing in the late 1800s as trade routes began providing access to European foods including sugar, flour, and dairy products, but prior to that their diet consisted primarily of animal protein and fat for most of the year.

East African herdsmen (Masai, Samburu and Rendille peoples) studied hailed from what are now Kenya and Tanzania, along the African equator. By tradition, males in these tribes ate only animal foods (meat and dairy products) from age 14 until at least age 28, when they completed their warrior years.

These unique groups of people were the subjects of intense medical investigation several decades ago, and there have been numerous scientific articles written about their diet and health.

Meat and heart disease

More than 40 years ago, the remote region of Point Hope, Alaska (where a mostly-meat diet was still being consumed due to its isolated location) was the subject of a research study published in 1972:

“The Point Hope inhabitants represent one of the few remnants of the Eskimo whale, sea, and walrus hunting cultures in the world . . . Average total daily caloric intake was approximately 3,000 kcal [calories] per person, ranging from 2,300 to 4,500 kcal. Approximately 50% of the calories were derived from fat and 30 to 35% from protein. Carbohydrate accounted for only 15 to 20% of their calories, largely in the form of glycogen [animal starch] from the meat they consumed. Grain products were scarce and although sucrose [table sugar] was not unknown, the average adult ingested less than 3 g/day, primarily for sweetening tea or coffee.”1

Researchers found that the incidence of heart disease among Point Hope residents was ten times lower than in the general Caucasian population of the United States. Not only that—their triglyceride levels (levels of fat in the bloodstream) averaged 85 mg/dL, whereas the average U.S. triglyceride levels at that time averaged over 100 mg/dL.

[To read more about why carbohydrates are not necessary in the diet and how carbohydrates cause the body to produce extra fat, please see my carbohydrates page]

Lest you think that these Alaskans were special—that their triglyceride levels were low because of genetic differences, or because they had become adapted over centuries to their meaty diet, and that it wasn’t fair to compare their triglyceride levels to those of mainland Americans—you may want to think twice.

A much more recent study conducted in remote areas of southwestern Alaska compared native people who reported eating the highest percentage of traditional animal foods to native people who reported eating the lowest percentage of traditional animal foods. Native Alaskans following a more traditional diet were eating much more animal protein and animal fat, yet had triglyceride levels on average 25 points lower than their more Westernized neighbors. 2

Even as recently as the 1980s, only 3.5% of all deaths in Greenland Eskimos were due to heart disease, despite a life span of more than 60 years.

Now, some Arctic peoples did have some cholesterol buildup in their arteries, but this was apparently mild and primarily seen in those who were eating a mixture of modern and traditional foods:

“The rarity of ischaemic heart disease has been repeatedly noted, with due allowance for the life-expectancy of Eskimos. Rabinowitch, discussing the contention of others that arteriosclerosis was rare in Eskimos, stated that this was not the case in those he examined in the eastern Arctic of Canada where contact with white man had altered the diet, but in the most northerly parts there was no evidence of arteriosclerosis; total cholesterol in serum was low. 18 necropsies by Gottman between 1956 and 1958, and by Arthaud between 1959 and 1968, on Alaskan Eskimos partly on European diets, showed that atherosclerosis was mild and not a major cause of death.”3

Meanwhile, back in Africa…

As for our pastoral African nomad friends, heart attacks were essentially unknown among Masai males, despite living well into their 60s. Researchers examined 600 living Masai men, more than half of whom were over 40 years old, and found that only one of them had ever had a heart attack. In fact, researchers went so far as to collect and examine the hearts of 50 Masai who had dropped dead, and found no evidence of a heart attack in a single one. Just as with Eskimos, they did find “fatty streaks” and some cholesterol deposits inside of their arteries, but not enough to cause any blockages.

It was estimated that these men obtained 66% of their daily calories from pure animal fat, eating about 300 grams of fat and 600 milligrams of cholesterol per day. Americans are advised to keep fat intake to 20 to 35% of calories and to keep cholesterol intake below 300 mg per day, therefore these men were eating twice as much cholesterol and 2 to 3 times as much fat as we are told to eat.

Meat and blood pressure

Once upon a time, there was a group of Inuit from Greenland who had been raised on a diet high in meat, fish, and animal fat, and very low in fruits, vegetables, and dairy products. In the 1980s and 1990s, some of them immigrated south to Denmark, and in the process, turned their diets upside-down. They started eating the way Danish people ate—adding lots more plant foods and dairy products to their menus, and eating fewer animal foods. This is the advice we are given by public health officials if we want to improve our health. So, did these transplanted Greenlanders become healthier? Researchers discovered that the Inuit who had moved to Denmark and changed their diets had blood pressures ten points higher than those who had stayed behind in Greenland. This was despite the fact that they weighed less, smoked less, drank less, and got the same amount of exercise as their Greenland brothers and sisters.

Unfortunately the researchers did not ask about junk food intake, so we don’t know if the Inuit were also eating more refined carbohydrates, salt, and chemicals after relocating to Denmark, although that would be a safe bet. My point is that simply eating less meat and eating more fruits and vegetables, which is what we are told we should do to be healthier, did not improve or protect their health–at least not when it came to blood pressure.

While back in the shadow of Mount Kilimanjaro . . .

Blood pressures among the Masai of East Africa averaged 120/80 in males ranging in age from 14 to over 55; only 1% of Masai men had high blood pressure. Among the Samburu, as well, blood pressures were excellent, averaging 112/76, with systolic (upper) blood pressure values tending to rise only a few points after the age of 60.

Meat and obesity

The problem of overweight and obesity did not exist among the Masai, Samburu, or Rendille people. The average Masai male measured approximately 5 feet 7 inches tall and weighed 134 pounds. The average Samburu man was equally as tall and weighed 126 pounds. The typical Rendille man weighed only 121 pounds. Weights within all of these groups of people remained stable throughout their lifetimes.

Out of Africa . . .

I just adore these passages written in 1936 by noted Canadian anthropologist Vilhjalmur Stefansson:

“Eskimos, when still on their native meats, are never corpulent—at least I have seen none. They may be well-fleshed. Some especially women, are notably heavier in middle age than when young. But they are not corpulent in our sense.

When you see Eskimos in their native garments you do get the impression of fat round faces on fat round bodies, but the roundness of face is a racial peculiarity and the rest of the effect is produced by loose and puffy garments. See them stripped and you do not find the abdominal protuberances and folds which are numerous at Coney Island beaches and so persuasive in arguments against nudism.

There is no racial immunity among Eskimos to corpulence. You prove that by how quickly they get fat and how fat they grow on European diets.”

I can relate…ich bin ein Eskimo…

Unanswered questions

If meat, saturated fat and cholesterol are supposed to cause heart disease, and if colorful, fiber-rich fruits and vegetables are supposed to protect us from heart disease, why didn’t these people, who were eating MUCH more meat and FAR less plant food than most of us ever will, suffer from heart disease and all of the health problems we associate with heart disease risk, such as high blood pressure, obesity, and high triglycerides?

This post was not designed to provide an airtight argument for meat and health, but I do hope that it has at least prompted those of you who remain skeptical about meat to rethink what you’ve been led to believe.

To read my detailed critique of the World Health Organization’s 2015 report claiming that red meat causes cancer, read my post “Who Says Meat Causes Cancer?“

If you’ve got a hankerin’ for more information about meat and health, take a look at my meats page.

What about cholesterol levels in carnivorous cultures? It turns out that cholesterol is the most complicated topic of all . . . as usual . . . but ask a silly question. . . . In the meantime, if you are worried that eating a high-cholesterol diet will raise your “bad” cholesterol, you may want to read my cholesterol page to see why you don’t need to worry about this.

Are you thinking of trying an all-meat diet?

Jessica Haggard recently (2019) published The Carnivore Cookbook. She has created many tasty recipes, and includes good tips for finding affordable meat and how best to use different cuts of meat. There is also an entire chapter on offal (organ meats). If you do try an all-meat diet, you should know that in order to get all of the nutrients you need to support your good health, it may be important to include organ meats in your diet. If not, you can be at risk for deficiency in retinol (vitamin A), folate, vitamin D3, vitamin K2, vitamin C, and the essential fatty acids EPA and DHA (although the fatty acids can also be found in fatty fish).

You may also want to check out my conversation with Tristan Haggard on his Primal Edge Health podcast about the benefits of eating meat for mental health. It is available both in audio and video format.

The dynamic duo Maria and Craig Emmerich also just released a brand new carnivore cookbook (2020) with over 100 tasty recipes that introduce creative ways to add flavor and variety to an all-meat diet. As with most of Maria’s cookbooks, they open this book with an in-depth introduction to the science behind carnivore diets, provide historical/anthropological context, and explain why some people might benefit from going plant-free. The book includes meal plans with grocery lists and tips for safely transitioning to the diet. I am a big fan of the Emmerichs’ other cookbooks and highly recommend this one for those interested in trying a  carnivore diet or are already enjoying the benefits of an all-meat diet.

Could a low-histamine diet be the solution to your health problems? Do you suffer from any of the following?

• Headaches/migraines
• Asthma
• Itching
• Puffy eyes
• Facial flushing
• Hives
• Pre-menstrual cramps
• Cough
• Palpitations or racing heart
• Swelling of ankles/feet
• Low blood pressure
• High blood pressure
• Insomnia
• Abdominal pain, gas, bloating, diarrhea

If so, you’re not alone. MANY people have at least one of the problems listed above but might never suspect that the culprit could be right in front of their noses—on their dinner plates! These symptoms can all be caused by a tiny but powerful natural substance called histamine.1

Anybody can have histamine intolerance, but you are at higher risk if you eat a GAPS diet or a low-carb diet, enjoy gourmet foods, or have been swept up in the current fermented foods fad. That’s because histamine is found lurking primarily in aged, fermented, cured, cultured, and smoked foods. Foods like aged beef, ripe cheeses, salami, sauerkraut, red wine, and natto can all be quite high in histamine.

Histamine intolerance symptoms tend to appear very soon after eating a high-histamine food, typically within less than two hours. Symptoms typically disappear in a matter of hours and rarely last longer than 24 hours.2 These symptoms aren’t proof positive of a histamine problem; it is also possible that you have other food sensitivities or health problems, which we’ll discuss later in this article.

This post is dedicated to the practical aspects of histamine intolerance, such as diagnosis, prevention, treatment, food choices, food handling/storage, and medications to avoid. To learn about the biology and chemistry behind this diagnosis—what histamine is, how it forms, how it behaves in our bodies and why some people are more sensitive to it than others, please see my companion post: “Histamine Intolerance: Understanding the Science.”

Histamine intolerance in a nutshell

Histamine is an important molecule used to regulate body functions, so it’s found naturally in our bodies in tiny amounts for good reason. The problem is that it is also found in aged foods. If you have healthy gut defenses, you can handle reasonable quantities of histamine in foods. However, more and more of us have compromised gastrointestinal systems and so have difficulty with even small quantities of natural food toxins like histamine. If too much histamine makes its way from foods into your bloodstream, it can cause a wide variety of unpleasant symptoms.

If you eat too much histamine or are sensitive to histamine, you can experience all kinds of annoying symptoms that most people wouldn’t think of as related to diet, including asthma, panic attacks, pre-menstrual cramps, and sleep disturbances.

My story

Histamine intolerance is much more common than most people realize. Most people who have it don’t realize it—I was one of them!

Years ago when I first turned my diet upside-down and started eating a low-carbohydrate, high-fat, mostly-meat diet, my health improved tremendously in every way. Yet there were still some frustrating symptoms that would crop up every once in a while: IBS, fatigue, insomnia, ankle swelling, itchy skin, dry cough, and environmental allergies. I couldn’t tell which foods were the culprits. Sometimes fish or beef or pork would bother me and other times it wouldn’t. Some processed meats agreed with me while others didn’t. In 2013 I started a blog series about a new ketogenic diet I was experimenting with, describing how I felt along the way. It was then that Dr. Judy Tsafrir wrote in and suggested I might have histamine intolerance. And by gum, she was right! This eureka moment was what inspired me to write these articles for you.

Who is at risk for histamine intolerance?

Histamine intolerance affects at LEAST 1% of us, but the majority of people with histamine intolerance go undiagnosed, so the actual prevalence is surely much higher. 1 Eighty percent of histamine intolerance sufferers are middle-aged, and the vast majority are female.2 Other risk factors for histamine intolerance include:3

• Gastrointestinal damage (crohn’s, celiac, intestinal surgery, chemotherapy)
• Deficiencies in vitamin B6, vitamin C, zinc, or copper
• Genetic abnormalities in DAO (diamine oxidase), the primary enzyme responsible for protecting us from histamine in foods
• Taking a medication that interferes with histamine metabolism

How much histamine can you tolerate?

Levels exceeding 2 mg/L in beverages and 50 mg/kg in foods are considered risky4 even for healthy individuals without histamine intolerance, because the human body has a limited capacity to handle histamine in foods. People with histamine intolerance tend to react to even lower levels because they are especially sensitive.

Foods high in histamine

Nearly all foods contain at least a small amount of histamine, so it’s impossible to completely avoid it. However, some foods are MUCH higher in histamine than others. Unfortunately, histamine levels in foods vary WIDELY. For example, like other animal foods, fresh tuna is very low in histamine, whereas levels in canned tuna can range anywhere from zero to as high as 40.5 mg/kg. So as you’ll notice, most histamine levels in the tables below are listed as ranges rather than absolute values.

Unless you have your own personal chemistry lab, it is simply impossible to know how much histamine is in any given food. However, there are general guidelines that can help you guess whether a food is likely to be lower or higher in histamine.

• Any high-protein food (meat, poultry, seafood) that isn’t absolutely fresh will contain rising levels of histamine. The less fresh it is, the more histamine it will contain. Examples include aged beef, leftover chicken salad stored for too long in the refrigerator, and fish that takes a long time to travel from the boat to the grocery store
• Most aged, cultured, fermented, smoked, and cured foods and even some cultured beverages
• A handful of fresh plant foods that are naturally high in histamine

Beverages

Champagne	670 mg/L
Red wine	up to 24 mg/L
Coffee	<2mg/L

Plant foods

Most (fresh) vegetables are very low in histamine, with levels ranging from 0 to 16 mg/kg. The notable exceptions are tomatoes, eggplant, and spinach:

Ketchup	22 mg/kg
Eggplant	26 mg/kg
Spinach	30 to 60 mg/kg
Avocado	23mg/kg
Sauerkraut (fermented cabbage)	up to 229 mg/kg
Miso (fermented soybeans)	3 to 6 mg/kg
Natto (fermented soybeans)	can reach over 50mg/kg

Dairy products

Uncultured dairy products such as milk and cream tend to be very low in histamine, with levels of less than 1 mg/kg. The same is true for fresh, unripened cheeses with short shelf-lives, such as fresh mozzarella and ricotta.

Sour cream	up to 7 mg/kg
Yogurt	up to 13 mg/kg
Ripened cheeses	2.21 – 2500 mg/kg (whoa…)

Meat

Most fresh meats are very low in histamine. Dry sausages such as salami, pepperoni, and chorizo, are the meat products highest in histamine content.

Dry aged sausages

up to 357 mg/kg

Fish

Certain kinds of fish are more likely to contain high amounts of histamine unless they are very fresh, because they are naturally higher in the amino acid histidine, which bacteria can turn into histamine.

Amberjack	Herring	Tuna
Anchovies	Mackerel	Pilchards
Bluefish	Mahi Mahi	Sardines
Cape Yellowtail	Marlin

Trigger foods

Some foods are suspected of triggering histamine release within some people’s bodies, even though they may not contain much histamine of their own.

Citrus fruits	Crustaceans	Spices
Peanuts	Fish	Chocolate
Additives	Strawberries	Licorice
Pineapple	Tomatoes	Egg white
Spinach	Papaya	Pork
Nuts

How is histamine intolerance diagnosed?

If you have at least two typical symptoms (listed at the top of this article) and they go away either with a low-histamine diet or with the use of antihistamine medications, then you probably have histamine intolerance. As with any food sensitivity issue, keeping a careful food-symptom diary is very important in noticing patterns. There are many possible food culprits in the world that have nothing to do with histamine intolerance, so you may discover some surprising food reactions if you pay close attention.

People who suspect they may have histamine intolerance should first be tested for true food allergies to rule those out before undergoing more specialized testing. Food allergies can cause a lot of the same symptoms that histamine intolerance can.

Other possible conditions that can mimic histamine intolerance Include:

• Non-histamine food intolerances
• Mast Cell Activation Syndrome, a condition in which histamine-producing mast cells in the immune system are too reactive1
• Mastocytosis, a rare genetic excess of mast cells

There is a variety of methods you and your doctor can use to figure out whether you might have histamine intolerance, but most available tests are imperfect. This means that even if you “test negative” for histamine intolerance, you could still have it. That’s why I believe the best approach is to eat a low-histamine diet for a few weeks to see if your symptoms go away. If they do, you’ve solved your own problem and you may decide you don’t need further proof or validation!

Serum DAO level

Activity levels of DAO—the enzyme that destroys histamine–can be measured using a blood test:

“Histamine intolerance is presumably highly likely in patients with DAO activity <3 U/mL, likely (but less likely) in patients with DAO activity <10 U/mL, and improbable in patients with DAO activity >10 U/mL.”2

However, this method is considered fairly unreliable, because blood levels of DAO are so unstable. Even if your DAO blood test comes back normal, there is still a 50% chance that you have histamine intolerance (false-negative). If your DAO blood test comes back abnormal, there is a 17% chance that you DON’T have histamine intolerance (false-positive).

Oral histamine challenge

Many physicians consider this test to be the gold standard for diagnosis of histamine intolerance. It involves following a strict low-histamine diet for four weeks, and then undergoing a “histamine challenge” in which you are asked to swallow capsules filled with pure histamine (typically a 75 mg dose) while a clinician monitors your medical reaction for signs and symptoms of histamine intolerance. Unfortunately, this test can also be misleading, because there are many people with histamine intolerance who do not react to pure histamine and pass this test with flying colors. They look and feel perfectly fine.

Why would that be? If you are sensitive to histamine, and someone gives you pure histamine, shouldn’t you have a bad reaction?

Here’s the thing: pure histamine does not exist in nature. In real life, histamine exists in foods, some of which can affect the way we respond to histamine. To make matters more complicated, histamine is always accompanied by related substances (other biogenic amines) in aged foods that magnify our reaction to histamine. There are also many other factors that can influence how you respond to histamine from one day to the next [see section below entitled confounding factors].

