Category: Nutrition

So, what if you already avoid refined carbs, eat the right kinds of fats, and still have ADHD symptoms? Perhaps you eat a Paleo diet, or a low-carb Paleo diet, or even a ketogenic diet, and are still troubled by ADHD . . . what then?

Food sensitivities can cause ADHD symptoms

In my work with children and adults with ADHD, I have seen some patients reduce or even cure their ADHD symptoms simply by removing certain foods from their diet. People are often completely unaware that they have a food sensitivity, especially if the food that bothers them is something they eat every day, like wheat or dairy products. Everybody is different, so food that is the culprit for one person may not bother another person at all. While any food can be problematic, the ones that have been shown by researchers to be the most commonly associated with ADHD symptoms are:

• Gluten (from wheat and related grains)*
• Dairy products (usually due to casein, a dairy protein)
• Soy
• Corn
• Legumes
• Oats
• Eggs
• Nuts and peanuts
• Citrus
• Chocolate
• Tomato
• Yeast
• Fish
• Shellfish

*People with Celiac Disease (an autoimmune disease associated with gluten) are more likely to have ADHD symptoms, and these symptoms usually improve on a gluten-free diet. However, people with ADHD are at no higher risk for Celiac Disease than people without ADHD.

Simplified diets shown to cure ADHD

Dietary studies have found a strong connection between food and ADHD symptoms. These studies are small and have their limitations, as most nutrition studies do, but they all produce remarkable results. These studies compared a standard diet to a special limited diet and found that the special diet resulted in a dramatic reduction in ADHD symptoms. Most people with ADHD are not aware of these studies (notice that all of them were conducted in Europe):

Egger 1985 (London)

Carter 1993 (London)

Schmidt 1997 (Germany)

Pelsser 2002 (Netherlands)

Pelsser 2009 (Netherlands)

What was so magical about these diets? These simple diets removed all of the common food culprits listed above, as well as sugar and processed foods. These diets have a lot in common with whole-foods, hunter-gatherer diets of meats, fruits, and vegetables. I personally believe the studies may have worked even better if researchers had also removed the fruit juice (high in sugars), margarine (high in omega-6 and trans fats), and white rice (high glycemic index), but nevertheless, these diets worked very well. 62% to 82% response rates in outpatients and a 24% response rate in inpatients—pretty impressive.

The Feingold Diet?

Ben Feingold, MD was a pediatric allergy specialist who wrote a book in 1975 called Why Your Child Is Hyperactive. He recommended a diet free of artificial flavors and colors, and advised avoiding foods containing salicylate, a naturally occurring plant chemical found in a wide variety of fruits, vegetables, and spices. He claimed that his special diet was effective for 50% of children with ADHD. This diet is referred to as the Feingold Diet, or as the “K-P Diet” (K-P for Kaiser-Permanente, the name of the medical center where he worked).

Plants use salicylates as signaling compounds and to protect themselves from infection and insects. Aspirin is a famous salicylate originally extracted from willow bark. Below are the foods Dr. Feingold thought to be high in salicylates, and therefore advised eliminating from the diet:

Improved food testing methods have since determined that the following foods contain the highest amounts of salicylates [Wood 2011]:

• Fruits: red grapes, lemons, peaches, pears, cherries. dried fruits typically much higher.
• Vegetables: asparagus, eggplant, broccoli, mushrooms, onions, green peppers
• Beverages: coffee, tea, beer, pineapple juice, tomato juice
• Herbs/Spices: All tested were extremely high, with exception of garlic which was extremely low

Legumes and grains are very low in salicylates. All animal foods, including meats, organ meats, and dairy products, contain little to no salicylate.

Does the Feingold Diet really work?

None of the studies of this diet were able to generate the impressive 50% cure rate that Feingold reported. However, some of the studies did find that a small number of children (11% to 33%) were significantly less hyperactive on his diet.

ADHD and artificial colors

An analysis [Schab 2004] of the 15 best studies done on food coloring and ADHD found a clear connection between artificial food colorings and hyperactivity in children with ADHD. A review of all studies [Stevens 2011] concluded that artificial food colorings can result in significant changes in behavior in people with ADHD, and two studies found that artificial colorings can even cause hyperactivity in people who do not have a history of ADHD. The vast majority of studies tested complicated mixtures of artificial colors rather than single additives, often in combination with sodium benzoate, a popular preservative. The artificial colors used in experiments are listed below. Those in italics are no longer approved for use in foods in the United States:

Tartrazine (Yellow #5)
Sunset Yellow (Yellow #6)
Quinoline Yellow (Yellow #10)
Allura Red (Red #40)
Erythrosine (Red #3)
Carmoisine (Red #10)
Ponceau 4R (a red dye)
Brilliant Blue (Blue #1)
Indigotine (Blue #2)
Fast Green (Green #3)
Orange B

Are people with ADHD more sensitive?

In my clinical experience I have found that many of my ADHD patients are more sensitive in general, not only to foods and medications, but also to other stimuli, such as scents and sounds. They can also be more socially sensitive, particularly to perceived judgment, exclusion, or rejection. The European studies detailed above make it clear that many children have food sensitivities that manifest themselves as ADHD symptoms. Could it be that some people with ADHD are simply reacting badly to certain foods? I know for myself that changing my diet significantly improved my concentration, productivity, motivation and energy, and eliminated my dependence on caffeine to get things done.

Your own body of evidence

While there are good medical tests available for true food allergies, there are no medical tests for food sensitivities. So how do you know if your ADHD symptoms are being caused by food sensitivities? There are many other bodily clues to food issues, such as asthma, eczema, fatigue, fluid retention, frequent headaches, or digestive problems. One possible sign of food sensitivity that is easy to recognize is the presence of dark circles under the eyes, which allergy specialists call “allergic shiners.” People often mistake dark circles for signs of poor sleep or fatigue, but dark circles are most often a sign of allergy or sensitivity.

An example from my own personal experience: I underwent complete food allergy (skin) testing and was found to have no allergies to any of the foods included in the panel, including nuts. However, whenever I ate something that contained small amounts of nuts, the next morning I would see dark circles under my eyes (along with a variety of other unhappy symptoms), which I did not normally have. 24% of people who do not have allergies have allergic shiners—how many of these non-allergic people have food sensitivities?

Unfortunately, the only way for you to discover whether or not your ADHD symptoms are due to a food sensitivity is to do your own dietary experiment. There are many ways to do this, but the two most popular are the all-at-once approach and the one-at-a-time approach. You may prefer to remove all of the most common culprits for two weeks and see if you feel better. If you do, then reintroduce one food at a time for at least three days in a row to try to identify the guilty food (or foods). Others prefer to remove one culprit at a time for two weeks to see if that single food is causing the problem. If it is not, that food can be added back, and the next suspect can be removed for two weeks, and so on. This approach takes much more time, but some people find it easier than removing so many culprits all at once.

The hypo-allergenic Paleo diet

When people ask me what diet I recommend to identify if food sensitivities may be causing ADHD, I recommend what I call a “hypo-allergenic” Paleo diet for two weeks. This diet consists of:

• Chicken, turkey, duck and/or lamb and their organ meats (no sauces or marinades)
• Any fresh/frozen vegetables you like (except for green beans, wax beans, sprouts, beets and white potato)
• Any whole fresh/frozen fruits you like except for citrus and tomato.
• Water, seltzer

No dairy, nuts, soy, grains, legumes, nuts, seeds, beef, pork, chocolate, eggs, yeast, coffee, tea, sugar, juices, processed foods, artificial ingredients, gum, sweeteners (whether natural or artificial), or cold cuts at first. Avoid preserved, fermented, canned, dried, smoked, pickled, and excessively salty foods.

After two weeks if you are feeling better, you can try adding back beef, pork, fish, citrus, tomato, coffee, tea, etc. one at a time for three days each to see if they bother you.

Keep in mind that any food can be a culprit, including any food on my hypo-allergenic Paleo diet, so some people may need to explore further, but the above diet removes all of the most common culprits.

These dietary experiments can be frustrating and difficult, but they can also be very illuminating. Once you have figured out your food sensitivities, it does not mean you can never eat that food again—that’s completely up to you—but at least you’ll have more control over how you feel from day to day if you want to!

What about you?

Have you been able to reduce your ADHD symptoms by making dietary changes? What has or has not worked for you?

If you are want to learn more more about ADHD and diet, you may be interested in my articles “Sugar and ADHD” and “Attention! Is Your Diet Causing ADHD?“

What is ADHD?

Attention deficit/hyperactivity disorder, or ADHD, affects about 4% of children and about 2% of adults. ADHD is a complex condition and poorly named, because it is not really an attention deficit—but rather an inability to regulate attention. People with ADHD have trouble directing attention to what’s most important and sustaining that attention for as long as required. This can cause all kinds of problems in school, at home, on the road, at work, and in relationships.

I would estimate that about a quarter of my students at Harvard University and Smith College present with a chief complaint of “difficulty concentrating.” When I worked at the Hallowell Center, which specializes in the treatment of people with attention-related disorders, 100% of clients came to me because of problems with focus and productivity. Nearly every psychiatric diagnosis—depression, anxiety, bipolar disorder, schizophrenia, substance abuse, and PTSD, just to name a few—can affect the ability to concentrate. Even common issues like stress or lack of sleep can impair attention. Therefore, the majority of people who have attention problems do not turn out to have ADHD after all, which is why a skilled psychiatric evaluation is so important in determining the underlying problem. Whether you are interested in treating ADHD with diet or simply improving your concentration, it is important to understand how diet affects attention regulation.

The chemistry of concentration

We psychiatrists are fond of saying that ADHD is caused by a chemical imbalance in the brain, and that medicines can help to correct the imbalance. There are at least two brain chemicals (or neurotransmitters) that seem to be involved in ADHD: dopamine and norepinephrine. These are tiny messengers that send signals from one brain cell to the next. If levels of dopamine or norepinephrine are too low, or if the system that processes these neurotransmitters is not functioning properly, a stimulant medication (like Ritalin or Adderall) might help by forcing brain cells to release higher amounts of these chemicals. But what causes the chemical imbalance in the first place? Why are the levels of these chemicals too low? And where do these chemicals come from?

Brain chemicals come from food.

After all, where else could they possibly come from? This seems so obvious, but many doctors don’t think about the connection. We are trained to think about which medications might correct the imbalance, not what causes it in the first place. So which foods does your body need to make these important chemicals?

Dopamine and norepinephrine are made from protein.

The body breaks down proteins in foods like fish, chicken, and beef into amino acids, and one of these amino acids is called tyrosine. The body then uses special chemical reactions to turn tyrosine into the dopamine and norepinephrine brain cells need to communicate with each other:

TYROSINE → DOPAMINE → NOREPINEPHRINE

Therefore, those not getting enough protein (especially at breakfast), may have difficulty concentrating. For more information about proteins and amino acids, including daily requirements and best food sources, see my Protein page.

The brain is mostly made of fat.

Yes, even yours. 🙂 About 2/3 of the brain is made of fat, and about 20% of that fat should consist of omega-3 fatty acids. Omega-3 fatty acids keep cell membranes flexible and healthy. Without these special polyunsaturated fats, brain cells become stiff and can’t communicate with each other easily. So even if there is plenty of dopamine and norepinephrine around, brain cells may not be able to pass these chemicals back and forth properly if the right fats aren’t built in to their membranes.

The brain is picky about omega-3s

There are 3 types of omega-3 fatty acids: ALA, DHA, and EPA. The brain’s favorite omega-3 fatty acid is called DHA. ALA is found in both plant and animal foods. Popular vegetarian sources of ALA include flaxseed, walnuts, and chia seeds. ALA is often called the “parent” omega-3 because of this pathway:

ALA → EPA → DHA

Looking at this pathway you might think that if you eat enough ALA, you’re all set. But here’s the problem—the body has a very hard time converting ALA to EPA and DHA, so about 95% of it remains stuck in the form of ALA. However, we convert EPA to DHA very easily. This means that in order to be sure our brain gets enough DHA, we need to eat EPA and DHA themselves. Plant foods do not contain any EPA or DHA. EPA and DHA are hard to find in the typical American diet because the best sources are wild animal foods, such as cold-water, fatty fish (like salmon and mackerel), and naturally-raised animals, such as grass-fed cows and pasture-raised chickens. This is why public health officials sometimes recommend omega-3 supplements. These supplements are typically in the form of fish oil, but there are also new vegan-friendly supplements available which are made from algae.

Omega-3s and ADHD

There have been many studies of omega-3 fatty acids in the treatment of ADHD, but most have shown no benefit or only modest improvement compared to medications. However, many experts seem to agree with this conclusion, quoted from a 2011 (Bloch) review:

“Based on the currently available evidence, using omega-3 fatty acid supplementation in lieu of traditional pharmacologic treatments is not recommended in children with significant ADHD symptoms. However, given the evidence of modest efficacy of omega-3 fatty acid supplementation and its relatively benign side-effect profile, omega-3 fatty acid supplementation, particularly with higher doses of EPA, is a reasonable treatment strategy as augmentation to traditional pharmacotherapy or for those families reticent to use psychopharmacologic agents.”

