Category: Nutrition

Type “is fructose bad for you” into your search engine and you’ll get a slew of articles telling you that fructose (aka fruit sugar) can cause diabetes, obesity, gout, fatty liver disease, and even cancer. If you believe the headlines, you might be worried that every time you bite into a banana, you’re hammering a big squishy yellow nail into your future fruity coffin. Yet public health officials, and even pediatric obesity specialist Dr. Robert Lustig, who goes so far as to call fructose a poison, continue to advise us to eat fruit. Confused? In this post, I provide a review of the science and clear, simple answers about the connection between fructose, glucose, and common health problems so that you have the information you need to make smart decisions about your health.

I put all of these diseases in a single blog post not to overwhelm you, but because they belong together. Although these conditions seem very different on the outside, as you’re about to see, they are actually just different faces of the same basic underlying metabolic problem: insulin resistance. You’ll also quickly discover that all kinds of sugar are risky when it comes to your health, and that fructose is probably the least of your worries.

[Note: this article is part three of a five-part series on sugar and health. To begin with article one, see “Has Fructose Been Framed?”]

Ok, so let’s get to the bottom of these, once and for all. [You can use the links below if you want to skip to a particular section.]

Note: Because fructose malabsorption differs metabolically from the above diseases, I decided to cover it in a separate post.

Q: Does fructose cause TYPE 2 (“adult-onset”) DIABETES?

A: There’s no evidence that reasonable amounts of fructose increase risk for diabetes more than other sugars do. Excessive intake of sugars of any kind can lead to high blood glucose levels and type 2 diabetes in susceptible people, but glucose raises blood glucose and insulin levels more than fructose does (except at very high doses), so glucose is arguably the more dangerous of the two sugars.

Type 2 diabetes is a disease characterized by “insulin resistance,” which can gradually lead to high insulin levels and high blood glucose levels. Insulin resistance means that your body has become less sensitive to the effects of insulin, a powerful hormone released after meals that tells your body what to do with the calories you eat. For example, after eating a meal, insulin tells muscle and liver cells to soak up excess glucose from your blood stream to keep your blood sugar from going too high. The most powerful trigger for insulin release is glucose (from sugars and starches); fructose does not directly stimulate insulin production.

If you eat too much sugar and/or starch too often, as most people do, your blood glucose will spike frequently and your body will have to release lots of insulin over and over again to deal with those glucose spikes. Eventually your cells can become so accustomed to insulin spikes that they become less responsive to insulin. If your cells become numbed to insulin’s signals, they can’t absorb extra glucose from the bloodstream as well, and your blood sugar could stay too high for too long after meals. In response, the body releases even more insulin to try to get cells to respond better. One result of this vicious cycle can be type 2 diabetes, a disease marked by high blood sugar and high insulin levels. I highly recommend this wonderful video of Dr. Andreas Eenfeldt interviewing kidney specialist Dr. Jason Fung explaining why it makes no sense to treat type 2 diabetes with insulin.

Excess consumption of sugars in general is well-established as a major risk factor in the development of insulin resistance, but is there quality evidence to suggest that fructose in particular is any more dangerous than any other sugar in this regard? Does fructose increase fasting insulin, fasting glucose, or insulin resistance more than glucose does?

It depends on who you ask and what kinds of doses we’re talking about.

It turns out that low to moderately high amounts of fructose are no worse than glucose and often are superior to glucose when it comes to these metabolic markers in human studies.1

That is to say that fasting insulin, fasting glucose, hemoglobin A1C (a measure of blood sugar over time) and insulin resistance often look better when people consume fructose than when they consume glucose. This makes sense because it is well-known that glucose is a far more powerful trigger of blood sugar and insulin spikes than fructose.

However, at very high doses (more than 100 grams per day) fructose actually starts to look a little worse than glucose.2

The fact that fructose behaves so differently at very high doses is responsible for some of the confusion and disagreement among scientists about whether fructose is worse than glucose for diabetes or not. [Read article two in this series to see how studies using excessively high doses of fructose produce unreliable results.]

There is no good scientific evidence to support the idea that sugar (which is a 50/50 mix of fructose and glucose) is metabolically any worse than starch (glucose) when appropriate amounts are considered.3

However, just because fructose is no worse than glucose does not mean that either one of them is innocent. When it comes to the big picture and common sense recommendations to reduce your risk for diabetes, I wholeheartedly agree with the conclusions reached by Dr. James DiNicolantonio and colleagues in a recent review of the subject:

“There is no need for added fructose or any added sugars in the diet; reducing intake to 5% of total calories (the level now suggested by the World Health Organization) has been shown to improve glucose tolerance in humans and decrease prevalence of diabetes and metabolic derangements that often precede and accompany it.”4

Q: Does fructose cause CANCER?

A: There’s no evidence that fructose causes cancer, however it may play a role in the spread of the disease. Cancer cells require glucose, not fructose, for energy and survival. High blood glucose and insulin levels set the stage for cancer growth in the body, so individuals with insulin resistance, high blood sugar, and type 2 diabetes are at higher risk. There is some evidence to support the notion that fructose may make it easier for certain kinds of cancer to spread, but no cancer cell can live without glucose.

It is an undisputed fact that cancer cells are addicted to glucose, which is found in virtually all sweet and starchy foods.

Cancer cells need a LOT more glucose than healthy cells because they rely mainly on a process called “anaerobic glycolysis” to fuel their furious growth rate. This means that instead of using oxygen to burn glucose for energy (aerobic glycolysis) like most healthy cells do, they ferment glucose into lactic acid for energy. Fermentation is very inefficient, so cancer cells demand high amounts of glucose to stay alive. [To learn more about how cancer cells operate, please see my series “What Causes Cancer?“]

Malignant cancer cells display high numbers of glucose transporters on their surfaces; without these special sugar transporters, glucose molecules would not be able to enter cancer cells from the bloodstream.

The more glucose you have in your bloodstream, the happier cancer cells are, so it makes perfect sense that high blood sugar levels would be a strong risk factor for cancer. Insulin resistance makes it hard to process glucose properly, so blood glucose levels rise. To make matters worse, cancer cells love high insulin levels, too, because insulin is a growth hormone that helps cells to grow. People with high insulin levels are at higher risk for cancer and have a worse prognosis once they develop cancer. High blood sugar and insulin levels are seen in people with insulin resistance, type 2 diabetes, and obesity, all of which belong to a group of related conditions collectively known as “metabolic syndrome.”

“Several studies indicate a strong association between MS [metabolic syndrome] and increased risk of cancer. The underlying mechanism of this association is not fully understood but, obesity, hyperglycemia, and hyperinsulinemic states are definitely involved. . . . Increased insulin levels in MS may lead not only to cancer initiation but also to its progression.”1

Okay, so when it comes to cancer, too much glucose in the blood is BAD. But what about fructose and cancer? Do tumor cells eat fructose, too? Do cancer cells have enough fructose transporters on their surfaces to use fructose as an energy source?

Yes, some cancer cells do eat fructose.

In humans, certain types of cancer cells are capable of sporting significant numbers of fructose transporters on their surfaces (in addition to the required high number of glucose receptors): certain kidney cancer cells,2 breast cancer cells, and certain brain cancer cells (gliomas).3

The most recent review of the possible role of fructose in cancer was written by scientists at the University of Maryland and Boston University in 2012 and is quite good.4

The authors of this review emphasize that it is well established that cancer cells love glucose and that excess glucose fuels cancer growth. However, they believe that fructose may be even more dangerous than glucose under certain circumstances. Almost all of the evidence used to support their argument against fructose comes either from epidemiological studies or from laboratory studies of specialized cell cultures under extreme conditions, but there are important exceptions that make their conclusions worth our attention:

• Interestingly, there is an autopsy study showing that lung cancer tumor cells that had metastasized (spread) to the liver displayed higher numbers of fructose transporters than the primary (original) lung tumor cells that hadn’t left the lung.
• Certain kidney cancer cells (clear cell renal carcinoma cells) display significant numbers of fructose transporters on their surfaces and have certain features that could make them more likely to metastasize (spread).
• In the laboratory, if you put cancer cells in Petri dishes and feed them fructose instead of glucose, they grow much more slowly than they do on glucose, but they also produce smaller amounts of self-destructive lactic acid, and produce more protein (via the pentose phosphate pathway—see article one). The thinking is this: If a cancer cell can use fructose in addition to glucose, it might be able to survive better because it produces less lactic acid, and its ability to crank out proteins may make it easier for it to break free and travel (metastasize).

“Fructose appears to be a superior precursor for protein synthesis over glucose by enhancing flux through biosynthetic pathways. Together, glucose and fructose may act synergistically to support malignant growth. . . . Fructose may also promote a more aggressive phenotype in cancer cells and increase the likelihood of metastasis. Further research into the specific effects of fructose, together with glucose, at physiologic levels on malignant growth is warranted.”5

Keep in mind that, unless you are in the habit of consuming high doses of fructose, most cancer cells are unlikely to be able to get much fructose out of your bloodstream. This is because, if you recall from article one, the liver sops up the vast majority of the fructose we absorb from foods and beverages before it has a chance to circulate, as long as the amount you consume is not too high. The only theoretical exception to this rule might be cancers of the digestive tract, which could be exposed to any fructose that you can’t absorb (we’ll look at fructose absorption problems in part four). Regardless, it appears that some cancer cells have come up with ways to exploit whatever fructose might be floating around and use it to their advantage.

Q: Does fructose cause OBESITY?

A: There’s no evidence that reasonable amounts of fructose cause more weight gain than other sugars. However, too many sugary calories (of any kind) can absolutely cause weight gain, especially in people with insulin resistance.

An excellent 2012 review of human studies funded by the Canadian Institutes of Health Research1 concludes convincingly that fructose does NOT cause weight gain compared to other sugars unless people are fed extra calories.

Yet, when high doses of fructose that add lots of extra calories to the diet are given to people, yes, some studies do show weight gain.

Given that only a tiny fraction of pure fructose is turned into fat (see article one), it’s unlikely that fructose on its own could be responsible for the obesity epidemic. HOWEVER, in real life, fructose and glucose are almost always eaten together. Fructose itself doesn’t cause much of an insulin response, but glucose certainly does, so when fructose and glucose are eaten together, insulin will spike and turn on fat building in the liver. It should be no surprise that big doses of fructose, when eaten with glucose, can make people fat.

But it’s important to point out that eating a big dose of glucose can make people just as fat.

A good example of a study that illustrates this point compared the effects of glucose drinks to fructose drinks on older overweight men and women. The sweetened drinks provided 25% of daily caloric intake (for a 2000 calorie/day diet, that would be 500 calories worth of fructose or glucose per day). Despite the fact that this study uses high doses of these sugars, it is interesting to note that, after 8 weeks, both glucose and fructose had caused the same amount of weight gain—more than 3 pounds,2 suggesting that overeating either type of sugar can make you fat.

There is a consensus building that “central obesity” is a disease of insulin resistance.3 This means that if you tend to gain weight around your middle, like an apple, you probably have insulin resistance and therefore your body will tend to turn sugars and starches into fat very easily and have a harder time burning it for energy. [Take my quiz: “How Carbohydrate Sensitive Are You?]”

Q:  Does fructose cause GOUT?

A: There’s no evidence that reasonable amounts of fructose raise uric acid levels, let alone cause gout. High doses of fructose do raise uric acid levels more than glucose does, but high uric acid levels alone are not enough to cause gout. In fact, most people with high uric acid levels will never develop gout.

Gout is a special type of arthritis marked by painful deposits of uric acid crystals in joints. Uric acid is a normal by-product of everyday cellular activity, so we all have uric acid in our blood all the time, whether we eat fructose or not, but some people have more uric acid floating around in their bloodstream than others do. It is unclear why some people are more prone to gout, but we do know that people with insulin resistance are at higher risk.1 This is partly because high insulin levels tell the kidney to hold on to extra uric acid instead of excreting it in the urine, the way it normally would.

Studies consistently show that very high doses of fructose do raise uric acid levels more than glucose does (see article one) However, when studies use a normal number of calories, fructose does not raise uric acid more than other sugars do.2 For more information about diet and gout, please see my post “Got Gout But Love Meat?“

Q:  Does fructose cause FATTY LIVER DISEASE?

A: There’s no evidence that reasonable amounts of fructose lead to fatty changes in the liver. However, excessive intake of sugar of any kind can lead to fatty changes in the liver.

Non-alcoholic fatty liver disease (NAFLD) affects 30% of Americans [wow!]. It is characterized by insulin resistance and fatty deposits in the liver, which can lead to liver damage over time.