In addition, oral challenge tests are expensive and time-consuming, so they may not be offered by your doctor’s office and/or may not be covered by your medical insurance plan.

Intestinal biopsy

DAO levels in the cells lining the gut can be measured directly if you undergo an endoscopy and have small samples of your intestinal cells biopsied for laboratory testing. This test is the real gold standard, because most cases of histamine intolerance are thought to be due to reduced levels of DAO in the cells lining the gastrointestinal tract.3 Naturally, the biopsy test is rarely performed, because:

• it is an invasive surgical procedure
• it is expensive
• it is highly unlikely that your insurance would cover it

Histamine skin-prick test

This is probably the best test available because it’s inexpensive, simpler, and more accurate than other readily available office tests.

In this test, your skin is punctured with histamine. If you develop a “wheal” (bump) on your skin that is still visible 50 minutes later, it is likely that you have histamine intolerance. Whether you test positive or negative for histamine intolerance by skin testing, there is about a 20% chance that the test result is wrong.4

Beyond histamine

Unfortunately, symptoms of histamine intolerance are not simply about how much histamine is in the foods we eat. There are many other things that influence how we respond to histamine in foods, which can make things quite confusing for patients and doctors alike. Below are common reasons why we might have different reactions to the same food on different days.

• Some medications interfere with DAO activity, including NSAIDS such as Ibuprofen5
• Estrogen stimulates histamine production6
• Stress and physical injury trigger immune cells to release histamine and other pro-inflammatory substances7
• Alcohol interferes with DAO activity, which can increase our exposure to histamine8
• Histamine is always accompanied by a posse of other “biogenic amines” which can worsen our response to histamine depending on which ones are present and how high the levels of each of them are.9

Is histamine intolerance real?

Although the concept of histamine intolerance is gaining ground, there is considerable controversy around this diagnosis, and many scientists and physicians still think of histamine intolerance as only weakly grounded in scientific evidence or perhaps even psychosomatic in nature. It is easy for doctors to be skeptical:

• Tests for histamine intolerance are often inaccurate
• A person’s reaction to high-histamine foods can vary from day to day
• Some doctors may not understand the complexity of the science behind histamine intolerance

My philosophy is this: if you notice that foods high in histamine bother you, you don’t need a scientist or a doctor to prove you right.

Food handling and storage tips to minimize histamine exposure

Of course, simple, natural, preventive measures are usually the wisest course of action. Understanding how histamine forms in foods can help you to minimize your exposure not just to histamine, but to all potentially irritating and/or toxic biogenic amines.

Once histamine is in a food, there’s no getting rid of it; it is not destroyed by cooking, freezing, hot smoking, or canning.

Histamine is indestructible. Once histamine develops in a food, there’s no getting rid of it. And if bacteria or yeast are still present in the food, histamine levels will only continue to rise. So here’s what you need to know:1

• Immediate storage of meats and fish on ice dramatically reduces the rate of histamine formation (but does not stop it completely). If you can bring a cooler with some ice in it to your grocery store, you can keep histamine levels from rising in your warm car on the way home.
• HDC (histidine decarboxylase) is the enzyme that bacteria and yeast use to create histamine from proteins in our foods. HDC can remain in foods even after the bacteria (or yeast) that produced that enzyme have died off. Therefore, HDC can remain active, turning proteins into histamine, long after the micro-organisms are dead and gone, leading to continued accumulation of histamine. Fortunately, HDC can be inactivated by freezing for 1-2 weeks, and is destroyed by cooking.
• Histamine itself is NOT destroyed by cooking, freezing, hot smoking, or canning. Therefore, once it has been produced, you are stuck with it.
• Histamine itself has no flavor and is odorless, so you can’t use the “smell test” to detect its presence.

Treatment of histamine intolerance

If you suspect you have histamine intolerance, here are some options which may help you to feel better:

1. Eat a low-histamine diet. Avoid cultured, processed, cured, fermented and aged foods. Choose fresh foods whenever possible. Look for the “packed on” date of the meat or fish being sold. “FAS” (frozen-at-sea) fish may be your best bet. Grass-fed and pastured meats are not necessarily better choices—it depends on how far they had to travel to get to your store. Also, it is important to know that nearly all beef sold in the U.S. “hangs” for at least two weeks before it is packaged, even if it comes from a local family farm that pastures their animals. Therefore virtually all beef is aged to some extent. Yasmina Ykelenstam’s website contains a wealth of information about low-histamine diets: http://thelowhistaminechef.com/
2. Occasional use of antihistamines such as Diphenhydramine (Benadryl) and Cetirizine (Zyrtec), or “mast cell stabilizers” such as Cromolyn Sodium (Gastrocrom) may be helpful if they don’t bother you.
3. Vitamin C, vitamin B6, zinc, and copper are all required for DAO to work properly. Addressing potential deficiencies in these may be helpful in resolving histamine intolerance.

4. DAO supplements are available and have been proven effective.1 The one I use is from Seeking Health. This supplement contains DAO enzymes isolated from pig kidney. It also contains a small amount of vitamin C, which helps DAO to work better. While I generally try to avoid high-histamine foods, life happens. When I’m traveling, eating at someone else’s home, or not sure about the histamine content of a food, I use this supplement to help minimize symptoms of histamine intolerance from foods I suspect may bother me. It needs to be taken right before you eat—no longer than 15 minutes– so that it will be in the right place at the right time—in your small intestine when the suspicious food arrives.

5. Some people, especially those with prominent gastrointestinal symptoms of histamine intolerance may benefit from pancreatic enzymes.1
6. Avoid alcohol—alcohol reduces DAO activity.
7. Be aware of medications that interfere with DAO activity. If you take any of the following medicines, discuss with your clinician how they may be affecting your histamine intolerance symptoms, to see if alternatives are available.2

Bottom line?

Eat fresh (and I don’t mean at Subway . . . )

Hungry for more histamine knowledge?

Please see my companion post: “Histamine Intolerance: Understanding the Science” which explores the fascinating world of biogenic amines, how histamine forms inside and outside of our bodies, how and why histamine affects our physical and mental health, why some people, especially women, are more sensitive to histamine than others, and why reactions to high-histamine foods can be so unpredictable and confusing.

To learn about the connection between food sensitivities and anxiety or insomnia, including the possibility that histamine is keeping you up at night or causing panic attacks, I recommend reading my Psychology Today article “5 Foods Proven to Cause Anxiety and Insomnia.”

You can also listen to my podcast interview with Yasmina Ykelenstam, the Low Histamine Chef, about the connection between histamine intolerance and mental health.

Could a low-histamine diet be the solution to your health problems? Do you suffer from any of the following?

• Headaches/migraines
• Asthma
• Itching
• Puffy eyes
• Facial flushing
• Hives
• Pre-menstrual cramps
• Cough
• Palpitations or racing heart
• Swelling of ankles/feet
• Low blood pressure
• High blood pressure
• Insomnia
• Abdominal pain, gas, bloating, diarrhea

If so, you’re not alone. MANY people have at least one of the problems listed above but might never suspect that the culprit could be right in front of their noses—on their dinner plates! These symptoms can all be caused by a tiny but powerful natural substance called histamine.1

Anybody can have histamine intolerance, but you are at higher risk if you eat a GAPS diet or a low-carb diet, enjoy gourmet foods, or have been swept up in the current fermented foods fad. That’s because histamine is found lurking primarily in aged, fermented, cured, cultured, and smoked foods. Foods like aged beef, ripe cheeses, salami, sauerkraut, red wine, and natto can all be quite high in histamine.

Histamine intolerance symptoms tend to appear very soon after eating a high-histamine food, typically within less than two hours. Symptoms typically disappear in a matter of hours and rarely last longer than 24 hours.2 These symptoms aren’t proof positive of a histamine problem; it is also possible that you have other food sensitivities or health problems, which we’ll discuss later in this article.

This post is dedicated to the practical aspects of histamine intolerance, such as diagnosis, prevention, treatment, food choices, food handling/storage, and medications to avoid. To learn about the biology and chemistry behind this diagnosis—what histamine is, how it forms, how it behaves in our bodies and why some people are more sensitive to it than others, please see my companion post: “Histamine Intolerance: Understanding the Science.”

Histamine intolerance in a nutshell

Histamine is an important molecule used to regulate body functions, so it’s found naturally in our bodies in tiny amounts for good reason. The problem is that it is also found in aged foods. If you have healthy gut defenses, you can handle reasonable quantities of histamine in foods. However, more and more of us have compromised gastrointestinal systems and so have difficulty with even small quantities of natural food toxins like histamine. If too much histamine makes its way from foods into your bloodstream, it can cause a wide variety of unpleasant symptoms.

If you eat too much histamine or are sensitive to histamine, you can experience all kinds of annoying symptoms that most people wouldn’t think of as related to diet, including asthma, panic attacks, pre-menstrual cramps, and sleep disturbances.

My story

Histamine intolerance is much more common than most people realize. Most people who have it don’t realize it—I was one of them!

Years ago when I first turned my diet upside-down and started eating a low-carbohydrate, high-fat, mostly-meat diet, my health improved tremendously in every way. Yet there were still some frustrating symptoms that would crop up every once in a while: IBS, fatigue, insomnia, ankle swelling, itchy skin, dry cough, and environmental allergies. I couldn’t tell which foods were the culprits. Sometimes fish or beef or pork would bother me and other times it wouldn’t. Some processed meats agreed with me while others didn’t. In 2013 I started a blog series about a new ketogenic diet I was experimenting with, describing how I felt along the way. It was then that Dr. Judy Tsafrir wrote in and suggested I might have histamine intolerance. And by gum, she was right! This eureka moment was what inspired me to write these articles for you.

Who is at risk for histamine intolerance?

Histamine intolerance affects at LEAST 1% of us, but the majority of people with histamine intolerance go undiagnosed, so the actual prevalence is surely much higher. 1 Eighty percent of histamine intolerance sufferers are middle-aged, and the vast majority are female.2 Other risk factors for histamine intolerance include:3

• Gastrointestinal damage (crohn’s, celiac, intestinal surgery, chemotherapy)
• Deficiencies in vitamin B6, vitamin C, zinc, or copper
• Genetic abnormalities in DAO (diamine oxidase), the primary enzyme responsible for protecting us from histamine in foods
• Taking a medication that interferes with histamine metabolism

How much histamine can you tolerate?

Levels exceeding 2 mg/L in beverages and 50 mg/kg in foods are considered risky4 even for healthy individuals without histamine intolerance, because the human body has a limited capacity to handle histamine in foods. People with histamine intolerance tend to react to even lower levels because they are especially sensitive.

Foods high in histamine

Nearly all foods contain at least a small amount of histamine, so it’s impossible to completely avoid it. However, some foods are MUCH higher in histamine than others. Unfortunately, histamine levels in foods vary WIDELY. For example, like other animal foods, fresh tuna is very low in histamine, whereas levels in canned tuna can range anywhere from zero to as high as 40.5 mg/kg. So as you’ll notice, most histamine levels in the tables below are listed as ranges rather than absolute values.

Unless you have your own personal chemistry lab, it is simply impossible to know how much histamine is in any given food. However, there are general guidelines that can help you guess whether a food is likely to be lower or higher in histamine.

• Any high-protein food (meat, poultry, seafood) that isn’t absolutely fresh will contain rising levels of histamine. The less fresh it is, the more histamine it will contain. Examples include aged beef, leftover chicken salad stored for too long in the refrigerator, and fish that takes a long time to travel from the boat to the grocery store
• Most aged, cultured, fermented, smoked, and cured foods and even some cultured beverages
• A handful of fresh plant foods that are naturally high in histamine

Beverages

Champagne	670 mg/L
Red wine	up to 24 mg/L
Coffee	<2mg/L

Plant foods

Most (fresh) vegetables are very low in histamine, with levels ranging from 0 to 16 mg/kg. The notable exceptions are tomatoes, eggplant, and spinach:

Ketchup	22 mg/kg
Eggplant	26 mg/kg
Spinach	30 to 60 mg/kg
Avocado	23mg/kg
Sauerkraut (fermented cabbage)	up to 229 mg/kg
Miso (fermented soybeans)	3 to 6 mg/kg
Natto (fermented soybeans)	can reach over 50mg/kg

Dairy products

Uncultured dairy products such as milk and cream tend to be very low in histamine, with levels of less than 1 mg/kg. The same is true for fresh, unripened cheeses with short shelf-lives, such as fresh mozzarella and ricotta.

Sour cream	up to 7 mg/kg
Yogurt	up to 13 mg/kg
Ripened cheeses	2.21 – 2500 mg/kg (whoa…)

Meat

Most fresh meats are very low in histamine. Dry sausages such as salami, pepperoni, and chorizo, are the meat products highest in histamine content.

Dry aged sausages

up to 357 mg/kg

Fish

Certain kinds of fish are more likely to contain high amounts of histamine unless they are very fresh, because they are naturally higher in the amino acid histidine, which bacteria can turn into histamine.

Amberjack	Herring	Tuna
Anchovies	Mackerel	Pilchards
Bluefish	Mahi Mahi	Sardines
Cape Yellowtail	Marlin

Trigger foods

Some foods are suspected of triggering histamine release within some people’s bodies, even though they may not contain much histamine of their own.

Citrus fruits	Crustaceans	Spices
Peanuts	Fish	Chocolate
Additives	Strawberries	Licorice
Pineapple	Tomatoes	Egg white
Spinach	Papaya	Pork
Nuts

How is histamine intolerance diagnosed?

If you have at least two typical symptoms (listed at the top of this article) and they go away either with a low-histamine diet or with the use of antihistamine medications, then you probably have histamine intolerance. As with any food sensitivity issue, keeping a careful food-symptom diary is very important in noticing patterns. There are many possible food culprits in the world that have nothing to do with histamine intolerance, so you may discover some surprising food reactions if you pay close attention.

People who suspect they may have histamine intolerance should first be tested for true food allergies to rule those out before undergoing more specialized testing. Food allergies can cause a lot of the same symptoms that histamine intolerance can.

Other possible conditions that can mimic histamine intolerance Include:

• Non-histamine food intolerances
• Mast Cell Activation Syndrome, a condition in which histamine-producing mast cells in the immune system are too reactive1
• Mastocytosis, a rare genetic excess of mast cells

There is a variety of methods you and your doctor can use to figure out whether you might have histamine intolerance, but most available tests are imperfect. This means that even if you “test negative” for histamine intolerance, you could still have it. That’s why I believe the best approach is to eat a low-histamine diet for a few weeks to see if your symptoms go away. If they do, you’ve solved your own problem and you may decide you don’t need further proof or validation!

Serum DAO level

Activity levels of DAO—the enzyme that destroys histamine–can be measured using a blood test:

“Histamine intolerance is presumably highly likely in patients with DAO activity <3 U/mL, likely (but less likely) in patients with DAO activity <10 U/mL, and improbable in patients with DAO activity >10 U/mL.”2

However, this method is considered fairly unreliable, because blood levels of DAO are so unstable. Even if your DAO blood test comes back normal, there is still a 50% chance that you have histamine intolerance (false-negative). If your DAO blood test comes back abnormal, there is a 17% chance that you DON’T have histamine intolerance (false-positive).

Oral histamine challenge

Many physicians consider this test to be the gold standard for diagnosis of histamine intolerance. It involves following a strict low-histamine diet for four weeks, and then undergoing a “histamine challenge” in which you are asked to swallow capsules filled with pure histamine (typically a 75 mg dose) while a clinician monitors your medical reaction for signs and symptoms of histamine intolerance. Unfortunately, this test can also be misleading, because there are many people with histamine intolerance who do not react to pure histamine and pass this test with flying colors. They look and feel perfectly fine.

Why would that be? If you are sensitive to histamine, and someone gives you pure histamine, shouldn’t you have a bad reaction?

Here’s the thing: pure histamine does not exist in nature. In real life, histamine exists in foods, some of which can affect the way we respond to histamine. To make matters more complicated, histamine is always accompanied by related substances (other biogenic amines) in aged foods that magnify our reaction to histamine. There are also many other factors that can influence how you respond to histamine from one day to the next [see section below entitled confounding factors].

In addition, oral challenge tests are expensive and time-consuming, so they may not be offered by your doctor’s office and/or may not be covered by your medical insurance plan.

Intestinal biopsy

DAO levels in the cells lining the gut can be measured directly if you undergo an endoscopy and have small samples of your intestinal cells biopsied for laboratory testing. This test is the real gold standard, because most cases of histamine intolerance are thought to be due to reduced levels of DAO in the cells lining the gastrointestinal tract.3 Naturally, the biopsy test is rarely performed, because:

• it is an invasive surgical procedure
• it is expensive
• it is highly unlikely that your insurance would cover it

Histamine skin-prick test

This is probably the best test available because it’s inexpensive, simpler, and more accurate than other readily available office tests.

In this test, your skin is punctured with histamine. If you develop a “wheal” (bump) on your skin that is still visible 50 minutes later, it is likely that you have histamine intolerance. Whether you test positive or negative for histamine intolerance by skin testing, there is about a 20% chance that the test result is wrong.4

Beyond histamine

Unfortunately, symptoms of histamine intolerance are not simply about how much histamine is in the foods we eat. There are many other things that influence how we respond to histamine in foods, which can make things quite confusing for patients and doctors alike. Below are common reasons why we might have different reactions to the same food on different days.

• Some medications interfere with DAO activity, including NSAIDS such as Ibuprofen5
• Estrogen stimulates histamine production6
• Stress and physical injury trigger immune cells to release histamine and other pro-inflammatory substances7
• Alcohol interferes with DAO activity, which can increase our exposure to histamine8
• Histamine is always accompanied by a posse of other “biogenic amines” which can worsen our response to histamine depending on which ones are present and how high the levels of each of them are.9

Is histamine intolerance real?

Although the concept of histamine intolerance is gaining ground, there is considerable controversy around this diagnosis, and many scientists and physicians still think of histamine intolerance as only weakly grounded in scientific evidence or perhaps even psychosomatic in nature. It is easy for doctors to be skeptical:

• Tests for histamine intolerance are often inaccurate
• A person’s reaction to high-histamine foods can vary from day to day
• Some doctors may not understand the complexity of the science behind histamine intolerance

My philosophy is this: if you notice that foods high in histamine bother you, you don’t need a scientist or a doctor to prove you right.

Food handling and storage tips to minimize histamine exposure

Of course, simple, natural, preventive measures are usually the wisest course of action. Understanding how histamine forms in foods can help you to minimize your exposure not just to histamine, but to all potentially irritating and/or toxic biogenic amines.