The bottom line is that medications seemed to work much better than omega-3 supplements. In the studies that did show a modest benefit from omega-3s, the doses of EPA that seemed to work best were between 300 and 600 mg per day. But wait . . . doesn’t the brain prefer DHA? Yes. Even though the brain loves and needs lots of DHA to work properly, researchers find that EPA supplements seem to work much better than DHA supplements. As these were short-term studies, the thinking is that EPA works better because of its fast-acting anti-inflammatory properties.

Is your brain unbalanced?

There’s another kind of essential polyunsaturated fatty acid we need to take into consideration: omega-6. Theoretically, if you eat too much omega-6 it is harder for the omega-3s to work properly because they compete with each other. Many scientists believe that these two types of polyunsaturated fats—the omega-3s and the omega-6s—need to be in balance for our brains and bodies to function at their best. Omega-6 fatty acids are found in a wide variety of plant and animal foods, but certain kinds of plant foods are extremely high in omega-6. Animal fats contain on average 10-20% omega-6, whereas vegetable oils, such as soybean, corn, peanut, and sunflower oils, contain 50-80% omega-6. The average American eats a diet that is far too high in omega-6 and far too low in omega-3. Would the omega-3 ADHD studies have been more impressive if the people in the experiments were also asked to reduce the amount of omega-6 they were eating? Hard to say . . .

For more information about omega-3 fatty acids, the difference between EPA and other omega-3s, best food sources, and how to improve your omega-3 balance, please see my Fats page.

Minerals are mandatory: iron and zinc

Iron is the most prevalent mineral in the body. When we think of iron, we usually think about its role in our red blood cells where it functions to carry oxygen from the lungs out to all of our cells. We don’t usually think of it as a brain mineral, but remember our neurotransmitter pathway from the top of this article? The first step on the road from tyrosine to dopamine and norepinephrine requires an enzyme called tyrosine hydroxylase, and this enzyme needs iron in order to do its job. Iron is also important in regulating dopamine function. Therefore, iron deficiency, which is relatively common, can impair concentration.

The second most common mineral in the body is zinc. Brain cells that release dopamine out into the synapse (space between cells where communication occurs) vacuum it back up using a dopamine transporter. This crucial transporter is regulated by zinc. Zinc binds to the dopamine transporter and slows it down, allowing dopamine to remain active in the synapse for a longer period of time before being pulled back into the cell to be recycled. It is essentially a natural dopamine reuptake inhibitor. Interestingly, this is also one of the ways in which stimulant medications work to improve dopamine activity.

There have been two clinical trials of zinc supplements in the treatment of ADHD, both of which noted some benefit. An Iranian study found that Ritalin + (15 mg of elemental) zinc given for six weeks worked twice as well as Ritalin + a sugar pill. A Turkish study found that (40 mg of elemental) zinc given for 12 weeks worked twice as well as a sugar pill.

Zinc and iron supplements can be hard to stomach. Zinc frequently causes nausea, and iron supplements can cause constipation and other gastrointestinal problems. Are there alternatives to supplements for people who have mineral deficiencies? What is causing these deficiencies in the first place? Are there dietary changes we can make that can improve our mineral status?

Plant foods are very low in zinc, whereas animal foods are excellent sources of zinc.

While both plant and animal foods contain iron, the type of iron found in animal foods (called heme iron) is 8 times more bioavailable (useful) to us than the type found in plant foods.

Seed foods (which include grains, beans, and nuts) contain phytic acid, which interferes with our ability to absorb essential minerals. For more information, including a surprising study illustrating the degree that phytic acid interferes in zinc absorption, see my “Micronutrients and Mental Health” article.

Some plant foods contain tannins, which interfere with iron absorption. For more information, please see my Fruits page.

Tips for treating ADHD with diet

• Be sure to eat some protein at breakfast
• Include foods rich in omega-3 fatty acids in your diet (healthy animal foods), or take a daily supplement containing at least 300 mg of EPA
• Reduce omega-6 intake by minimizing vegetable oils, nuts, and seeds
• Improve mineral absorption by reducing phytic acid intake (minimize grains, beans, nuts and seeds)
• If you have iron deficiency, increase meat intake and reduce phytic acid intake (grains, beans, nuts, and seeds) and/or take a heme iron supplement.
• Improve zinc status by reducing phytic acid intake (minimize grains, beans, nuts, and seeds), and including animal foods in your diet. Zinc supplements may also be helpful.
• If you eat a vegan or vegetarian diet, please see my see my “Micronutrients and Mental Health” article for information about how to optimize your mineral status.

So, paying more attention to the quality of your diet just might help you pay more attention to . . . everything.

Learn more about how to treat your ADHD with diet in my posts “Sugar and ADHD” and “Food Sensitivities and ADHD.”

What is ADHD?

Attention deficit/hyperactivity disorder, or ADHD, affects about 4% of children and about 2% of adults. ADHD is a complex condition and poorly named, because it is not really an attention deficit—but rather an inability to regulate attention. People with ADHD have trouble directing attention to what’s most important and sustaining that attention for as long as required. This can cause all kinds of problems in school, at home, on the road, at work, and in relationships.

I would estimate that about a quarter of my students at Harvard University and Smith College present with a chief complaint of “difficulty concentrating.” When I worked at the Hallowell Center, which specializes in the treatment of people with attention-related disorders, 100% of clients came to me because of problems with focus and productivity. Nearly every psychiatric diagnosis—depression, anxiety, bipolar disorder, schizophrenia, substance abuse, and PTSD, just to name a few—can affect the ability to concentrate. Even common issues like stress or lack of sleep can impair attention. Therefore, the majority of people who have attention problems do not turn out to have ADHD after all, which is why a skilled psychiatric evaluation is so important in determining the underlying problem. Whether you are interested in treating ADHD with diet or simply improving your concentration, it is important to understand how diet affects attention regulation.

The chemistry of concentration

We psychiatrists are fond of saying that ADHD is caused by a chemical imbalance in the brain, and that medicines can help to correct the imbalance. There are at least two brain chemicals (or neurotransmitters) that seem to be involved in ADHD: dopamine and norepinephrine. These are tiny messengers that send signals from one brain cell to the next. If levels of dopamine or norepinephrine are too low, or if the system that processes these neurotransmitters is not functioning properly, a stimulant medication (like Ritalin or Adderall) might help by forcing brain cells to release higher amounts of these chemicals. But what causes the chemical imbalance in the first place? Why are the levels of these chemicals too low? And where do these chemicals come from?

Brain chemicals come from food.

After all, where else could they possibly come from? This seems so obvious, but many doctors don’t think about the connection. We are trained to think about which medications might correct the imbalance, not what causes it in the first place. So which foods does your body need to make these important chemicals?

Dopamine and norepinephrine are made from protein.

The body breaks down proteins in foods like fish, chicken, and beef into amino acids, and one of these amino acids is called tyrosine. The body then uses special chemical reactions to turn tyrosine into the dopamine and norepinephrine brain cells need to communicate with each other:

TYROSINE → DOPAMINE → NOREPINEPHRINE

Therefore, those not getting enough protein (especially at breakfast), may have difficulty concentrating. For more information about proteins and amino acids, including daily requirements and best food sources, see my Protein page.

The brain is mostly made of fat.

Yes, even yours. 🙂 About 2/3 of the brain is made of fat, and about 20% of that fat should consist of omega-3 fatty acids. Omega-3 fatty acids keep cell membranes flexible and healthy. Without these special polyunsaturated fats, brain cells become stiff and can’t communicate with each other easily. So even if there is plenty of dopamine and norepinephrine around, brain cells may not be able to pass these chemicals back and forth properly if the right fats aren’t built in to their membranes.

The brain is picky about omega-3s

There are 3 types of omega-3 fatty acids: ALA, DHA, and EPA. The brain’s favorite omega-3 fatty acid is called DHA. ALA is found in both plant and animal foods. Popular vegetarian sources of ALA include flaxseed, walnuts, and chia seeds. ALA is often called the “parent” omega-3 because of this pathway:

ALA → EPA → DHA

Looking at this pathway you might think that if you eat enough ALA, you’re all set. But here’s the problem—the body has a very hard time converting ALA to EPA and DHA, so about 95% of it remains stuck in the form of ALA. However, we convert EPA to DHA very easily. This means that in order to be sure our brain gets enough DHA, we need to eat EPA and DHA themselves. Plant foods do not contain any EPA or DHA. EPA and DHA are hard to find in the typical American diet because the best sources are wild animal foods, such as cold-water, fatty fish (like salmon and mackerel), and naturally-raised animals, such as grass-fed cows and pasture-raised chickens. This is why public health officials sometimes recommend omega-3 supplements. These supplements are typically in the form of fish oil, but there are also new vegan-friendly supplements available which are made from algae.

Omega-3s and ADHD

There have been many studies of omega-3 fatty acids in the treatment of ADHD, but most have shown no benefit or only modest improvement compared to medications. However, many experts seem to agree with this conclusion, quoted from a 2011 (Bloch) review:

“Based on the currently available evidence, using omega-3 fatty acid supplementation in lieu of traditional pharmacologic treatments is not recommended in children with significant ADHD symptoms. However, given the evidence of modest efficacy of omega-3 fatty acid supplementation and its relatively benign side-effect profile, omega-3 fatty acid supplementation, particularly with higher doses of EPA, is a reasonable treatment strategy as augmentation to traditional pharmacotherapy or for those families reticent to use psychopharmacologic agents.”

The bottom line is that medications seemed to work much better than omega-3 supplements. In the studies that did show a modest benefit from omega-3s, the doses of EPA that seemed to work best were between 300 and 600 mg per day. But wait . . . doesn’t the brain prefer DHA? Yes. Even though the brain loves and needs lots of DHA to work properly, researchers find that EPA supplements seem to work much better than DHA supplements. As these were short-term studies, the thinking is that EPA works better because of its fast-acting anti-inflammatory properties.

Is your brain unbalanced?

There’s another kind of essential polyunsaturated fatty acid we need to take into consideration: omega-6. Theoretically, if you eat too much omega-6 it is harder for the omega-3s to work properly because they compete with each other. Many scientists believe that these two types of polyunsaturated fats—the omega-3s and the omega-6s—need to be in balance for our brains and bodies to function at their best. Omega-6 fatty acids are found in a wide variety of plant and animal foods, but certain kinds of plant foods are extremely high in omega-6. Animal fats contain on average 10-20% omega-6, whereas vegetable oils, such as soybean, corn, peanut, and sunflower oils, contain 50-80% omega-6. The average American eats a diet that is far too high in omega-6 and far too low in omega-3. Would the omega-3 ADHD studies have been more impressive if the people in the experiments were also asked to reduce the amount of omega-6 they were eating? Hard to say . . .

For more information about omega-3 fatty acids, the difference between EPA and other omega-3s, best food sources, and how to improve your omega-3 balance, please see my Fats page.

Minerals are mandatory: iron and zinc

Iron is the most prevalent mineral in the body. When we think of iron, we usually think about its role in our red blood cells where it functions to carry oxygen from the lungs out to all of our cells. We don’t usually think of it as a brain mineral, but remember our neurotransmitter pathway from the top of this article? The first step on the road from tyrosine to dopamine and norepinephrine requires an enzyme called tyrosine hydroxylase, and this enzyme needs iron in order to do its job. Iron is also important in regulating dopamine function. Therefore, iron deficiency, which is relatively common, can impair concentration.

The second most common mineral in the body is zinc. Brain cells that release dopamine out into the synapse (space between cells where communication occurs) vacuum it back up using a dopamine transporter. This crucial transporter is regulated by zinc. Zinc binds to the dopamine transporter and slows it down, allowing dopamine to remain active in the synapse for a longer period of time before being pulled back into the cell to be recycled. It is essentially a natural dopamine reuptake inhibitor. Interestingly, this is also one of the ways in which stimulant medications work to improve dopamine activity.

There have been two clinical trials of zinc supplements in the treatment of ADHD, both of which noted some benefit. An Iranian study found that Ritalin + (15 mg of elemental) zinc given for six weeks worked twice as well as Ritalin + a sugar pill. A Turkish study found that (40 mg of elemental) zinc given for 12 weeks worked twice as well as a sugar pill.

Zinc and iron supplements can be hard to stomach. Zinc frequently causes nausea, and iron supplements can cause constipation and other gastrointestinal problems. Are there alternatives to supplements for people who have mineral deficiencies? What is causing these deficiencies in the first place? Are there dietary changes we can make that can improve our mineral status?

Plant foods are very low in zinc, whereas animal foods are excellent sources of zinc.

While both plant and animal foods contain iron, the type of iron found in animal foods (called heme iron) is 8 times more bioavailable (useful) to us than the type found in plant foods.

Seed foods (which include grains, beans, and nuts) contain phytic acid, which interferes with our ability to absorb essential minerals. For more information, including a surprising study illustrating the degree that phytic acid interferes in zinc absorption, see my “Micronutrients and Mental Health” article.