A recent review of all available controlled feeding studies in humans concluded that there is no evidence that fructose at ordinary doses can cause fatty liver changes in healthy people.1

It is important to point out that when certain people (typically people with insulin resistance) overeat sugars of any kind, the liver can start to become fatty, because insulin orchestrates the movement, usage, and storage of sugars and fats throughout the body. If insulin signaling isn’t working properly, fats can end up in the wrong places. In one study, when overweight men drank 25% of their daily calories as either glucose or fructose, after two weeks BOTH groups exhibited the kinds of changes that can lead to fatty liver, not just the fructose group.2

Q:  Does fructose raise your blood pressure, cholesterol and triglyceride levels, increasing your risk for HEART DISEASE?

A: Fructose is no worse than glucose for your overall cardiovascular health, and may even have some advantages over glucose when it comes to blood pressure.

An excellent review about this topic1 summarizes what is currently known about the effects of fructose on various heart health markers. Unfortunately most of the human evidence comes from studies using too many calories, but nevertheless, even when high doses of fructose are compared to equally high doses of glucose, some differences do appear.

Cholesterol levels (fasting): There are no differences between fructose and glucose when it comes to LDL (so-called “bad cholesterol”) or HDL (so-called “good cholesterol”). However, fructose does raise total cholesterol in some people more than glucose does. But total cholesterol levels do not tell us anything about our risk for heart disease. When it comes to standard cholesterol test results, HDL is the only number worth paying attention to in estimating heart disease risk.

Triglyceride levels: Fructose temporarily raises triglycerides (blood fats) after eating more than glucose does, but does not affect fasting triglyceride levels any differently than glucose does, and it is fasting triglycerides that are used to help predict heart attack risk. If you already read article one, you saw that pure fructose has almost no effect on fat production in the liver, so you may wonder how fructose can raise blood fats, even temporarily. If fructose is eaten in combination with glucose (which is almost always the case in the real world and in human experiments), then glucose will trigger an insulin spike, and insulin will tell the liver to build fat (triglycerides). Fructose also temporarily slows down the removal of triglycerides from the blood, so the level can appear to rise even if the liver isn’t making any more triglycerides than usual.2

Blood pressure: Diets high in sugars in general can raise blood pressure,3 at least partly because sugar can raise adrenaline levels.4 However, glucose raises blood pressure more than fructose in some people.5 This makes sense because hypertension is known to be an insulin-resistant condition, and it is high levels of glucose that overtax insulin.6

So, is fructose bad for you?

It turns out that excess GLUCOSE, the source of most of the sugar in our diet, is just as risky, and often riskier than fructose when it comes to these health conditions, primarily because of how glucose affects insulin and blood sugar. However, fructose at very high doses, or in people with cancer, poses health risks as well, so both of these sugars are worth minimizing.

Each and every single one of these health problems—type 2 diabetes, cancer, obesity, gout, fatty liver disease, and heart disease—is an insulin-resistant condition. Insulin resistance, which leads to high blood glucose and high insulin levels, is the scourge of our time.

Any lifestyle change you can make to improve insulin resistance, lower insulin levels and lower blood sugar, is well worth making, and will go a long way toward protecting and perhaps even completely restoring your good health. I can think of no better target, no better use of your time and energy.

In article five of this series: “How to Diagnose, Prevent, and Treat Insulin Resistance” we finally crawl out of the test tube and back into reality. I’ll show you which of your favorite foods and beverages contain the most glucose and fructose and share with you strategies you can use to improve your insulin sensitivity (including some recommendations that may surprise you). But first, we’ll take a quick detour and look at the one health problem that is absolutely caused by fructose and not glucose: fructose malabsorption. Until then, how about you?

What do you think about the connection between fructose and these common diseases? Are you any more or less afraid of fructose than you were before? Have you tried a low-fructose, low-sugar, or low-carbohydrate diet for diabetes, gout, weight loss, fatty liver, high blood pressure, or even cancer? What has your experience been?

Type “is fructose bad for you” into your search engine and you’ll get a slew of articles telling you that fructose (aka fruit sugar) can cause diabetes, obesity, gout, fatty liver disease, and even cancer. If you believe the headlines, you might be worried that every time you bite into a banana, you’re hammering a big squishy yellow nail into your future fruity coffin. Yet public health officials, and even pediatric obesity specialist Dr. Robert Lustig, who goes so far as to call fructose a poison, continue to advise us to eat fruit. Confused? In this post, I provide a review of the science and clear, simple answers about the connection between fructose, glucose, and common health problems so that you have the information you need to make smart decisions about your health.

I put all of these diseases in a single blog post not to overwhelm you, but because they belong together. Although these conditions seem very different on the outside, as you’re about to see, they are actually just different faces of the same basic underlying metabolic problem: insulin resistance. You’ll also quickly discover that all kinds of sugar are risky when it comes to your health, and that fructose is probably the least of your worries.

[Note: this article is part three of a five-part series on sugar and health. To begin with article one, see “Has Fructose Been Framed?”]

Ok, so let’s get to the bottom of these, once and for all. [You can use the links below if you want to skip to a particular section.]

Note: Because fructose malabsorption differs metabolically from the above diseases, I decided to cover it in a separate post.

Q: Does fructose cause TYPE 2 (“adult-onset”) DIABETES?

A: There’s no evidence that reasonable amounts of fructose increase risk for diabetes more than other sugars do. Excessive intake of sugars of any kind can lead to high blood glucose levels and type 2 diabetes in susceptible people, but glucose raises blood glucose and insulin levels more than fructose does (except at very high doses), so glucose is arguably the more dangerous of the two sugars.

Type 2 diabetes is a disease characterized by “insulin resistance,” which can gradually lead to high insulin levels and high blood glucose levels. Insulin resistance means that your body has become less sensitive to the effects of insulin, a powerful hormone released after meals that tells your body what to do with the calories you eat. For example, after eating a meal, insulin tells muscle and liver cells to soak up excess glucose from your blood stream to keep your blood sugar from going too high. The most powerful trigger for insulin release is glucose (from sugars and starches); fructose does not directly stimulate insulin production.

If you eat too much sugar and/or starch too often, as most people do, your blood glucose will spike frequently and your body will have to release lots of insulin over and over again to deal with those glucose spikes. Eventually your cells can become so accustomed to insulin spikes that they become less responsive to insulin. If your cells become numbed to insulin’s signals, they can’t absorb extra glucose from the bloodstream as well, and your blood sugar could stay too high for too long after meals. In response, the body releases even more insulin to try to get cells to respond better. One result of this vicious cycle can be type 2 diabetes, a disease marked by high blood sugar and high insulin levels. I highly recommend this wonderful video of Dr. Andreas Eenfeldt interviewing kidney specialist Dr. Jason Fung explaining why it makes no sense to treat type 2 diabetes with insulin.

Excess consumption of sugars in general is well-established as a major risk factor in the development of insulin resistance, but is there quality evidence to suggest that fructose in particular is any more dangerous than any other sugar in this regard? Does fructose increase fasting insulin, fasting glucose, or insulin resistance more than glucose does?

It depends on who you ask and what kinds of doses we’re talking about.

It turns out that low to moderately high amounts of fructose are no worse than glucose and often are superior to glucose when it comes to these metabolic markers in human studies.1

That is to say that fasting insulin, fasting glucose, hemoglobin A1C (a measure of blood sugar over time) and insulin resistance often look better when people consume fructose than when they consume glucose. This makes sense because it is well-known that glucose is a far more powerful trigger of blood sugar and insulin spikes than fructose.

However, at very high doses (more than 100 grams per day) fructose actually starts to look a little worse than glucose.2

The fact that fructose behaves so differently at very high doses is responsible for some of the confusion and disagreement among scientists about whether fructose is worse than glucose for diabetes or not. [Read article two in this series to see how studies using excessively high doses of fructose produce unreliable results.]

There is no good scientific evidence to support the idea that sugar (which is a 50/50 mix of fructose and glucose) is metabolically any worse than starch (glucose) when appropriate amounts are considered.3

However, just because fructose is no worse than glucose does not mean that either one of them is innocent. When it comes to the big picture and common sense recommendations to reduce your risk for diabetes, I wholeheartedly agree with the conclusions reached by Dr. James DiNicolantonio and colleagues in a recent review of the subject:

“There is no need for added fructose or any added sugars in the diet; reducing intake to 5% of total calories (the level now suggested by the World Health Organization) has been shown to improve glucose tolerance in humans and decrease prevalence of diabetes and metabolic derangements that often precede and accompany it.”4

Q: Does fructose cause CANCER?

A: There’s no evidence that fructose causes cancer, however it may play a role in the spread of the disease. Cancer cells require glucose, not fructose, for energy and survival. High blood glucose and insulin levels set the stage for cancer growth in the body, so individuals with insulin resistance, high blood sugar, and type 2 diabetes are at higher risk. There is some evidence to support the notion that fructose may make it easier for certain kinds of cancer to spread, but no cancer cell can live without glucose.

It is an undisputed fact that cancer cells are addicted to glucose, which is found in virtually all sweet and starchy foods.

Cancer cells need a LOT more glucose than healthy cells because they rely mainly on a process called “anaerobic glycolysis” to fuel their furious growth rate. This means that instead of using oxygen to burn glucose for energy (aerobic glycolysis) like most healthy cells do, they ferment glucose into lactic acid for energy. Fermentation is very inefficient, so cancer cells demand high amounts of glucose to stay alive. [To learn more about how cancer cells operate, please see my series “What Causes Cancer?“]

Malignant cancer cells display high numbers of glucose transporters on their surfaces; without these special sugar transporters, glucose molecules would not be able to enter cancer cells from the bloodstream.

The more glucose you have in your bloodstream, the happier cancer cells are, so it makes perfect sense that high blood sugar levels would be a strong risk factor for cancer. Insulin resistance makes it hard to process glucose properly, so blood glucose levels rise. To make matters worse, cancer cells love high insulin levels, too, because insulin is a growth hormone that helps cells to grow. People with high insulin levels are at higher risk for cancer and have a worse prognosis once they develop cancer. High blood sugar and insulin levels are seen in people with insulin resistance, type 2 diabetes, and obesity, all of which belong to a group of related conditions collectively known as “metabolic syndrome.”

“Several studies indicate a strong association between MS [metabolic syndrome] and increased risk of cancer. The underlying mechanism of this association is not fully understood but, obesity, hyperglycemia, and hyperinsulinemic states are definitely involved. . . . Increased insulin levels in MS may lead not only to cancer initiation but also to its progression.”1

Okay, so when it comes to cancer, too much glucose in the blood is BAD. But what about fructose and cancer? Do tumor cells eat fructose, too? Do cancer cells have enough fructose transporters on their surfaces to use fructose as an energy source?

Yes, some cancer cells do eat fructose.

In humans, certain types of cancer cells are capable of sporting significant numbers of fructose transporters on their surfaces (in addition to the required high number of glucose receptors): certain kidney cancer cells,2 breast cancer cells, and certain brain cancer cells (gliomas).3

The most recent review of the possible role of fructose in cancer was written by scientists at the University of Maryland and Boston University in 2012 and is quite good.4

The authors of this review emphasize that it is well established that cancer cells love glucose and that excess glucose fuels cancer growth. However, they believe that fructose may be even more dangerous than glucose under certain circumstances. Almost all of the evidence used to support their argument against fructose comes either from epidemiological studies or from laboratory studies of specialized cell cultures under extreme conditions, but there are important exceptions that make their conclusions worth our attention:

• Interestingly, there is an autopsy study showing that lung cancer tumor cells that had metastasized (spread) to the liver displayed higher numbers of fructose transporters than the primary (original) lung tumor cells that hadn’t left the lung.
• Certain kidney cancer cells (clear cell renal carcinoma cells) display significant numbers of fructose transporters on their surfaces and have certain features that could make them more likely to metastasize (spread).
• In the laboratory, if you put cancer cells in Petri dishes and feed them fructose instead of glucose, they grow much more slowly than they do on glucose, but they also produce smaller amounts of self-destructive lactic acid, and produce more protein (via the pentose phosphate pathway—see article one). The thinking is this: If a cancer cell can use fructose in addition to glucose, it might be able to survive better because it produces less lactic acid, and its ability to crank out proteins may make it easier for it to break free and travel (metastasize).

“Fructose appears to be a superior precursor for protein synthesis over glucose by enhancing flux through biosynthetic pathways. Together, glucose and fructose may act synergistically to support malignant growth. . . . Fructose may also promote a more aggressive phenotype in cancer cells and increase the likelihood of metastasis. Further research into the specific effects of fructose, together with glucose, at physiologic levels on malignant growth is warranted.”5

Keep in mind that, unless you are in the habit of consuming high doses of fructose, most cancer cells are unlikely to be able to get much fructose out of your bloodstream. This is because, if you recall from article one, the liver sops up the vast majority of the fructose we absorb from foods and beverages before it has a chance to circulate, as long as the amount you consume is not too high. The only theoretical exception to this rule might be cancers of the digestive tract, which could be exposed to any fructose that you can’t absorb (we’ll look at fructose absorption problems in part four). Regardless, it appears that some cancer cells have come up with ways to exploit whatever fructose might be floating around and use it to their advantage.