Once histamine is in a food, there’s no getting rid of it; it is not destroyed by cooking, freezing, hot smoking, or canning.

Histamine is indestructible. Once histamine develops in a food, there’s no getting rid of it. And if bacteria or yeast are still present in the food, histamine levels will only continue to rise. So here’s what you need to know:1

• Immediate storage of meats and fish on ice dramatically reduces the rate of histamine formation (but does not stop it completely). If you can bring a cooler with some ice in it to your grocery store, you can keep histamine levels from rising in your warm car on the way home.
• HDC (histidine decarboxylase) is the enzyme that bacteria and yeast use to create histamine from proteins in our foods. HDC can remain in foods even after the bacteria (or yeast) that produced that enzyme have died off. Therefore, HDC can remain active, turning proteins into histamine, long after the micro-organisms are dead and gone, leading to continued accumulation of histamine. Fortunately, HDC can be inactivated by freezing for 1-2 weeks, and is destroyed by cooking.
• Histamine itself is NOT destroyed by cooking, freezing, hot smoking, or canning. Therefore, once it has been produced, you are stuck with it.
• Histamine itself has no flavor and is odorless, so you can’t use the “smell test” to detect its presence.

Treatment of histamine intolerance

If you suspect you have histamine intolerance, here are some options which may help you to feel better:

1. Eat a low-histamine diet. Avoid cultured, processed, cured, fermented and aged foods. Choose fresh foods whenever possible. Look for the “packed on” date of the meat or fish being sold. “FAS” (frozen-at-sea) fish may be your best bet. Grass-fed and pastured meats are not necessarily better choices—it depends on how far they had to travel to get to your store. Also, it is important to know that nearly all beef sold in the U.S. “hangs” for at least two weeks before it is packaged, even if it comes from a local family farm that pastures their animals. Therefore virtually all beef is aged to some extent. Yasmina Ykelenstam’s website contains a wealth of information about low-histamine diets: http://thelowhistaminechef.com/
2. Occasional use of antihistamines such as Diphenhydramine (Benadryl) and Cetirizine (Zyrtec), or “mast cell stabilizers” such as Cromolyn Sodium (Gastrocrom) may be helpful if they don’t bother you.
3. Vitamin C, vitamin B6, zinc, and copper are all required for DAO to work properly. Addressing potential deficiencies in these may be helpful in resolving histamine intolerance.

4. DAO supplements are available and have been proven effective.1 The one I use is from Seeking Health. This supplement contains DAO enzymes isolated from pig kidney. It also contains a small amount of vitamin C, which helps DAO to work better. While I generally try to avoid high-histamine foods, life happens. When I’m traveling, eating at someone else’s home, or not sure about the histamine content of a food, I use this supplement to help minimize symptoms of histamine intolerance from foods I suspect may bother me. It needs to be taken right before you eat—no longer than 15 minutes– so that it will be in the right place at the right time—in your small intestine when the suspicious food arrives.

5. Some people, especially those with prominent gastrointestinal symptoms of histamine intolerance may benefit from pancreatic enzymes.1
6. Avoid alcohol—alcohol reduces DAO activity.
7. Be aware of medications that interfere with DAO activity. If you take any of the following medicines, discuss with your clinician how they may be affecting your histamine intolerance symptoms, to see if alternatives are available.2

Bottom line?

Eat fresh (and I don’t mean at Subway . . . )

Hungry for more histamine knowledge?

Please see my companion post: “Histamine Intolerance: Understanding the Science” which explores the fascinating world of biogenic amines, how histamine forms inside and outside of our bodies, how and why histamine affects our physical and mental health, why some people, especially women, are more sensitive to histamine than others, and why reactions to high-histamine foods can be so unpredictable and confusing.

To learn about the connection between food sensitivities and anxiety or insomnia, including the possibility that histamine is keeping you up at night or causing panic attacks, I recommend reading my Psychology Today article “5 Foods Proven to Cause Anxiety and Insomnia.”

You can also listen to my podcast interview with Yasmina Ykelenstam, the Low Histamine Chef, about the connection between histamine intolerance and mental health.

Could a low-histamine diet be the solution to your health problems? Do you suffer from any of the following?

• Headaches/migraines
• Asthma
• Itching
• Puffy eyes
• Facial flushing
• Hives
• Pre-menstrual cramps
• Cough
• Palpitations or racing heart
• Swelling of ankles/feet
• Low blood pressure
• High blood pressure
• Insomnia
• Abdominal pain, gas, bloating, diarrhea

If so, you’re not alone. MANY people have at least one of the problems listed above but might never suspect that the culprit could be right in front of their noses—on their dinner plates! These symptoms can all be caused by a tiny but powerful natural substance called histamine.1

Anybody can have histamine intolerance, but you are at higher risk if you eat a GAPS diet or a low-carb diet, enjoy gourmet foods, or have been swept up in the current fermented foods fad. That’s because histamine is found lurking primarily in aged, fermented, cured, cultured, and smoked foods. Foods like aged beef, ripe cheeses, salami, sauerkraut, red wine, and natto can all be quite high in histamine.

Histamine intolerance symptoms tend to appear very soon after eating a high-histamine food, typically within less than two hours. Symptoms typically disappear in a matter of hours and rarely last longer than 24 hours.2 These symptoms aren’t proof positive of a histamine problem; it is also possible that you have other food sensitivities or health problems, which we’ll discuss later in this article.

This post is dedicated to the practical aspects of histamine intolerance, such as diagnosis, prevention, treatment, food choices, food handling/storage, and medications to avoid. To learn about the biology and chemistry behind this diagnosis—what histamine is, how it forms, how it behaves in our bodies and why some people are more sensitive to it than others, please see my companion post: “Histamine Intolerance: Understanding the Science.”

Histamine intolerance in a nutshell

Histamine is an important molecule used to regulate body functions, so it’s found naturally in our bodies in tiny amounts for good reason. The problem is that it is also found in aged foods. If you have healthy gut defenses, you can handle reasonable quantities of histamine in foods. However, more and more of us have compromised gastrointestinal systems and so have difficulty with even small quantities of natural food toxins like histamine. If too much histamine makes its way from foods into your bloodstream, it can cause a wide variety of unpleasant symptoms.

If you eat too much histamine or are sensitive to histamine, you can experience all kinds of annoying symptoms that most people wouldn’t think of as related to diet, including asthma, panic attacks, pre-menstrual cramps, and sleep disturbances.

My story

Histamine intolerance is much more common than most people realize. Most people who have it don’t realize it—I was one of them!

Years ago when I first turned my diet upside-down and started eating a low-carbohydrate, high-fat, mostly-meat diet, my health improved tremendously in every way. Yet there were still some frustrating symptoms that would crop up every once in a while: IBS, fatigue, insomnia, ankle swelling, itchy skin, dry cough, and environmental allergies. I couldn’t tell which foods were the culprits. Sometimes fish or beef or pork would bother me and other times it wouldn’t. Some processed meats agreed with me while others didn’t. In 2013 I started a blog series about a new ketogenic diet I was experimenting with, describing how I felt along the way. It was then that Dr. Judy Tsafrir wrote in and suggested I might have histamine intolerance. And by gum, she was right! This eureka moment was what inspired me to write these articles for you.

Who is at risk for histamine intolerance?

Histamine intolerance affects at LEAST 1% of us, but the majority of people with histamine intolerance go undiagnosed, so the actual prevalence is surely much higher. 1 Eighty percent of histamine intolerance sufferers are middle-aged, and the vast majority are female.2 Other risk factors for histamine intolerance include:3

• Gastrointestinal damage (crohn’s, celiac, intestinal surgery, chemotherapy)
• Deficiencies in vitamin B6, vitamin C, zinc, or copper
• Genetic abnormalities in DAO (diamine oxidase), the primary enzyme responsible for protecting us from histamine in foods
• Taking a medication that interferes with histamine metabolism

How much histamine can you tolerate?

Levels exceeding 2 mg/L in beverages and 50 mg/kg in foods are considered risky4 even for healthy individuals without histamine intolerance, because the human body has a limited capacity to handle histamine in foods. People with histamine intolerance tend to react to even lower levels because they are especially sensitive.

Foods high in histamine

Nearly all foods contain at least a small amount of histamine, so it’s impossible to completely avoid it. However, some foods are MUCH higher in histamine than others. Unfortunately, histamine levels in foods vary WIDELY. For example, like other animal foods, fresh tuna is very low in histamine, whereas levels in canned tuna can range anywhere from zero to as high as 40.5 mg/kg. So as you’ll notice, most histamine levels in the tables below are listed as ranges rather than absolute values.

Unless you have your own personal chemistry lab, it is simply impossible to know how much histamine is in any given food. However, there are general guidelines that can help you guess whether a food is likely to be lower or higher in histamine.

• Any high-protein food (meat, poultry, seafood) that isn’t absolutely fresh will contain rising levels of histamine. The less fresh it is, the more histamine it will contain. Examples include aged beef, leftover chicken salad stored for too long in the refrigerator, and fish that takes a long time to travel from the boat to the grocery store
• Most aged, cultured, fermented, smoked, and cured foods and even some cultured beverages
• A handful of fresh plant foods that are naturally high in histamine

Beverages

Champagne	670 mg/L
Red wine	up to 24 mg/L
Coffee	<2mg/L

Plant foods

Most (fresh) vegetables are very low in histamine, with levels ranging from 0 to 16 mg/kg. The notable exceptions are tomatoes, eggplant, and spinach:

Ketchup	22 mg/kg
Eggplant	26 mg/kg
Spinach	30 to 60 mg/kg
Avocado	23mg/kg
Sauerkraut (fermented cabbage)	up to 229 mg/kg
Miso (fermented soybeans)	3 to 6 mg/kg
Natto (fermented soybeans)	can reach over 50mg/kg

Dairy products

Uncultured dairy products such as milk and cream tend to be very low in histamine, with levels of less than 1 mg/kg. The same is true for fresh, unripened cheeses with short shelf-lives, such as fresh mozzarella and ricotta.

Sour cream	up to 7 mg/kg
Yogurt	up to 13 mg/kg
Ripened cheeses	2.21 – 2500 mg/kg (whoa…)

Meat

Most fresh meats are very low in histamine. Dry sausages such as salami, pepperoni, and chorizo, are the meat products highest in histamine content.

Dry aged sausages

up to 357 mg/kg

Fish

Certain kinds of fish are more likely to contain high amounts of histamine unless they are very fresh, because they are naturally higher in the amino acid histidine, which bacteria can turn into histamine.

Amberjack	Herring	Tuna
Anchovies	Mackerel	Pilchards
Bluefish	Mahi Mahi	Sardines
Cape Yellowtail	Marlin

Trigger foods

Some foods are suspected of triggering histamine release within some people’s bodies, even though they may not contain much histamine of their own.

Citrus fruits	Crustaceans	Spices
Peanuts	Fish	Chocolate
Additives	Strawberries	Licorice
Pineapple	Tomatoes	Egg white
Spinach	Papaya	Pork
Nuts

How is histamine intolerance diagnosed?

If you have at least two typical symptoms (listed at the top of this article) and they go away either with a low-histamine diet or with the use of antihistamine medications, then you probably have histamine intolerance. As with any food sensitivity issue, keeping a careful food-symptom diary is very important in noticing patterns. There are many possible food culprits in the world that have nothing to do with histamine intolerance, so you may discover some surprising food reactions if you pay close attention.

People who suspect they may have histamine intolerance should first be tested for true food allergies to rule those out before undergoing more specialized testing. Food allergies can cause a lot of the same symptoms that histamine intolerance can.

Other possible conditions that can mimic histamine intolerance Include:

• Non-histamine food intolerances
• Mast Cell Activation Syndrome, a condition in which histamine-producing mast cells in the immune system are too reactive1
• Mastocytosis, a rare genetic excess of mast cells

There is a variety of methods you and your doctor can use to figure out whether you might have histamine intolerance, but most available tests are imperfect. This means that even if you “test negative” for histamine intolerance, you could still have it. That’s why I believe the best approach is to eat a low-histamine diet for a few weeks to see if your symptoms go away. If they do, you’ve solved your own problem and you may decide you don’t need further proof or validation!

Serum DAO level

Activity levels of DAO—the enzyme that destroys histamine–can be measured using a blood test:

“Histamine intolerance is presumably highly likely in patients with DAO activity <3 U/mL, likely (but less likely) in patients with DAO activity <10 U/mL, and improbable in patients with DAO activity >10 U/mL.”2

However, this method is considered fairly unreliable, because blood levels of DAO are so unstable. Even if your DAO blood test comes back normal, there is still a 50% chance that you have histamine intolerance (false-negative). If your DAO blood test comes back abnormal, there is a 17% chance that you DON’T have histamine intolerance (false-positive).

Oral histamine challenge

Many physicians consider this test to be the gold standard for diagnosis of histamine intolerance. It involves following a strict low-histamine diet for four weeks, and then undergoing a “histamine challenge” in which you are asked to swallow capsules filled with pure histamine (typically a 75 mg dose) while a clinician monitors your medical reaction for signs and symptoms of histamine intolerance. Unfortunately, this test can also be misleading, because there are many people with histamine intolerance who do not react to pure histamine and pass this test with flying colors. They look and feel perfectly fine.

Why would that be? If you are sensitive to histamine, and someone gives you pure histamine, shouldn’t you have a bad reaction?

Here’s the thing: pure histamine does not exist in nature. In real life, histamine exists in foods, some of which can affect the way we respond to histamine. To make matters more complicated, histamine is always accompanied by related substances (other biogenic amines) in aged foods that magnify our reaction to histamine. There are also many other factors that can influence how you respond to histamine from one day to the next [see section below entitled confounding factors].

In addition, oral challenge tests are expensive and time-consuming, so they may not be offered by your doctor’s office and/or may not be covered by your medical insurance plan.

Intestinal biopsy

DAO levels in the cells lining the gut can be measured directly if you undergo an endoscopy and have small samples of your intestinal cells biopsied for laboratory testing. This test is the real gold standard, because most cases of histamine intolerance are thought to be due to reduced levels of DAO in the cells lining the gastrointestinal tract.3 Naturally, the biopsy test is rarely performed, because:

• it is an invasive surgical procedure
• it is expensive
• it is highly unlikely that your insurance would cover it

Histamine skin-prick test

This is probably the best test available because it’s inexpensive, simpler, and more accurate than other readily available office tests.

In this test, your skin is punctured with histamine. If you develop a “wheal” (bump) on your skin that is still visible 50 minutes later, it is likely that you have histamine intolerance. Whether you test positive or negative for histamine intolerance by skin testing, there is about a 20% chance that the test result is wrong.4

Beyond histamine

Unfortunately, symptoms of histamine intolerance are not simply about how much histamine is in the foods we eat. There are many other things that influence how we respond to histamine in foods, which can make things quite confusing for patients and doctors alike. Below are common reasons why we might have different reactions to the same food on different days.

• Some medications interfere with DAO activity, including NSAIDS such as Ibuprofen5
• Estrogen stimulates histamine production6
• Stress and physical injury trigger immune cells to release histamine and other pro-inflammatory substances7
• Alcohol interferes with DAO activity, which can increase our exposure to histamine8
• Histamine is always accompanied by a posse of other “biogenic amines” which can worsen our response to histamine depending on which ones are present and how high the levels of each of them are.9

Is histamine intolerance real?

Although the concept of histamine intolerance is gaining ground, there is considerable controversy around this diagnosis, and many scientists and physicians still think of histamine intolerance as only weakly grounded in scientific evidence or perhaps even psychosomatic in nature. It is easy for doctors to be skeptical:

• Tests for histamine intolerance are often inaccurate
• A person’s reaction to high-histamine foods can vary from day to day
• Some doctors may not understand the complexity of the science behind histamine intolerance

My philosophy is this: if you notice that foods high in histamine bother you, you don’t need a scientist or a doctor to prove you right.

Food handling and storage tips to minimize histamine exposure

Of course, simple, natural, preventive measures are usually the wisest course of action. Understanding how histamine forms in foods can help you to minimize your exposure not just to histamine, but to all potentially irritating and/or toxic biogenic amines.

Once histamine is in a food, there’s no getting rid of it; it is not destroyed by cooking, freezing, hot smoking, or canning.

Histamine is indestructible. Once histamine develops in a food, there’s no getting rid of it. And if bacteria or yeast are still present in the food, histamine levels will only continue to rise. So here’s what you need to know:1

• Immediate storage of meats and fish on ice dramatically reduces the rate of histamine formation (but does not stop it completely). If you can bring a cooler with some ice in it to your grocery store, you can keep histamine levels from rising in your warm car on the way home.
• HDC (histidine decarboxylase) is the enzyme that bacteria and yeast use to create histamine from proteins in our foods. HDC can remain in foods even after the bacteria (or yeast) that produced that enzyme have died off. Therefore, HDC can remain active, turning proteins into histamine, long after the micro-organisms are dead and gone, leading to continued accumulation of histamine. Fortunately, HDC can be inactivated by freezing for 1-2 weeks, and is destroyed by cooking.
• Histamine itself is NOT destroyed by cooking, freezing, hot smoking, or canning. Therefore, once it has been produced, you are stuck with it.
• Histamine itself has no flavor and is odorless, so you can’t use the “smell test” to detect its presence.

Treatment of histamine intolerance

If you suspect you have histamine intolerance, here are some options which may help you to feel better:

1. Eat a low-histamine diet. Avoid cultured, processed, cured, fermented and aged foods. Choose fresh foods whenever possible. Look for the “packed on” date of the meat or fish being sold. “FAS” (frozen-at-sea) fish may be your best bet. Grass-fed and pastured meats are not necessarily better choices—it depends on how far they had to travel to get to your store. Also, it is important to know that nearly all beef sold in the U.S. “hangs” for at least two weeks before it is packaged, even if it comes from a local family farm that pastures their animals. Therefore virtually all beef is aged to some extent. Yasmina Ykelenstam’s website contains a wealth of information about low-histamine diets: http://thelowhistaminechef.com/
2. Occasional use of antihistamines such as Diphenhydramine (Benadryl) and Cetirizine (Zyrtec), or “mast cell stabilizers” such as Cromolyn Sodium (Gastrocrom) may be helpful if they don’t bother you.
3. Vitamin C, vitamin B6, zinc, and copper are all required for DAO to work properly. Addressing potential deficiencies in these may be helpful in resolving histamine intolerance.