Some plant foods contain tannins, which interfere with iron absorption. For more information, please see my Fruits page.

Tips for treating ADHD with diet

• Be sure to eat some protein at breakfast
• Include foods rich in omega-3 fatty acids in your diet (healthy animal foods), or take a daily supplement containing at least 300 mg of EPA
• Reduce omega-6 intake by minimizing vegetable oils, nuts, and seeds
• Improve mineral absorption by reducing phytic acid intake (minimize grains, beans, nuts and seeds)
• If you have iron deficiency, increase meat intake and reduce phytic acid intake (grains, beans, nuts, and seeds) and/or take a heme iron supplement.
• Improve zinc status by reducing phytic acid intake (minimize grains, beans, nuts, and seeds), and including animal foods in your diet. Zinc supplements may also be helpful.
• If you eat a vegan or vegetarian diet, please see my see my “Micronutrients and Mental Health” article for information about how to optimize your mineral status.

So, paying more attention to the quality of your diet just might help you pay more attention to . . . everything.

Learn more about how to treat your ADHD with diet in my posts “Sugar and ADHD” and “Food Sensitivities and ADHD.”

The holiday table would look dull, lifeless, and naked without an intensely colorful, jellied, saucy, free-form, or cylindrical cranberry side dish. We believe in the festive and medicinal properties of these sour little berries, so let’s take a closer look and see whether they are truly the crimson crusaders of our dreams.

Why aren’t cranberries sweet?

Berries begin their lives tart, to discourage animals from eating them before their seeds are mature. Then, when the time is right, most berries become sweet to entice hungry animals to munch upon them, but not so the cranberry. I was fascinated to learn that cranberry bushes do not use animals to spread their seeds; they use water! Cranberries are very light and contain inner air pockets. When cranberry bogs flood, or if the ripe buoyant berries fall off the cranberry bush, they simply float away with the current in hopes of being deposited on a distant bank. They don’t need animals to help them reproduce, so they don’t need to go to the trouble of sweetening their fruits. Nature is amazing.

Since we’re not designated by the cranberry plant as preferred seed carriers, clearly we are not “meant” to eat cranberries. However, that doesn’t necessarily mean that they are bad for us. In fact, there are many studies which suggest they may be good for us under certain conditions—most famously in the case of urinary tract infections (or UTIs). Is that true? If so, what is their secret ingredient?

Cranberry ingredient list

Cranberries contain numerous chemicals with interesting properties: proanthocyanidins, triterpenoids, lectins, catechins, ascorbic acid, benzoic acid, quinic acid, oxalic acid, citric acid and malic acid. Of these, the ones that have been the most intensely studied are the proanthocyanidins, or PAs for short. PAs are also commonly referred to as tannins, and it is the presence of these chemicals that gives cranberries their astringency (they make your mouth feel dry). PAs belong to the polyphenol (aka flavonoid) family of plant compounds. Plants use these bitter chemicals to ward off hungry creatures such as bacteria and insects and to protect themselves from harsh weather. Plants can also break PAs down into a rainbow of colorful pigments. PAs can be grouped into two major categories, depending on their chemical structure: A-type and B-type. B-types are found in a wide variety of foods, including red wine (grape skins), coffee, tea and chocolate. A-type PAs are uncommon, being found only in cinnamon, plum, peanut, and our friend, the cranberry.

A-type PAs are special in that they can prevent many types of bacteria, including E. coli (the most common bacteria found in UTIs), from attaching to certain surfaces, including the cell surfaces lining the urinary tract. Aha!

How might cranberries fight urinary tract infections?

There have been numerous clinical human studies of cranberry juices and cranberry extracts in the prevention of UTIs in all kinds of patients—children, adults, pregnant women, seniors, and people with bladder conditions that require the use of catheters. These studies vary widely in the types of cranberry products tested and the doses of active ingredients used and have generated very mixed results. A Cochrane review conducted in 2008 concluded:

“Given the large number of dropouts/withdrawals from studies (mainly attributed to the acceptability of consuming cranberry products particularly juice, over long periods), and the evidence that the benefit for preventing UTI is small, cranberry juice cannot currently be recommended for the prevention of UTIs. Other preparations (such as powders) need to be quantified using standardised methods to ensure the potency, and contain enough of the ‘active’ ingredient, before being evaluated in clinical studies or recommended for use.”1

A review of randomized controlled trials2 noted the following trends, but they were not strong enough to be statistically significant:

• Cranberry juice is more effective than tablets or capsules of cranberry extract
• Cranberry products work best if taken at least every 8 hours
• Women and children are the most likely to benefit from cranberry treatments.

Cranberry juice treatments are hard to stomach, with up to 50% of subjects dropping out of studies due to side effects (nausea, vomiting, diarrhea, unpleasant taste).

Prevention or cure?

Cranberry PAs have the power to prevent bacterial attachment, but they probably do not have the ability to dislodge bacteria once they have set up shop, therefore cranberry juice cannot be recommended for treatment of existing UTIs. The weak/mixed evidence suggesting that they may help to prevent UTIs in susceptible individuals indicates that one would need to drink cranberry juice 3 times a day every day to reduce risk of future UTIs. It is not yet known what dose of PAs or what volume of cranberry juice may work best, if PAs even work at all.

Is it all just juicy gossip?

It could be that we simply need more robust studies to prove the might of our sour little Cape Crusader. But there may be other factors at play.

We know that cranberries are high in PAs, and that they survive cooking and digestion, but the vast majority of cranberry PAs are not absorbed into the bloodstream and therefore do not make it to the urethra (urinary tract). On average, less than 1% of cranberry juice PAs show up in the urine. Is that a high enough concentration to ward off bacteria? We don’t know. If it isn’t, it could be that the PAs are NOT the secret ingredient in cranberries after all. The fact that cranberry juice seems more effective than cranberry capsules suggests that an ingredient present in the juice that is not present in raw cranberries might be playing a role behind the scenes.

If it’s not the PAs, what is it?

What else is in cranberry juice?

Fructose itself can prevent E. coli from attaching to cells. The vast majority of cranberry juice drinks available are sweetened with corn syrup and/or sugar, both of which contain about 50% fructose (fruit sugar). How much of the power of cranberry juice might be due to the fructose content? We don’t know. However, a large study showed that a low-calorie cranberry juice sweetened with sucralose (Splenda) did not reduce UTI risk any more than a cranberry-free beverage did.1 The authors don’t specify whether the control beverage was also sweetened with sucralose, but I assume that it was. The authors note that the rate of UTI was about 50% lower than expected in BOTH groups, suggesting that both beverages were equally effective. The authors wondered if perhaps it was the vitamin C content in both drinks that was responsible for the possible reduction in UTIs.

Bottom line about cranberries

• The jury is out as to whether cranberry juice is effective in the prevention of UTIs.
• It remains unclear which ingredient(s) in cranberry juice may be helpful in preventing UTIs.
• The tannins/proanthocyanidins within cranberries, which are there for the protection of the fruit in the wilderness, have so far been shown to be non-toxic, probably because they are very poorly absorbed. However, tannins are known “anti-nutrients”, and can interfere with the absorption of dietary iron and protein. For more information about tannins, please see my Fruits page.
• The risk of drinking traditionally sweetened cranberry juice three times a day, which is very high in sugar and can therefore increase risk of obesity, diabetes, heart disease, and other chronic health problems, probably outweighs any potential reduction in UTI risk.
• Oh, and most importantly, cranberries are cool cuz they float:)

The holiday table would look dull, lifeless, and naked without an intensely colorful, jellied, saucy, free-form, or cylindrical cranberry side dish. We believe in the festive and medicinal properties of these sour little berries, so let’s take a closer look and see whether they are truly the crimson crusaders of our dreams.

Why aren’t cranberries sweet?

Berries begin their lives tart, to discourage animals from eating them before their seeds are mature. Then, when the time is right, most berries become sweet to entice hungry animals to munch upon them, but not so the cranberry. I was fascinated to learn that cranberry bushes do not use animals to spread their seeds; they use water! Cranberries are very light and contain inner air pockets. When cranberry bogs flood, or if the ripe buoyant berries fall off the cranberry bush, they simply float away with the current in hopes of being deposited on a distant bank. They don’t need animals to help them reproduce, so they don’t need to go to the trouble of sweetening their fruits. Nature is amazing.

Since we’re not designated by the cranberry plant as preferred seed carriers, clearly we are not “meant” to eat cranberries. However, that doesn’t necessarily mean that they are bad for us. In fact, there are many studies which suggest they may be good for us under certain conditions—most famously in the case of urinary tract infections (or UTIs). Is that true? If so, what is their secret ingredient?

Cranberry ingredient list

Cranberries contain numerous chemicals with interesting properties: proanthocyanidins, triterpenoids, lectins, catechins, ascorbic acid, benzoic acid, quinic acid, oxalic acid, citric acid and malic acid. Of these, the ones that have been the most intensely studied are the proanthocyanidins, or PAs for short. PAs are also commonly referred to as tannins, and it is the presence of these chemicals that gives cranberries their astringency (they make your mouth feel dry). PAs belong to the polyphenol (aka flavonoid) family of plant compounds. Plants use these bitter chemicals to ward off hungry creatures such as bacteria and insects and to protect themselves from harsh weather. Plants can also break PAs down into a rainbow of colorful pigments. PAs can be grouped into two major categories, depending on their chemical structure: A-type and B-type. B-types are found in a wide variety of foods, including red wine (grape skins), coffee, tea and chocolate. A-type PAs are uncommon, being found only in cinnamon, plum, peanut, and our friend, the cranberry.

A-type PAs are special in that they can prevent many types of bacteria, including E. coli (the most common bacteria found in UTIs), from attaching to certain surfaces, including the cell surfaces lining the urinary tract. Aha!

How might cranberries fight urinary tract infections?

There have been numerous clinical human studies of cranberry juices and cranberry extracts in the prevention of UTIs in all kinds of patients—children, adults, pregnant women, seniors, and people with bladder conditions that require the use of catheters. These studies vary widely in the types of cranberry products tested and the doses of active ingredients used and have generated very mixed results. A Cochrane review conducted in 2008 concluded:

“Given the large number of dropouts/withdrawals from studies (mainly attributed to the acceptability of consuming cranberry products particularly juice, over long periods), and the evidence that the benefit for preventing UTI is small, cranberry juice cannot currently be recommended for the prevention of UTIs. Other preparations (such as powders) need to be quantified using standardised methods to ensure the potency, and contain enough of the ‘active’ ingredient, before being evaluated in clinical studies or recommended for use.”1

A review of randomized controlled trials2 noted the following trends, but they were not strong enough to be statistically significant:

• Cranberry juice is more effective than tablets or capsules of cranberry extract
• Cranberry products work best if taken at least every 8 hours
• Women and children are the most likely to benefit from cranberry treatments.

Cranberry juice treatments are hard to stomach, with up to 50% of subjects dropping out of studies due to side effects (nausea, vomiting, diarrhea, unpleasant taste).

Prevention or cure?

Cranberry PAs have the power to prevent bacterial attachment, but they probably do not have the ability to dislodge bacteria once they have set up shop, therefore cranberry juice cannot be recommended for treatment of existing UTIs. The weak/mixed evidence suggesting that they may help to prevent UTIs in susceptible individuals indicates that one would need to drink cranberry juice 3 times a day every day to reduce risk of future UTIs. It is not yet known what dose of PAs or what volume of cranberry juice may work best, if PAs even work at all.

Is it all just juicy gossip?

It could be that we simply need more robust studies to prove the might of our sour little Cape Crusader. But there may be other factors at play.

We know that cranberries are high in PAs, and that they survive cooking and digestion, but the vast majority of cranberry PAs are not absorbed into the bloodstream and therefore do not make it to the urethra (urinary tract). On average, less than 1% of cranberry juice PAs show up in the urine. Is that a high enough concentration to ward off bacteria? We don’t know. If it isn’t, it could be that the PAs are NOT the secret ingredient in cranberries after all. The fact that cranberry juice seems more effective than cranberry capsules suggests that an ingredient present in the juice that is not present in raw cranberries might be playing a role behind the scenes.

If it’s not the PAs, what is it?

What else is in cranberry juice?

Fructose itself can prevent E. coli from attaching to cells. The vast majority of cranberry juice drinks available are sweetened with corn syrup and/or sugar, both of which contain about 50% fructose (fruit sugar). How much of the power of cranberry juice might be due to the fructose content? We don’t know. However, a large study showed that a low-calorie cranberry juice sweetened with sucralose (Splenda) did not reduce UTI risk any more than a cranberry-free beverage did.1 The authors don’t specify whether the control beverage was also sweetened with sucralose, but I assume that it was. The authors note that the rate of UTI was about 50% lower than expected in BOTH groups, suggesting that both beverages were equally effective. The authors wondered if perhaps it was the vitamin C content in both drinks that was responsible for the possible reduction in UTIs.