Q: Does fructose cause OBESITY?

A: There’s no evidence that reasonable amounts of fructose cause more weight gain than other sugars. However, too many sugary calories (of any kind) can absolutely cause weight gain, especially in people with insulin resistance.

An excellent 2012 review of human studies funded by the Canadian Institutes of Health Research1 concludes convincingly that fructose does NOT cause weight gain compared to other sugars unless people are fed extra calories.

Yet, when high doses of fructose that add lots of extra calories to the diet are given to people, yes, some studies do show weight gain.

Given that only a tiny fraction of pure fructose is turned into fat (see article one), it’s unlikely that fructose on its own could be responsible for the obesity epidemic. HOWEVER, in real life, fructose and glucose are almost always eaten together. Fructose itself doesn’t cause much of an insulin response, but glucose certainly does, so when fructose and glucose are eaten together, insulin will spike and turn on fat building in the liver. It should be no surprise that big doses of fructose, when eaten with glucose, can make people fat.

But it’s important to point out that eating a big dose of glucose can make people just as fat.

A good example of a study that illustrates this point compared the effects of glucose drinks to fructose drinks on older overweight men and women. The sweetened drinks provided 25% of daily caloric intake (for a 2000 calorie/day diet, that would be 500 calories worth of fructose or glucose per day). Despite the fact that this study uses high doses of these sugars, it is interesting to note that, after 8 weeks, both glucose and fructose had caused the same amount of weight gain—more than 3 pounds,2 suggesting that overeating either type of sugar can make you fat.

There is a consensus building that “central obesity” is a disease of insulin resistance.3 This means that if you tend to gain weight around your middle, like an apple, you probably have insulin resistance and therefore your body will tend to turn sugars and starches into fat very easily and have a harder time burning it for energy. [Take my quiz: “How Carbohydrate Sensitive Are You?]”

Q:  Does fructose cause GOUT?

A: There’s no evidence that reasonable amounts of fructose raise uric acid levels, let alone cause gout. High doses of fructose do raise uric acid levels more than glucose does, but high uric acid levels alone are not enough to cause gout. In fact, most people with high uric acid levels will never develop gout.

Gout is a special type of arthritis marked by painful deposits of uric acid crystals in joints. Uric acid is a normal by-product of everyday cellular activity, so we all have uric acid in our blood all the time, whether we eat fructose or not, but some people have more uric acid floating around in their bloodstream than others do. It is unclear why some people are more prone to gout, but we do know that people with insulin resistance are at higher risk.1 This is partly because high insulin levels tell the kidney to hold on to extra uric acid instead of excreting it in the urine, the way it normally would.

Studies consistently show that very high doses of fructose do raise uric acid levels more than glucose does (see article one) However, when studies use a normal number of calories, fructose does not raise uric acid more than other sugars do.2 For more information about diet and gout, please see my post “Got Gout But Love Meat?“

Q:  Does fructose cause FATTY LIVER DISEASE?

A: There’s no evidence that reasonable amounts of fructose lead to fatty changes in the liver. However, excessive intake of sugar of any kind can lead to fatty changes in the liver.

Non-alcoholic fatty liver disease (NAFLD) affects 30% of Americans [wow!]. It is characterized by insulin resistance and fatty deposits in the liver, which can lead to liver damage over time.

A recent review of all available controlled feeding studies in humans concluded that there is no evidence that fructose at ordinary doses can cause fatty liver changes in healthy people.1

It is important to point out that when certain people (typically people with insulin resistance) overeat sugars of any kind, the liver can start to become fatty, because insulin orchestrates the movement, usage, and storage of sugars and fats throughout the body. If insulin signaling isn’t working properly, fats can end up in the wrong places. In one study, when overweight men drank 25% of their daily calories as either glucose or fructose, after two weeks BOTH groups exhibited the kinds of changes that can lead to fatty liver, not just the fructose group.2

Q:  Does fructose raise your blood pressure, cholesterol and triglyceride levels, increasing your risk for HEART DISEASE?

A: Fructose is no worse than glucose for your overall cardiovascular health, and may even have some advantages over glucose when it comes to blood pressure.

An excellent review about this topic1 summarizes what is currently known about the effects of fructose on various heart health markers. Unfortunately most of the human evidence comes from studies using too many calories, but nevertheless, even when high doses of fructose are compared to equally high doses of glucose, some differences do appear.

Cholesterol levels (fasting): There are no differences between fructose and glucose when it comes to LDL (so-called “bad cholesterol”) or HDL (so-called “good cholesterol”). However, fructose does raise total cholesterol in some people more than glucose does. But total cholesterol levels do not tell us anything about our risk for heart disease. When it comes to standard cholesterol test results, HDL is the only number worth paying attention to in estimating heart disease risk.

Triglyceride levels: Fructose temporarily raises triglycerides (blood fats) after eating more than glucose does, but does not affect fasting triglyceride levels any differently than glucose does, and it is fasting triglycerides that are used to help predict heart attack risk. If you already read article one, you saw that pure fructose has almost no effect on fat production in the liver, so you may wonder how fructose can raise blood fats, even temporarily. If fructose is eaten in combination with glucose (which is almost always the case in the real world and in human experiments), then glucose will trigger an insulin spike, and insulin will tell the liver to build fat (triglycerides). Fructose also temporarily slows down the removal of triglycerides from the blood, so the level can appear to rise even if the liver isn’t making any more triglycerides than usual.2

Blood pressure: Diets high in sugars in general can raise blood pressure,3 at least partly because sugar can raise adrenaline levels.4 However, glucose raises blood pressure more than fructose in some people.5 This makes sense because hypertension is known to be an insulin-resistant condition, and it is high levels of glucose that overtax insulin.6

So, is fructose bad for you?

It turns out that excess GLUCOSE, the source of most of the sugar in our diet, is just as risky, and often riskier than fructose when it comes to these health conditions, primarily because of how glucose affects insulin and blood sugar. However, fructose at very high doses, or in people with cancer, poses health risks as well, so both of these sugars are worth minimizing.

Each and every single one of these health problems—type 2 diabetes, cancer, obesity, gout, fatty liver disease, and heart disease—is an insulin-resistant condition. Insulin resistance, which leads to high blood glucose and high insulin levels, is the scourge of our time.

Any lifestyle change you can make to improve insulin resistance, lower insulin levels and lower blood sugar, is well worth making, and will go a long way toward protecting and perhaps even completely restoring your good health. I can think of no better target, no better use of your time and energy.

In article five of this series: “How to Diagnose, Prevent, and Treat Insulin Resistance” we finally crawl out of the test tube and back into reality. I’ll show you which of your favorite foods and beverages contain the most glucose and fructose and share with you strategies you can use to improve your insulin sensitivity (including some recommendations that may surprise you). But first, we’ll take a quick detour and look at the one health problem that is absolutely caused by fructose and not glucose: fructose malabsorption. Until then, how about you?

What do you think about the connection between fructose and these common diseases? Are you any more or less afraid of fructose than you were before? Have you tried a low-fructose, low-sugar, or low-carbohydrate diet for diabetes, gout, weight loss, fatty liver, high blood pressure, or even cancer? What has your experience been?

Type “is fructose bad for you” into your search engine and you’ll get a slew of articles telling you that fructose (aka fruit sugar) can cause diabetes, obesity, gout, fatty liver disease, and even cancer. If you believe the headlines, you might be worried that every time you bite into a banana, you’re hammering a big squishy yellow nail into your future fruity coffin. Yet public health officials, and even pediatric obesity specialist Dr. Robert Lustig, who goes so far as to call fructose a poison, continue to advise us to eat fruit. Confused? In this post, I provide a review of the science and clear, simple answers about the connection between fructose, glucose, and common health problems so that you have the information you need to make smart decisions about your health.

I put all of these diseases in a single blog post not to overwhelm you, but because they belong together. Although these conditions seem very different on the outside, as you’re about to see, they are actually just different faces of the same basic underlying metabolic problem: insulin resistance. You’ll also quickly discover that all kinds of sugar are risky when it comes to your health, and that fructose is probably the least of your worries.

[Note: this article is part three of a five-part series on sugar and health. To begin with article one, see “Has Fructose Been Framed?”]

Ok, so let’s get to the bottom of these, once and for all. [You can use the links below if you want to skip to a particular section.]

Note: Because fructose malabsorption differs metabolically from the above diseases, I decided to cover it in a separate post.

Q: Does fructose cause TYPE 2 (“adult-onset”) DIABETES?

A: There’s no evidence that reasonable amounts of fructose increase risk for diabetes more than other sugars do. Excessive intake of sugars of any kind can lead to high blood glucose levels and type 2 diabetes in susceptible people, but glucose raises blood glucose and insulin levels more than fructose does (except at very high doses), so glucose is arguably the more dangerous of the two sugars.

Type 2 diabetes is a disease characterized by “insulin resistance,” which can gradually lead to high insulin levels and high blood glucose levels. Insulin resistance means that your body has become less sensitive to the effects of insulin, a powerful hormone released after meals that tells your body what to do with the calories you eat. For example, after eating a meal, insulin tells muscle and liver cells to soak up excess glucose from your blood stream to keep your blood sugar from going too high. The most powerful trigger for insulin release is glucose (from sugars and starches); fructose does not directly stimulate insulin production.

If you eat too much sugar and/or starch too often, as most people do, your blood glucose will spike frequently and your body will have to release lots of insulin over and over again to deal with those glucose spikes. Eventually your cells can become so accustomed to insulin spikes that they become less responsive to insulin. If your cells become numbed to insulin’s signals, they can’t absorb extra glucose from the bloodstream as well, and your blood sugar could stay too high for too long after meals. In response, the body releases even more insulin to try to get cells to respond better. One result of this vicious cycle can be type 2 diabetes, a disease marked by high blood sugar and high insulin levels. I highly recommend this wonderful video of Dr. Andreas Eenfeldt interviewing kidney specialist Dr. Jason Fung explaining why it makes no sense to treat type 2 diabetes with insulin.

Excess consumption of sugars in general is well-established as a major risk factor in the development of insulin resistance, but is there quality evidence to suggest that fructose in particular is any more dangerous than any other sugar in this regard? Does fructose increase fasting insulin, fasting glucose, or insulin resistance more than glucose does?

It depends on who you ask and what kinds of doses we’re talking about.

It turns out that low to moderately high amounts of fructose are no worse than glucose and often are superior to glucose when it comes to these metabolic markers in human studies.1

That is to say that fasting insulin, fasting glucose, hemoglobin A1C (a measure of blood sugar over time) and insulin resistance often look better when people consume fructose than when they consume glucose. This makes sense because it is well-known that glucose is a far more powerful trigger of blood sugar and insulin spikes than fructose.

However, at very high doses (more than 100 grams per day) fructose actually starts to look a little worse than glucose.2

The fact that fructose behaves so differently at very high doses is responsible for some of the confusion and disagreement among scientists about whether fructose is worse than glucose for diabetes or not. [Read article two in this series to see how studies using excessively high doses of fructose produce unreliable results.]

There is no good scientific evidence to support the idea that sugar (which is a 50/50 mix of fructose and glucose) is metabolically any worse than starch (glucose) when appropriate amounts are considered.3

However, just because fructose is no worse than glucose does not mean that either one of them is innocent. When it comes to the big picture and common sense recommendations to reduce your risk for diabetes, I wholeheartedly agree with the conclusions reached by Dr. James DiNicolantonio and colleagues in a recent review of the subject:

“There is no need for added fructose or any added sugars in the diet; reducing intake to 5% of total calories (the level now suggested by the World Health Organization) has been shown to improve glucose tolerance in humans and decrease prevalence of diabetes and metabolic derangements that often precede and accompany it.”4

Q: Does fructose cause CANCER?

A: There’s no evidence that fructose causes cancer, however it may play a role in the spread of the disease. Cancer cells require glucose, not fructose, for energy and survival. High blood glucose and insulin levels set the stage for cancer growth in the body, so individuals with insulin resistance, high blood sugar, and type 2 diabetes are at higher risk. There is some evidence to support the notion that fructose may make it easier for certain kinds of cancer to spread, but no cancer cell can live without glucose.

It is an undisputed fact that cancer cells are addicted to glucose, which is found in virtually all sweet and starchy foods.

Cancer cells need a LOT more glucose than healthy cells because they rely mainly on a process called “anaerobic glycolysis” to fuel their furious growth rate. This means that instead of using oxygen to burn glucose for energy (aerobic glycolysis) like most healthy cells do, they ferment glucose into lactic acid for energy. Fermentation is very inefficient, so cancer cells demand high amounts of glucose to stay alive. [To learn more about how cancer cells operate, please see my series “What Causes Cancer?“]

Malignant cancer cells display high numbers of glucose transporters on their surfaces; without these special sugar transporters, glucose molecules would not be able to enter cancer cells from the bloodstream.