4. DAO supplements are available and have been proven effective.1 The one I use is from Seeking Health. This supplement contains DAO enzymes isolated from pig kidney. It also contains a small amount of vitamin C, which helps DAO to work better. While I generally try to avoid high-histamine foods, life happens. When I’m traveling, eating at someone else’s home, or not sure about the histamine content of a food, I use this supplement to help minimize symptoms of histamine intolerance from foods I suspect may bother me. It needs to be taken right before you eat—no longer than 15 minutes– so that it will be in the right place at the right time—in your small intestine when the suspicious food arrives.

5. Some people, especially those with prominent gastrointestinal symptoms of histamine intolerance may benefit from pancreatic enzymes.1
6. Avoid alcohol—alcohol reduces DAO activity.
7. Be aware of medications that interfere with DAO activity. If you take any of the following medicines, discuss with your clinician how they may be affecting your histamine intolerance symptoms, to see if alternatives are available.2

Bottom line?

Eat fresh (and I don’t mean at Subway . . . )

Hungry for more histamine knowledge?

Please see my companion post: “Histamine Intolerance: Understanding the Science” which explores the fascinating world of biogenic amines, how histamine forms inside and outside of our bodies, how and why histamine affects our physical and mental health, why some people, especially women, are more sensitive to histamine than others, and why reactions to high-histamine foods can be so unpredictable and confusing.

To learn about the connection between food sensitivities and anxiety or insomnia, including the possibility that histamine is keeping you up at night or causing panic attacks, I recommend reading my Psychology Today article “5 Foods Proven to Cause Anxiety and Insomnia.”

You can also listen to my podcast interview with Yasmina Ykelenstam, the Low Histamine Chef, about the connection between histamine intolerance and mental health.

Today we have an inspiring real world “n=1” example of how a ketogenic diet can be successfully used by a real woman to easily and happily lose weight!

I thought it would be nice to give you all a much-deserved break from my own dietary misadventures and stop to appreciate the beauty of a well-done ketogenic diet. My recent experiment with Professor Seyfried’s dietary recommendations for cancer was one of extreme ketosis for the explicit purpose of cancer treatment. However, most people who decide to try a ketogenic diet do so with the goal of losing weight, and they use a more moderate plan, such as the one recommended by Drs. Phinney and Volek in their book The Art and Science of Low Carbohydrate Living or the one recommended by Dr. Ron Rosedale in his book The Rosedale Diet. It is this kind of plan I intend to try myself soon, motivated in no small part by my friend Anne, who has successfully applied ketogenic dietary theory to her own life, and who has generously agreed to share her inspirational story here with us. But first, a bit of context.

On a beautiful autumn day last October, I was sitting on a beach in picturesque Rockport, Massachusetts with two friends, babbling incessantly about some of the talks I had heard at the 2012 Ancestral Health Symposium. In particular, I was waxing poetic about Dr. Rosedale’s presentation about high fat/adequate protein/low carbohydrate diets being the key not only to weight loss but also to overall health, optimal function, and longevity.

When carbohydrates are restricted and protein is limited to daily requirements, the body has no choice but to burn fat for energy—this is what people who want to lose weight actually want to do—they want to burn fat. While I personally had lots of positive experience with very low carbohydrate diets, I had reached a weight loss wall, and had never tried to limit protein before. Dr. Rosedale’s logic seemed airtight and I was very intrigued—maybe protein limitation would be the key to my own weight loss challenges.

So, there I was, droning on and on about the virtues of nutritional ketosis to my friends. But did I start a ketogenic diet myself? Nope . . . at least not right away. But Anne did. Anne is the kind of person who embodies clarity and decisiveness. If she’s on board with something, she launches into it. If not, she dismisses it and moves on, without any angst or regret. She’s also really good with data and technology, so she’s included some terrific graphics.

So, ladies and gentlemen, without further ado, I give you: Real Woman Anne.

Anne’s Story

I’m approaching almost five months on a ketogenic diet. But before I talk about keto, I’ll give you some background information about me. I’m female, 46 years old, and 5 ft tall. I was not an overweight kid, but my diet as a child was processed everything. I loved Velveeta, canned ravioli, marshmallow fluff, boxed macaroni and cheese, etc. You get the picture. When I hit my 30s, my metabolism changed and I began gaining weight. My love for processed foods and chips and dip were at an all-time high. For emotional reasons I would turn to these foods to feel better, however briefly. I have been dieting off and on for the last 6 or 7 years.

The only other specific diet I have tried is Weight Watchers (WW). I have had success with WW in that I do lose weight, but I struggle to stick with it. One of the reasons I loved WW was that I was able to eat anything I wanted—I just had to count it. So I didn’t have to give up my favorite carbs, I just had to moderate. Well, moderation is not my strong suit. When low, feeling fat, whatever, I would go on a happy bender of a bag of chips with dip.

I have tracked my weight since December 2006 when I was at my heaviest (153.4 lbs). On WW the lowest weight I reached was 126.4 lbs back in October of 2010, but I quickly gained weight again. My weight has yo-yoed ever since, but never again coming close to the low 126.4 weight. That is until now. One afternoon in October 2012, Georgia mentioned Dr. Rosedale’s diet to me. Something struck a chord and I started the diet just a few days later. With winter fast approaching and me almost at my heaviest weight again, something had to be done. I weighed 149 lbs; my BMI was 29.1.

So I began my keto diet October 15, 2012. Interestingly Dr. Rosedale never mentions ketosis in his book, but his diet recommendations put you into ketosis. Georgia had also mentioned Jimmy Moore’s Livin’ La Vida Low Carb blog so I checked that out too and learned more about keto and ketone strips. Since I was ready to diet again, and I had to strike while the desire iron was hot, I started the diet without blood ketone strips in hand. So I do not have the before numbers or know when I first reached ketosis. I followed Rosedale’s first 3 weeks pretty closely, avoiding any starchy vegetables, rice, flour, sugar, fruit, and fake sugars.

I ordered my blood ketone strips and tester and began testing my ketones on November 6, 2012. At three weeks on keto, my ketones were at 5.4, blood glucose 73 (testing always occurred first thing in the morning before breakfast). That was the highest ketone measurement I ever had, and my ketones quickly came down to 2.8 in a couple of days. I ranged from a high of 5.4 to a low of 0.3 blood ketones while I was testing. I ran out of expensive ketone strips on January 4, 2013. Since things were going great—I was losing weight, I was satisfied and not hungry for many hours—I no longer cared about my ketones. Or at least not enough to keep spending the money.

I have written down my food, protein, fat, carbs, and calories each day and tracked my weight. Upon review I see the first 3 weeks I was really trying to not eat many saturated fats, a recommendation from Dr. Rosedale. I vaguely remember being tired for the first few days on keto but hung in there. My target protein has been 66 grams/day and I try to keep the carbs down to 50 grams or less/day. I have days when I do go over on one or the other, but for the most part I’ve been pretty steady. Over these 5 months, I have averaged 1,160 calories, 42 g of carbs, 82 g of fat, and 73 g of protein a day.

As of today March 11, 2013, I weigh 121.4 lbs, a loss of 27.6 lbs in less than 5 months. My BMI is 23.6. I’ve gone from a size 12 to a size 8; a few pairs of pants are a size 6. My initial goal is to reach 120 lbs. I’m just 1.4 lbs away, but I’m not going to stop there. I’m thinking once I reach the 120 goal, I’ll go for a goal of 115 lbs and see how I feel at that weight. I still have more fat on me than I’d like. I’ve never dieted without an intense desire to reach the end of the diet before. Nutritional ketosis is so different for me. I’m happy on this diet. I don’t have the cravings for any of those foods that have been my comfort and my downfall. My low level depression is gone. I have energy. I’m not hungry. I don’t covet the foods other people are eating. I find this diet just amazing. I never thought any of this would be possible. My impatience is only around my intense curiosity of what this old body could look like again.

As for exercise, I have been much more active in the past. With a current hip problem, my activity level has slowed to a crawl. I do a little biking (10-15 min/day and a little Pilates (5-10 min/day). Two years ago when I reached 126 pounds, I was playing tennis 3-4 times a week, biking, and hiking.I have found that I can have ½ of an apple, berries with heavy cream or sugar free chocolate as my treats in the evening with no ill effects. It hasn’t made me crave more sweets or carbs. Life is good. Of course, what I don’t know is the sustainability of this weight loss. What will maintenance look like once I’ve reached my weight goal? How many more carbs and protein can I have without triggering the old cravings or gaining weight? I’m going for blood tests tomorrow to make sure my cholesterol isn’t sky high. I eat a lot of saturated fats now and hope I’m not hurting myself. Stay tuned, I’ll keep Georgia apprised.

UPDATE: March 2013

Anne tells me she has continued to lose weight, and is now at 118 lbs, which is 8 pounds lighter than she was able to achieve with Weight Watchers plus exercise two years ago. She has surpassed her original goal of 120 lbs and has set her sights on 115.

She had labs drawn in March of 2011 (while eating a standard diet, not during her Weight Watchers diet) and again in March of 2013, while on a ketogenic diet. I have excluded electrolytes, blood count, kidney and liver function tests because they were normal and unchanged.

Reflections on Anne’s results

Anne’s fasting blood sugar is much better on a ketogenic diet, but her lipid profile has “worsened.” Anne is eating a standard ketogenic diet—high fat, moderate protein, low carb, and not exercising much these days due to a hip problem. She includes dairy and some processed foods in her diet, as the vast majority of people who eat a ketogenic diet do. Her triglycerides, while still in the normal range, have increased significantly, and her HDL has fallen. I will not venture to form a conclusion about these results except to say that they may or may not be due to a) the high fat content of a ketogenic diet, b) the process of fat burning, c) the presence of dairy, d) low activity levels (HDL in particular).

My own (much more extreme) version of a ketogenic diet earlier this year, with little/no dairy or processed foods, and almost no exercise, produced the following lipid profile:

• Total cholesterol: 260
• LDL: 170
• HDL: 70
• Triglycerides: 99

[For my complete lab results, see my post “Keto for Cancer: Week 5.”]

Her primary care doctor was very concerned about the trend in her lipid profile. She recommended she reduce her saturated fat intake, and start taking red rice yeast daily. What do you think of Anne’s lab test results?

If you are interested in starting a ketogenic diet yourself, see my online guide: “Ketogenic Diets 101.”

Today we have an inspiring real world “n=1” example of how a ketogenic diet can be successfully used by a real woman to easily and happily lose weight!

I thought it would be nice to give you all a much-deserved break from my own dietary misadventures and stop to appreciate the beauty of a well-done ketogenic diet. My recent experiment with Professor Seyfried’s dietary recommendations for cancer was one of extreme ketosis for the explicit purpose of cancer treatment. However, most people who decide to try a ketogenic diet do so with the goal of losing weight, and they use a more moderate plan, such as the one recommended by Drs. Phinney and Volek in their book The Art and Science of Low Carbohydrate Living or the one recommended by Dr. Ron Rosedale in his book The Rosedale Diet. It is this kind of plan I intend to try myself soon, motivated in no small part by my friend Anne, who has successfully applied ketogenic dietary theory to her own life, and who has generously agreed to share her inspirational story here with us. But first, a bit of context.

On a beautiful autumn day last October, I was sitting on a beach in picturesque Rockport, Massachusetts with two friends, babbling incessantly about some of the talks I had heard at the 2012 Ancestral Health Symposium. In particular, I was waxing poetic about Dr. Rosedale’s presentation about high fat/adequate protein/low carbohydrate diets being the key not only to weight loss but also to overall health, optimal function, and longevity.

When carbohydrates are restricted and protein is limited to daily requirements, the body has no choice but to burn fat for energy—this is what people who want to lose weight actually want to do—they want to burn fat. While I personally had lots of positive experience with very low carbohydrate diets, I had reached a weight loss wall, and had never tried to limit protein before. Dr. Rosedale’s logic seemed airtight and I was very intrigued—maybe protein limitation would be the key to my own weight loss challenges.

So, there I was, droning on and on about the virtues of nutritional ketosis to my friends. But did I start a ketogenic diet myself? Nope . . . at least not right away. But Anne did. Anne is the kind of person who embodies clarity and decisiveness. If she’s on board with something, she launches into it. If not, she dismisses it and moves on, without any angst or regret. She’s also really good with data and technology, so she’s included some terrific graphics.

So, ladies and gentlemen, without further ado, I give you: Real Woman Anne.

Anne’s Story

I’m approaching almost five months on a ketogenic diet. But before I talk about keto, I’ll give you some background information about me. I’m female, 46 years old, and 5 ft tall. I was not an overweight kid, but my diet as a child was processed everything. I loved Velveeta, canned ravioli, marshmallow fluff, boxed macaroni and cheese, etc. You get the picture. When I hit my 30s, my metabolism changed and I began gaining weight. My love for processed foods and chips and dip were at an all-time high. For emotional reasons I would turn to these foods to feel better, however briefly. I have been dieting off and on for the last 6 or 7 years.

The only other specific diet I have tried is Weight Watchers (WW). I have had success with WW in that I do lose weight, but I struggle to stick with it. One of the reasons I loved WW was that I was able to eat anything I wanted—I just had to count it. So I didn’t have to give up my favorite carbs, I just had to moderate. Well, moderation is not my strong suit. When low, feeling fat, whatever, I would go on a happy bender of a bag of chips with dip.

I have tracked my weight since December 2006 when I was at my heaviest (153.4 lbs). On WW the lowest weight I reached was 126.4 lbs back in October of 2010, but I quickly gained weight again. My weight has yo-yoed ever since, but never again coming close to the low 126.4 weight. That is until now. One afternoon in October 2012, Georgia mentioned Dr. Rosedale’s diet to me. Something struck a chord and I started the diet just a few days later. With winter fast approaching and me almost at my heaviest weight again, something had to be done. I weighed 149 lbs; my BMI was 29.1.

So I began my keto diet October 15, 2012. Interestingly Dr. Rosedale never mentions ketosis in his book, but his diet recommendations put you into ketosis. Georgia had also mentioned Jimmy Moore’s Livin’ La Vida Low Carb blog so I checked that out too and learned more about keto and ketone strips. Since I was ready to diet again, and I had to strike while the desire iron was hot, I started the diet without blood ketone strips in hand. So I do not have the before numbers or know when I first reached ketosis. I followed Rosedale’s first 3 weeks pretty closely, avoiding any starchy vegetables, rice, flour, sugar, fruit, and fake sugars.

I ordered my blood ketone strips and tester and began testing my ketones on November 6, 2012. At three weeks on keto, my ketones were at 5.4, blood glucose 73 (testing always occurred first thing in the morning before breakfast). That was the highest ketone measurement I ever had, and my ketones quickly came down to 2.8 in a couple of days. I ranged from a high of 5.4 to a low of 0.3 blood ketones while I was testing. I ran out of expensive ketone strips on January 4, 2013. Since things were going great—I was losing weight, I was satisfied and not hungry for many hours—I no longer cared about my ketones. Or at least not enough to keep spending the money.

I have written down my food, protein, fat, carbs, and calories each day and tracked my weight. Upon review I see the first 3 weeks I was really trying to not eat many saturated fats, a recommendation from Dr. Rosedale. I vaguely remember being tired for the first few days on keto but hung in there. My target protein has been 66 grams/day and I try to keep the carbs down to 50 grams or less/day. I have days when I do go over on one or the other, but for the most part I’ve been pretty steady. Over these 5 months, I have averaged 1,160 calories, 42 g of carbs, 82 g of fat, and 73 g of protein a day.

As of today March 11, 2013, I weigh 121.4 lbs, a loss of 27.6 lbs in less than 5 months. My BMI is 23.6. I’ve gone from a size 12 to a size 8; a few pairs of pants are a size 6. My initial goal is to reach 120 lbs. I’m just 1.4 lbs away, but I’m not going to stop there. I’m thinking once I reach the 120 goal, I’ll go for a goal of 115 lbs and see how I feel at that weight. I still have more fat on me than I’d like. I’ve never dieted without an intense desire to reach the end of the diet before. Nutritional ketosis is so different for me. I’m happy on this diet. I don’t have the cravings for any of those foods that have been my comfort and my downfall. My low level depression is gone. I have energy. I’m not hungry. I don’t covet the foods other people are eating. I find this diet just amazing. I never thought any of this would be possible. My impatience is only around my intense curiosity of what this old body could look like again.

As for exercise, I have been much more active in the past. With a current hip problem, my activity level has slowed to a crawl. I do a little biking (10-15 min/day and a little Pilates (5-10 min/day). Two years ago when I reached 126 pounds, I was playing tennis 3-4 times a week, biking, and hiking.I have found that I can have ½ of an apple, berries with heavy cream or sugar free chocolate as my treats in the evening with no ill effects. It hasn’t made me crave more sweets or carbs. Life is good. Of course, what I don’t know is the sustainability of this weight loss. What will maintenance look like once I’ve reached my weight goal? How many more carbs and protein can I have without triggering the old cravings or gaining weight? I’m going for blood tests tomorrow to make sure my cholesterol isn’t sky high. I eat a lot of saturated fats now and hope I’m not hurting myself. Stay tuned, I’ll keep Georgia apprised.

UPDATE: March 2013

Anne tells me she has continued to lose weight, and is now at 118 lbs, which is 8 pounds lighter than she was able to achieve with Weight Watchers plus exercise two years ago. She has surpassed her original goal of 120 lbs and has set her sights on 115.

She had labs drawn in March of 2011 (while eating a standard diet, not during her Weight Watchers diet) and again in March of 2013, while on a ketogenic diet. I have excluded electrolytes, blood count, kidney and liver function tests because they were normal and unchanged.

Reflections on Anne’s results

Anne’s fasting blood sugar is much better on a ketogenic diet, but her lipid profile has “worsened.” Anne is eating a standard ketogenic diet—high fat, moderate protein, low carb, and not exercising much these days due to a hip problem. She includes dairy and some processed foods in her diet, as the vast majority of people who eat a ketogenic diet do. Her triglycerides, while still in the normal range, have increased significantly, and her HDL has fallen. I will not venture to form a conclusion about these results except to say that they may or may not be due to a) the high fat content of a ketogenic diet, b) the process of fat burning, c) the presence of dairy, d) low activity levels (HDL in particular).

My own (much more extreme) version of a ketogenic diet earlier this year, with little/no dairy or processed foods, and almost no exercise, produced the following lipid profile:

• Total cholesterol: 260
• LDL: 170
• HDL: 70
• Triglycerides: 99

[For my complete lab results, see my post “Keto for Cancer: Week 5.”]