Bottom line about cranberries

• The jury is out as to whether cranberry juice is effective in the prevention of UTIs.
• It remains unclear which ingredient(s) in cranberry juice may be helpful in preventing UTIs.
• The tannins/proanthocyanidins within cranberries, which are there for the protection of the fruit in the wilderness, have so far been shown to be non-toxic, probably because they are very poorly absorbed. However, tannins are known “anti-nutrients”, and can interfere with the absorption of dietary iron and protein. For more information about tannins, please see my Fruits page.
• The risk of drinking traditionally sweetened cranberry juice three times a day, which is very high in sugar and can therefore increase risk of obesity, diabetes, heart disease, and other chronic health problems, probably outweighs any potential reduction in UTI risk.
• Oh, and most importantly, cranberries are cool cuz they float:)

We think of fruits as being sweet and juicy, yet the two fruits Americans love to eat most on Thanksgiving are neither. Intensely colorful and tart cranberries, despite being so dry and sour that they taste absolutely terrible in their natural state, are always invited to Thanksgiving dinner. But cranberries are not the only unusual fruits donning the Thanksgiving dinner table—what fall feast would be complete without a bright orange member of the squash family?

Squashes are fruits

We think of most squashes as vegetables because they are dry and starchy rather than sweet and juicy. However, because they contain seeds, they are actually fruits in disguise. The Cucurbita family (squash family) includes not only squashes, pumpkins, and gourds, but also zucchini, yellow squash, cucumbers, and melons. Let’s take a closer look at these vibrant autumn unfruity fruits.

Fruits vs. vegetables

Those of you familiar with my philosophy about vegetables know that I view them as untrustworthy and deserving of suspicion (see my Vegetables page)—but what about fruits? Plants that rely on animals to disperse their seeds tend to wrap their seeds in fruits to entice hungry mobile sorts. If all goes as planned, an unsuspecting creature will eat the seedy fruit, walk away, digest the fruit, and later deposit the seeds, along with a nice meadow-muffin of natural fertilizer, in just the right spot so they can germinate and grow into mature plants. Not the most romantic method of reproduction, but so effective that it’s been around for hundreds of millions of years. Plants want and need animals to eat their fruits, so it would not be in their best interest to invest fruits with toxic compounds—it would be unwise to sicken or kill your reproductive helpers. Therefore, hypothetically speaking, the chemicals in fruits should be gentler on our systems than those in vegetables.

Pumpkins and other squashes are not particularly appealing fruits in their natural state—they generally need to be cooked in order to be palatable. Of course plants in the squash family also have vegetable parts—stems, roots, and leaves, but we don’t tend to eat those parts, probably because they don’t taste very good. In fact, even many fruits in this family don’t taste very good—when was the last time you enjoyed a nice steaming helping of gourd?

Pumpkins and squashes, deconstructed

The Cucurbita moschata include several varieties of pumpkins and squashes, including butternut squash. The poor pumpkin family—they have had every inch of their beings, from stem to seeds, violated by scientists who hope to discover magical, life-saving ingredients. In this post we’ll focus only on the fruit flesh of pumpkins and squashes, since that’s what we like to eat on Thanksgiving.

Does orange = vitamin A?

Carotenoids (such as alpha and beta carotene) are responsible for the beautiful orange color of pumpkins and squashes. We think of orange foods like carrots and sweet potatoes as excellent sources of vitamin A, but you may be surprised to learn that plant foods contain no vitamin A at all, at least as far as humans are concerned. Herbivores (vegan animals) and many other animals possess an enzyme that can convert carotenoids to vitamin A, but we don’t. In our bodies, plant carotenoids have to jump through a series of biological hoops in order to become the active form of vitamin A (retinol) that our bodies can use.

Carotenoids in fibrous foods like pumpkin are trapped within plant cell walls made of indigestible cellulose (insoluble fiber), so that even after cooking and digesting pumpkin, a maximum of only 25% of the carotenoids are freed from its rigid fibrous matrix. Fat is then required to absorb carotenoids (pass the butter please), but even if we eat enough fat with our pumpkin or squash, we can only absorb about 8% of the carotenoids within. Furthermore, once it’s inside our bloodstream, we can only convert about 50% of the beta carotene into active vitamin A. The conversion rate varies widely from one plant food to another. The National Institutes of Health estimate that it is 12 to 24 times more difficult for our bodies to extract vitamin A out of plant foods than from animal foods. Vitamin A from animal sources is in the form of retinyl esters, not carotenoids, and we easily convert these to active vitamin A; therefore, they are completely bio-available. Good food sources of vitamin A include egg yolks and dairy products, but the best source of vitamin A is actually liver. Unfortunately liver is not a pretty orange vegetable, but hey, looks aren’t everything.

Can pumpkins cure cancer?

Well, maybe . . . if you drop one directly on top of a tumor . . .

Pumpkin’s latest claim to fame is cucurmosin, a chemical within pumpkin flesh that is toxic to cancer cells under laboratory conditions. Cucurmosin is a “Ribosome Inactivating Protein”, RIP for short. RIPs are aptly named because they are deadly. RIP’s kill cells by stopping their ribosomes dead in their tracks. Ribosomes are the protein manufacturing assembly lines within all cells (not just cancerous cells), so if they are taken out of commission, all cellular activity grinds to a screeching halt, killing the cell. Two especially potent RIPs are notorious poisons—Shiga toxin (from bacteria) and ricin (from castor beans). Luckily, cucurmosin is a kinder, gentler variety of RIP, because it has a harder time breaking into cells to get at their ribosomes. However, when it does, it is just as merciless as other RIPs. Pumpkins and squashes use cucurmosin to ward off invaders such as bacteria and viruses.

But wait . . . healthy cells also contain ribosomes—does cucurmosin kill them too?

It may be reassuring to know that, in laboratory studies, it takes a much higher dose of cucurmosin to kill healthy cells than to kill cancer cells. But most importantly, and very reassuringly, cooking destroys cucurmosin.

The bottom line

Happily I have found no evidence that compounds within the fruity flesh of pumpkins and related squashes are harmful to our health, provided we eat them cooked. This is in keeping with my theory that the fruity parts of edible plants are usually less likely to irritate our bodies than the vegetable bodies of plants. So chances are excellent that you can enjoy your beautiful, bountiful, colorful, giant pumpkins with wild abandon! Just remember to cook them first, use plenty of delicious fat, and keep the added sugar to a minimum:)

Next up, we explore the magical healing powers of our other holiday favorite in “Cranberries for UTI prevention: Crimson Crusader or Juicy Gossip?“

We think of fruits as being sweet and juicy, yet the two fruits Americans love to eat most on Thanksgiving are neither. Intensely colorful and tart cranberries, despite being so dry and sour that they taste absolutely terrible in their natural state, are always invited to Thanksgiving dinner. But cranberries are not the only unusual fruits donning the Thanksgiving dinner table—what fall feast would be complete without a bright orange member of the squash family?

Squashes are fruits

We think of most squashes as vegetables because they are dry and starchy rather than sweet and juicy. However, because they contain seeds, they are actually fruits in disguise. The Cucurbita family (squash family) includes not only squashes, pumpkins, and gourds, but also zucchini, yellow squash, cucumbers, and melons. Let’s take a closer look at these vibrant autumn unfruity fruits.

Fruits vs. vegetables

Those of you familiar with my philosophy about vegetables know that I view them as untrustworthy and deserving of suspicion (see my Vegetables page)—but what about fruits? Plants that rely on animals to disperse their seeds tend to wrap their seeds in fruits to entice hungry mobile sorts. If all goes as planned, an unsuspecting creature will eat the seedy fruit, walk away, digest the fruit, and later deposit the seeds, along with a nice meadow-muffin of natural fertilizer, in just the right spot so they can germinate and grow into mature plants. Not the most romantic method of reproduction, but so effective that it’s been around for hundreds of millions of years. Plants want and need animals to eat their fruits, so it would not be in their best interest to invest fruits with toxic compounds—it would be unwise to sicken or kill your reproductive helpers. Therefore, hypothetically speaking, the chemicals in fruits should be gentler on our systems than those in vegetables.

Pumpkins and other squashes are not particularly appealing fruits in their natural state—they generally need to be cooked in order to be palatable. Of course plants in the squash family also have vegetable parts—stems, roots, and leaves, but we don’t tend to eat those parts, probably because they don’t taste very good. In fact, even many fruits in this family don’t taste very good—when was the last time you enjoyed a nice steaming helping of gourd?

Pumpkins and squashes, deconstructed

The Cucurbita moschata include several varieties of pumpkins and squashes, including butternut squash. The poor pumpkin family—they have had every inch of their beings, from stem to seeds, violated by scientists who hope to discover magical, life-saving ingredients. In this post we’ll focus only on the fruit flesh of pumpkins and squashes, since that’s what we like to eat on Thanksgiving.

Does orange = vitamin A?

Carotenoids (such as alpha and beta carotene) are responsible for the beautiful orange color of pumpkins and squashes. We think of orange foods like carrots and sweet potatoes as excellent sources of vitamin A, but you may be surprised to learn that plant foods contain no vitamin A at all, at least as far as humans are concerned. Herbivores (vegan animals) and many other animals possess an enzyme that can convert carotenoids to vitamin A, but we don’t. In our bodies, plant carotenoids have to jump through a series of biological hoops in order to become the active form of vitamin A (retinol) that our bodies can use.

Carotenoids in fibrous foods like pumpkin are trapped within plant cell walls made of indigestible cellulose (insoluble fiber), so that even after cooking and digesting pumpkin, a maximum of only 25% of the carotenoids are freed from its rigid fibrous matrix. Fat is then required to absorb carotenoids (pass the butter please), but even if we eat enough fat with our pumpkin or squash, we can only absorb about 8% of the carotenoids within. Furthermore, once it’s inside our bloodstream, we can only convert about 50% of the beta carotene into active vitamin A. The conversion rate varies widely from one plant food to another. The National Institutes of Health estimate that it is 12 to 24 times more difficult for our bodies to extract vitamin A out of plant foods than from animal foods. Vitamin A from animal sources is in the form of retinyl esters, not carotenoids, and we easily convert these to active vitamin A; therefore, they are completely bio-available. Good food sources of vitamin A include egg yolks and dairy products, but the best source of vitamin A is actually liver. Unfortunately liver is not a pretty orange vegetable, but hey, looks aren’t everything.

Can pumpkins cure cancer?

Well, maybe . . . if you drop one directly on top of a tumor . . .

Pumpkin’s latest claim to fame is cucurmosin, a chemical within pumpkin flesh that is toxic to cancer cells under laboratory conditions. Cucurmosin is a “Ribosome Inactivating Protein”, RIP for short. RIPs are aptly named because they are deadly. RIP’s kill cells by stopping their ribosomes dead in their tracks. Ribosomes are the protein manufacturing assembly lines within all cells (not just cancerous cells), so if they are taken out of commission, all cellular activity grinds to a screeching halt, killing the cell. Two especially potent RIPs are notorious poisons—Shiga toxin (from bacteria) and ricin (from castor beans). Luckily, cucurmosin is a kinder, gentler variety of RIP, because it has a harder time breaking into cells to get at their ribosomes. However, when it does, it is just as merciless as other RIPs. Pumpkins and squashes use cucurmosin to ward off invaders such as bacteria and viruses.

But wait . . . healthy cells also contain ribosomes—does cucurmosin kill them too?

It may be reassuring to know that, in laboratory studies, it takes a much higher dose of cucurmosin to kill healthy cells than to kill cancer cells. But most importantly, and very reassuringly, cooking destroys cucurmosin.

The bottom line

Happily I have found no evidence that compounds within the fruity flesh of pumpkins and related squashes are harmful to our health, provided we eat them cooked. This is in keeping with my theory that the fruity parts of edible plants are usually less likely to irritate our bodies than the vegetable bodies of plants. So chances are excellent that you can enjoy your beautiful, bountiful, colorful, giant pumpkins with wild abandon! Just remember to cook them first, use plenty of delicious fat, and keep the added sugar to a minimum:)

Next up, we explore the magical healing powers of our other holiday favorite in “Cranberries for UTI prevention: Crimson Crusader or Juicy Gossip?“

Once called “the ailment of kings” because it mainly afflicted those who could afford a rich diet, gout now affects more than 8 million non-royal Americans. To what do we owe this dubious honor? Is it because we are eating more meat than ever before?

What is gout?

Gout is a special type of arthritis in which certain joints fill up with microscopic shards of uric acid, becoming red, swollen, and exquisitely sensitive to the touch. Most people with gout have too much uric acid in their blood—higher than 6 mg/dl in women and 7 mg/dl in men (levels can reach 12 mg/dl or more in some cases). Uric acid crystals can also cause kidney stones and kidney damage. More than 20% of Americans now have abnormally high uric acid levels.

What is uric acid?