The more glucose you have in your bloodstream, the happier cancer cells are, so it makes perfect sense that high blood sugar levels would be a strong risk factor for cancer. Insulin resistance makes it hard to process glucose properly, so blood glucose levels rise. To make matters worse, cancer cells love high insulin levels, too, because insulin is a growth hormone that helps cells to grow. People with high insulin levels are at higher risk for cancer and have a worse prognosis once they develop cancer. High blood sugar and insulin levels are seen in people with insulin resistance, type 2 diabetes, and obesity, all of which belong to a group of related conditions collectively known as “metabolic syndrome.”

“Several studies indicate a strong association between MS [metabolic syndrome] and increased risk of cancer. The underlying mechanism of this association is not fully understood but, obesity, hyperglycemia, and hyperinsulinemic states are definitely involved. . . . Increased insulin levels in MS may lead not only to cancer initiation but also to its progression.”1

Okay, so when it comes to cancer, too much glucose in the blood is BAD. But what about fructose and cancer? Do tumor cells eat fructose, too? Do cancer cells have enough fructose transporters on their surfaces to use fructose as an energy source?

Yes, some cancer cells do eat fructose.

In humans, certain types of cancer cells are capable of sporting significant numbers of fructose transporters on their surfaces (in addition to the required high number of glucose receptors): certain kidney cancer cells,2 breast cancer cells, and certain brain cancer cells (gliomas).3

The most recent review of the possible role of fructose in cancer was written by scientists at the University of Maryland and Boston University in 2012 and is quite good.4

The authors of this review emphasize that it is well established that cancer cells love glucose and that excess glucose fuels cancer growth. However, they believe that fructose may be even more dangerous than glucose under certain circumstances. Almost all of the evidence used to support their argument against fructose comes either from epidemiological studies or from laboratory studies of specialized cell cultures under extreme conditions, but there are important exceptions that make their conclusions worth our attention:

• Interestingly, there is an autopsy study showing that lung cancer tumor cells that had metastasized (spread) to the liver displayed higher numbers of fructose transporters than the primary (original) lung tumor cells that hadn’t left the lung.
• Certain kidney cancer cells (clear cell renal carcinoma cells) display significant numbers of fructose transporters on their surfaces and have certain features that could make them more likely to metastasize (spread).
• In the laboratory, if you put cancer cells in Petri dishes and feed them fructose instead of glucose, they grow much more slowly than they do on glucose, but they also produce smaller amounts of self-destructive lactic acid, and produce more protein (via the pentose phosphate pathway—see article one). The thinking is this: If a cancer cell can use fructose in addition to glucose, it might be able to survive better because it produces less lactic acid, and its ability to crank out proteins may make it easier for it to break free and travel (metastasize).

“Fructose appears to be a superior precursor for protein synthesis over glucose by enhancing flux through biosynthetic pathways. Together, glucose and fructose may act synergistically to support malignant growth. . . . Fructose may also promote a more aggressive phenotype in cancer cells and increase the likelihood of metastasis. Further research into the specific effects of fructose, together with glucose, at physiologic levels on malignant growth is warranted.”5

Keep in mind that, unless you are in the habit of consuming high doses of fructose, most cancer cells are unlikely to be able to get much fructose out of your bloodstream. This is because, if you recall from article one, the liver sops up the vast majority of the fructose we absorb from foods and beverages before it has a chance to circulate, as long as the amount you consume is not too high. The only theoretical exception to this rule might be cancers of the digestive tract, which could be exposed to any fructose that you can’t absorb (we’ll look at fructose absorption problems in part four). Regardless, it appears that some cancer cells have come up with ways to exploit whatever fructose might be floating around and use it to their advantage.

Q: Does fructose cause OBESITY?

A: There’s no evidence that reasonable amounts of fructose cause more weight gain than other sugars. However, too many sugary calories (of any kind) can absolutely cause weight gain, especially in people with insulin resistance.

An excellent 2012 review of human studies funded by the Canadian Institutes of Health Research1 concludes convincingly that fructose does NOT cause weight gain compared to other sugars unless people are fed extra calories.

Yet, when high doses of fructose that add lots of extra calories to the diet are given to people, yes, some studies do show weight gain.

Given that only a tiny fraction of pure fructose is turned into fat (see article one), it’s unlikely that fructose on its own could be responsible for the obesity epidemic. HOWEVER, in real life, fructose and glucose are almost always eaten together. Fructose itself doesn’t cause much of an insulin response, but glucose certainly does, so when fructose and glucose are eaten together, insulin will spike and turn on fat building in the liver. It should be no surprise that big doses of fructose, when eaten with glucose, can make people fat.

But it’s important to point out that eating a big dose of glucose can make people just as fat.

A good example of a study that illustrates this point compared the effects of glucose drinks to fructose drinks on older overweight men and women. The sweetened drinks provided 25% of daily caloric intake (for a 2000 calorie/day diet, that would be 500 calories worth of fructose or glucose per day). Despite the fact that this study uses high doses of these sugars, it is interesting to note that, after 8 weeks, both glucose and fructose had caused the same amount of weight gain—more than 3 pounds,2 suggesting that overeating either type of sugar can make you fat.

There is a consensus building that “central obesity” is a disease of insulin resistance.3 This means that if you tend to gain weight around your middle, like an apple, you probably have insulin resistance and therefore your body will tend to turn sugars and starches into fat very easily and have a harder time burning it for energy. [Take my quiz: “How Carbohydrate Sensitive Are You?]”

Q:  Does fructose cause GOUT?

A: There’s no evidence that reasonable amounts of fructose raise uric acid levels, let alone cause gout. High doses of fructose do raise uric acid levels more than glucose does, but high uric acid levels alone are not enough to cause gout. In fact, most people with high uric acid levels will never develop gout.

Gout is a special type of arthritis marked by painful deposits of uric acid crystals in joints. Uric acid is a normal by-product of everyday cellular activity, so we all have uric acid in our blood all the time, whether we eat fructose or not, but some people have more uric acid floating around in their bloodstream than others do. It is unclear why some people are more prone to gout, but we do know that people with insulin resistance are at higher risk.1 This is partly because high insulin levels tell the kidney to hold on to extra uric acid instead of excreting it in the urine, the way it normally would.

Studies consistently show that very high doses of fructose do raise uric acid levels more than glucose does (see article one) However, when studies use a normal number of calories, fructose does not raise uric acid more than other sugars do.2 For more information about diet and gout, please see my post “Got Gout But Love Meat?“

Q:  Does fructose cause FATTY LIVER DISEASE?

A: There’s no evidence that reasonable amounts of fructose lead to fatty changes in the liver. However, excessive intake of sugar of any kind can lead to fatty changes in the liver.

Non-alcoholic fatty liver disease (NAFLD) affects 30% of Americans [wow!]. It is characterized by insulin resistance and fatty deposits in the liver, which can lead to liver damage over time.

A recent review of all available controlled feeding studies in humans concluded that there is no evidence that fructose at ordinary doses can cause fatty liver changes in healthy people.1

It is important to point out that when certain people (typically people with insulin resistance) overeat sugars of any kind, the liver can start to become fatty, because insulin orchestrates the movement, usage, and storage of sugars and fats throughout the body. If insulin signaling isn’t working properly, fats can end up in the wrong places. In one study, when overweight men drank 25% of their daily calories as either glucose or fructose, after two weeks BOTH groups exhibited the kinds of changes that can lead to fatty liver, not just the fructose group.2

Q:  Does fructose raise your blood pressure, cholesterol and triglyceride levels, increasing your risk for HEART DISEASE?

A: Fructose is no worse than glucose for your overall cardiovascular health, and may even have some advantages over glucose when it comes to blood pressure.

An excellent review about this topic1 summarizes what is currently known about the effects of fructose on various heart health markers. Unfortunately most of the human evidence comes from studies using too many calories, but nevertheless, even when high doses of fructose are compared to equally high doses of glucose, some differences do appear.

Cholesterol levels (fasting): There are no differences between fructose and glucose when it comes to LDL (so-called “bad cholesterol”) or HDL (so-called “good cholesterol”). However, fructose does raise total cholesterol in some people more than glucose does. But total cholesterol levels do not tell us anything about our risk for heart disease. When it comes to standard cholesterol test results, HDL is the only number worth paying attention to in estimating heart disease risk.

Triglyceride levels: Fructose temporarily raises triglycerides (blood fats) after eating more than glucose does, but does not affect fasting triglyceride levels any differently than glucose does, and it is fasting triglycerides that are used to help predict heart attack risk. If you already read article one, you saw that pure fructose has almost no effect on fat production in the liver, so you may wonder how fructose can raise blood fats, even temporarily. If fructose is eaten in combination with glucose (which is almost always the case in the real world and in human experiments), then glucose will trigger an insulin spike, and insulin will tell the liver to build fat (triglycerides). Fructose also temporarily slows down the removal of triglycerides from the blood, so the level can appear to rise even if the liver isn’t making any more triglycerides than usual.2

Blood pressure: Diets high in sugars in general can raise blood pressure,3 at least partly because sugar can raise adrenaline levels.4 However, glucose raises blood pressure more than fructose in some people.5 This makes sense because hypertension is known to be an insulin-resistant condition, and it is high levels of glucose that overtax insulin.6

So, is fructose bad for you?

It turns out that excess GLUCOSE, the source of most of the sugar in our diet, is just as risky, and often riskier than fructose when it comes to these health conditions, primarily because of how glucose affects insulin and blood sugar. However, fructose at very high doses, or in people with cancer, poses health risks as well, so both of these sugars are worth minimizing.

Each and every single one of these health problems—type 2 diabetes, cancer, obesity, gout, fatty liver disease, and heart disease—is an insulin-resistant condition. Insulin resistance, which leads to high blood glucose and high insulin levels, is the scourge of our time.

Any lifestyle change you can make to improve insulin resistance, lower insulin levels and lower blood sugar, is well worth making, and will go a long way toward protecting and perhaps even completely restoring your good health. I can think of no better target, no better use of your time and energy.

In article five of this series: “How to Diagnose, Prevent, and Treat Insulin Resistance” we finally crawl out of the test tube and back into reality. I’ll show you which of your favorite foods and beverages contain the most glucose and fructose and share with you strategies you can use to improve your insulin sensitivity (including some recommendations that may surprise you). But first, we’ll take a quick detour and look at the one health problem that is absolutely caused by fructose and not glucose: fructose malabsorption. Until then, how about you?

What do you think about the connection between fructose and these common diseases? Are you any more or less afraid of fructose than you were before? Have you tried a low-fructose, low-sugar, or low-carbohydrate diet for diabetes, gout, weight loss, fatty liver, high blood pressure, or even cancer? What has your experience been?

Fructose: the new F word

We used to be told that fructose (aka “fruit sugar”) was the ideal sweetener for people with diabetes because it doesn’t cause blood sugar spikes. However, in recent years its reputation has tanked, as some experts have decided that fructose is the silently sinister sister of the sugar family, single-handedly responsible for obesity, diabetes, heart disease, fatty liver disease, gout, cancer, and worldwide destruction. In this popular lecture about the perils of fructose fructose has even been dubbed a poison largely responsible for the epidemic of childhood obesity.

Just a few weeks ago, yet another fructose study1 made headlines, including this New York Times article and a nicely balanced report in Science News claiming that fructose may make it harder to control appetite and food cravings than glucose, paving the way to overeating and obesity. [See article two in this series for a full breakdown of this study.]

Many of us had finally come to understand that excess refined carbohydrate intake, not saturated fat, is endangering our health, and some of us started cutting back on sugar and flour to protect ourselves. These changes aren’t easy—baked goods, pasta, ice cream and candy are cheap, convenient, and delicious! I personally would love to be told that I can safely eat all sugars except for fructose, and I bet I’m not alone. So what’s going on here?

It turns out that fructose is a fascinating and complicated topic, so what started out as a single blog post became a five-part series (my condolences in advance). Those of you already familiar with my pro-meat, pro-saturated fat, pro-cholesterol, anti-carbohydrate, plant-foods-are-not-to-be-trusted nutritional philosophy might guess fructose would be an easy target for me, but to my own surprise, the more I dug into the science, the more I found myself defending the the fruity little guy. Fructose is no health food, but it’s no poison either. Well, no more poisonous than any other sugar has the potential to be, anyway. Come with me to discover what fructose is, how it compares to other sugars, and how much you can safely consume. No time for details?