Her primary care doctor was very concerned about the trend in her lipid profile. She recommended she reduce her saturated fat intake, and start taking red rice yeast daily. What do you think of Anne’s lab test results?

If you are interested in starting a ketogenic diet yourself, see my online guide: “Ketogenic Diets 101.”

Today we have an inspiring real world “n=1” example of how a ketogenic diet can be successfully used by a real woman to easily and happily lose weight!

I thought it would be nice to give you all a much-deserved break from my own dietary misadventures and stop to appreciate the beauty of a well-done ketogenic diet. My recent experiment with Professor Seyfried’s dietary recommendations for cancer was one of extreme ketosis for the explicit purpose of cancer treatment. However, most people who decide to try a ketogenic diet do so with the goal of losing weight, and they use a more moderate plan, such as the one recommended by Drs. Phinney and Volek in their book The Art and Science of Low Carbohydrate Living or the one recommended by Dr. Ron Rosedale in his book The Rosedale Diet. It is this kind of plan I intend to try myself soon, motivated in no small part by my friend Anne, who has successfully applied ketogenic dietary theory to her own life, and who has generously agreed to share her inspirational story here with us. But first, a bit of context.

On a beautiful autumn day last October, I was sitting on a beach in picturesque Rockport, Massachusetts with two friends, babbling incessantly about some of the talks I had heard at the 2012 Ancestral Health Symposium. In particular, I was waxing poetic about Dr. Rosedale’s presentation about high fat/adequate protein/low carbohydrate diets being the key not only to weight loss but also to overall health, optimal function, and longevity.

When carbohydrates are restricted and protein is limited to daily requirements, the body has no choice but to burn fat for energy—this is what people who want to lose weight actually want to do—they want to burn fat. While I personally had lots of positive experience with very low carbohydrate diets, I had reached a weight loss wall, and had never tried to limit protein before. Dr. Rosedale’s logic seemed airtight and I was very intrigued—maybe protein limitation would be the key to my own weight loss challenges.

So, there I was, droning on and on about the virtues of nutritional ketosis to my friends. But did I start a ketogenic diet myself? Nope . . . at least not right away. But Anne did. Anne is the kind of person who embodies clarity and decisiveness. If she’s on board with something, she launches into it. If not, she dismisses it and moves on, without any angst or regret. She’s also really good with data and technology, so she’s included some terrific graphics.

So, ladies and gentlemen, without further ado, I give you: Real Woman Anne.

Anne’s Story

I’m approaching almost five months on a ketogenic diet. But before I talk about keto, I’ll give you some background information about me. I’m female, 46 years old, and 5 ft tall. I was not an overweight kid, but my diet as a child was processed everything. I loved Velveeta, canned ravioli, marshmallow fluff, boxed macaroni and cheese, etc. You get the picture. When I hit my 30s, my metabolism changed and I began gaining weight. My love for processed foods and chips and dip were at an all-time high. For emotional reasons I would turn to these foods to feel better, however briefly. I have been dieting off and on for the last 6 or 7 years.

The only other specific diet I have tried is Weight Watchers (WW). I have had success with WW in that I do lose weight, but I struggle to stick with it. One of the reasons I loved WW was that I was able to eat anything I wanted—I just had to count it. So I didn’t have to give up my favorite carbs, I just had to moderate. Well, moderation is not my strong suit. When low, feeling fat, whatever, I would go on a happy bender of a bag of chips with dip.

I have tracked my weight since December 2006 when I was at my heaviest (153.4 lbs). On WW the lowest weight I reached was 126.4 lbs back in October of 2010, but I quickly gained weight again. My weight has yo-yoed ever since, but never again coming close to the low 126.4 weight. That is until now. One afternoon in October 2012, Georgia mentioned Dr. Rosedale’s diet to me. Something struck a chord and I started the diet just a few days later. With winter fast approaching and me almost at my heaviest weight again, something had to be done. I weighed 149 lbs; my BMI was 29.1.

So I began my keto diet October 15, 2012. Interestingly Dr. Rosedale never mentions ketosis in his book, but his diet recommendations put you into ketosis. Georgia had also mentioned Jimmy Moore’s Livin’ La Vida Low Carb blog so I checked that out too and learned more about keto and ketone strips. Since I was ready to diet again, and I had to strike while the desire iron was hot, I started the diet without blood ketone strips in hand. So I do not have the before numbers or know when I first reached ketosis. I followed Rosedale’s first 3 weeks pretty closely, avoiding any starchy vegetables, rice, flour, sugar, fruit, and fake sugars.

I ordered my blood ketone strips and tester and began testing my ketones on November 6, 2012. At three weeks on keto, my ketones were at 5.4, blood glucose 73 (testing always occurred first thing in the morning before breakfast). That was the highest ketone measurement I ever had, and my ketones quickly came down to 2.8 in a couple of days. I ranged from a high of 5.4 to a low of 0.3 blood ketones while I was testing. I ran out of expensive ketone strips on January 4, 2013. Since things were going great—I was losing weight, I was satisfied and not hungry for many hours—I no longer cared about my ketones. Or at least not enough to keep spending the money.

I have written down my food, protein, fat, carbs, and calories each day and tracked my weight. Upon review I see the first 3 weeks I was really trying to not eat many saturated fats, a recommendation from Dr. Rosedale. I vaguely remember being tired for the first few days on keto but hung in there. My target protein has been 66 grams/day and I try to keep the carbs down to 50 grams or less/day. I have days when I do go over on one or the other, but for the most part I’ve been pretty steady. Over these 5 months, I have averaged 1,160 calories, 42 g of carbs, 82 g of fat, and 73 g of protein a day.

As of today March 11, 2013, I weigh 121.4 lbs, a loss of 27.6 lbs in less than 5 months. My BMI is 23.6. I’ve gone from a size 12 to a size 8; a few pairs of pants are a size 6. My initial goal is to reach 120 lbs. I’m just 1.4 lbs away, but I’m not going to stop there. I’m thinking once I reach the 120 goal, I’ll go for a goal of 115 lbs and see how I feel at that weight. I still have more fat on me than I’d like. I’ve never dieted without an intense desire to reach the end of the diet before. Nutritional ketosis is so different for me. I’m happy on this diet. I don’t have the cravings for any of those foods that have been my comfort and my downfall. My low level depression is gone. I have energy. I’m not hungry. I don’t covet the foods other people are eating. I find this diet just amazing. I never thought any of this would be possible. My impatience is only around my intense curiosity of what this old body could look like again.

As for exercise, I have been much more active in the past. With a current hip problem, my activity level has slowed to a crawl. I do a little biking (10-15 min/day and a little Pilates (5-10 min/day). Two years ago when I reached 126 pounds, I was playing tennis 3-4 times a week, biking, and hiking.I have found that I can have ½ of an apple, berries with heavy cream or sugar free chocolate as my treats in the evening with no ill effects. It hasn’t made me crave more sweets or carbs. Life is good. Of course, what I don’t know is the sustainability of this weight loss. What will maintenance look like once I’ve reached my weight goal? How many more carbs and protein can I have without triggering the old cravings or gaining weight? I’m going for blood tests tomorrow to make sure my cholesterol isn’t sky high. I eat a lot of saturated fats now and hope I’m not hurting myself. Stay tuned, I’ll keep Georgia apprised.

UPDATE: March 2013

Anne tells me she has continued to lose weight, and is now at 118 lbs, which is 8 pounds lighter than she was able to achieve with Weight Watchers plus exercise two years ago. She has surpassed her original goal of 120 lbs and has set her sights on 115.

She had labs drawn in March of 2011 (while eating a standard diet, not during her Weight Watchers diet) and again in March of 2013, while on a ketogenic diet. I have excluded electrolytes, blood count, kidney and liver function tests because they were normal and unchanged.

Reflections on Anne’s results

Anne’s fasting blood sugar is much better on a ketogenic diet, but her lipid profile has “worsened.” Anne is eating a standard ketogenic diet—high fat, moderate protein, low carb, and not exercising much these days due to a hip problem. She includes dairy and some processed foods in her diet, as the vast majority of people who eat a ketogenic diet do. Her triglycerides, while still in the normal range, have increased significantly, and her HDL has fallen. I will not venture to form a conclusion about these results except to say that they may or may not be due to a) the high fat content of a ketogenic diet, b) the process of fat burning, c) the presence of dairy, d) low activity levels (HDL in particular).

My own (much more extreme) version of a ketogenic diet earlier this year, with little/no dairy or processed foods, and almost no exercise, produced the following lipid profile:

• Total cholesterol: 260
• LDL: 170
• HDL: 70
• Triglycerides: 99

[For my complete lab results, see my post “Keto for Cancer: Week 5.”]

Her primary care doctor was very concerned about the trend in her lipid profile. She recommended she reduce her saturated fat intake, and start taking red rice yeast daily. What do you think of Anne’s lab test results?

If you are interested in starting a ketogenic diet yourself, see my online guide: “Ketogenic Diets 101.”

Note: this post was originally published on Aug 1, 2013. It was edited to streamline content and improve graphics in June 2016; therefore some older comments may pertain to content that was removed during revision.

This post is part of a series describing my attempt to follow Dr. Seyfried’s dietary recommendations for cancer. To start at the beginning, please go to the first post: “Seyfried’s Ketogenic Cancer Diet: My Fasting Jump-Start to Ketosis.“

My deep ketosis experiment went down in flames this week, but not before I had my blood drawn. I share my ketogenic diet blood tests with you as compared to results from a year ago. So, even though hunger eventually got the best of me, I learned a lot in the process, and hope you did too! Links to my moderate ketosis experiment are provided if you’d like to see what a more successful approach looks like.

Oh the humanity . . .

It was the best of times, it was the worst of times . . .

Call me Ishmael . . .

Oh, wait, that last one is completely irrelevant . . .

Before I begin my sorry tale, let me reassure you that I’m feeling much better now. And I have some very interesting lab test results to report. But the previous Thursday was a terrible, horrible, no good, very bad day. It started off with my posting about my unhappy fourth week on my modified version of Dr. Seyfried’s ketogenic diet. Here’s my data from that Thursday morning:

Day 29 (2/28/13)

(Food not included because I didn’t keep track.)

So off I went to my primary care center, in my fasting state, with my blood sugar at 81 and my ketones at 5.2 (too high to be comfortable), hoping to be back home within an hour or so to eat breakfast and get ready for work. After having my blood drawn, I discovered that my doctor had not been willing to order all of the tests I requested, so I wrote myself a second set of orders and headed off to a different lab, on the other side of town, to have a second set of labs drawn.

Unfortunately, there was a wait of about an hour at the second lab. I had never been so hungry in my whole life. I would have eaten any one of you in a heartbeat, had you been willing to be grilled. Anyway, I got my blood drawn, but no time to go back home to eat—I had to go straight to the office—where there was no food . . . and I had a full day of patients ahead of me.

The only thing I had time to do was stop in the hospital gift shop on my way out and hope that something they sold was not made of carbohydrate. After a month of working so hard on this diet I really didn’t want to lose whatever keto-adaptation status I may have gained by eating carbs. All I could find was mozzarella sticks, which don’t agree with me, but any port in a storm . . .

By the end of the day I was still very hungry, so I ate chicken without counting protein grams until I felt better.

Day 30 (3/1/13)

Notes: Still feeling off, despite eating as much as I wanted yesterday. So today I decided to continue eating as much as I want until I feel normal again.

At some point succumbed to a scoop of Ben and Jerry’s sugar-free ice cream, which ultimately triggered carbohydrate cravings. And so it was that my human ketosis experiment went down in flames like a lumbering inflatable airbus . . .

So, I wondered—how can I use this failure to educate myself—and those of you who were hoping to learn something from my experiment? You’ll notice that some values along the way are missing. This is because I was initially ambivalent at first about how to proceed, but by the end of the week I had settled on a way forward.

Day 31 (3/2/13)

Notes: I was concerned about my lingering lightheadedness/dizziness and low energy, despite eating plenty of food for three days in a row, including carbs, that I wrote to Dr. Rosedale through his website for advice. We don’t know each other, so I was pleasantly surprised and very grateful when he wrote me back. One of the things he advised me to do was to begin taking potassium and magnesium supplements, so I started taking them this evening.

Day 32 (3/3/13)

Notes: I woke up lightheaded, with low energy. I decided to try coffee.

Day 33 (3/4/13)

Notes: Woke up lightheaded, but otherwise ok. Strong carbohydrate cravings towards evening. Didn’t even try to fight them.

Day 34 (3/5/13)

Notes: Woke with mild low back pain and mild sinus congestion (dairy protein effects from ice cream) Above average appetite with carb cravings all day.

Day 35 (3/6/13)

Notes: Hungry all day long—ate about twice as much at each meal as I normally would, and still couldn’t get the carb cravings or hunger to go away, so I gave in again to the carbs . . .

Day 36 (3/7/13)

I feel fine this morning, actually—that lightheaded/dizzy feeling is completely gone, finally! Maybe I just needed a lot of calories yesterday, who knows? I want to try to get these carbs back out of my diet . . . maybe if I stick with the coffee for another day or two it will help to resist them. Anyway, I’m curious about coffee’s effects on blood sugar, so I tried a mini-experiment before breakfast.

• Morning blood sugar: 105
• Blood sugar 1 hour after 1 cup of unsweetened black coffee: 94
• Blood sugar 2 hours after coffee: 88

Well, plain coffee certainly didn’t raise blood sugar, but in order to know whether it lowered blood sugar, I’d need to do a control experiment where I test my blood sugar one and two hours after drinking water, to see if the drop was just the natural effect of not having any calories.

Ketogenic diet blood tests: results from 2/28/13 (day 29)

I wish it had occurred to me to have blood work drawn just prior to starting my experiment. Instead, I am using test results from last April for comparison. At that time, I was eating a modified Paleo diet of mostly meat, plus a few fruits and vegetables. I limited calories to 1200–1400 per day, and exercised vigorously for 45 to 90 mins, 5-7 times per week. I’ve only listed those comparison values that are significantly different from last year’s results or are of particular interest. Otherwise you can assume they were about the same. Abnormal values from 2/28 are in red.

Reflections on “abnormal” ketogenic lab results

Blood sugar & insulin

Clearly this diet had powerful effects on blood sugar and insulin levels. According to the lab, both of these values were abnormally low. It is certainly possible for blood sugar to be too low, and we do need some insulin in our bodies at all time, but lab ranges for normal values tend to reflect the normal values found in the population—not the ideal ranges associated with optimal health. Was my insulin too low to be healthy, or just lower than it is for most people?

Homocysteine and vitamin B12

It is strange that both of these were elevated, because they often tend to go in opposite directions. In fact, LOW B12 levels are a commonly linked to HIGH homocysteine levels—clearly not the case for me. Other vitamin deficiencies can also be associated with high homocysteine levels, including low B6 and low folate. I don’t have low folate levels, and I did not have my B6 level checked, but B vitamins are plentiful in animal foods, so I doubt my B6 would be low.

It makes sense that my B12 level would be high, because my diet is very high in animal foods, which are rich sources of B12. I am not aware of any negative consequences of having a somewhat higher level of B12 than the average population. In epidemiological studies, high homocysteine levels have been observed to be associated with higher risk for heart disease, but keep in mind that epidemiological studies cannot prove cause and effect (for more info about this topic, see my brief post about this: “The Problem with Epidemiology.”) In clinical studies, lowering homocysteine levels turned out not to reduce risk for heart disease. Some people have genetic differences in enzymes that cause homocysteine to accumulate, so perhaps that is true for me.

Anion gap

This just means that there are extra charged particles in the bloodstream that were not directly measured. The ones that are directly measured are sodium, chloride, and CO2 (carbon dioxide). It is common for people in ketosis to have a bit of an anion gap because ketones are charged particles. Note that my CO2 level was normal, which means that I was in ketosis, not ketoacidosis. In ketoacidosis, the CO2 level would be LOW.

Cholesterol and triglycerides

Elevated total cholesterol or elevated LDL do not concern me (for more information about this, please see my cholesterol page). I care much more about my HDL (pretty good, but it was even better last year when I was exercising regularly) and my triglycerides (again, also pretty good, but even better last year).

Apolipoprotein B

Nicknamed “ApoB” for short, Apolipoprotein B is a fatty protein on the outside of LDL particles. The more ApoB you have, the more LDL particles you have. Higher numbers are usually considered bad, because what we want are small numbers of big fluffy LDL particles, not large numbers of small, dense LDL particles. It is unclear to me precisely how ApoB and LDL particle size are related, but my basic understanding of this relationship is that people with insulin resistance are more likely to have high ApoB values.

I believe I am more insulin resistant than the average person, given my high fasting and post-meal blood sugar values when eating a diet containing typical amounts of protein and carbohydrate. It seems that high ApoB levels are not uncommon in people eating a ketogenic diet, and that cardiologists are unsure whether this is unhealthy. Listen to Jimmy Moore’s interview with Dr. Thomas Dayspring for his take on this issue.

Thyroid tests and ketogenic diets

My TSH (thyroid stimulating hormone) level was normal, and that is the test that most doctors currently use to screen for low thyroid hormone activity. However, my circulating levels of T3 (the most active form of thyroid hormone) and reverse T3 (the deactivated form of rT3) are both “abnormal”, and most importantly, the ratio between them is very low. This may help to explain why my energy was low during this diet, although I have to keep in mind that I have never had T3 and reverse T3 measured before, so there is no way for me to know what my levels were before this diet.

When the body is stressed or undernourished, it will work to lower thyroid hormone activity to slow metabolism. It is definitely possible that my low thyroid hormone activity could have been caused by an extreme ketogenic diet. Whether low thyroid activity (without symptoms of hypothyrodism) is ultimately a good or bad thing for the body is debatable, as some (most notably Dr. Rosedale) believe that a “cooler” metabolic rate may be beneficial.

Folate

Folate (aka Folic Acid) is famous for being found in green leafy vegetables. One problem with my 90-day all-meat diet last summer was that my folate level dropped to below normal. I tried to supplement with folic acid tablets but couldn’t tolerate them, so I added occasional chicken liver to my diet last summer and that seemed to correct the problem.

Vitamin D

My levels have improved since last summer, when I started taking Vitamin D supplements.

Where to from here?

I continue to believe in the promise of ketogenic diets for overall health, mental health, appetite control, and weight management. However, I personally was not able to tolerate the diet recommended by Dr. Seyfried for cancer treatment—at least not as I had constructed it. If any of you have ever reached ketones of 4.0 and blood sugars of 55-65 and had a different experience, I would love to hear from you. I hope that people with cancer may achieve important benefits from a less extreme ketogenic diet, but I do not know if that is true.