Uric acid is a breakdown product of purines—molecules that help make up some vitally important compounds present in the cells of all plants and animals, including DNA (genes), RNA (protein manufacturing) and ATP (energy). The following are the most familiar purines:

• Adenine
• Guanine
• Caffeine
• Theobromine (cocoa beans, tea leaves, kola nuts, yerba mate)

Low-purine diets

Low-purine diets (in combination with medication) have been prescribed for gout since the middle of the 20th century. This dietary advice is based on the belief that too many purines in the diet cause high uric acid in the blood. Now, since all plants and animals are made of cells, and all cells contain purines, asking someone to eat fewer purines is a tall order. However, since most animal foods are higher in purines than most plant foods (animal foods are denser and contain more cells per unit weight), doctors advise people with gout to eat less meat. You could also lower purines in your diet by simply eating fewer whole foods of all kinds. [Actually, the best advice, if you follow this reasoning to its logical conclusion, would be to eat a 100% junk food diet of flour, sugar, candy, soda, ice cream, and fruit juice—foods that have had their cells destroyed or removed in the refining process—because these foods contain few if any purines at all—sound like a plan?] The below list is adapted from Emmerson 1996:1

High-Purine Foods

• All meats, including organ meats, and seafood
• Meat extracts and gravies
• Yeast and yeast extracts
• Beer, and other alcoholic beverages
• Beans, peas, lentils, oatmeal, spinach, asparagus, cauliflower, and mushrooms

Low-Purine Foods

• Refined cereals and cereal products, such as cornflakes, white bread, pasta, flour, and tapioca
• Milk, milk products, and eggs
• Sugar, sweets, and gelatin
• Butter, polyunsaturated margarine, and all other fats
• Fruit, nuts, and peanut butter
• Lettuce, tomatoes, and green vegetables (except spinach and asparagus)
• Vegetarian cream soups made with low-purine vegetables
• Water, fruit juice, cordials, and carbonated drinks

In actuality, scientists admit that it is impossible to know the true purine content of any food, but even if we did, purines are not the only problem.

Those kings of old must have known how to party.

It has been known for centuries that alcohol consumption can trigger gouty attacks. This connection is now well supported by scientific studies. Two 12 oz beers can raise uric acid levels in healthy men by about 10%, and drinking to intoxication doubles uric acid levels in alcoholics. Interestingly, most alcoholic drinks contain no purines, so how does alcohol raise uric acid levels?

1. Alcohol cuts the kidney’s ability to rid the blood of excess purines by at least 50%.
2. When the liver processes alcohol, lots of ATP (an energy molecule) is used up in the process; ATP contains purines that get broken down into uric acid.
3. Beer is especially risky because it contains alcohol AND purines (derived from brewer’s yeast).

Fructose raises uric acid levels

It has been known since the late 1960s that fructose raises uric acid levels. Examples of foods which contain fructose are fresh fruit (max 10% fructose), dried fruit (max 40% fructose), table sugar (50% fructose) and corn syrup (55% fructose). Uric acid levels rise about 13% after eating meals containing fructose. People with gout have more exaggerated responses to fructose than healthy controls.

“subjects prone to developing gout in the 1700s and 1800s tended to be wealthy and sedentary, often with the ability to afford sugar, the latter of which is known to raise uric acid. Indeed, today gout is increasing in all populations, and if anything, is more common among the poor and less educated.”1

Yet, as you can see in this 2007 New York Times article, fructose is not even on the list of possible dietary factors in gout, which may be why celebrated NY Times food writer Frank Bruni continues to suffer with some symptoms of gout, despite following his doctors’ advice to limit meat and alcohol and to take medication:

“I’ve noticed discernible changes in my health—or at least in the way I feel. How much of that is attributable to my reduced alcohol intake and how much to the exodus of red meat is impossible to say. I haven’t lost more than a pound or two, because carbs have rushed in where protein isn’t permitted to treat . . . the flare-ups [of gout] are subtle now that I’m medicated and reformed.”2

Aye, there’s the rub! Mr. Bruni has gotten right to the meat of the problem—low-purine diets can be high in refined carbohydrates, such as sugar and flour, which raise insulin levels, and now not only do you have gout, but you have a hard time losing weight and you’ve further increased your risk for all kinds of other chronic diseases:

“Fructose is unique among sugars in that it rapidly causes features of metabolic syndrome both in experimental animals and humans. Fructose ingestion also leads to fatty liver and elevated triglycerides in humans and can also raise blood pressure. Intriguingly, fructose is a sugar that has the unique ability to raise serum uric acid. Serum uric acid levels rise within minutes of fructose ingestion… the increase in fructose intake closely parallels the rise in gout, obesity and metabolic syndrome that has occurred over the last two centuries. Serum uric acid levels increased from <3.5 mg/dl in the early twentieth century to over 6 mg/dl today in adult males.”3

How does fructose raise uric acid levels?

“The specific reason why fructose is superior than glucose in increasing fat stores likely relates to the unique first steps in fructose metabolism. When fructose enters the hepatocyte, it is metabolized by a specific enzyme, fructokinase C. Unlike glucokinase, which has a negative feedback system to prevent excessive phosphorylation, the phosphorylation of fructose by fructokinase will proceed uninterrupted, and as a consequence intracellular phosphate depletion and ATP depletion frequently occur. The fall in intracellular phosphate results in the stimulation of AMP deaminase that helps accelerate the degradation of AMP to IMP and later to uric acid. In turn, the intracellular generation of uric acid results in oxidative stress.”1

Translation: Fructose is especially good at turning into fat. The enzymes in the liver that turn fructose into fat use up lots of ATP in the process. ATP contains purines that get broken down into uric acid.

Both alcohol and fructose burn through ATP like kindling. Metabolically speaking, fructose and alcohol have a lot in common, which is why Dr. Robert Lustig mentions them both in the same breath as poisons.

But there’s more to the sugar story

Rapidly digestible carbohydrates such as sugar, flour, starch, fruit juice, and white potato are notorious for causing insulin spikes. Insulin tells the kidneys to reabsorb uric acid into the blood instead of excreting it into the urine. Why? Because insulin is, first and foremost, a growth hormone. In order to grow you need to build more cells, and to build more cells you need more purines.

Thus our dear meat-mourning Mr. Bruni is dutifully eating a low-purine, high-refined carb diet, which both lowers and raises uric acid. As comedian Steven Wright would have said, that’s like putting a humidifier and a dehumidifier in the same room and letting them fight it out.

So what is he supposed to do? What foods would he be left with if we told him he can’t eat carbs, meat, or alcohol? Fat and low-purine vegetables? Unfortunately that diet is dangerously devoid of nutrients. Which is worse for gout—meat or carbs?

My beef with the meat-purine-gout hypothesis

• We are not eating any more meat now than we did 100 years ago.
• Some cultures eating lots of meat, including 19th century Arctic peoples who lived on a diet of nearly 100% animal foods, did not develop gout. “Gout is unknown in Eskimos and Northern Indians despite their purine-rich diet.”1
• Animal foods are higher in protein than plant foods. Proteins increase the elimination of purines in the urine, which can actually lower uric acid levels.
• Some plant foods are rich in purines, including legumes, spinach, asparagus, and mushrooms (dense or rapidly growing plants).
• Purines in the diet do not have much of an effect on uric acid levels, because most of the uric acid in the blood comes from inside the body, as part of everyday cell turnover: “The purine content of the diet does not usually contribute more than 1 mg/dl to the serum urate concentration.”2

Studies tying animal foods to gout have been epidemiological studies which have observed that people who eat more meat tend to have higher uric acid levels and/or a higher risk of gout. These studies have not taken carbohydrate in general, nor fructose in particular, into consideration. Therefore we have no idea whether people who reported eating more meat also happened to eat more fructose, which is, in my opinion, a critical omission given that we have known since 1967 that fructose can raise uric acid levels. Furthermore there are some epidemiological studies that find no association whatsoever between meat and uric acid levels.3 Either way, as many of you know, epidemiological studies are not experiments and correlation does not equal causation.

What do the clinical studies show? 

Unfortunately, as is the case with so many diseases, when the use of drugs to treat gout became popular in the 1950s, interest in dietary strategies fizzled. So we only have a wee handful of small, flawed studies to guide us:

There are ZERO studies that have attempted to prevent gout with diet.

I could only locate a grand total of ONE study of the oft-recommended low-purine, alcohol-free diet that is relevant to our question.1 In this study, 55 Brazilian adults with both high blood pressure and high uric acid levels were divided into three groups— diet alone, low-purine diet plus medication, and medication alone—for three months. Uric acid levels fell by about 2 mg/dl in all three groups by week six. However, people in this study were not gout patients, there was no control group, and the composition of the diet was not described (we are only told what was excluded from the diet), therefore we do not know if this diet contained less fructose and/or less refined carbohydrate than a standard diet. Without that information, we can’t be sure that it was the lack of purines that may have been responsible for the decrease in uric acid.

I located only ONE small pilot study exploring the role of refined carbohydrate in gout.2 Thirteen South African men with gout were placed on a 1600 calorie diet containing 40% unrefined carbohydrate, 30% protein, and 30% (unsaturated) fat, including four servings of fish per week. Purines were unlimited and alcohol was not restricted. Here are the results, on average, after 16 weeks:

• uric acid levels fell by 18%, from 10.3 mg/dl to 8.5 mg/dl on average; seven men had a normal uric acid level by the end of the study.
• frequency of gout attacks was reduced by 72%
• weight dropped by 17 lbs

This study is very promising, but unfortunately it is hard to know which of the interventions was responsible for the positive benefits—was it the lack of refined carbohydrate, reduction in saturated fat, or the weight loss itself? Even more confusing is that it is unclear whether these patients were eating much less meat than usual, given that they were told to avoid saturated fat. Uric acid levels fell by about 2 points, which is about the same as in the Peixoto low-purine diet study, although that group had much lower uric acid levels to begin with.

So, what should you do if you have gout?

The answer is that the research doesn’t have a clear answer for you yet. Many questions remain. We still don’t understand exactly why alcohol raises uric acid levels, why only a small percentage of people with high uric acid levels get gout, or even which carbohydrates might aggravate gout and why. For example, a brand new analysis of all available fructose studies calls into question whether fructose raises uric acid any more than any other kind of sugar.1

But here’s what we do know. When we combine the available science with common sense, we can say that:

• Human beings must be well-adapted, as all animals must be, to eating purines, which are found in all whole foods.
• It is highly likely that we are poorly adapted to be able to handle much refined carbohydrate or alcohol, which have never existed in nature in significant amounts.

Dietary tips for managing gout

1. Stabilize and lower your blood sugar and insulin levels by reducing carbohydrate intake, especially refined carbohydrate intake. A low glycemic index diet would be a good place to start. Depending on your chemistry, you may even need to consider a very low carbohydrate diet or ketogenic diet. Refined carbohydrate and high insulin levels have been strongly linked to metabolic syndrome and most diseases of Western civilization, and gout is probably just one more sugar-tipped arrow in the quiver of the Western diet. There is no evidence that lowering the amount of meat in your diet will protect you from these diseases, whereas there is plenty of evidence to suggest that lowering refined carbohydrate intake can. Even if it doesn’t completely cure your gout, you’ll be a lot healthier for it.
2. Minimize alcohol intake, especially beer.
3. Consider taking a vitamin C supplement. A single randomized controlled trial found that taking 500 mg of vitamin C per day for two months reduced uric acid levels by 1.5 mg/dl.

If you focus on these goals, you may be able to have your meat and eat it too 🙂

Want to learn more?

For more reassuring facts about meat and health, including information about kidney disease, heart disease, and nitrites/nitrates, please see my meats page. You may be interested to read about the history of mostly-meat diets, including the diets of Arctic and African peoples. I also recently wrote a critique of the latest study trying to connect the carnitine in red meat to heart disease.

In 2015, I wrote a five-part series about fructose, how it gets processed in our bodies compared to how we process glucose, if it is more dangerous than glucose, and how some of the fructose studies use questionable methods to single out fructose as more harmful than other forms of sugar. The series begins with the biochemistry of sugar in a post entitled: “Has Fructose Been Framed“. I dedicate a portion of part 3 “Why Sugar Is Bad for You: A Summary of the Research” specifically to sugar consumption and gout.

What about you? Have you tried any dietary strategies for gout that have worked?

Once called “the ailment of kings” because it mainly afflicted those who could afford a rich diet, gout now affects more than 8 million non-royal Americans. To what do we owe this dubious honor? Is it because we are eating more meat than ever before?

What is gout?

Gout is a special type of arthritis in which certain joints fill up with microscopic shards of uric acid, becoming red, swollen, and exquisitely sensitive to the touch. Most people with gout have too much uric acid in their blood—higher than 6 mg/dl in women and 7 mg/dl in men (levels can reach 12 mg/dl or more in some cases). Uric acid crystals can also cause kidney stones and kidney damage. More than 20% of Americans now have abnormally high uric acid levels.

What is uric acid?