I’ve broken up the fructose fun into five articles to aid digestion:

1. Fructose metabolism vs glucose metabolism. Today’s article reveals fun facts about fructose and how it behaves in your body compared to other sugars. If you had as much trouble following Dr. Lustig’s chemistry lesson as I did, read on to understand what the real differences are between fructose and glucose processing.
2. Does fructose make you hungrier? In article two, “Fructose Raises Appetite . . . for Better Science,” we look under the hood of the new study that claims fructose can cause overeating to see if we should be concerned.
3. Fructose and your health. In article three, “Why Sugar Is Bad for You: A Summary of the Research,” I review and summarize for you the latest research about fructose and diabetes, obesity, fatty liver, gout, heart disease and cancer.
4. Fructose malabsorption. In article four, “Is Fructose Malabsorption Causing Your IBS?” we look at how to find out if fructose is the culprit of your IBS symptoms, and if so, how you can minimize fructose in your diet.
5. Fructose in the real world. In the fifth article, “How to Diagnose, Prevent, and Treat Insulin Resistance,” we finally look at real foods! We examine your favorite sweeteners, fruits, vegetables, grains and legumes to see how they measure up. I’ll share with you my dietary recommendations, provide a downloadable PDF with medical tests for insulin resistance that you can discuss with your health care provider, and include an infographic with helpful tips to guide you in your dietary decisions.

And away we go!

First, a bit of context. Where does fructose stand in relation to its natural simple sugar sisters?

Simple sugars: short and sweet

Glucose: aka blood sugar. A 6-carbon monosaccharide (single sugar ring) used by all plants and animals as their primary energy source, and therefore critically important to life. Glucose is not very sweet—less than half as sweet as fructose—which is why glucose isn’t used as a sweetener. All plants contain some pure glucose, and some plants also contain glucose linked together in long chains in the form of starch (amylose), which is not sweet at all. Dextrose is simply the name given to the glucose extracted from plant starch.

Fructose: aka fruit sugar. A 6-carbon monosaccharide (single sugar ring) used by plants to sweeten their fruits and make them more appealing to animals. Fructose is the sweetest of all the natural sugars and is found in its free form primarily in sweet fruits and vegetables. In humans, fructose is used by only a few cell types in the body for energy (notably sperm cells), but the body can make fructose from glucose where necessary.

Sucrose: aka table sugar, white sugar, cane sugar, beet sugar, or just plain old sugar. Sucrose is a disaccharide (double sugar ring) used by plants to transport and store energy. Each sucrose molecule consists of one glucose molecule bonded to one fructose molecule. We break this bond easily during digestion to free up glucose and fructose for absorption:

There are a few other simple natural sugars I’m not describing here for the sake of brevity: lactose and galactose (from milk), maltose (see article four), and trehalose (from mushrooms). All of them turn into glucose in our bodies. Even unnatural sugars such as high fructose corn syrup, brown rice syrup and agave syrup all turn into glucose and/or fructose in our bodies. [There’ll be more details about these sweeteners in article four.]

Since all of the sugars we eat ultimately break down into glucose, fructose, or some combination of the two, from here on we will focus on the differences between fructose and glucose.

The arguments in the fructose vs glucose war center around differences in how fructose and glucose are handled by the liver, so we unfortunately have to review some biochemistry. I’ll make this as painless as possible. Pretty pictures are included. Sit back, have yourself a nice baked potato, and we’ll get started.

Glucose metabolism

You can think of your baked potato as a lovely lump of glucose. Baked potatoes are full of a starch called amylose, which is just long chains of glucose molecules. Your intestinal enzymes rapidly digest potato starch into pure glucose and your intestinal cells absorb it completely, causing your blood glucose (blood sugar) to spike. Fast on its heels, insulin rushes into your bloodstream to direct glucose traffic and bring your blood sugar back down.

Your liver is the first organ to see the blood glucose wave, and soaks up about 1/3 of the glucose for processing.1 The remaining 2/3 of the glucose circulates throughout your body to feed your cells. The absorption of glucose by liver cells does NOT require insulin,2 but insulin is required to keep the glucose inside liver cells.

Insulin is not simply a blood sugar regulator; it is a powerful growth hormone.

Once glucose is locked inside a liver cell, the cell can do a variety of things with it, depending on the circumstances. Remember that you have an insulin spike travelling with your glucose. Insulin is not simply a blood sugar regulator; it is a powerful growth hormone. Insulin sets the stage in the body for growth, and one of the ways it does this is by telling your liver: “build, grow and store!” If insulin is present, it will crank up the activity of a series of enzymes in the liver cell needed to process all the glucose rushing in.

The first liver cell enzyme turned on by insulin is glucokinase, which immediately slaps a phosphate onto glucose, trapping glucose inside the cell so it can’t leak back into the bloodstream.3 The phosphate comes from a molecule called ATP (adenosine TRI-phosphate), our body’s chief energy storage molecule. After ATP sacrifices one of its phosphates to glucose, it is then called ADP (adenosine DI-phosphate). When your insulin level is low, as it should be between meals, glucokinase will turn off so that the liver can release glucose back into the bloodstream to keep your blood sugar from dropping.

Which pathway glucose takes once it’s captured by a liver cell depends on MANY things, including levels of insulin, ATP, and a variety of other molecules that help the liver cell know what its needs are at any given moment. These molecules control glucose processing by turning enzymes on and off. The master regulator enzyme on the glucose conveyor belt is called PFK-1. One of the things that turns PFK-1 on is insulin, and one of the things that turns it off is ATP. When PFK-1 is turned on, glucose will be sent to the chopping block to be cut in half for further processing.

Under the influence of insulin, your liver can do any of following things with the new glucose load, depending on your body’s needs at the time:4

Burn it or ferment it for energy (ATP). If liver cells need energy to conduct their cellular business, glucose will be chopped in half in preparation for burning in the mitochondria (your cellular furnace). Mitochondria require oxygen to turn glucose fragments into ATP; this process is called aerobic glycolysis. If there’s not enough oxygen around to burn it, glucose will be fermented instead, producing lactic acid (anaerobic glycolysis). The liver can release lactic acid into the bloodstream to be burned by working muscle or other oxygen-starved cells for energy.

Transform it into 5-carbon building blocks (ribulose-5-phosphate) plus powerful helper molecules (NADPH) required to build components of new or growing cells, such as proteins, RNA, and DNA. This “build and grow” route is called the “pentose phosphate pathway.”

Store it as glycogen or fat. In a process called glycogenesis, the liver strings glucose molecules into long chains of animal starch called glycogen, which is stored in the liver. If the liver’s glycogen tank is already full, glucose can be turned into fat instead (lipogenesis). The healthy liver doesn’t store much fat; it prefers to ship it out to other cells by releasing it into the bloodstream as triglycerides.

So, as you can see, glucose is a versatile molecule whose destiny depends on sophisticated signals between food, hormones, the liver, and the rest of the body. How is fructose different? Have a nice big swig of agave syrup (mostly fructose, as you’ll see in article four) and we’ll get started.

Differences between glucose and fructose metabolism

Difference #1: The intestine does not absorb fructose as well as it absorbs glucose. There’ll be more details about fructose absorption issues in articles two and three, but for now suffice it to say that pure fructose is difficult for most of us to absorb completely.

Difference #2: The liver absorbs a LOT more fructose than glucose. Since you don’t need fructose to feed your cells, there’s no need to keep any of it in circulation, so your liver removes as much of it as it possibly can, like a big sponge.1

Difference #3: Glucose triggers insulin release, but fructose doesn’t.2 Insulin plays a major role in turning key enzymes on or off, so without an insulin spike, the enzyme environment within the liver cell may be very different, and therefore the processing pathways available to fructose bits may be very different. (The important truth is that all foods that contain fructose also contain glucose, and some fructose gets converted into glucose, so when you consume fructose there usually WILL be some insulin around, but just for now, let’s stick with pure fructose for now to highlight the metabolic differences).

Difference #4: The first two steps in fructose processing are completely separate from glucose processing, unregulated, and irreversible. Once inside the liver cell, ATP tags fructose with a phosphate no matter what, trapping it inside the cell. The enzyme responsible for this step is fructokinase, which is turned on by fructose, and doesn’t listen to insulin. Next, an enzyme called aldolase B unceremoniously chops fructose in half. These first two steps completely bypass PFK-1, the master enzyme that controls glucose processing, so regardless of what your body needs or wants at the moment, fructose will be broken down, because, unlike glucose, fructose molecules can’t be stored, and can’t be released back into the bloodstream. The liver cell has no choice but to break down every molecule of fructose it receives.

Similarities between glucose and fructose metabolism

Glucose and fructose travel separate roads for just the first few steps of processing. However, as soon as fructose gets chopped in half, it turns into the very same 3-carbon molecule that glucose forms when glucose is chopped in half (glyceraldehyde-3-phosphate, or G3P for short). All G3P molecules, whether they come from fructose or glucose, get funneled into a single common pathway. From that point on, you can’t tell the difference between them; fructose bits can turn into ATP, lactic acid, building blocks, glycogen, or fat, just like glucose bits can, because the bits are identical. Fructose pieces can even turn into glucose! Which pathway fructose and glucose take is determined by your body’s needs at that moment and by the amount of fructose and glucose you eat.3

This illustration highlights the key differences between glucose and fructose metabolism in the liver. Fructose follows its own unidirectional, unregulated pathway until it is cleaved into Glyceraldehyde-3-Phosphate (G3P), which is identical to G3P from glucose. At that point, the G3P from fructose enters the glucose metabolic pathway and can become lactic acid, ATP, or fat, or can cycle back through the glucose pathway to enter the Pentose Phosphate Pathway, become glycogen, or re-enter the bloodstream as glucose.

Fructophobic claims

The gist of the fructophobes’ argument is that fructose is dangerous because it bypasses the usual checks and balances that control glucose (namely insulin and PFK-1), heads straight to the liver, and turns instantly into fat, slashing and burning precious ATP (energy molecules) along the way, leaving piles of toxic waste (uric acid) in its wake.1

Uric acid? What’s that? Under normal circumstances, whenever ATP donates a phosphate to fructose or glucose, the ADP leftover is recycled back into ATP. However, the liver absorbs only a portion of the glucose you consume, whereas it absorbs almost all of the fructose you consume. If too many fructose molecules flood the liver, they could theoretically use up too much ATP too fast, and ADP leftovers could overwhelm the recycling machinery. If ADP can’t be recycled, cells can turn it into a waste product called uric acid and send it out via the bloodstream to the kidneys for removal from the body. High levels of uric acid in the blood can trigger gout in some people. For more information about gout see article three of this series, and also my post “Got Gout but Love Meat?“

Scary claim #1: Fructose is fast fat

Those in the fructose-phobia camp would say that the liver turns all the fructose we eat instantly into fat, and that the fat either pours into the bloodstream (raising bad cholesterol and triglyceride levels and increasing risk for heart disease) or getting trapped in the liver, causing fatty liver disease.

As you now know, fructose can turn into anything that glucose can. There’s no evidence in humans that a realistic amount of fructose under ordinary circumstances causes an increase in fat production by the liver compared to glucose.1

In fact, a review of studies that used radioactive tracers to stalk fructose as it traveled through people’s bodies found that less than 1% of the fructose consumed by the research subjects ended up as fat!3 A decent amount of the fructose, as much as 54%, actually turned into glucose! Why did so little of the fructose turn into fat? Fructose doesn’t trigger insulin spikes, and you need insulin to turn on fat-building pathways. Insulin is a growth hormone that tells the liver to grow and store; when insulin levels are low, fat-building pathways are turned off.

Scary claim #2: Fructose drains cells of ATP, our precious energy molecules

There is no evidence that ATP depletion occurs in humans except when fructose is injected directly into someone’s veins (don’t try this at home . . .).4

Scary claim #3: Fructose raises uric acid levels, which can cause gout.

While there are human studies showing that fructose can raise uric acid levels more than glucose can, all of these studies used extremely high doses of fructose (approximately 215 grams)—this is roughly the amount of fructose in 2-1/2 liters of Mountain Dew or grape juice (don’t try this at home either). In addition, people in these studies were given these mega-doses of fructose on top of their usual diet, increasing their daily calorie intake by about 1/3. Therefore it is impossible to say whether it was the extreme fructose exposure or simply the excess calories that caused uric acid levels to rise in these cases. Human studies of fructose under normal calorie conditions found no increase in uric acid production.5

Summary of key points

• All of the sugars and starches in our diet, whether natural or artificial, ultimately break down into glucose, fructose, or a combination of the two.
• Glucose from sweets and starches spike in the bloodstream, triggering an insulin spike. Fructose spikes in the liver, and does not directly trigger an insulin response.
• Insulin is a powerful hormone that puts your liver in growth and storage mode.
• The first phase of glucose processing is very tightly controlled because glucose must obey both insulin and the regulatory enzyme PFK-1, whereas fructose bypasses these important checks and balances.
• The remaining phases of glucose and fructose processing merge and become identical. Therefore both glucose and fructose can turn into ATP (energy), lactic acid (energy), glycogen (storage), ribulose-5-phosphate (building blocks for new/growing cells), or fat, depending on the body’s needs.
• Very little of the fructose we eat turns into fat in the absence of glucose/insulin.
• There is no evidence that fructose drains cells of ATP unless you inject it into your veins.
• Fructose only raises uric acid levels in the blood at high doses under high calorie conditions.