I went back through Seyfried’s book again last week and found that, in one place he refers to a target ketone zone of 3.0 mM to 5.0 mM (whereas he usually used 4.0mM as his minimum target zone); 3.0 would have been easier, because I could have eaten a little more protein. Theoretically, a standard ketogenic diet (aka “nutritional ketosis, such as that recommended by Phinney & Volek, which aims for ketones in the 0.5 to 3.0 mM range) or the Rosedale Diet (which does not recommend testing ketone levels at all), should provide benefits to all and should not be harmful, but whether they pack the punch necessary to fight cancer or control seizures is unclear.

For the sake of my own future health, and to satisfy my intellectual curiosity, I would like to try a standard ketogenic diet, and had hoped to gradually transition into such a diet this past week without going out of ketosis, but unfortunately, that didn’t happen.

Ketogenic diet experiment, take 2

So, what to do now? I’d like to try moderate nutritional ketosis using the mostly-meat diet that worked so well for me last summer. However, I don’t know if I’ll be able to limit my protein enough to get my ketones into the target range without getting hungry.

I know people who have been very successful at managing weight and controlling appetite using a standard ketogenic diet, including a friend of mine whose progress has been inspiring to me. She has been following a ketogenic diet since October and agreed to let me post about her experience. Her post provides more promising and hopeful results than those I personally have yet to offer. . . . Read a terrific guest post by Anne, who successfully and happily lost weight using nutritional ketosis.

I hope you have enjoyed witnessing the launch and demise of my ketogenic Hindenburg . . .

If you are interested in starting a ketogenic diet yourself, see my online guide: “Ketogenic Diets 101.”

Note: this post was originally published on Aug 1, 2013. It was edited to streamline content and improve graphics in June 2016; therefore some older comments may pertain to content that was removed during revision.

This post is part of a series describing my attempt to follow Dr. Seyfried’s dietary recommendations for cancer. To start at the beginning, please go to the first post: “Seyfried’s Ketogenic Cancer Diet: My Fasting Jump-Start to Ketosis.“

My deep ketosis experiment went down in flames this week, but not before I had my blood drawn. I share my ketogenic diet blood tests with you as compared to results from a year ago. So, even though hunger eventually got the best of me, I learned a lot in the process, and hope you did too! Links to my moderate ketosis experiment are provided if you’d like to see what a more successful approach looks like.

Oh the humanity . . .

It was the best of times, it was the worst of times . . .

Call me Ishmael . . .

Oh, wait, that last one is completely irrelevant . . .

Before I begin my sorry tale, let me reassure you that I’m feeling much better now. And I have some very interesting lab test results to report. But the previous Thursday was a terrible, horrible, no good, very bad day. It started off with my posting about my unhappy fourth week on my modified version of Dr. Seyfried’s ketogenic diet. Here’s my data from that Thursday morning:

Day 29 (2/28/13)

(Food not included because I didn’t keep track.)

So off I went to my primary care center, in my fasting state, with my blood sugar at 81 and my ketones at 5.2 (too high to be comfortable), hoping to be back home within an hour or so to eat breakfast and get ready for work. After having my blood drawn, I discovered that my doctor had not been willing to order all of the tests I requested, so I wrote myself a second set of orders and headed off to a different lab, on the other side of town, to have a second set of labs drawn.

Unfortunately, there was a wait of about an hour at the second lab. I had never been so hungry in my whole life. I would have eaten any one of you in a heartbeat, had you been willing to be grilled. Anyway, I got my blood drawn, but no time to go back home to eat—I had to go straight to the office—where there was no food . . . and I had a full day of patients ahead of me.

The only thing I had time to do was stop in the hospital gift shop on my way out and hope that something they sold was not made of carbohydrate. After a month of working so hard on this diet I really didn’t want to lose whatever keto-adaptation status I may have gained by eating carbs. All I could find was mozzarella sticks, which don’t agree with me, but any port in a storm . . .

By the end of the day I was still very hungry, so I ate chicken without counting protein grams until I felt better.

Day 30 (3/1/13)

Notes: Still feeling off, despite eating as much as I wanted yesterday. So today I decided to continue eating as much as I want until I feel normal again.

At some point succumbed to a scoop of Ben and Jerry’s sugar-free ice cream, which ultimately triggered carbohydrate cravings. And so it was that my human ketosis experiment went down in flames like a lumbering inflatable airbus . . .

So, I wondered—how can I use this failure to educate myself—and those of you who were hoping to learn something from my experiment? You’ll notice that some values along the way are missing. This is because I was initially ambivalent at first about how to proceed, but by the end of the week I had settled on a way forward.

Day 31 (3/2/13)

Notes: I was concerned about my lingering lightheadedness/dizziness and low energy, despite eating plenty of food for three days in a row, including carbs, that I wrote to Dr. Rosedale through his website for advice. We don’t know each other, so I was pleasantly surprised and very grateful when he wrote me back. One of the things he advised me to do was to begin taking potassium and magnesium supplements, so I started taking them this evening.

Day 32 (3/3/13)

Notes: I woke up lightheaded, with low energy. I decided to try coffee.

Day 33 (3/4/13)

Notes: Woke up lightheaded, but otherwise ok. Strong carbohydrate cravings towards evening. Didn’t even try to fight them.

Day 34 (3/5/13)

Notes: Woke with mild low back pain and mild sinus congestion (dairy protein effects from ice cream) Above average appetite with carb cravings all day.

Day 35 (3/6/13)

Notes: Hungry all day long—ate about twice as much at each meal as I normally would, and still couldn’t get the carb cravings or hunger to go away, so I gave in again to the carbs . . .

Day 36 (3/7/13)

I feel fine this morning, actually—that lightheaded/dizzy feeling is completely gone, finally! Maybe I just needed a lot of calories yesterday, who knows? I want to try to get these carbs back out of my diet . . . maybe if I stick with the coffee for another day or two it will help to resist them. Anyway, I’m curious about coffee’s effects on blood sugar, so I tried a mini-experiment before breakfast.

• Morning blood sugar: 105
• Blood sugar 1 hour after 1 cup of unsweetened black coffee: 94
• Blood sugar 2 hours after coffee: 88

Well, plain coffee certainly didn’t raise blood sugar, but in order to know whether it lowered blood sugar, I’d need to do a control experiment where I test my blood sugar one and two hours after drinking water, to see if the drop was just the natural effect of not having any calories.

Ketogenic diet blood tests: results from 2/28/13 (day 29)

I wish it had occurred to me to have blood work drawn just prior to starting my experiment. Instead, I am using test results from last April for comparison. At that time, I was eating a modified Paleo diet of mostly meat, plus a few fruits and vegetables. I limited calories to 1200–1400 per day, and exercised vigorously for 45 to 90 mins, 5-7 times per week. I’ve only listed those comparison values that are significantly different from last year’s results or are of particular interest. Otherwise you can assume they were about the same. Abnormal values from 2/28 are in red.

Reflections on “abnormal” ketogenic lab results

Blood sugar & insulin

Clearly this diet had powerful effects on blood sugar and insulin levels. According to the lab, both of these values were abnormally low. It is certainly possible for blood sugar to be too low, and we do need some insulin in our bodies at all time, but lab ranges for normal values tend to reflect the normal values found in the population—not the ideal ranges associated with optimal health. Was my insulin too low to be healthy, or just lower than it is for most people?

Homocysteine and vitamin B12

It is strange that both of these were elevated, because they often tend to go in opposite directions. In fact, LOW B12 levels are a commonly linked to HIGH homocysteine levels—clearly not the case for me. Other vitamin deficiencies can also be associated with high homocysteine levels, including low B6 and low folate. I don’t have low folate levels, and I did not have my B6 level checked, but B vitamins are plentiful in animal foods, so I doubt my B6 would be low.

It makes sense that my B12 level would be high, because my diet is very high in animal foods, which are rich sources of B12. I am not aware of any negative consequences of having a somewhat higher level of B12 than the average population. In epidemiological studies, high homocysteine levels have been observed to be associated with higher risk for heart disease, but keep in mind that epidemiological studies cannot prove cause and effect (for more info about this topic, see my brief post about this: “The Problem with Epidemiology.”) In clinical studies, lowering homocysteine levels turned out not to reduce risk for heart disease. Some people have genetic differences in enzymes that cause homocysteine to accumulate, so perhaps that is true for me.

Anion gap

This just means that there are extra charged particles in the bloodstream that were not directly measured. The ones that are directly measured are sodium, chloride, and CO2 (carbon dioxide). It is common for people in ketosis to have a bit of an anion gap because ketones are charged particles. Note that my CO2 level was normal, which means that I was in ketosis, not ketoacidosis. In ketoacidosis, the CO2 level would be LOW.

Cholesterol and triglycerides

Elevated total cholesterol or elevated LDL do not concern me (for more information about this, please see my cholesterol page). I care much more about my HDL (pretty good, but it was even better last year when I was exercising regularly) and my triglycerides (again, also pretty good, but even better last year).

Apolipoprotein B

Nicknamed “ApoB” for short, Apolipoprotein B is a fatty protein on the outside of LDL particles. The more ApoB you have, the more LDL particles you have. Higher numbers are usually considered bad, because what we want are small numbers of big fluffy LDL particles, not large numbers of small, dense LDL particles. It is unclear to me precisely how ApoB and LDL particle size are related, but my basic understanding of this relationship is that people with insulin resistance are more likely to have high ApoB values.

I believe I am more insulin resistant than the average person, given my high fasting and post-meal blood sugar values when eating a diet containing typical amounts of protein and carbohydrate. It seems that high ApoB levels are not uncommon in people eating a ketogenic diet, and that cardiologists are unsure whether this is unhealthy. Listen to Jimmy Moore’s interview with Dr. Thomas Dayspring for his take on this issue.

Thyroid tests and ketogenic diets

My TSH (thyroid stimulating hormone) level was normal, and that is the test that most doctors currently use to screen for low thyroid hormone activity. However, my circulating levels of T3 (the most active form of thyroid hormone) and reverse T3 (the deactivated form of rT3) are both “abnormal”, and most importantly, the ratio between them is very low. This may help to explain why my energy was low during this diet, although I have to keep in mind that I have never had T3 and reverse T3 measured before, so there is no way for me to know what my levels were before this diet.

When the body is stressed or undernourished, it will work to lower thyroid hormone activity to slow metabolism. It is definitely possible that my low thyroid hormone activity could have been caused by an extreme ketogenic diet. Whether low thyroid activity (without symptoms of hypothyrodism) is ultimately a good or bad thing for the body is debatable, as some (most notably Dr. Rosedale) believe that a “cooler” metabolic rate may be beneficial.

Folate

Folate (aka Folic Acid) is famous for being found in green leafy vegetables. One problem with my 90-day all-meat diet last summer was that my folate level dropped to below normal. I tried to supplement with folic acid tablets but couldn’t tolerate them, so I added occasional chicken liver to my diet last summer and that seemed to correct the problem.

Vitamin D

My levels have improved since last summer, when I started taking Vitamin D supplements.

Where to from here?

I continue to believe in the promise of ketogenic diets for overall health, mental health, appetite control, and weight management. However, I personally was not able to tolerate the diet recommended by Dr. Seyfried for cancer treatment—at least not as I had constructed it. If any of you have ever reached ketones of 4.0 and blood sugars of 55-65 and had a different experience, I would love to hear from you. I hope that people with cancer may achieve important benefits from a less extreme ketogenic diet, but I do not know if that is true.

I went back through Seyfried’s book again last week and found that, in one place he refers to a target ketone zone of 3.0 mM to 5.0 mM (whereas he usually used 4.0mM as his minimum target zone); 3.0 would have been easier, because I could have eaten a little more protein. Theoretically, a standard ketogenic diet (aka “nutritional ketosis, such as that recommended by Phinney & Volek, which aims for ketones in the 0.5 to 3.0 mM range) or the Rosedale Diet (which does not recommend testing ketone levels at all), should provide benefits to all and should not be harmful, but whether they pack the punch necessary to fight cancer or control seizures is unclear.

For the sake of my own future health, and to satisfy my intellectual curiosity, I would like to try a standard ketogenic diet, and had hoped to gradually transition into such a diet this past week without going out of ketosis, but unfortunately, that didn’t happen.

Ketogenic diet experiment, take 2

So, what to do now? I’d like to try moderate nutritional ketosis using the mostly-meat diet that worked so well for me last summer. However, I don’t know if I’ll be able to limit my protein enough to get my ketones into the target range without getting hungry.

I know people who have been very successful at managing weight and controlling appetite using a standard ketogenic diet, including a friend of mine whose progress has been inspiring to me. She has been following a ketogenic diet since October and agreed to let me post about her experience. Her post provides more promising and hopeful results than those I personally have yet to offer. . . . Read a terrific guest post by Anne, who successfully and happily lost weight using nutritional ketosis.

I hope you have enjoyed witnessing the launch and demise of my ketogenic Hindenburg . . .

If you are interested in starting a ketogenic diet yourself, see my online guide: “Ketogenic Diets 101.”

Note: this post was originally published on Aug 1, 2013. It was edited to streamline content and improve graphics in June 2016; therefore some older comments may pertain to content that was removed during revision.

This post is part of a series describing my attempt to follow Dr. Seyfried’s dietary recommendations for cancer. To start at the beginning, please go to the first post: “Seyfried’s Ketogenic Cancer Diet: My Fasting Jump-Start to Ketosis.“

My deep ketosis experiment went down in flames this week, but not before I had my blood drawn. I share my ketogenic diet blood tests with you as compared to results from a year ago. So, even though hunger eventually got the best of me, I learned a lot in the process, and hope you did too! Links to my moderate ketosis experiment are provided if you’d like to see what a more successful approach looks like.

Oh the humanity . . .

It was the best of times, it was the worst of times . . .

Call me Ishmael . . .

Oh, wait, that last one is completely irrelevant . . .

Before I begin my sorry tale, let me reassure you that I’m feeling much better now. And I have some very interesting lab test results to report. But the previous Thursday was a terrible, horrible, no good, very bad day. It started off with my posting about my unhappy fourth week on my modified version of Dr. Seyfried’s ketogenic diet. Here’s my data from that Thursday morning:

Day 29 (2/28/13)

(Food not included because I didn’t keep track.)

So off I went to my primary care center, in my fasting state, with my blood sugar at 81 and my ketones at 5.2 (too high to be comfortable), hoping to be back home within an hour or so to eat breakfast and get ready for work. After having my blood drawn, I discovered that my doctor had not been willing to order all of the tests I requested, so I wrote myself a second set of orders and headed off to a different lab, on the other side of town, to have a second set of labs drawn.

Unfortunately, there was a wait of about an hour at the second lab. I had never been so hungry in my whole life. I would have eaten any one of you in a heartbeat, had you been willing to be grilled. Anyway, I got my blood drawn, but no time to go back home to eat—I had to go straight to the office—where there was no food . . . and I had a full day of patients ahead of me.

The only thing I had time to do was stop in the hospital gift shop on my way out and hope that something they sold was not made of carbohydrate. After a month of working so hard on this diet I really didn’t want to lose whatever keto-adaptation status I may have gained by eating carbs. All I could find was mozzarella sticks, which don’t agree with me, but any port in a storm . . .

By the end of the day I was still very hungry, so I ate chicken without counting protein grams until I felt better.

Day 30 (3/1/13)

Notes: Still feeling off, despite eating as much as I wanted yesterday. So today I decided to continue eating as much as I want until I feel normal again.

At some point succumbed to a scoop of Ben and Jerry’s sugar-free ice cream, which ultimately triggered carbohydrate cravings. And so it was that my human ketosis experiment went down in flames like a lumbering inflatable airbus . . .

So, I wondered—how can I use this failure to educate myself—and those of you who were hoping to learn something from my experiment? You’ll notice that some values along the way are missing. This is because I was initially ambivalent at first about how to proceed, but by the end of the week I had settled on a way forward.

Day 31 (3/2/13)

Notes: I was concerned about my lingering lightheadedness/dizziness and low energy, despite eating plenty of food for three days in a row, including carbs, that I wrote to Dr. Rosedale through his website for advice. We don’t know each other, so I was pleasantly surprised and very grateful when he wrote me back. One of the things he advised me to do was to begin taking potassium and magnesium supplements, so I started taking them this evening.

Day 32 (3/3/13)

Notes: I woke up lightheaded, with low energy. I decided to try coffee.

Day 33 (3/4/13)

Notes: Woke up lightheaded, but otherwise ok. Strong carbohydrate cravings towards evening. Didn’t even try to fight them.

Day 34 (3/5/13)

Notes: Woke with mild low back pain and mild sinus congestion (dairy protein effects from ice cream) Above average appetite with carb cravings all day.

Day 35 (3/6/13)

Notes: Hungry all day long—ate about twice as much at each meal as I normally would, and still couldn’t get the carb cravings or hunger to go away, so I gave in again to the carbs . . .

Day 36 (3/7/13)

I feel fine this morning, actually—that lightheaded/dizzy feeling is completely gone, finally! Maybe I just needed a lot of calories yesterday, who knows? I want to try to get these carbs back out of my diet . . . maybe if I stick with the coffee for another day or two it will help to resist them. Anyway, I’m curious about coffee’s effects on blood sugar, so I tried a mini-experiment before breakfast.

• Morning blood sugar: 105
• Blood sugar 1 hour after 1 cup of unsweetened black coffee: 94
• Blood sugar 2 hours after coffee: 88

Well, plain coffee certainly didn’t raise blood sugar, but in order to know whether it lowered blood sugar, I’d need to do a control experiment where I test my blood sugar one and two hours after drinking water, to see if the drop was just the natural effect of not having any calories.

Ketogenic diet blood tests: results from 2/28/13 (day 29)

I wish it had occurred to me to have blood work drawn just prior to starting my experiment. Instead, I am using test results from last April for comparison. At that time, I was eating a modified Paleo diet of mostly meat, plus a few fruits and vegetables. I limited calories to 1200–1400 per day, and exercised vigorously for 45 to 90 mins, 5-7 times per week. I’ve only listed those comparison values that are significantly different from last year’s results or are of particular interest. Otherwise you can assume they were about the same. Abnormal values from 2/28 are in red.

Reflections on “abnormal” ketogenic lab results

Blood sugar & insulin

Clearly this diet had powerful effects on blood sugar and insulin levels. According to the lab, both of these values were abnormally low. It is certainly possible for blood sugar to be too low, and we do need some insulin in our bodies at all time, but lab ranges for normal values tend to reflect the normal values found in the population—not the ideal ranges associated with optimal health. Was my insulin too low to be healthy, or just lower than it is for most people?