Uric acid is a breakdown product of purines—molecules that help make up some vitally important compounds present in the cells of all plants and animals, including DNA (genes), RNA (protein manufacturing) and ATP (energy). The following are the most familiar purines:

• Adenine
• Guanine
• Caffeine
• Theobromine (cocoa beans, tea leaves, kola nuts, yerba mate)

Low-purine diets

Low-purine diets (in combination with medication) have been prescribed for gout since the middle of the 20th century. This dietary advice is based on the belief that too many purines in the diet cause high uric acid in the blood. Now, since all plants and animals are made of cells, and all cells contain purines, asking someone to eat fewer purines is a tall order. However, since most animal foods are higher in purines than most plant foods (animal foods are denser and contain more cells per unit weight), doctors advise people with gout to eat less meat. You could also lower purines in your diet by simply eating fewer whole foods of all kinds. [Actually, the best advice, if you follow this reasoning to its logical conclusion, would be to eat a 100% junk food diet of flour, sugar, candy, soda, ice cream, and fruit juice—foods that have had their cells destroyed or removed in the refining process—because these foods contain few if any purines at all—sound like a plan?] The below list is adapted from Emmerson 1996:1

High-Purine Foods

• All meats, including organ meats, and seafood
• Meat extracts and gravies
• Yeast and yeast extracts
• Beer, and other alcoholic beverages
• Beans, peas, lentils, oatmeal, spinach, asparagus, cauliflower, and mushrooms

Low-Purine Foods

• Refined cereals and cereal products, such as cornflakes, white bread, pasta, flour, and tapioca
• Milk, milk products, and eggs
• Sugar, sweets, and gelatin
• Butter, polyunsaturated margarine, and all other fats
• Fruit, nuts, and peanut butter
• Lettuce, tomatoes, and green vegetables (except spinach and asparagus)
• Vegetarian cream soups made with low-purine vegetables
• Water, fruit juice, cordials, and carbonated drinks

In actuality, scientists admit that it is impossible to know the true purine content of any food, but even if we did, purines are not the only problem.

Those kings of old must have known how to party.

It has been known for centuries that alcohol consumption can trigger gouty attacks. This connection is now well supported by scientific studies. Two 12 oz beers can raise uric acid levels in healthy men by about 10%, and drinking to intoxication doubles uric acid levels in alcoholics. Interestingly, most alcoholic drinks contain no purines, so how does alcohol raise uric acid levels?

1. Alcohol cuts the kidney’s ability to rid the blood of excess purines by at least 50%.
2. When the liver processes alcohol, lots of ATP (an energy molecule) is used up in the process; ATP contains purines that get broken down into uric acid.
3. Beer is especially risky because it contains alcohol AND purines (derived from brewer’s yeast).

Fructose raises uric acid levels

It has been known since the late 1960s that fructose raises uric acid levels. Examples of foods which contain fructose are fresh fruit (max 10% fructose), dried fruit (max 40% fructose), table sugar (50% fructose) and corn syrup (55% fructose). Uric acid levels rise about 13% after eating meals containing fructose. People with gout have more exaggerated responses to fructose than healthy controls.

“subjects prone to developing gout in the 1700s and 1800s tended to be wealthy and sedentary, often with the ability to afford sugar, the latter of which is known to raise uric acid. Indeed, today gout is increasing in all populations, and if anything, is more common among the poor and less educated.”1

Yet, as you can see in this 2007 New York Times article, fructose is not even on the list of possible dietary factors in gout, which may be why celebrated NY Times food writer Frank Bruni continues to suffer with some symptoms of gout, despite following his doctors’ advice to limit meat and alcohol and to take medication:

“I’ve noticed discernible changes in my health—or at least in the way I feel. How much of that is attributable to my reduced alcohol intake and how much to the exodus of red meat is impossible to say. I haven’t lost more than a pound or two, because carbs have rushed in where protein isn’t permitted to treat . . . the flare-ups [of gout] are subtle now that I’m medicated and reformed.”2

Aye, there’s the rub! Mr. Bruni has gotten right to the meat of the problem—low-purine diets can be high in refined carbohydrates, such as sugar and flour, which raise insulin levels, and now not only do you have gout, but you have a hard time losing weight and you’ve further increased your risk for all kinds of other chronic diseases:

“Fructose is unique among sugars in that it rapidly causes features of metabolic syndrome both in experimental animals and humans. Fructose ingestion also leads to fatty liver and elevated triglycerides in humans and can also raise blood pressure. Intriguingly, fructose is a sugar that has the unique ability to raise serum uric acid. Serum uric acid levels rise within minutes of fructose ingestion… the increase in fructose intake closely parallels the rise in gout, obesity and metabolic syndrome that has occurred over the last two centuries. Serum uric acid levels increased from <3.5 mg/dl in the early twentieth century to over 6 mg/dl today in adult males.”3

How does fructose raise uric acid levels?

“The specific reason why fructose is superior than glucose in increasing fat stores likely relates to the unique first steps in fructose metabolism. When fructose enters the hepatocyte, it is metabolized by a specific enzyme, fructokinase C. Unlike glucokinase, which has a negative feedback system to prevent excessive phosphorylation, the phosphorylation of fructose by fructokinase will proceed uninterrupted, and as a consequence intracellular phosphate depletion and ATP depletion frequently occur. The fall in intracellular phosphate results in the stimulation of AMP deaminase that helps accelerate the degradation of AMP to IMP and later to uric acid. In turn, the intracellular generation of uric acid results in oxidative stress.”1

Translation: Fructose is especially good at turning into fat. The enzymes in the liver that turn fructose into fat use up lots of ATP in the process. ATP contains purines that get broken down into uric acid.

Both alcohol and fructose burn through ATP like kindling. Metabolically speaking, fructose and alcohol have a lot in common, which is why Dr. Robert Lustig mentions them both in the same breath as poisons.

But there’s more to the sugar story

Rapidly digestible carbohydrates such as sugar, flour, starch, fruit juice, and white potato are notorious for causing insulin spikes. Insulin tells the kidneys to reabsorb uric acid into the blood instead of excreting it into the urine. Why? Because insulin is, first and foremost, a growth hormone. In order to grow you need to build more cells, and to build more cells you need more purines.

Thus our dear meat-mourning Mr. Bruni is dutifully eating a low-purine, high-refined carb diet, which both lowers and raises uric acid. As comedian Steven Wright would have said, that’s like putting a humidifier and a dehumidifier in the same room and letting them fight it out.

So what is he supposed to do? What foods would he be left with if we told him he can’t eat carbs, meat, or alcohol? Fat and low-purine vegetables? Unfortunately that diet is dangerously devoid of nutrients. Which is worse for gout—meat or carbs?

My beef with the meat-purine-gout hypothesis

• We are not eating any more meat now than we did 100 years ago.
• Some cultures eating lots of meat, including 19th century Arctic peoples who lived on a diet of nearly 100% animal foods, did not develop gout. “Gout is unknown in Eskimos and Northern Indians despite their purine-rich diet.”1
• Animal foods are higher in protein than plant foods. Proteins increase the elimination of purines in the urine, which can actually lower uric acid levels.
• Some plant foods are rich in purines, including legumes, spinach, asparagus, and mushrooms (dense or rapidly growing plants).
• Purines in the diet do not have much of an effect on uric acid levels, because most of the uric acid in the blood comes from inside the body, as part of everyday cell turnover: “The purine content of the diet does not usually contribute more than 1 mg/dl to the serum urate concentration.”2

Studies tying animal foods to gout have been epidemiological studies which have observed that people who eat more meat tend to have higher uric acid levels and/or a higher risk of gout. These studies have not taken carbohydrate in general, nor fructose in particular, into consideration. Therefore we have no idea whether people who reported eating more meat also happened to eat more fructose, which is, in my opinion, a critical omission given that we have known since 1967 that fructose can raise uric acid levels. Furthermore there are some epidemiological studies that find no association whatsoever between meat and uric acid levels.3 Either way, as many of you know, epidemiological studies are not experiments and correlation does not equal causation.

What do the clinical studies show? 

Unfortunately, as is the case with so many diseases, when the use of drugs to treat gout became popular in the 1950s, interest in dietary strategies fizzled. So we only have a wee handful of small, flawed studies to guide us:

There are ZERO studies that have attempted to prevent gout with diet.

I could only locate a grand total of ONE study of the oft-recommended low-purine, alcohol-free diet that is relevant to our question.1 In this study, 55 Brazilian adults with both high blood pressure and high uric acid levels were divided into three groups— diet alone, low-purine diet plus medication, and medication alone—for three months. Uric acid levels fell by about 2 mg/dl in all three groups by week six. However, people in this study were not gout patients, there was no control group, and the composition of the diet was not described (we are only told what was excluded from the diet), therefore we do not know if this diet contained less fructose and/or less refined carbohydrate than a standard diet. Without that information, we can’t be sure that it was the lack of purines that may have been responsible for the decrease in uric acid.

I located only ONE small pilot study exploring the role of refined carbohydrate in gout.2 Thirteen South African men with gout were placed on a 1600 calorie diet containing 40% unrefined carbohydrate, 30% protein, and 30% (unsaturated) fat, including four servings of fish per week. Purines were unlimited and alcohol was not restricted. Here are the results, on average, after 16 weeks:

• uric acid levels fell by 18%, from 10.3 mg/dl to 8.5 mg/dl on average; seven men had a normal uric acid level by the end of the study.
• frequency of gout attacks was reduced by 72%
• weight dropped by 17 lbs

This study is very promising, but unfortunately it is hard to know which of the interventions was responsible for the positive benefits—was it the lack of refined carbohydrate, reduction in saturated fat, or the weight loss itself? Even more confusing is that it is unclear whether these patients were eating much less meat than usual, given that they were told to avoid saturated fat. Uric acid levels fell by about 2 points, which is about the same as in the Peixoto low-purine diet study, although that group had much lower uric acid levels to begin with.

So, what should you do if you have gout?

The answer is that the research doesn’t have a clear answer for you yet. Many questions remain. We still don’t understand exactly why alcohol raises uric acid levels, why only a small percentage of people with high uric acid levels get gout, or even which carbohydrates might aggravate gout and why. For example, a brand new analysis of all available fructose studies calls into question whether fructose raises uric acid any more than any other kind of sugar.1

But here’s what we do know. When we combine the available science with common sense, we can say that:

• Human beings must be well-adapted, as all animals must be, to eating purines, which are found in all whole foods.
• It is highly likely that we are poorly adapted to be able to handle much refined carbohydrate or alcohol, which have never existed in nature in significant amounts.

Dietary tips for managing gout

1. Stabilize and lower your blood sugar and insulin levels by reducing carbohydrate intake, especially refined carbohydrate intake. A low glycemic index diet would be a good place to start. Depending on your chemistry, you may even need to consider a very low carbohydrate diet or ketogenic diet. Refined carbohydrate and high insulin levels have been strongly linked to metabolic syndrome and most diseases of Western civilization, and gout is probably just one more sugar-tipped arrow in the quiver of the Western diet. There is no evidence that lowering the amount of meat in your diet will protect you from these diseases, whereas there is plenty of evidence to suggest that lowering refined carbohydrate intake can. Even if it doesn’t completely cure your gout, you’ll be a lot healthier for it.
2. Minimize alcohol intake, especially beer.
3. Consider taking a vitamin C supplement. A single randomized controlled trial found that taking 500 mg of vitamin C per day for two months reduced uric acid levels by 1.5 mg/dl.

If you focus on these goals, you may be able to have your meat and eat it too 🙂

Want to learn more?

For more reassuring facts about meat and health, including information about kidney disease, heart disease, and nitrites/nitrates, please see my meats page. You may be interested to read about the history of mostly-meat diets, including the diets of Arctic and African peoples. I also recently wrote a critique of the latest study trying to connect the carnitine in red meat to heart disease.

In 2015, I wrote a five-part series about fructose, how it gets processed in our bodies compared to how we process glucose, if it is more dangerous than glucose, and how some of the fructose studies use questionable methods to single out fructose as more harmful than other forms of sugar. The series begins with the biochemistry of sugar in a post entitled: “Has Fructose Been Framed“. I dedicate a portion of part 3 “Why Sugar Is Bad for You: A Summary of the Research” specifically to sugar consumption and gout.

What about you? Have you tried any dietary strategies for gout that have worked?

Public health officials and nutrition experts love to sing the praises of the virtuous cruciferous vegetable family. We are told that these pungent plants can fight off cancer, strengthen our immune system, and leap tall buildings in a single bound. But could crucifers have a dark side?

Meet the crucifer family

Cruciferous veggies (the Brassica family) dominate the produce aisle; many people may not realize how many familiar vegetables belong to this family.

These mustard family members are notorious for giving off a strong odor that sends children ducking for cover underneath the dinner table. That lovely aroma is due to the presence of sulfur-containing chemicals called “thiocyanates.” These are natural plant defense compounds, designed to protect the plant from potential invaders.

Plant psychology and defense

Plants are cunning. If they need us to help them disperse their seeds, they will package the seeds in a colorful, appealing fruit and fill it with the sweet sugars we love to eat. However, they do not want us to eat their stalks, roots, stems, and leaves—the vital body parts that keep the plant alive, so they tend to make those parts bitter. Plants do not want to be eaten any more than animals do, but since they can’t run, growl, bite, or claw at creatures that want to feast upon them, they have evolved, over hundreds of millions of years, some very sophistical chemical weapons to ward off hungry passers-by.