Conclusions

Yes, fructose is handled differently by the body than glucose in a variety of ways. It is absorbed less well by the intestines, absorbed in far greater amounts by the liver, and the first two steps of its processing in the liver are unregulated, meaning that fructose gets broken down by the liver no matter what. However, there is no reason to believe that these metabolic differences make ordinary amounts of fructose any worse than ordinary amounts of glucose when it comes to ATP reserves, fat production, or uric acid levels. Fructose byproducts are identical to glucose byproducts and can turn into all of the same things that glucose can. Fructose is primarily just another source of glucose in the diet.

How do I know fructose is not a poison? The body has a variety of sugar receptor molecules that help simple sugars enter cells. One of them, called GLUT-5, is specific for fructose alone.6 We also turn a good deal of the fructose we eat into glucose, a molecule critical to life. We do not require fructose (or any sugar) to live or be healthy, but fructose can certainly be used as a source of nourishment, and in my book, that means it’s not a poison. If fructose were an actual poison, Mother Nature would not have installed receptors in our intestines designed specifically to welcome fructose into our bodies. Yes, too much fructose, like too much of anything, can be potentially harmful, but that doesn’t make it poisonous. If you drink too much water, your sodium levels will drop, you will have a seizure, and you could die. But water is clearly not a poison. In the case of fructose, as in the case of water, the dose makes the poison. How much fructose can you safely eat? it all depends on who you are…find out more in article four!

Bottom line

I don’t believe that the fact that fructose is handled differently than glucose by the body makes fructose any worse than glucose when it comes to the health of our cells. As you’ll see in the rest of the series (if you’re still alive after having slogged through this basic science article), fructose is not the nutritional super-villain it’s been made out to be. What is the dietary scourge of our time? Sugar. Excessive sugar of any type, including fructose, but perhaps glucose worst of all. If you don’t believe me, stay tuned for more!

There you have it. Did that make sense? Are you any more or less afraid of fructose than you were before? Please share your thoughts and questions below so we can continue to learn from one another.

In article two, “Fructose Raises Appetite . . . for Better Science,” we answer the following questions:

Is the new study about fructose and appetite worth your attention? How good are scientific studies of fructose in general? Can we count on them to give us useful information about what we should eat to be healthy?

Fructose: the new F word

We used to be told that fructose (aka “fruit sugar”) was the ideal sweetener for people with diabetes because it doesn’t cause blood sugar spikes. However, in recent years its reputation has tanked, as some experts have decided that fructose is the silently sinister sister of the sugar family, single-handedly responsible for obesity, diabetes, heart disease, fatty liver disease, gout, cancer, and worldwide destruction. In this popular lecture about the perils of fructose fructose has even been dubbed a poison largely responsible for the epidemic of childhood obesity.

Just a few weeks ago, yet another fructose study1 made headlines, including this New York Times article and a nicely balanced report in Science News claiming that fructose may make it harder to control appetite and food cravings than glucose, paving the way to overeating and obesity. [See article two in this series for a full breakdown of this study.]

Many of us had finally come to understand that excess refined carbohydrate intake, not saturated fat, is endangering our health, and some of us started cutting back on sugar and flour to protect ourselves. These changes aren’t easy—baked goods, pasta, ice cream and candy are cheap, convenient, and delicious! I personally would love to be told that I can safely eat all sugars except for fructose, and I bet I’m not alone. So what’s going on here?

It turns out that fructose is a fascinating and complicated topic, so what started out as a single blog post became a five-part series (my condolences in advance). Those of you already familiar with my pro-meat, pro-saturated fat, pro-cholesterol, anti-carbohydrate, plant-foods-are-not-to-be-trusted nutritional philosophy might guess fructose would be an easy target for me, but to my own surprise, the more I dug into the science, the more I found myself defending the the fruity little guy. Fructose is no health food, but it’s no poison either. Well, no more poisonous than any other sugar has the potential to be, anyway. Come with me to discover what fructose is, how it compares to other sugars, and how much you can safely consume. No time for details?

I’ve broken up the fructose fun into five articles to aid digestion:

1. Fructose metabolism vs glucose metabolism. Today’s article reveals fun facts about fructose and how it behaves in your body compared to other sugars. If you had as much trouble following Dr. Lustig’s chemistry lesson as I did, read on to understand what the real differences are between fructose and glucose processing.
2. Does fructose make you hungrier? In article two, “Fructose Raises Appetite . . . for Better Science,” we look under the hood of the new study that claims fructose can cause overeating to see if we should be concerned.
3. Fructose and your health. In article three, “Why Sugar Is Bad for You: A Summary of the Research,” I review and summarize for you the latest research about fructose and diabetes, obesity, fatty liver, gout, heart disease and cancer.
4. Fructose malabsorption. In article four, “Is Fructose Malabsorption Causing Your IBS?” we look at how to find out if fructose is the culprit of your IBS symptoms, and if so, how you can minimize fructose in your diet.
5. Fructose in the real world. In the fifth article, “How to Diagnose, Prevent, and Treat Insulin Resistance,” we finally look at real foods! We examine your favorite sweeteners, fruits, vegetables, grains and legumes to see how they measure up. I’ll share with you my dietary recommendations, provide a downloadable PDF with medical tests for insulin resistance that you can discuss with your health care provider, and include an infographic with helpful tips to guide you in your dietary decisions.

And away we go!

First, a bit of context. Where does fructose stand in relation to its natural simple sugar sisters?

Simple sugars: short and sweet

Glucose: aka blood sugar. A 6-carbon monosaccharide (single sugar ring) used by all plants and animals as their primary energy source, and therefore critically important to life. Glucose is not very sweet—less than half as sweet as fructose—which is why glucose isn’t used as a sweetener. All plants contain some pure glucose, and some plants also contain glucose linked together in long chains in the form of starch (amylose), which is not sweet at all. Dextrose is simply the name given to the glucose extracted from plant starch.

Fructose: aka fruit sugar. A 6-carbon monosaccharide (single sugar ring) used by plants to sweeten their fruits and make them more appealing to animals. Fructose is the sweetest of all the natural sugars and is found in its free form primarily in sweet fruits and vegetables. In humans, fructose is used by only a few cell types in the body for energy (notably sperm cells), but the body can make fructose from glucose where necessary.

Sucrose: aka table sugar, white sugar, cane sugar, beet sugar, or just plain old sugar. Sucrose is a disaccharide (double sugar ring) used by plants to transport and store energy. Each sucrose molecule consists of one glucose molecule bonded to one fructose molecule. We break this bond easily during digestion to free up glucose and fructose for absorption:

There are a few other simple natural sugars I’m not describing here for the sake of brevity: lactose and galactose (from milk), maltose (see article four), and trehalose (from mushrooms). All of them turn into glucose in our bodies. Even unnatural sugars such as high fructose corn syrup, brown rice syrup and agave syrup all turn into glucose and/or fructose in our bodies. [There’ll be more details about these sweeteners in article four.]

Since all of the sugars we eat ultimately break down into glucose, fructose, or some combination of the two, from here on we will focus on the differences between fructose and glucose.

The arguments in the fructose vs glucose war center around differences in how fructose and glucose are handled by the liver, so we unfortunately have to review some biochemistry. I’ll make this as painless as possible. Pretty pictures are included. Sit back, have yourself a nice baked potato, and we’ll get started.

Glucose metabolism

You can think of your baked potato as a lovely lump of glucose. Baked potatoes are full of a starch called amylose, which is just long chains of glucose molecules. Your intestinal enzymes rapidly digest potato starch into pure glucose and your intestinal cells absorb it completely, causing your blood glucose (blood sugar) to spike. Fast on its heels, insulin rushes into your bloodstream to direct glucose traffic and bring your blood sugar back down.

Your liver is the first organ to see the blood glucose wave, and soaks up about 1/3 of the glucose for processing.1 The remaining 2/3 of the glucose circulates throughout your body to feed your cells. The absorption of glucose by liver cells does NOT require insulin,2 but insulin is required to keep the glucose inside liver cells.

Insulin is not simply a blood sugar regulator; it is a powerful growth hormone.

Once glucose is locked inside a liver cell, the cell can do a variety of things with it, depending on the circumstances. Remember that you have an insulin spike travelling with your glucose. Insulin is not simply a blood sugar regulator; it is a powerful growth hormone. Insulin sets the stage in the body for growth, and one of the ways it does this is by telling your liver: “build, grow and store!” If insulin is present, it will crank up the activity of a series of enzymes in the liver cell needed to process all the glucose rushing in.

The first liver cell enzyme turned on by insulin is glucokinase, which immediately slaps a phosphate onto glucose, trapping glucose inside the cell so it can’t leak back into the bloodstream.3 The phosphate comes from a molecule called ATP (adenosine TRI-phosphate), our body’s chief energy storage molecule. After ATP sacrifices one of its phosphates to glucose, it is then called ADP (adenosine DI-phosphate). When your insulin level is low, as it should be between meals, glucokinase will turn off so that the liver can release glucose back into the bloodstream to keep your blood sugar from dropping.

Which pathway glucose takes once it’s captured by a liver cell depends on MANY things, including levels of insulin, ATP, and a variety of other molecules that help the liver cell know what its needs are at any given moment. These molecules control glucose processing by turning enzymes on and off. The master regulator enzyme on the glucose conveyor belt is called PFK-1. One of the things that turns PFK-1 on is insulin, and one of the things that turns it off is ATP. When PFK-1 is turned on, glucose will be sent to the chopping block to be cut in half for further processing.

Under the influence of insulin, your liver can do any of following things with the new glucose load, depending on your body’s needs at the time:4

Burn it or ferment it for energy (ATP). If liver cells need energy to conduct their cellular business, glucose will be chopped in half in preparation for burning in the mitochondria (your cellular furnace). Mitochondria require oxygen to turn glucose fragments into ATP; this process is called aerobic glycolysis. If there’s not enough oxygen around to burn it, glucose will be fermented instead, producing lactic acid (anaerobic glycolysis). The liver can release lactic acid into the bloodstream to be burned by working muscle or other oxygen-starved cells for energy.

Transform it into 5-carbon building blocks (ribulose-5-phosphate) plus powerful helper molecules (NADPH) required to build components of new or growing cells, such as proteins, RNA, and DNA. This “build and grow” route is called the “pentose phosphate pathway.”

Store it as glycogen or fat. In a process called glycogenesis, the liver strings glucose molecules into long chains of animal starch called glycogen, which is stored in the liver. If the liver’s glycogen tank is already full, glucose can be turned into fat instead (lipogenesis). The healthy liver doesn’t store much fat; it prefers to ship it out to other cells by releasing it into the bloodstream as triglycerides.

So, as you can see, glucose is a versatile molecule whose destiny depends on sophisticated signals between food, hormones, the liver, and the rest of the body. How is fructose different? Have a nice big swig of agave syrup (mostly fructose, as you’ll see in article four) and we’ll get started.

Differences between glucose and fructose metabolism

Difference #1: The intestine does not absorb fructose as well as it absorbs glucose. There’ll be more details about fructose absorption issues in articles two and three, but for now suffice it to say that pure fructose is difficult for most of us to absorb completely.

Difference #2: The liver absorbs a LOT more fructose than glucose. Since you don’t need fructose to feed your cells, there’s no need to keep any of it in circulation, so your liver removes as much of it as it possibly can, like a big sponge.1

Difference #3: Glucose triggers insulin release, but fructose doesn’t.2 Insulin plays a major role in turning key enzymes on or off, so without an insulin spike, the enzyme environment within the liver cell may be very different, and therefore the processing pathways available to fructose bits may be very different. (The important truth is that all foods that contain fructose also contain glucose, and some fructose gets converted into glucose, so when you consume fructose there usually WILL be some insulin around, but just for now, let’s stick with pure fructose for now to highlight the metabolic differences).

Difference #4: The first two steps in fructose processing are completely separate from glucose processing, unregulated, and irreversible. Once inside the liver cell, ATP tags fructose with a phosphate no matter what, trapping it inside the cell. The enzyme responsible for this step is fructokinase, which is turned on by fructose, and doesn’t listen to insulin. Next, an enzyme called aldolase B unceremoniously chops fructose in half. These first two steps completely bypass PFK-1, the master enzyme that controls glucose processing, so regardless of what your body needs or wants at the moment, fructose will be broken down, because, unlike glucose, fructose molecules can’t be stored, and can’t be released back into the bloodstream. The liver cell has no choice but to break down every molecule of fructose it receives.