Homocysteine and vitamin B12

It is strange that both of these were elevated, because they often tend to go in opposite directions. In fact, LOW B12 levels are a commonly linked to HIGH homocysteine levels—clearly not the case for me. Other vitamin deficiencies can also be associated with high homocysteine levels, including low B6 and low folate. I don’t have low folate levels, and I did not have my B6 level checked, but B vitamins are plentiful in animal foods, so I doubt my B6 would be low.

It makes sense that my B12 level would be high, because my diet is very high in animal foods, which are rich sources of B12. I am not aware of any negative consequences of having a somewhat higher level of B12 than the average population. In epidemiological studies, high homocysteine levels have been observed to be associated with higher risk for heart disease, but keep in mind that epidemiological studies cannot prove cause and effect (for more info about this topic, see my brief post about this: “The Problem with Epidemiology.”) In clinical studies, lowering homocysteine levels turned out not to reduce risk for heart disease. Some people have genetic differences in enzymes that cause homocysteine to accumulate, so perhaps that is true for me.

Anion gap

This just means that there are extra charged particles in the bloodstream that were not directly measured. The ones that are directly measured are sodium, chloride, and CO2 (carbon dioxide). It is common for people in ketosis to have a bit of an anion gap because ketones are charged particles. Note that my CO2 level was normal, which means that I was in ketosis, not ketoacidosis. In ketoacidosis, the CO2 level would be LOW.

Cholesterol and triglycerides

Elevated total cholesterol or elevated LDL do not concern me (for more information about this, please see my cholesterol page). I care much more about my HDL (pretty good, but it was even better last year when I was exercising regularly) and my triglycerides (again, also pretty good, but even better last year).

Apolipoprotein B

Nicknamed “ApoB” for short, Apolipoprotein B is a fatty protein on the outside of LDL particles. The more ApoB you have, the more LDL particles you have. Higher numbers are usually considered bad, because what we want are small numbers of big fluffy LDL particles, not large numbers of small, dense LDL particles. It is unclear to me precisely how ApoB and LDL particle size are related, but my basic understanding of this relationship is that people with insulin resistance are more likely to have high ApoB values.

I believe I am more insulin resistant than the average person, given my high fasting and post-meal blood sugar values when eating a diet containing typical amounts of protein and carbohydrate. It seems that high ApoB levels are not uncommon in people eating a ketogenic diet, and that cardiologists are unsure whether this is unhealthy. Listen to Jimmy Moore’s interview with Dr. Thomas Dayspring for his take on this issue.

Thyroid tests and ketogenic diets

My TSH (thyroid stimulating hormone) level was normal, and that is the test that most doctors currently use to screen for low thyroid hormone activity. However, my circulating levels of T3 (the most active form of thyroid hormone) and reverse T3 (the deactivated form of rT3) are both “abnormal”, and most importantly, the ratio between them is very low. This may help to explain why my energy was low during this diet, although I have to keep in mind that I have never had T3 and reverse T3 measured before, so there is no way for me to know what my levels were before this diet.

When the body is stressed or undernourished, it will work to lower thyroid hormone activity to slow metabolism. It is definitely possible that my low thyroid hormone activity could have been caused by an extreme ketogenic diet. Whether low thyroid activity (without symptoms of hypothyrodism) is ultimately a good or bad thing for the body is debatable, as some (most notably Dr. Rosedale) believe that a “cooler” metabolic rate may be beneficial.

Folate

Folate (aka Folic Acid) is famous for being found in green leafy vegetables. One problem with my 90-day all-meat diet last summer was that my folate level dropped to below normal. I tried to supplement with folic acid tablets but couldn’t tolerate them, so I added occasional chicken liver to my diet last summer and that seemed to correct the problem.

Vitamin D

My levels have improved since last summer, when I started taking Vitamin D supplements.

Where to from here?

I continue to believe in the promise of ketogenic diets for overall health, mental health, appetite control, and weight management. However, I personally was not able to tolerate the diet recommended by Dr. Seyfried for cancer treatment—at least not as I had constructed it. If any of you have ever reached ketones of 4.0 and blood sugars of 55-65 and had a different experience, I would love to hear from you. I hope that people with cancer may achieve important benefits from a less extreme ketogenic diet, but I do not know if that is true.

I went back through Seyfried’s book again last week and found that, in one place he refers to a target ketone zone of 3.0 mM to 5.0 mM (whereas he usually used 4.0mM as his minimum target zone); 3.0 would have been easier, because I could have eaten a little more protein. Theoretically, a standard ketogenic diet (aka “nutritional ketosis, such as that recommended by Phinney & Volek, which aims for ketones in the 0.5 to 3.0 mM range) or the Rosedale Diet (which does not recommend testing ketone levels at all), should provide benefits to all and should not be harmful, but whether they pack the punch necessary to fight cancer or control seizures is unclear.

For the sake of my own future health, and to satisfy my intellectual curiosity, I would like to try a standard ketogenic diet, and had hoped to gradually transition into such a diet this past week without going out of ketosis, but unfortunately, that didn’t happen.

Ketogenic diet experiment, take 2

So, what to do now? I’d like to try moderate nutritional ketosis using the mostly-meat diet that worked so well for me last summer. However, I don’t know if I’ll be able to limit my protein enough to get my ketones into the target range without getting hungry.

I know people who have been very successful at managing weight and controlling appetite using a standard ketogenic diet, including a friend of mine whose progress has been inspiring to me. She has been following a ketogenic diet since October and agreed to let me post about her experience. Her post provides more promising and hopeful results than those I personally have yet to offer. . . . Read a terrific guest post by Anne, who successfully and happily lost weight using nutritional ketosis.

I hope you have enjoyed witnessing the launch and demise of my ketogenic Hindenburg . . .

If you are interested in starting a ketogenic diet yourself, see my online guide: “Ketogenic Diets 101.”

No shortage of lessons this week in my little Ketogenic Klassroom. Viruses, hormones, hunger, red meat, and a long-awaited dairy experiment! I wasn’t the happiest of campers this week and had difficulty figuring out what more I could eat to stave off hunger without falling out of ketosis. While I’m hopeful that keto-adaptation will occur if I stick with it and remain patient, this experiment is becoming more challenging with time, which is precisely the opposite of what I’d expected.

Note: this post was originally published on Aug 1, 2013. It was edited to streamline content and improve graphics in June 2016; therefore some older comments may pertain to content that was removed during revision.

This post is part of a series describing my attempt to follow Dr. Seyfried’s dietary recommendations for cancer. To start at the beginning, please go to the first post: “Seyfried’s Ketogenic Cancer Diet: My Fasting Jump-Start to Ketosis.“

Day 22 (2/21/13)

Notes: Woke up feeling fine other than minor residual cold symptoms. Wasn’t hungry.

Day 23 (2/22/13)

Notes: Eyes dry and vision slightly blurry for about a half hour after waking; then fine after eating. Lethargic, heavy, slow, drained today but mentally clear, focused, and productive. Appetite was fine until evening, when it became very strong. I wasn’t exactly sure how to count values for the roasted chicken skin, so I may have under-eaten today. Stomach growly, cold, tired, heart poundy. Slept from 9:30 pm to 1:30 am and woke up extremely hungry, so I tested my blood ketones and blood sugar:

So I ate more chicken skin and some tuna fish + olive oil, which helped. Because it was the middle of the night, I added the chicken skin and 1/2 of the tuna values to Fri and the other half of the tuna values to Saturday. Went back to sleep from 4:30 am to 6:15 am (poor quality, light sleep). The roasted chicken skin weighed 50 g but I was unable to locate any nutrition data for roasted chicken skin by weight on the internet. (The day’s food stats don’t include the chicken skin.)

Day 24 (2/23/13)

Notes: Woke feeling unrefreshed, very hungry, slightly lightheaded, lethargic, heartbeat strong. I ate my entire protein allotment for the day by 10 am because I was so hungry. It helped a lot. I’m clearly not getting enough of something lately—not enough calories? Not enough protein? Not enough fat? Who knows . . . I’m starting by adding more fat calories, but if that doesn’t do the trick, I’ll need to increase protein.

Afternoon/evening appetite was low, but I ate some beef fat anyway as an experiment to raise my calories. It made me feel a little queasy and gave me a mild headache, but it took away the heart pounding sensation I’ve had for the past 3 weeks . . . interesting . . . and took my appetite down to zero. My energy improved a bit, as well, but my sleep quality was poor.

Day 25 (2/24/13)

Morning notes: Woke feeling unrested. No ravenous hunger or pounding heart, but somewhat hungry with low energy. My cold symptoms are almost entirely gone.

Mid-morning notes: Two hours after eating a breakfast of chicken and duckfat (21 grams of protein + 29 grams of fat for a total of 374 calories), I still felt a bit lightheaded and cold and fuzzy-headed, so I purchased some beef fat from the local butcher. Before eating it, I checked my values:

In honor of Pippin (from The Fellowship of the Ring), and my time living in Germany, I decided to have a “second breakfast” (or “zweites Frühstück”). This consisted of tunafish and duck fat (13 g protein and 227 g fat). Then I checked my values after two more hours:

Now for brunch I’m going to have the rest of my protein grams (chicken) and the same amount of fat grams as in the first two breakfasts, but in the form of heavy cream. I’ve wanted to do a dairy experiment for a long time, but wanted to wait until I was firmly in ketosis first. I have long suspected that dairy can throw some people out of ketosis but have never tested this idea before. I waited two more hours and re-tested everything:

The cream caused a bit of upper respiratory irritation, making me feel like coughing whenever I took a deep breath. It also gave me a very mild headache and I felt warm. Those are the highest blood sugar and lowest ketone readings in a while. Was it the cream? We can’t be sure yet, because, as you know, I haven’t been testing my values throughout the day like this, so this may be a normal trend, but a few more experiments will give us better clues.

I will eat the rest of my fat calories as heavy cream today, and we’ll see if my values continue to go down. It will be especially interesting to see what my values are tomorrow morning, since I have lots of previous data for morning values. I won’t go any higher on my fat grams today than yesterday, so that we can do the cleanest experiment possible.

Evening notes: In the afternoon and evening, I was distracted by thoughts of food—dancing through my head were images of chocolate cupcakes, giant balls of fresh mozzarella cheese, grilled burgers, and all kinds of yummy things. I told myself that if I don’t eat dairy tomorrow, I should be free of these intrusive, delectable daydreams. Productivity and mental energy was pretty good today.

Day 26 (2/25/13)

Notes: I did not have hunger signals this morning—no lightheadedness, lethargy, or pounding heart. Also no food cravings. While I can’t be 100% sure that it was the cream that caused my food cravings yesterday, it seemed to spike my blood sugar a bit, and dropped my ketones this morning. I have no other explanation—especially for the ketones.

Day 27 (2/26/13)

Notes: Felt a bit lightheaded mid-morning so ate some more food.

I’ve been trying to use roasted beef fat for extra fat/calories but if I eat more than a little bit, my stomach feels quite queasy and I get a mild headache.

I had eaten all my protein and fat calories by 1 pm, felt lousy for a few hours, napped briefly a couple of times midday. Then my mind felt more awake and I was not lightheaded anymore.

Day 28 (2/27/13)

Morning notes: Heart pounding, mild tinnitus (ear ringing), and sl bloated/heavy feeling. I am attributing these effects to beef products, which I usually avoid, but I’m having a hard time finding fat that is appealing to eat on its own. I am envious of those of you who can eat cheese, cream, coconut oil, nuts, and eggs. Any ONE of those things would make this diet much easier.

Evening notes: I was fairly hungry by early evening but was still able to concentrate and function very well at work. Dry cough, dry eyes, poor sleep.

Keto-adaptation and reflections on week 4

Keto-adaptation

This current plan is not sustainable for me and is clearly not healthy. Perhaps if I’d been able to comfortably eat more fat, it would have worked. I would have been willing to tolerate some fatigue and some hunger, which some people experience during the first two to three weeks of ketoadaptation, but it’s been more than three weeks and these have not been the only worrisome signs, so time to increase protein intake.

Food sensitivities and ketosis

My original goal for this week was to eat the same things every day to make for a cleaner experiment, but when I was eating only chicken, turkey, tuna, and duck fat, I felt I wasn’t getting enough nutrition, so I wanted to add some red meat. Beef seems to bother me, so I added lamb. Unfortunately, one can’t buy lamb fat, and I needed to add fat to manage hunger.

Energy and ketosis

I may not have been in ketosis long enough (it’s been 25 days) to be fully adapted—for some it can take up to five weeks. I hope that this is why my physical energy is generally low. It may be that, despite the fact that I’m generating plenty o’ ketones, my cells are not yet good at burning them for fuel. I had originally intended to add some exercise this week, but I didn’t feel like I could do that yet.

Virus

My cold virus lingers. Although symptoms are very mild, they are not completely gone.

Hormones and ketosis

I was not expecting to have a practically nonexistent cycle this month. I have never experienced that before. When I looked into it online, it turns out to be a well-known side effect of ketogenic diets for women, yet there is not a single word about this potential issue in either Dr. Rosedale’s book nor in Phinney and Volek’s books. However, these experts don’t ask people to aim for ketones of 4+ mM, either. According to Dr. Rosedale, when one loses weight on his diet, the body naturally focuses on maintenance and repair, not on reproduction. That all makes sense, but I am not interested in extreme dieting to the detriment of normal body function.

Blood sugar

My blood sugar occasionally flirts with 65 mg/dL (the upper end of Dr. Seyfried’s “zone of metabolic management” for cancer patients), but it only goes that low when I haven’t been eating enough. I may need to abandon this goal, since the only way I can think of to reduce my blood sugar even further would be to reduce protein even further, and I can’t do that.

Can ketones be too high?

When ketones are in the 5+ range, it feels more like starvation (based on my experiences with fasting on days 1 through 4) than dieting, and doesn’t feel healthy. I feel cold, sluggish, and can’t sleep.

For people without cancer or seizures, who are just using this diet to lose weight, improve function/performance, manage mood swings, or manage appetite, does the degree of ketosis matter? Most people seem to report good weight loss and energy with ketone levels in Phinney & Volek’s recommended range of 0.5 to 3.0 mM.

Sleep and ketosis

My sleep could have been affected by my red meat experiments this week (beef, lamb) and/or by the diet itself, which does cause insomnia for some people. Given that I’ve had some good nights of sleep on this diet when I avoid foods that tend to bother me and my ketones are under 5, I’m inclined to think the majority of the blame for this week’s lousy sleep belongs to red meat.

Dairy and ketosis

I found the dairy experiment very interesting. The carbohydrate cravings were strong, and dairy did seem to lower ketones and raise blood sugar. However, a single days’ experiment is not much to go on, so I may need to repeat this experiment from time to time.

Timing of meals and ketosis

My tendency was to want to eat most or all of my food in the morning. Dr. Rosedale recommends dividing meals throughout day, but I was too hungry in the morning to be able to do that. In an interview on Jimmy Moore’s podcast, Ask the Low-Carb Experts, Dr. Phinney said it is unknown whether dividing meals or to eating once a day is better.

Protein vs. fat vs. calories

I’ve tried increasing fat and calories to increase my energy, blood pressure, and ketones and reduce the hunger I’ve had this past week, but I haven’t been very successful. I am very concerned that I’m not getting enough protein—as evidenced by nearly nonexistent hormonal cycle, low energy, and poor/slow recovery from cold virus.

What does this mean for cancer patients?

I wish I were a better guinea pig for those of you considering ketogenic diets for cancer treatment, but it appears as if my food sensitivities may be affecting my keto-adaptation course and therefore make it difficult for you to use my experiences to tell you what this kind of diet would be like for you. However, if you can tolerate fats like coconut oil, butter, cheese, sour cream, mayonnaise, etc., you may be able to achieve Seyfried’s target zone without raising your protein intake.

Goals for week 5

• Increase protein to see if I can improve my blood pressure and energy.
• No red meat—to see if my sleep will normalize without it.

To see whether I reached either of these goals, go to the next post “Keto for Cancer: Week 5—Ketogenic Diet Blood Tests.” If you are interested in starting a ketogenic diet yourself, see my online guide: “Ketogenic Diets 101.”

No shortage of lessons this week in my little Ketogenic Klassroom. Viruses, hormones, hunger, red meat, and a long-awaited dairy experiment! I wasn’t the happiest of campers this week and had difficulty figuring out what more I could eat to stave off hunger without falling out of ketosis. While I’m hopeful that keto-adaptation will occur if I stick with it and remain patient, this experiment is becoming more challenging with time, which is precisely the opposite of what I’d expected.

Note: this post was originally published on Aug 1, 2013. It was edited to streamline content and improve graphics in June 2016; therefore some older comments may pertain to content that was removed during revision.

This post is part of a series describing my attempt to follow Dr. Seyfried’s dietary recommendations for cancer. To start at the beginning, please go to the first post: “Seyfried’s Ketogenic Cancer Diet: My Fasting Jump-Start to Ketosis.“

Day 22 (2/21/13)

Notes: Woke up feeling fine other than minor residual cold symptoms. Wasn’t hungry.

Day 23 (2/22/13)

Notes: Eyes dry and vision slightly blurry for about a half hour after waking; then fine after eating. Lethargic, heavy, slow, drained today but mentally clear, focused, and productive. Appetite was fine until evening, when it became very strong. I wasn’t exactly sure how to count values for the roasted chicken skin, so I may have under-eaten today. Stomach growly, cold, tired, heart poundy. Slept from 9:30 pm to 1:30 am and woke up extremely hungry, so I tested my blood ketones and blood sugar:

So I ate more chicken skin and some tuna fish + olive oil, which helped. Because it was the middle of the night, I added the chicken skin and 1/2 of the tuna values to Fri and the other half of the tuna values to Saturday. Went back to sleep from 4:30 am to 6:15 am (poor quality, light sleep). The roasted chicken skin weighed 50 g but I was unable to locate any nutrition data for roasted chicken skin by weight on the internet. (The day’s food stats don’t include the chicken skin.)

Day 24 (2/23/13)

Notes: Woke feeling unrefreshed, very hungry, slightly lightheaded, lethargic, heartbeat strong. I ate my entire protein allotment for the day by 10 am because I was so hungry. It helped a lot. I’m clearly not getting enough of something lately—not enough calories? Not enough protein? Not enough fat? Who knows . . . I’m starting by adding more fat calories, but if that doesn’t do the trick, I’ll need to increase protein.