Let’s use broccoli as our signature crucifer, as it is the best-studied. Like all cruciferous veggies, broccoli uses isothiocyanates to protect itself. The one it happens to use is called sulforaphane, which is made this way:

Glucosinolate + Myrosinase (enzyme) = SULFORAPHANE

When broccoli is sitting peacefully in a field (cue the flute solo), it does not contain any sulforaphane. This pungent molecule is so toxic to living cells (including broccoli’s own cells) that the two harmless ingredients needed to make it are stored in separate compartments within broccoli cells. However, if the cells’ defenses are breached—if the vegetable is cut or bruised or if an insect or small animal comes along and bites into its flesh (cue the ominous organ music)—the individual compartments break open, the two ingredients mix together, and POOF! Sulforaphane—a chemical weapon with the power to kill things like insects, bacteria, and worms.

How does sulforaphane kill tiny living creatures and why should you care?

You should care because sulforaphane can do the very same things to your cells that it does to the cells of the little guys:

• poisons mitochondria (cell energy generators)
• inhibits microsomal enzymes in the endoplasmic reticulum (cellular manufacturing and detoxifying centers)
• generates reactive oxygen species (these are damaging pro-oxidants)
• interferes with thyroid iodine absorption
• disrupts epithelial barriers (can poke holes in sheets of cells)
• depletes glutathione levels (the most important antioxidant inside our cells)

All of the above mechanisms explain how sulforaphane can kill small living creatures. In research studies it has also been demonstrated that sulforaphane can kill healthy human cells and can cause cancerous changes in human cells.

Plant paradox?

It may come as a surprise to you to learn that this sulforaphane is the very same broccoli ingredient that we are told is responsible for the health benefits of broccoli. The reason for these health claims lies in the other things that sulforaphane does in research studies:

• induces cancer cell apoptosis (causes cancer cells to commit suicide)
• inhibits angiogenesis (slows new blood vessel formation, which is how cancers grow)
• induces “phase II enzymes” (fires up human immune system antioxidants)
• kills bacteria (natural antibiotic)

So, as you can see, sulforaphane is a double-edged sword, capable of killing bacteria and cancer cells, as well as killing healthy cells and even causing cancer. Just like any form of chemotherapy, this compound does not do a very good job of distinguishing between cancerous cells and healthy cells, so collateral damage (friendly fire) may occur.

Believing is seeing

Why do we only hear about broccoli’s superhero side, and not its villainous dark side? As a psychiatrist and someone who has read far too many nutrition articles, I can confidently say this: when it comes to food and health, believing is seeing. If we believe something is good for us, we only see evidence to support that belief and are almost incapable of seeing evidence to the contrary. The belief that vegetables are good for us comes entirely from epidemiological studies, which are only capable of generating untested theories about food and health. Scientific experiments are then conducted to try to support those beliefs, and the truth is that these experiments yield very mixed results about how broccoli affects us.

Scientists who are aware of the dark side of crucifers defend them as superfoods by invoking the concept of hormesis. The hormesis theory essentially says that small amounts of toxic compounds can actually be good for you—this is the “what does not kill you makes you stronger” argument. However, when it comes to crucifers and health, this is just a hypothesis. What’s more, even if it were true, then the best advice about crucifers would be to eat them in small amounts to ensure tiny doses of isothiocyanates. Instead, the prevailing wisdom about crucifers is “the more, the merrier.”

Sulforaphane 101

• Sprouts contain 20 to 100 times more glucosinolate than mature vegetables (to protect the baby plant).
• Freezing crucifers or boiling them for 10 minutes reduces glucosinolate concentrations by about 50%.
• Steaming reduces glucosinolate concentrations by about 2/3.
• Heat completely destroys myrosinase. However, the bacteria in our gastrointestinal tract contain enzymes that mimic myrosinase, so sulforaphane will still be generated in the process of digestion.
• About 75% of all sulforaphane in the digestive tract is absorbed into the bloodstream and taken up by cells throughout the body. Blood levels peak about two hours after eating crucifers.
• Once inside cells, our own natural cellular antioxidant, glutathione, rapidly binds to sulforaphane and escorts it out of cells to be eliminated within three hours.

Some scientists have postulated that our cells get rid of sulforaphane as quickly as possible precisely because it is an unwanted guest—an irritant, rather than a helpful tool in our cancer-fighting arsenal.

So, is broccoli good for you?

We really don’t know. I was unable to find any convincing clinical evidence to support the health benefits of crucifers, but I did find enough interesting scientific evidence to at least call their health benefits into question. Most humans and their ancestors have been eating vegetables for tens if not hundreds of thousands of years. Therefore, even if broccoli may be potentially harmful to us, we have likely evolved ways to minimize any damage it may cause. Case in point: although we do absorb significant amounts of sulforaphane, our cells rapidly evict it. However, individuals with chemical sensitivities, weakened immune systems, liver disease, and/or gastrointestinal problems may be more likely to experience symptoms related to the natural chemicals in certain vegetables, which are usually not suspected as potential culprits. People with hypothyroidism (under-active thyroid) may also want to consider removing cruciferous vegetables due to their potential to interfere with normal thyroid activity.

Are children who hate broccoli onto something? Out of the mouths of babes . . .

For information about how cruciferous vegetables can aggravate IBS in some people, read my blog post: “Common Constipation Culprits.”

To read more about vegetables in general, visit my Vegetables page or watch my 20-minute presentation below, given at the 2012 Ancestral Health Symposium.

Public health officials and nutrition experts love to sing the praises of the virtuous cruciferous vegetable family. We are told that these pungent plants can fight off cancer, strengthen our immune system, and leap tall buildings in a single bound. But could crucifers have a dark side?

Meet the crucifer family

Cruciferous veggies (the Brassica family) dominate the produce aisle; many people may not realize how many familiar vegetables belong to this family.

These mustard family members are notorious for giving off a strong odor that sends children ducking for cover underneath the dinner table. That lovely aroma is due to the presence of sulfur-containing chemicals called “thiocyanates.” These are natural plant defense compounds, designed to protect the plant from potential invaders.

Plant psychology and defense

Plants are cunning. If they need us to help them disperse their seeds, they will package the seeds in a colorful, appealing fruit and fill it with the sweet sugars we love to eat. However, they do not want us to eat their stalks, roots, stems, and leaves—the vital body parts that keep the plant alive, so they tend to make those parts bitter. Plants do not want to be eaten any more than animals do, but since they can’t run, growl, bite, or claw at creatures that want to feast upon them, they have evolved, over hundreds of millions of years, some very sophistical chemical weapons to ward off hungry passers-by.

Let’s use broccoli as our signature crucifer, as it is the best-studied. Like all cruciferous veggies, broccoli uses isothiocyanates to protect itself. The one it happens to use is called sulforaphane, which is made this way:

Glucosinolate + Myrosinase (enzyme) = SULFORAPHANE

When broccoli is sitting peacefully in a field (cue the flute solo), it does not contain any sulforaphane. This pungent molecule is so toxic to living cells (including broccoli’s own cells) that the two harmless ingredients needed to make it are stored in separate compartments within broccoli cells. However, if the cells’ defenses are breached—if the vegetable is cut or bruised or if an insect or small animal comes along and bites into its flesh (cue the ominous organ music)—the individual compartments break open, the two ingredients mix together, and POOF! Sulforaphane—a chemical weapon with the power to kill things like insects, bacteria, and worms.

How does sulforaphane kill tiny living creatures and why should you care?

You should care because sulforaphane can do the very same things to your cells that it does to the cells of the little guys:

• poisons mitochondria (cell energy generators)
• inhibits microsomal enzymes in the endoplasmic reticulum (cellular manufacturing and detoxifying centers)
• generates reactive oxygen species (these are damaging pro-oxidants)
• interferes with thyroid iodine absorption
• disrupts epithelial barriers (can poke holes in sheets of cells)
• depletes glutathione levels (the most important antioxidant inside our cells)

All of the above mechanisms explain how sulforaphane can kill small living creatures. In research studies it has also been demonstrated that sulforaphane can kill healthy human cells and can cause cancerous changes in human cells.

Plant paradox?

It may come as a surprise to you to learn that this sulforaphane is the very same broccoli ingredient that we are told is responsible for the health benefits of broccoli. The reason for these health claims lies in the other things that sulforaphane does in research studies:

• induces cancer cell apoptosis (causes cancer cells to commit suicide)
• inhibits angiogenesis (slows new blood vessel formation, which is how cancers grow)
• induces “phase II enzymes” (fires up human immune system antioxidants)
• kills bacteria (natural antibiotic)

So, as you can see, sulforaphane is a double-edged sword, capable of killing bacteria and cancer cells, as well as killing healthy cells and even causing cancer. Just like any form of chemotherapy, this compound does not do a very good job of distinguishing between cancerous cells and healthy cells, so collateral damage (friendly fire) may occur.

Believing is seeing

Why do we only hear about broccoli’s superhero side, and not its villainous dark side? As a psychiatrist and someone who has read far too many nutrition articles, I can confidently say this: when it comes to food and health, believing is seeing. If we believe something is good for us, we only see evidence to support that belief and are almost incapable of seeing evidence to the contrary. The belief that vegetables are good for us comes entirely from epidemiological studies, which are only capable of generating untested theories about food and health. Scientific experiments are then conducted to try to support those beliefs, and the truth is that these experiments yield very mixed results about how broccoli affects us.

Scientists who are aware of the dark side of crucifers defend them as superfoods by invoking the concept of hormesis. The hormesis theory essentially says that small amounts of toxic compounds can actually be good for you—this is the “what does not kill you makes you stronger” argument. However, when it comes to crucifers and health, this is just a hypothesis. What’s more, even if it were true, then the best advice about crucifers would be to eat them in small amounts to ensure tiny doses of isothiocyanates. Instead, the prevailing wisdom about crucifers is “the more, the merrier.”

Sulforaphane 101

• Sprouts contain 20 to 100 times more glucosinolate than mature vegetables (to protect the baby plant).
• Freezing crucifers or boiling them for 10 minutes reduces glucosinolate concentrations by about 50%.
• Steaming reduces glucosinolate concentrations by about 2/3.
• Heat completely destroys myrosinase. However, the bacteria in our gastrointestinal tract contain enzymes that mimic myrosinase, so sulforaphane will still be generated in the process of digestion.
• About 75% of all sulforaphane in the digestive tract is absorbed into the bloodstream and taken up by cells throughout the body. Blood levels peak about two hours after eating crucifers.
• Once inside cells, our own natural cellular antioxidant, glutathione, rapidly binds to sulforaphane and escorts it out of cells to be eliminated within three hours.

Some scientists have postulated that our cells get rid of sulforaphane as quickly as possible precisely because it is an unwanted guest—an irritant, rather than a helpful tool in our cancer-fighting arsenal.

So, is broccoli good for you?

We really don’t know. I was unable to find any convincing clinical evidence to support the health benefits of crucifers, but I did find enough interesting scientific evidence to at least call their health benefits into question. Most humans and their ancestors have been eating vegetables for tens if not hundreds of thousands of years. Therefore, even if broccoli may be potentially harmful to us, we have likely evolved ways to minimize any damage it may cause. Case in point: although we do absorb significant amounts of sulforaphane, our cells rapidly evict it. However, individuals with chemical sensitivities, weakened immune systems, liver disease, and/or gastrointestinal problems may be more likely to experience symptoms related to the natural chemicals in certain vegetables, which are usually not suspected as potential culprits. People with hypothyroidism (under-active thyroid) may also want to consider removing cruciferous vegetables due to their potential to interfere with normal thyroid activity.

Are children who hate broccoli onto something? Out of the mouths of babes . . .

For information about how cruciferous vegetables can aggravate IBS in some people, read my blog post: “Common Constipation Culprits.”

To read more about vegetables in general, visit my Vegetables page or watch my 20-minute presentation below, given at the 2012 Ancestral Health Symposium.

Can food stabilize mood? Is there a diet out there that could prevent mania, mood swings, deep depressions, and uncomfortably anxious and agitated states? Sound far-fetched? Maybe not. Dietary changes can have very powerful effects on brain chemistry. Low carbohydrate diets, in particular, are fascinating.

Ketogenic diets and epilepsy

When most people think of low-carbohydrate diets, they think of weight loss. But did you know that neurologists have been successfully treating severe cases of epilepsy with low-carbohydrate (“ketogenic”) diets for nearly 100 years? Ketogenic diets are specially designed low-carbohydrate diets that typically contain between 60-80% fat, with the remainder consisting of roughly equal amounts of protein and carbohydrate. In most cases, patients in clinical studies were hospitalized children whose seizures could not be controlled with anticonvulsant medications. Yet, with diet alone:

• nearly all patients achieve more than a 50% reduction in seizures
• with 33% experiencing a 90% reduction in seizures
• and 10 to 15% achieving complete remission from seizures

What more powerful evidence could there be for the role of diet in brain chemistry? Not only is this phenomenon remarkable in its own right, but it also has potentially powerful implications for the treatment of a wide variety of neurological disorders.