Similarities between glucose and fructose metabolism

Glucose and fructose travel separate roads for just the first few steps of processing. However, as soon as fructose gets chopped in half, it turns into the very same 3-carbon molecule that glucose forms when glucose is chopped in half (glyceraldehyde-3-phosphate, or G3P for short). All G3P molecules, whether they come from fructose or glucose, get funneled into a single common pathway. From that point on, you can’t tell the difference between them; fructose bits can turn into ATP, lactic acid, building blocks, glycogen, or fat, just like glucose bits can, because the bits are identical. Fructose pieces can even turn into glucose! Which pathway fructose and glucose take is determined by your body’s needs at that moment and by the amount of fructose and glucose you eat.3

This illustration highlights the key differences between glucose and fructose metabolism in the liver. Fructose follows its own unidirectional, unregulated pathway until it is cleaved into Glyceraldehyde-3-Phosphate (G3P), which is identical to G3P from glucose. At that point, the G3P from fructose enters the glucose metabolic pathway and can become lactic acid, ATP, or fat, or can cycle back through the glucose pathway to enter the Pentose Phosphate Pathway, become glycogen, or re-enter the bloodstream as glucose.

Fructophobic claims

The gist of the fructophobes’ argument is that fructose is dangerous because it bypasses the usual checks and balances that control glucose (namely insulin and PFK-1), heads straight to the liver, and turns instantly into fat, slashing and burning precious ATP (energy molecules) along the way, leaving piles of toxic waste (uric acid) in its wake.1

Uric acid? What’s that? Under normal circumstances, whenever ATP donates a phosphate to fructose or glucose, the ADP leftover is recycled back into ATP. However, the liver absorbs only a portion of the glucose you consume, whereas it absorbs almost all of the fructose you consume. If too many fructose molecules flood the liver, they could theoretically use up too much ATP too fast, and ADP leftovers could overwhelm the recycling machinery. If ADP can’t be recycled, cells can turn it into a waste product called uric acid and send it out via the bloodstream to the kidneys for removal from the body. High levels of uric acid in the blood can trigger gout in some people. For more information about gout see article three of this series, and also my post “Got Gout but Love Meat?“

Scary claim #1: Fructose is fast fat

Those in the fructose-phobia camp would say that the liver turns all the fructose we eat instantly into fat, and that the fat either pours into the bloodstream (raising bad cholesterol and triglyceride levels and increasing risk for heart disease) or getting trapped in the liver, causing fatty liver disease.

As you now know, fructose can turn into anything that glucose can. There’s no evidence in humans that a realistic amount of fructose under ordinary circumstances causes an increase in fat production by the liver compared to glucose.1

In fact, a review of studies that used radioactive tracers to stalk fructose as it traveled through people’s bodies found that less than 1% of the fructose consumed by the research subjects ended up as fat!3 A decent amount of the fructose, as much as 54%, actually turned into glucose! Why did so little of the fructose turn into fat? Fructose doesn’t trigger insulin spikes, and you need insulin to turn on fat-building pathways. Insulin is a growth hormone that tells the liver to grow and store; when insulin levels are low, fat-building pathways are turned off.

Scary claim #2: Fructose drains cells of ATP, our precious energy molecules

There is no evidence that ATP depletion occurs in humans except when fructose is injected directly into someone’s veins (don’t try this at home . . .).4

Scary claim #3: Fructose raises uric acid levels, which can cause gout.

While there are human studies showing that fructose can raise uric acid levels more than glucose can, all of these studies used extremely high doses of fructose (approximately 215 grams)—this is roughly the amount of fructose in 2-1/2 liters of Mountain Dew or grape juice (don’t try this at home either). In addition, people in these studies were given these mega-doses of fructose on top of their usual diet, increasing their daily calorie intake by about 1/3. Therefore it is impossible to say whether it was the extreme fructose exposure or simply the excess calories that caused uric acid levels to rise in these cases. Human studies of fructose under normal calorie conditions found no increase in uric acid production.5

Summary of key points

• All of the sugars and starches in our diet, whether natural or artificial, ultimately break down into glucose, fructose, or a combination of the two.
• Glucose from sweets and starches spike in the bloodstream, triggering an insulin spike. Fructose spikes in the liver, and does not directly trigger an insulin response.
• Insulin is a powerful hormone that puts your liver in growth and storage mode.
• The first phase of glucose processing is very tightly controlled because glucose must obey both insulin and the regulatory enzyme PFK-1, whereas fructose bypasses these important checks and balances.
• The remaining phases of glucose and fructose processing merge and become identical. Therefore both glucose and fructose can turn into ATP (energy), lactic acid (energy), glycogen (storage), ribulose-5-phosphate (building blocks for new/growing cells), or fat, depending on the body’s needs.
• Very little of the fructose we eat turns into fat in the absence of glucose/insulin.
• There is no evidence that fructose drains cells of ATP unless you inject it into your veins.
• Fructose only raises uric acid levels in the blood at high doses under high calorie conditions.

Conclusions

Yes, fructose is handled differently by the body than glucose in a variety of ways. It is absorbed less well by the intestines, absorbed in far greater amounts by the liver, and the first two steps of its processing in the liver are unregulated, meaning that fructose gets broken down by the liver no matter what. However, there is no reason to believe that these metabolic differences make ordinary amounts of fructose any worse than ordinary amounts of glucose when it comes to ATP reserves, fat production, or uric acid levels. Fructose byproducts are identical to glucose byproducts and can turn into all of the same things that glucose can. Fructose is primarily just another source of glucose in the diet.

How do I know fructose is not a poison? The body has a variety of sugar receptor molecules that help simple sugars enter cells. One of them, called GLUT-5, is specific for fructose alone.6 We also turn a good deal of the fructose we eat into glucose, a molecule critical to life. We do not require fructose (or any sugar) to live or be healthy, but fructose can certainly be used as a source of nourishment, and in my book, that means it’s not a poison. If fructose were an actual poison, Mother Nature would not have installed receptors in our intestines designed specifically to welcome fructose into our bodies. Yes, too much fructose, like too much of anything, can be potentially harmful, but that doesn’t make it poisonous. If you drink too much water, your sodium levels will drop, you will have a seizure, and you could die. But water is clearly not a poison. In the case of fructose, as in the case of water, the dose makes the poison. How much fructose can you safely eat? it all depends on who you are…find out more in article four!

Bottom line

I don’t believe that the fact that fructose is handled differently than glucose by the body makes fructose any worse than glucose when it comes to the health of our cells. As you’ll see in the rest of the series (if you’re still alive after having slogged through this basic science article), fructose is not the nutritional super-villain it’s been made out to be. What is the dietary scourge of our time? Sugar. Excessive sugar of any type, including fructose, but perhaps glucose worst of all. If you don’t believe me, stay tuned for more!

There you have it. Did that make sense? Are you any more or less afraid of fructose than you were before? Please share your thoughts and questions below so we can continue to learn from one another.

In article two, “Fructose Raises Appetite . . . for Better Science,” we answer the following questions:

Is the new study about fructose and appetite worth your attention? How good are scientific studies of fructose in general? Can we count on them to give us useful information about what we should eat to be healthy?

Fructose: the new F word

We used to be told that fructose (aka “fruit sugar”) was the ideal sweetener for people with diabetes because it doesn’t cause blood sugar spikes. However, in recent years its reputation has tanked, as some experts have decided that fructose is the silently sinister sister of the sugar family, single-handedly responsible for obesity, diabetes, heart disease, fatty liver disease, gout, cancer, and worldwide destruction. In this popular lecture about the perils of fructose fructose has even been dubbed a poison largely responsible for the epidemic of childhood obesity.

Just a few weeks ago, yet another fructose study1 made headlines, including this New York Times article and a nicely balanced report in Science News claiming that fructose may make it harder to control appetite and food cravings than glucose, paving the way to overeating and obesity. [See article two in this series for a full breakdown of this study.]

Many of us had finally come to understand that excess refined carbohydrate intake, not saturated fat, is endangering our health, and some of us started cutting back on sugar and flour to protect ourselves. These changes aren’t easy—baked goods, pasta, ice cream and candy are cheap, convenient, and delicious! I personally would love to be told that I can safely eat all sugars except for fructose, and I bet I’m not alone. So what’s going on here?

It turns out that fructose is a fascinating and complicated topic, so what started out as a single blog post became a five-part series (my condolences in advance). Those of you already familiar with my pro-meat, pro-saturated fat, pro-cholesterol, anti-carbohydrate, plant-foods-are-not-to-be-trusted nutritional philosophy might guess fructose would be an easy target for me, but to my own surprise, the more I dug into the science, the more I found myself defending the the fruity little guy. Fructose is no health food, but it’s no poison either. Well, no more poisonous than any other sugar has the potential to be, anyway. Come with me to discover what fructose is, how it compares to other sugars, and how much you can safely consume. No time for details?

I’ve broken up the fructose fun into five articles to aid digestion:

1. Fructose metabolism vs glucose metabolism. Today’s article reveals fun facts about fructose and how it behaves in your body compared to other sugars. If you had as much trouble following Dr. Lustig’s chemistry lesson as I did, read on to understand what the real differences are between fructose and glucose processing.
2. Does fructose make you hungrier? In article two, “Fructose Raises Appetite . . . for Better Science,” we look under the hood of the new study that claims fructose can cause overeating to see if we should be concerned.
3. Fructose and your health. In article three, “Why Sugar Is Bad for You: A Summary of the Research,” I review and summarize for you the latest research about fructose and diabetes, obesity, fatty liver, gout, heart disease and cancer.
4. Fructose malabsorption. In article four, “Is Fructose Malabsorption Causing Your IBS?” we look at how to find out if fructose is the culprit of your IBS symptoms, and if so, how you can minimize fructose in your diet.
5. Fructose in the real world. In the fifth article, “How to Diagnose, Prevent, and Treat Insulin Resistance,” we finally look at real foods! We examine your favorite sweeteners, fruits, vegetables, grains and legumes to see how they measure up. I’ll share with you my dietary recommendations, provide a downloadable PDF with medical tests for insulin resistance that you can discuss with your health care provider, and include an infographic with helpful tips to guide you in your dietary decisions.

And away we go!

First, a bit of context. Where does fructose stand in relation to its natural simple sugar sisters?

Simple sugars: short and sweet

Glucose: aka blood sugar. A 6-carbon monosaccharide (single sugar ring) used by all plants and animals as their primary energy source, and therefore critically important to life. Glucose is not very sweet—less than half as sweet as fructose—which is why glucose isn’t used as a sweetener. All plants contain some pure glucose, and some plants also contain glucose linked together in long chains in the form of starch (amylose), which is not sweet at all. Dextrose is simply the name given to the glucose extracted from plant starch.

Fructose: aka fruit sugar. A 6-carbon monosaccharide (single sugar ring) used by plants to sweeten their fruits and make them more appealing to animals. Fructose is the sweetest of all the natural sugars and is found in its free form primarily in sweet fruits and vegetables. In humans, fructose is used by only a few cell types in the body for energy (notably sperm cells), but the body can make fructose from glucose where necessary.

Sucrose: aka table sugar, white sugar, cane sugar, beet sugar, or just plain old sugar. Sucrose is a disaccharide (double sugar ring) used by plants to transport and store energy. Each sucrose molecule consists of one glucose molecule bonded to one fructose molecule. We break this bond easily during digestion to free up glucose and fructose for absorption:

There are a few other simple natural sugars I’m not describing here for the sake of brevity: lactose and galactose (from milk), maltose (see article four), and trehalose (from mushrooms). All of them turn into glucose in our bodies. Even unnatural sugars such as high fructose corn syrup, brown rice syrup and agave syrup all turn into glucose and/or fructose in our bodies. [There’ll be more details about these sweeteners in article four.]

Since all of the sugars we eat ultimately break down into glucose, fructose, or some combination of the two, from here on we will focus on the differences between fructose and glucose.

The arguments in the fructose vs glucose war center around differences in how fructose and glucose are handled by the liver, so we unfortunately have to review some biochemistry. I’ll make this as painless as possible. Pretty pictures are included. Sit back, have yourself a nice baked potato, and we’ll get started.

Glucose metabolism

You can think of your baked potato as a lovely lump of glucose. Baked potatoes are full of a starch called amylose, which is just long chains of glucose molecules. Your intestinal enzymes rapidly digest potato starch into pure glucose and your intestinal cells absorb it completely, causing your blood glucose (blood sugar) to spike. Fast on its heels, insulin rushes into your bloodstream to direct glucose traffic and bring your blood sugar back down.

Your liver is the first organ to see the blood glucose wave, and soaks up about 1/3 of the glucose for processing.1 The remaining 2/3 of the glucose circulates throughout your body to feed your cells. The absorption of glucose by liver cells does NOT require insulin,2 but insulin is required to keep the glucose inside liver cells.

Insulin is not simply a blood sugar regulator; it is a powerful growth hormone.