Afternoon/evening appetite was low, but I ate some beef fat anyway as an experiment to raise my calories. It made me feel a little queasy and gave me a mild headache, but it took away the heart pounding sensation I’ve had for the past 3 weeks . . . interesting . . . and took my appetite down to zero. My energy improved a bit, as well, but my sleep quality was poor.

Day 25 (2/24/13)

Morning notes: Woke feeling unrested. No ravenous hunger or pounding heart, but somewhat hungry with low energy. My cold symptoms are almost entirely gone.

Mid-morning notes: Two hours after eating a breakfast of chicken and duckfat (21 grams of protein + 29 grams of fat for a total of 374 calories), I still felt a bit lightheaded and cold and fuzzy-headed, so I purchased some beef fat from the local butcher. Before eating it, I checked my values:

In honor of Pippin (from The Fellowship of the Ring), and my time living in Germany, I decided to have a “second breakfast” (or “zweites Frühstück”). This consisted of tunafish and duck fat (13 g protein and 227 g fat). Then I checked my values after two more hours:

Now for brunch I’m going to have the rest of my protein grams (chicken) and the same amount of fat grams as in the first two breakfasts, but in the form of heavy cream. I’ve wanted to do a dairy experiment for a long time, but wanted to wait until I was firmly in ketosis first. I have long suspected that dairy can throw some people out of ketosis but have never tested this idea before. I waited two more hours and re-tested everything:

The cream caused a bit of upper respiratory irritation, making me feel like coughing whenever I took a deep breath. It also gave me a very mild headache and I felt warm. Those are the highest blood sugar and lowest ketone readings in a while. Was it the cream? We can’t be sure yet, because, as you know, I haven’t been testing my values throughout the day like this, so this may be a normal trend, but a few more experiments will give us better clues.

I will eat the rest of my fat calories as heavy cream today, and we’ll see if my values continue to go down. It will be especially interesting to see what my values are tomorrow morning, since I have lots of previous data for morning values. I won’t go any higher on my fat grams today than yesterday, so that we can do the cleanest experiment possible.

Evening notes: In the afternoon and evening, I was distracted by thoughts of food—dancing through my head were images of chocolate cupcakes, giant balls of fresh mozzarella cheese, grilled burgers, and all kinds of yummy things. I told myself that if I don’t eat dairy tomorrow, I should be free of these intrusive, delectable daydreams. Productivity and mental energy was pretty good today.

Day 26 (2/25/13)

Notes: I did not have hunger signals this morning—no lightheadedness, lethargy, or pounding heart. Also no food cravings. While I can’t be 100% sure that it was the cream that caused my food cravings yesterday, it seemed to spike my blood sugar a bit, and dropped my ketones this morning. I have no other explanation—especially for the ketones.

Day 27 (2/26/13)

Notes: Felt a bit lightheaded mid-morning so ate some more food.

I’ve been trying to use roasted beef fat for extra fat/calories but if I eat more than a little bit, my stomach feels quite queasy and I get a mild headache.

I had eaten all my protein and fat calories by 1 pm, felt lousy for a few hours, napped briefly a couple of times midday. Then my mind felt more awake and I was not lightheaded anymore.

Day 28 (2/27/13)

Morning notes: Heart pounding, mild tinnitus (ear ringing), and sl bloated/heavy feeling. I am attributing these effects to beef products, which I usually avoid, but I’m having a hard time finding fat that is appealing to eat on its own. I am envious of those of you who can eat cheese, cream, coconut oil, nuts, and eggs. Any ONE of those things would make this diet much easier.

Evening notes: I was fairly hungry by early evening but was still able to concentrate and function very well at work. Dry cough, dry eyes, poor sleep.

Keto-adaptation and reflections on week 4

Keto-adaptation

This current plan is not sustainable for me and is clearly not healthy. Perhaps if I’d been able to comfortably eat more fat, it would have worked. I would have been willing to tolerate some fatigue and some hunger, which some people experience during the first two to three weeks of ketoadaptation, but it’s been more than three weeks and these have not been the only worrisome signs, so time to increase protein intake.

Food sensitivities and ketosis

My original goal for this week was to eat the same things every day to make for a cleaner experiment, but when I was eating only chicken, turkey, tuna, and duck fat, I felt I wasn’t getting enough nutrition, so I wanted to add some red meat. Beef seems to bother me, so I added lamb. Unfortunately, one can’t buy lamb fat, and I needed to add fat to manage hunger.

Energy and ketosis

I may not have been in ketosis long enough (it’s been 25 days) to be fully adapted—for some it can take up to five weeks. I hope that this is why my physical energy is generally low. It may be that, despite the fact that I’m generating plenty o’ ketones, my cells are not yet good at burning them for fuel. I had originally intended to add some exercise this week, but I didn’t feel like I could do that yet.

Virus

My cold virus lingers. Although symptoms are very mild, they are not completely gone.

Hormones and ketosis

I was not expecting to have a practically nonexistent cycle this month. I have never experienced that before. When I looked into it online, it turns out to be a well-known side effect of ketogenic diets for women, yet there is not a single word about this potential issue in either Dr. Rosedale’s book nor in Phinney and Volek’s books. However, these experts don’t ask people to aim for ketones of 4+ mM, either. According to Dr. Rosedale, when one loses weight on his diet, the body naturally focuses on maintenance and repair, not on reproduction. That all makes sense, but I am not interested in extreme dieting to the detriment of normal body function.

Blood sugar

My blood sugar occasionally flirts with 65 mg/dL (the upper end of Dr. Seyfried’s “zone of metabolic management” for cancer patients), but it only goes that low when I haven’t been eating enough. I may need to abandon this goal, since the only way I can think of to reduce my blood sugar even further would be to reduce protein even further, and I can’t do that.

Can ketones be too high?

When ketones are in the 5+ range, it feels more like starvation (based on my experiences with fasting on days 1 through 4) than dieting, and doesn’t feel healthy. I feel cold, sluggish, and can’t sleep.

For people without cancer or seizures, who are just using this diet to lose weight, improve function/performance, manage mood swings, or manage appetite, does the degree of ketosis matter? Most people seem to report good weight loss and energy with ketone levels in Phinney & Volek’s recommended range of 0.5 to 3.0 mM.

Sleep and ketosis

My sleep could have been affected by my red meat experiments this week (beef, lamb) and/or by the diet itself, which does cause insomnia for some people. Given that I’ve had some good nights of sleep on this diet when I avoid foods that tend to bother me and my ketones are under 5, I’m inclined to think the majority of the blame for this week’s lousy sleep belongs to red meat.

Dairy and ketosis

I found the dairy experiment very interesting. The carbohydrate cravings were strong, and dairy did seem to lower ketones and raise blood sugar. However, a single days’ experiment is not much to go on, so I may need to repeat this experiment from time to time.

Timing of meals and ketosis

My tendency was to want to eat most or all of my food in the morning. Dr. Rosedale recommends dividing meals throughout day, but I was too hungry in the morning to be able to do that. In an interview on Jimmy Moore’s podcast, Ask the Low-Carb Experts, Dr. Phinney said it is unknown whether dividing meals or to eating once a day is better.

Protein vs. fat vs. calories

I’ve tried increasing fat and calories to increase my energy, blood pressure, and ketones and reduce the hunger I’ve had this past week, but I haven’t been very successful. I am very concerned that I’m not getting enough protein—as evidenced by nearly nonexistent hormonal cycle, low energy, and poor/slow recovery from cold virus.

What does this mean for cancer patients?

I wish I were a better guinea pig for those of you considering ketogenic diets for cancer treatment, but it appears as if my food sensitivities may be affecting my keto-adaptation course and therefore make it difficult for you to use my experiences to tell you what this kind of diet would be like for you. However, if you can tolerate fats like coconut oil, butter, cheese, sour cream, mayonnaise, etc., you may be able to achieve Seyfried’s target zone without raising your protein intake.

Goals for week 5

• Increase protein to see if I can improve my blood pressure and energy.
• No red meat—to see if my sleep will normalize without it.

To see whether I reached either of these goals, go to the next post “Keto for Cancer: Week 5—Ketogenic Diet Blood Tests.” If you are interested in starting a ketogenic diet yourself, see my online guide: “Ketogenic Diets 101.”

No shortage of lessons this week in my little Ketogenic Klassroom. Viruses, hormones, hunger, red meat, and a long-awaited dairy experiment! I wasn’t the happiest of campers this week and had difficulty figuring out what more I could eat to stave off hunger without falling out of ketosis. While I’m hopeful that keto-adaptation will occur if I stick with it and remain patient, this experiment is becoming more challenging with time, which is precisely the opposite of what I’d expected.

Note: this post was originally published on Aug 1, 2013. It was edited to streamline content and improve graphics in June 2016; therefore some older comments may pertain to content that was removed during revision.

This post is part of a series describing my attempt to follow Dr. Seyfried’s dietary recommendations for cancer. To start at the beginning, please go to the first post: “Seyfried’s Ketogenic Cancer Diet: My Fasting Jump-Start to Ketosis.“

Day 22 (2/21/13)

Notes: Woke up feeling fine other than minor residual cold symptoms. Wasn’t hungry.

Day 23 (2/22/13)

Notes: Eyes dry and vision slightly blurry for about a half hour after waking; then fine after eating. Lethargic, heavy, slow, drained today but mentally clear, focused, and productive. Appetite was fine until evening, when it became very strong. I wasn’t exactly sure how to count values for the roasted chicken skin, so I may have under-eaten today. Stomach growly, cold, tired, heart poundy. Slept from 9:30 pm to 1:30 am and woke up extremely hungry, so I tested my blood ketones and blood sugar:

So I ate more chicken skin and some tuna fish + olive oil, which helped. Because it was the middle of the night, I added the chicken skin and 1/2 of the tuna values to Fri and the other half of the tuna values to Saturday. Went back to sleep from 4:30 am to 6:15 am (poor quality, light sleep). The roasted chicken skin weighed 50 g but I was unable to locate any nutrition data for roasted chicken skin by weight on the internet. (The day’s food stats don’t include the chicken skin.)

Day 24 (2/23/13)

Notes: Woke feeling unrefreshed, very hungry, slightly lightheaded, lethargic, heartbeat strong. I ate my entire protein allotment for the day by 10 am because I was so hungry. It helped a lot. I’m clearly not getting enough of something lately—not enough calories? Not enough protein? Not enough fat? Who knows . . . I’m starting by adding more fat calories, but if that doesn’t do the trick, I’ll need to increase protein.

Afternoon/evening appetite was low, but I ate some beef fat anyway as an experiment to raise my calories. It made me feel a little queasy and gave me a mild headache, but it took away the heart pounding sensation I’ve had for the past 3 weeks . . . interesting . . . and took my appetite down to zero. My energy improved a bit, as well, but my sleep quality was poor.

Day 25 (2/24/13)

Morning notes: Woke feeling unrested. No ravenous hunger or pounding heart, but somewhat hungry with low energy. My cold symptoms are almost entirely gone.

Mid-morning notes: Two hours after eating a breakfast of chicken and duckfat (21 grams of protein + 29 grams of fat for a total of 374 calories), I still felt a bit lightheaded and cold and fuzzy-headed, so I purchased some beef fat from the local butcher. Before eating it, I checked my values:

In honor of Pippin (from The Fellowship of the Ring), and my time living in Germany, I decided to have a “second breakfast” (or “zweites Frühstück”). This consisted of tunafish and duck fat (13 g protein and 227 g fat). Then I checked my values after two more hours:

Now for brunch I’m going to have the rest of my protein grams (chicken) and the same amount of fat grams as in the first two breakfasts, but in the form of heavy cream. I’ve wanted to do a dairy experiment for a long time, but wanted to wait until I was firmly in ketosis first. I have long suspected that dairy can throw some people out of ketosis but have never tested this idea before. I waited two more hours and re-tested everything:

The cream caused a bit of upper respiratory irritation, making me feel like coughing whenever I took a deep breath. It also gave me a very mild headache and I felt warm. Those are the highest blood sugar and lowest ketone readings in a while. Was it the cream? We can’t be sure yet, because, as you know, I haven’t been testing my values throughout the day like this, so this may be a normal trend, but a few more experiments will give us better clues.

I will eat the rest of my fat calories as heavy cream today, and we’ll see if my values continue to go down. It will be especially interesting to see what my values are tomorrow morning, since I have lots of previous data for morning values. I won’t go any higher on my fat grams today than yesterday, so that we can do the cleanest experiment possible.

Evening notes: In the afternoon and evening, I was distracted by thoughts of food—dancing through my head were images of chocolate cupcakes, giant balls of fresh mozzarella cheese, grilled burgers, and all kinds of yummy things. I told myself that if I don’t eat dairy tomorrow, I should be free of these intrusive, delectable daydreams. Productivity and mental energy was pretty good today.

Day 26 (2/25/13)

Notes: I did not have hunger signals this morning—no lightheadedness, lethargy, or pounding heart. Also no food cravings. While I can’t be 100% sure that it was the cream that caused my food cravings yesterday, it seemed to spike my blood sugar a bit, and dropped my ketones this morning. I have no other explanation—especially for the ketones.

Day 27 (2/26/13)

Notes: Felt a bit lightheaded mid-morning so ate some more food.

I’ve been trying to use roasted beef fat for extra fat/calories but if I eat more than a little bit, my stomach feels quite queasy and I get a mild headache.

I had eaten all my protein and fat calories by 1 pm, felt lousy for a few hours, napped briefly a couple of times midday. Then my mind felt more awake and I was not lightheaded anymore.

Day 28 (2/27/13)

Morning notes: Heart pounding, mild tinnitus (ear ringing), and sl bloated/heavy feeling. I am attributing these effects to beef products, which I usually avoid, but I’m having a hard time finding fat that is appealing to eat on its own. I am envious of those of you who can eat cheese, cream, coconut oil, nuts, and eggs. Any ONE of those things would make this diet much easier.

Evening notes: I was fairly hungry by early evening but was still able to concentrate and function very well at work. Dry cough, dry eyes, poor sleep.

Keto-adaptation and reflections on week 4

Keto-adaptation

This current plan is not sustainable for me and is clearly not healthy. Perhaps if I’d been able to comfortably eat more fat, it would have worked. I would have been willing to tolerate some fatigue and some hunger, which some people experience during the first two to three weeks of ketoadaptation, but it’s been more than three weeks and these have not been the only worrisome signs, so time to increase protein intake.

Food sensitivities and ketosis

My original goal for this week was to eat the same things every day to make for a cleaner experiment, but when I was eating only chicken, turkey, tuna, and duck fat, I felt I wasn’t getting enough nutrition, so I wanted to add some red meat. Beef seems to bother me, so I added lamb. Unfortunately, one can’t buy lamb fat, and I needed to add fat to manage hunger.

Energy and ketosis

I may not have been in ketosis long enough (it’s been 25 days) to be fully adapted—for some it can take up to five weeks. I hope that this is why my physical energy is generally low. It may be that, despite the fact that I’m generating plenty o’ ketones, my cells are not yet good at burning them for fuel. I had originally intended to add some exercise this week, but I didn’t feel like I could do that yet.

Virus

My cold virus lingers. Although symptoms are very mild, they are not completely gone.

Hormones and ketosis

I was not expecting to have a practically nonexistent cycle this month. I have never experienced that before. When I looked into it online, it turns out to be a well-known side effect of ketogenic diets for women, yet there is not a single word about this potential issue in either Dr. Rosedale’s book nor in Phinney and Volek’s books. However, these experts don’t ask people to aim for ketones of 4+ mM, either. According to Dr. Rosedale, when one loses weight on his diet, the body naturally focuses on maintenance and repair, not on reproduction. That all makes sense, but I am not interested in extreme dieting to the detriment of normal body function.

Blood sugar

My blood sugar occasionally flirts with 65 mg/dL (the upper end of Dr. Seyfried’s “zone of metabolic management” for cancer patients), but it only goes that low when I haven’t been eating enough. I may need to abandon this goal, since the only way I can think of to reduce my blood sugar even further would be to reduce protein even further, and I can’t do that.

Can ketones be too high?

When ketones are in the 5+ range, it feels more like starvation (based on my experiences with fasting on days 1 through 4) than dieting, and doesn’t feel healthy. I feel cold, sluggish, and can’t sleep.

For people without cancer or seizures, who are just using this diet to lose weight, improve function/performance, manage mood swings, or manage appetite, does the degree of ketosis matter? Most people seem to report good weight loss and energy with ketone levels in Phinney & Volek’s recommended range of 0.5 to 3.0 mM.

Sleep and ketosis

My sleep could have been affected by my red meat experiments this week (beef, lamb) and/or by the diet itself, which does cause insomnia for some people. Given that I’ve had some good nights of sleep on this diet when I avoid foods that tend to bother me and my ketones are under 5, I’m inclined to think the majority of the blame for this week’s lousy sleep belongs to red meat.

Dairy and ketosis

I found the dairy experiment very interesting. The carbohydrate cravings were strong, and dairy did seem to lower ketones and raise blood sugar. However, a single days’ experiment is not much to go on, so I may need to repeat this experiment from time to time.

Timing of meals and ketosis

My tendency was to want to eat most or all of my food in the morning. Dr. Rosedale recommends dividing meals throughout day, but I was too hungry in the morning to be able to do that. In an interview on Jimmy Moore’s podcast, Ask the Low-Carb Experts, Dr. Phinney said it is unknown whether dividing meals or to eating once a day is better.

Protein vs. fat vs. calories

I’ve tried increasing fat and calories to increase my energy, blood pressure, and ketones and reduce the hunger I’ve had this past week, but I haven’t been very successful. I am very concerned that I’m not getting enough protein—as evidenced by nearly nonexistent hormonal cycle, low energy, and poor/slow recovery from cold virus.

What does this mean for cancer patients?

I wish I were a better guinea pig for those of you considering ketogenic diets for cancer treatment, but it appears as if my food sensitivities may be affecting my keto-adaptation course and therefore make it difficult for you to use my experiences to tell you what this kind of diet would be like for you. However, if you can tolerate fats like coconut oil, butter, cheese, sour cream, mayonnaise, etc., you may be able to achieve Seyfried’s target zone without raising your protein intake.

Goals for week 5

• Increase protein to see if I can improve my blood pressure and energy.
• No red meat—to see if my sleep will normalize without it.

To see whether I reached either of these goals, go to the next post “Keto for Cancer: Week 5—Ketogenic Diet Blood Tests.” If you are interested in starting a ketogenic diet yourself, see my online guide: “Ketogenic Diets 101.”