Ketogenic diets have magical healing properties

All of the following conditions have been shown in animal models or in human studies to improve on a ketogenic diet:

• Autism
• Traumatic Brain Injury
• Alzheimer’s Disease
• Parkinson’s Disease
• Brain Cancer
• Diabetes
• Prostate Cancer
• Obesity
• Chronic Pain/Inflammation
• Multiple Sclerosis
• Insomnia/Circadian Rhythm disorders

How do ketogenic diets work?

Nobody knows. It is a subject of intense research, and there are many theories. Ketogenic diets restrict carbohydrate intake to 10-20 grams per day (the typical American diet contains at least 200 grams per day), and limit protein to just what’s needed. Therefore, the body has no choice but to burn fat for energy. Fat from the diet or from excess body fat gets broken down into three “ketone bodies” [“ketogenic” means that the diet generates ketones]: acetone, acetoacetate, and beta-hydroxybutyrate. Acetone leaves the body, but the other two compounds circulate in the blood and serve as fuel sources for our cells.

Ketogenic diets are very low in carbohydrate, therefore blood sugar and insulin levels are lower and much more stable than on standard “balanced” diets that are high in carbohydrate. We do not know whether it is the presence of ketone bodies in the blood, or the stabilization of blood sugar levels, or the reduction in blood sugar and insulin levels, or some combination of these changes that is responsible for the therapeutic effects of the ketogenic diet.

What we do know is that epilepsy and other neurodegenerative diseases are all associated with “mitochondrial dysfunction”. Mitochondria are the miniature generators inside of our cells, so when they are not working properly, energy production is disrupted, and all cell activities can be affected as a result. Studies consistently find that mitochondria produce more energy (ATP) more efficiently on ketogenic diets than on standard “balanced” diets which force cells to burn glucose (sugar) for energy. Put simply, most of our cells work best when they burn fat instead of carbohydrate.

We also know that epilepsy and other neurodegenerative diseases are universally associated with inflammation. Diets rich in sweets and refined starches that cause high, unstable blood sugar and insulin levels are well known for their ability to set the stage for inflammation throughout the body, therefore diets that are low in refined carbohydrates tend to quiet inflammation.

Bipolar disorder and diet

So, what does all of this have to do with bipolar disorder? It is well-established that epilepsy and bipolar disorder share many biological features, including:

• similar neurotransmitter imbalances (serotonin, norepinephrine, GABA, and glutamate)
• alterations in sodium and calcium distribution
• changes in chemical messenger activity

In fact, it just so happens that many of the mood stabilizing medications we psychiatrists prescribe for bipolar disorder are anticonvulsants that were originally designed to treat seizures—Depakote (Valproate), Lamictal (Lamotrigine) and Trileptal (Oxcarbazepine), to name a few. The fact that epilepsy and bipolar disorder have so much in common begs the question of whether perhaps a low-carb diet could be useful for mood stabilization, as well. Unfortunately, there has yet to be a single scientific study of ketogenic diets in bipolar disorder. I have not yet had a patient in my practice who has been willing to try a strict ketogenic diet, which not only limits carbohydrate, but also limits protein and requires blood monitoring of ketone levels.

However, I can tell you that my patients who have been willing to try low carbohydrate “modified Atkins” diets, low carbohydrate “Paleo” diets, or low glycemic index diets for mood problems—from depression to anxiety to eating disorders to bipolar disorders—report significant improvement in their symptoms. It stands to reason that these dietary changes, which have profound effects on other neurological disorders, would have the potential for profound effects on psychiatric disorders, as well.

Yet, even if a ketogenic diet worked beautifully for all cases of bipolar disorders of all types, I doubt that most people would choose to commit to a lifetime of eating a ketogenic diet. These diets are very restrictive and require major lifestyle changes. Most foods that people are accustomed to eating all day long are off-limits on this diet. For this reason, neurologists have recently begun to experiment with more relaxed versions of the diet to see how much carbohydrate patients can consume and still have good seizure control.

Studies of low glycemic index diets and modified Atkins diets (Atkins diets that allow unlimited protein and fat) look very promising but do not seem to work quite as well for seizures as ketogenic diets do. However, bipolar mood disorders and seizures are different in that seizures are black and white phenomena, whereas mood swings are a matter of degree. Perhaps people with bipolar mood disorders would be satisfied with less than perfect control over their mood swings in exchange for wider dietary variety?

If you have a bipolar mood disorder should you change your diet?

That’s up to you. While there are no scientific studies to support this idea yet, if you wait for the science to properly test the theory, you could be waiting for many years. You have nothing to lose by doing your own individual experiments, because it is well established that low glycemic index diets, Atkins diets, and ketogenic diets are safe. In fact, it is likely that they are far healthier than the low-fat, high-carb, low-meat diets recommended by public health officials, which are the very same diets that have worsened our collective health over the past four decades. If you do decide to try a dietary change, just keep in mind that it can take three to four weeks before potential benefits become noticeable.

A few words of caution

Dietary changes are difficult to make, and benefits can be slow to take effect, therefore nutritional approaches are not recommended in emergency situations.

If you are currently taking a mood stabilizing medication, please do not make any changes to your medications without discussing it with your clinician. Please see my article “Ketogenic Diets and Psychiatric Medications” for important information about drug interactions.

Very low-carbohydrate diets can alter the way medications are processed by the body, so if you are taking medications of any kind (including blood pressure and diabetes medications) and decide to try a low-carbohydrate diet, please do so with close medical supervision.

*If you are taking Depakote (Valproate), please be aware that there is a case report in the literature of a man who became manic and psychotic after starting a ketogenic diet, despite taking Depakote. The reason may have been that the diet reduced his Depakote levels (Depakote is a fatty acid, and the ketogenic diet is a fat-burning diet).

How about you?

Have you ever tried a low glycemic index diet or low carbohydrate diet? If so, did you notice any effects on your mood?

To learn more about about how diet can impact bipolar disorder, read my blog post “Bipolar Disorder and Diet Part I: Omega 3 Fatty Acids.”

Can food stabilize mood? Is there a diet out there that could prevent mania, mood swings, deep depressions, and uncomfortably anxious and agitated states? Sound far-fetched? Maybe not. Dietary changes can have very powerful effects on brain chemistry. Low carbohydrate diets, in particular, are fascinating.

Ketogenic diets and epilepsy

When most people think of low-carbohydrate diets, they think of weight loss. But did you know that neurologists have been successfully treating severe cases of epilepsy with low-carbohydrate (“ketogenic”) diets for nearly 100 years? Ketogenic diets are specially designed low-carbohydrate diets that typically contain between 60-80% fat, with the remainder consisting of roughly equal amounts of protein and carbohydrate. In most cases, patients in clinical studies were hospitalized children whose seizures could not be controlled with anticonvulsant medications. Yet, with diet alone:

• nearly all patients achieve more than a 50% reduction in seizures
• with 33% experiencing a 90% reduction in seizures
• and 10 to 15% achieving complete remission from seizures

What more powerful evidence could there be for the role of diet in brain chemistry? Not only is this phenomenon remarkable in its own right, but it also has potentially powerful implications for the treatment of a wide variety of neurological disorders.

Ketogenic diets have magical healing properties

All of the following conditions have been shown in animal models or in human studies to improve on a ketogenic diet:

• Autism
• Traumatic Brain Injury
• Alzheimer’s Disease
• Parkinson’s Disease
• Brain Cancer
• Diabetes
• Prostate Cancer
• Obesity
• Chronic Pain/Inflammation
• Multiple Sclerosis
• Insomnia/Circadian Rhythm disorders

How do ketogenic diets work?

Nobody knows. It is a subject of intense research, and there are many theories. Ketogenic diets restrict carbohydrate intake to 10-20 grams per day (the typical American diet contains at least 200 grams per day), and limit protein to just what’s needed. Therefore, the body has no choice but to burn fat for energy. Fat from the diet or from excess body fat gets broken down into three “ketone bodies” [“ketogenic” means that the diet generates ketones]: acetone, acetoacetate, and beta-hydroxybutyrate. Acetone leaves the body, but the other two compounds circulate in the blood and serve as fuel sources for our cells.

Ketogenic diets are very low in carbohydrate, therefore blood sugar and insulin levels are lower and much more stable than on standard “balanced” diets that are high in carbohydrate. We do not know whether it is the presence of ketone bodies in the blood, or the stabilization of blood sugar levels, or the reduction in blood sugar and insulin levels, or some combination of these changes that is responsible for the therapeutic effects of the ketogenic diet.

What we do know is that epilepsy and other neurodegenerative diseases are all associated with “mitochondrial dysfunction”. Mitochondria are the miniature generators inside of our cells, so when they are not working properly, energy production is disrupted, and all cell activities can be affected as a result. Studies consistently find that mitochondria produce more energy (ATP) more efficiently on ketogenic diets than on standard “balanced” diets which force cells to burn glucose (sugar) for energy. Put simply, most of our cells work best when they burn fat instead of carbohydrate.

We also know that epilepsy and other neurodegenerative diseases are universally associated with inflammation. Diets rich in sweets and refined starches that cause high, unstable blood sugar and insulin levels are well known for their ability to set the stage for inflammation throughout the body, therefore diets that are low in refined carbohydrates tend to quiet inflammation.

Bipolar disorder and diet

So, what does all of this have to do with bipolar disorder? It is well-established that epilepsy and bipolar disorder share many biological features, including:

• similar neurotransmitter imbalances (serotonin, norepinephrine, GABA, and glutamate)
• alterations in sodium and calcium distribution
• changes in chemical messenger activity

In fact, it just so happens that many of the mood stabilizing medications we psychiatrists prescribe for bipolar disorder are anticonvulsants that were originally designed to treat seizures—Depakote (Valproate), Lamictal (Lamotrigine) and Trileptal (Oxcarbazepine), to name a few. The fact that epilepsy and bipolar disorder have so much in common begs the question of whether perhaps a low-carb diet could be useful for mood stabilization, as well. Unfortunately, there has yet to be a single scientific study of ketogenic diets in bipolar disorder. I have not yet had a patient in my practice who has been willing to try a strict ketogenic diet, which not only limits carbohydrate, but also limits protein and requires blood monitoring of ketone levels.

However, I can tell you that my patients who have been willing to try low carbohydrate “modified Atkins” diets, low carbohydrate “Paleo” diets, or low glycemic index diets for mood problems—from depression to anxiety to eating disorders to bipolar disorders—report significant improvement in their symptoms. It stands to reason that these dietary changes, which have profound effects on other neurological disorders, would have the potential for profound effects on psychiatric disorders, as well.

Yet, even if a ketogenic diet worked beautifully for all cases of bipolar disorders of all types, I doubt that most people would choose to commit to a lifetime of eating a ketogenic diet. These diets are very restrictive and require major lifestyle changes. Most foods that people are accustomed to eating all day long are off-limits on this diet. For this reason, neurologists have recently begun to experiment with more relaxed versions of the diet to see how much carbohydrate patients can consume and still have good seizure control.

Studies of low glycemic index diets and modified Atkins diets (Atkins diets that allow unlimited protein and fat) look very promising but do not seem to work quite as well for seizures as ketogenic diets do. However, bipolar mood disorders and seizures are different in that seizures are black and white phenomena, whereas mood swings are a matter of degree. Perhaps people with bipolar mood disorders would be satisfied with less than perfect control over their mood swings in exchange for wider dietary variety?

If you have a bipolar mood disorder should you change your diet?

That’s up to you. While there are no scientific studies to support this idea yet, if you wait for the science to properly test the theory, you could be waiting for many years. You have nothing to lose by doing your own individual experiments, because it is well established that low glycemic index diets, Atkins diets, and ketogenic diets are safe. In fact, it is likely that they are far healthier than the low-fat, high-carb, low-meat diets recommended by public health officials, which are the very same diets that have worsened our collective health over the past four decades. If you do decide to try a dietary change, just keep in mind that it can take three to four weeks before potential benefits become noticeable.

A few words of caution

Dietary changes are difficult to make, and benefits can be slow to take effect, therefore nutritional approaches are not recommended in emergency situations.

If you are currently taking a mood stabilizing medication, please do not make any changes to your medications without discussing it with your clinician. Please see my article “Ketogenic Diets and Psychiatric Medications” for important information about drug interactions.

Very low-carbohydrate diets can alter the way medications are processed by the body, so if you are taking medications of any kind (including blood pressure and diabetes medications) and decide to try a low-carbohydrate diet, please do so with close medical supervision.

*If you are taking Depakote (Valproate), please be aware that there is a case report in the literature of a man who became manic and psychotic after starting a ketogenic diet, despite taking Depakote. The reason may have been that the diet reduced his Depakote levels (Depakote is a fatty acid, and the ketogenic diet is a fat-burning diet).

How about you?

Have you ever tried a low glycemic index diet or low carbohydrate diet? If so, did you notice any effects on your mood?

To learn more about about how diet can impact bipolar disorder, read my blog post “Bipolar Disorder and Diet Part I: Omega 3 Fatty Acids.”