Once glucose is locked inside a liver cell, the cell can do a variety of things with it, depending on the circumstances. Remember that you have an insulin spike travelling with your glucose. Insulin is not simply a blood sugar regulator; it is a powerful growth hormone. Insulin sets the stage in the body for growth, and one of the ways it does this is by telling your liver: “build, grow and store!” If insulin is present, it will crank up the activity of a series of enzymes in the liver cell needed to process all the glucose rushing in.

The first liver cell enzyme turned on by insulin is glucokinase, which immediately slaps a phosphate onto glucose, trapping glucose inside the cell so it can’t leak back into the bloodstream.3 The phosphate comes from a molecule called ATP (adenosine TRI-phosphate), our body’s chief energy storage molecule. After ATP sacrifices one of its phosphates to glucose, it is then called ADP (adenosine DI-phosphate). When your insulin level is low, as it should be between meals, glucokinase will turn off so that the liver can release glucose back into the bloodstream to keep your blood sugar from dropping.

Which pathway glucose takes once it’s captured by a liver cell depends on MANY things, including levels of insulin, ATP, and a variety of other molecules that help the liver cell know what its needs are at any given moment. These molecules control glucose processing by turning enzymes on and off. The master regulator enzyme on the glucose conveyor belt is called PFK-1. One of the things that turns PFK-1 on is insulin, and one of the things that turns it off is ATP. When PFK-1 is turned on, glucose will be sent to the chopping block to be cut in half for further processing.

Under the influence of insulin, your liver can do any of following things with the new glucose load, depending on your body’s needs at the time:4

Burn it or ferment it for energy (ATP). If liver cells need energy to conduct their cellular business, glucose will be chopped in half in preparation for burning in the mitochondria (your cellular furnace). Mitochondria require oxygen to turn glucose fragments into ATP; this process is called aerobic glycolysis. If there’s not enough oxygen around to burn it, glucose will be fermented instead, producing lactic acid (anaerobic glycolysis). The liver can release lactic acid into the bloodstream to be burned by working muscle or other oxygen-starved cells for energy.

Transform it into 5-carbon building blocks (ribulose-5-phosphate) plus powerful helper molecules (NADPH) required to build components of new or growing cells, such as proteins, RNA, and DNA. This “build and grow” route is called the “pentose phosphate pathway.”

Store it as glycogen or fat. In a process called glycogenesis, the liver strings glucose molecules into long chains of animal starch called glycogen, which is stored in the liver. If the liver’s glycogen tank is already full, glucose can be turned into fat instead (lipogenesis). The healthy liver doesn’t store much fat; it prefers to ship it out to other cells by releasing it into the bloodstream as triglycerides.

So, as you can see, glucose is a versatile molecule whose destiny depends on sophisticated signals between food, hormones, the liver, and the rest of the body. How is fructose different? Have a nice big swig of agave syrup (mostly fructose, as you’ll see in article four) and we’ll get started.

Differences between glucose and fructose metabolism

Difference #1: The intestine does not absorb fructose as well as it absorbs glucose. There’ll be more details about fructose absorption issues in articles two and three, but for now suffice it to say that pure fructose is difficult for most of us to absorb completely.

Difference #2: The liver absorbs a LOT more fructose than glucose. Since you don’t need fructose to feed your cells, there’s no need to keep any of it in circulation, so your liver removes as much of it as it possibly can, like a big sponge.1

Difference #3: Glucose triggers insulin release, but fructose doesn’t.2 Insulin plays a major role in turning key enzymes on or off, so without an insulin spike, the enzyme environment within the liver cell may be very different, and therefore the processing pathways available to fructose bits may be very different. (The important truth is that all foods that contain fructose also contain glucose, and some fructose gets converted into glucose, so when you consume fructose there usually WILL be some insulin around, but just for now, let’s stick with pure fructose for now to highlight the metabolic differences).

Difference #4: The first two steps in fructose processing are completely separate from glucose processing, unregulated, and irreversible. Once inside the liver cell, ATP tags fructose with a phosphate no matter what, trapping it inside the cell. The enzyme responsible for this step is fructokinase, which is turned on by fructose, and doesn’t listen to insulin. Next, an enzyme called aldolase B unceremoniously chops fructose in half. These first two steps completely bypass PFK-1, the master enzyme that controls glucose processing, so regardless of what your body needs or wants at the moment, fructose will be broken down, because, unlike glucose, fructose molecules can’t be stored, and can’t be released back into the bloodstream. The liver cell has no choice but to break down every molecule of fructose it receives.

Similarities between glucose and fructose metabolism

Glucose and fructose travel separate roads for just the first few steps of processing. However, as soon as fructose gets chopped in half, it turns into the very same 3-carbon molecule that glucose forms when glucose is chopped in half (glyceraldehyde-3-phosphate, or G3P for short). All G3P molecules, whether they come from fructose or glucose, get funneled into a single common pathway. From that point on, you can’t tell the difference between them; fructose bits can turn into ATP, lactic acid, building blocks, glycogen, or fat, just like glucose bits can, because the bits are identical. Fructose pieces can even turn into glucose! Which pathway fructose and glucose take is determined by your body’s needs at that moment and by the amount of fructose and glucose you eat.3

This illustration highlights the key differences between glucose and fructose metabolism in the liver. Fructose follows its own unidirectional, unregulated pathway until it is cleaved into Glyceraldehyde-3-Phosphate (G3P), which is identical to G3P from glucose. At that point, the G3P from fructose enters the glucose metabolic pathway and can become lactic acid, ATP, or fat, or can cycle back through the glucose pathway to enter the Pentose Phosphate Pathway, become glycogen, or re-enter the bloodstream as glucose.

Fructophobic claims

The gist of the fructophobes’ argument is that fructose is dangerous because it bypasses the usual checks and balances that control glucose (namely insulin and PFK-1), heads straight to the liver, and turns instantly into fat, slashing and burning precious ATP (energy molecules) along the way, leaving piles of toxic waste (uric acid) in its wake.1

Uric acid? What’s that? Under normal circumstances, whenever ATP donates a phosphate to fructose or glucose, the ADP leftover is recycled back into ATP. However, the liver absorbs only a portion of the glucose you consume, whereas it absorbs almost all of the fructose you consume. If too many fructose molecules flood the liver, they could theoretically use up too much ATP too fast, and ADP leftovers could overwhelm the recycling machinery. If ADP can’t be recycled, cells can turn it into a waste product called uric acid and send it out via the bloodstream to the kidneys for removal from the body. High levels of uric acid in the blood can trigger gout in some people. For more information about gout see article three of this series, and also my post “Got Gout but Love Meat?“

Scary claim #1: Fructose is fast fat

Those in the fructose-phobia camp would say that the liver turns all the fructose we eat instantly into fat, and that the fat either pours into the bloodstream (raising bad cholesterol and triglyceride levels and increasing risk for heart disease) or getting trapped in the liver, causing fatty liver disease.

As you now know, fructose can turn into anything that glucose can. There’s no evidence in humans that a realistic amount of fructose under ordinary circumstances causes an increase in fat production by the liver compared to glucose.1

In fact, a review of studies that used radioactive tracers to stalk fructose as it traveled through people’s bodies found that less than 1% of the fructose consumed by the research subjects ended up as fat!3 A decent amount of the fructose, as much as 54%, actually turned into glucose! Why did so little of the fructose turn into fat? Fructose doesn’t trigger insulin spikes, and you need insulin to turn on fat-building pathways. Insulin is a growth hormone that tells the liver to grow and store; when insulin levels are low, fat-building pathways are turned off.

Scary claim #2: Fructose drains cells of ATP, our precious energy molecules

There is no evidence that ATP depletion occurs in humans except when fructose is injected directly into someone’s veins (don’t try this at home . . .).4

Scary claim #3: Fructose raises uric acid levels, which can cause gout.

While there are human studies showing that fructose can raise uric acid levels more than glucose can, all of these studies used extremely high doses of fructose (approximately 215 grams)—this is roughly the amount of fructose in 2-1/2 liters of Mountain Dew or grape juice (don’t try this at home either). In addition, people in these studies were given these mega-doses of fructose on top of their usual diet, increasing their daily calorie intake by about 1/3. Therefore it is impossible to say whether it was the extreme fructose exposure or simply the excess calories that caused uric acid levels to rise in these cases. Human studies of fructose under normal calorie conditions found no increase in uric acid production.5

Summary of key points

• All of the sugars and starches in our diet, whether natural or artificial, ultimately break down into glucose, fructose, or a combination of the two.
• Glucose from sweets and starches spike in the bloodstream, triggering an insulin spike. Fructose spikes in the liver, and does not directly trigger an insulin response.
• Insulin is a powerful hormone that puts your liver in growth and storage mode.
• The first phase of glucose processing is very tightly controlled because glucose must obey both insulin and the regulatory enzyme PFK-1, whereas fructose bypasses these important checks and balances.
• The remaining phases of glucose and fructose processing merge and become identical. Therefore both glucose and fructose can turn into ATP (energy), lactic acid (energy), glycogen (storage), ribulose-5-phosphate (building blocks for new/growing cells), or fat, depending on the body’s needs.
• Very little of the fructose we eat turns into fat in the absence of glucose/insulin.
• There is no evidence that fructose drains cells of ATP unless you inject it into your veins.
• Fructose only raises uric acid levels in the blood at high doses under high calorie conditions.

Conclusions

Yes, fructose is handled differently by the body than glucose in a variety of ways. It is absorbed less well by the intestines, absorbed in far greater amounts by the liver, and the first two steps of its processing in the liver are unregulated, meaning that fructose gets broken down by the liver no matter what. However, there is no reason to believe that these metabolic differences make ordinary amounts of fructose any worse than ordinary amounts of glucose when it comes to ATP reserves, fat production, or uric acid levels. Fructose byproducts are identical to glucose byproducts and can turn into all of the same things that glucose can. Fructose is primarily just another source of glucose in the diet.

How do I know fructose is not a poison? The body has a variety of sugar receptor molecules that help simple sugars enter cells. One of them, called GLUT-5, is specific for fructose alone.6 We also turn a good deal of the fructose we eat into glucose, a molecule critical to life. We do not require fructose (or any sugar) to live or be healthy, but fructose can certainly be used as a source of nourishment, and in my book, that means it’s not a poison. If fructose were an actual poison, Mother Nature would not have installed receptors in our intestines designed specifically to welcome fructose into our bodies. Yes, too much fructose, like too much of anything, can be potentially harmful, but that doesn’t make it poisonous. If you drink too much water, your sodium levels will drop, you will have a seizure, and you could die. But water is clearly not a poison. In the case of fructose, as in the case of water, the dose makes the poison. How much fructose can you safely eat? it all depends on who you are…find out more in article four!

Bottom line

I don’t believe that the fact that fructose is handled differently than glucose by the body makes fructose any worse than glucose when it comes to the health of our cells. As you’ll see in the rest of the series (if you’re still alive after having slogged through this basic science article), fructose is not the nutritional super-villain it’s been made out to be. What is the dietary scourge of our time? Sugar. Excessive sugar of any type, including fructose, but perhaps glucose worst of all. If you don’t believe me, stay tuned for more!

There you have it. Did that make sense? Are you any more or less afraid of fructose than you were before? Please share your thoughts and questions below so we can continue to learn from one another.

In article two, “Fructose Raises Appetite . . . for Better Science,” we answer the following questions:

Is the new study about fructose and appetite worth your attention? How good are scientific studies of fructose in general? Can we count on them to give us useful information about what we should eat to be healthy?

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

Hypothyroidism 101

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

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

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

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

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

Iodine requirements

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

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

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

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

Plant goitrogens

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

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

Goitrin

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

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

Thiocyanates

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

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

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

Foods that form thiocyanates:

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

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

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

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

Flavonoids

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

Soy flavonoids (genistein, daidzein)

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

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

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

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

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

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

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

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

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

Cooking does not destroy the goitrogenic activity of soy isoflavones.

Millet flavonoids (apigenin, glucosylorientine, vitexin)

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

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

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

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

Other foods containing apigenin include:

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

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

Quercetin and friends

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

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

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

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

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

Can you eat too much iodine?

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

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

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

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

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

Dietary recommendations for hypothyroidism

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

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

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

Hypothyroidism 101

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

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

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

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

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

Iodine requirements

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

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

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

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

Plant goitrogens

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

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

Goitrin

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

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

Thiocyanates

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

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

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

Foods that form thiocyanates:

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

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

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

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

Flavonoids

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

Soy flavonoids (genistein, daidzein)

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

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

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

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

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

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

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

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

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

Cooking does not destroy the goitrogenic activity of soy isoflavones.

Millet flavonoids (apigenin, glucosylorientine, vitexin)

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

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

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

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

Other foods containing apigenin include:

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

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

Quercetin and friends

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

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

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

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

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

Can you eat too much iodine?

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

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

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

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

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

Dietary recommendations for hypothyroidism

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

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