Reversing Diabetic Blindness with Diet

Reversing Diabetic Blindness with Diet.jpeg

Though many reported feeling better on Dr. Walter Kempner's rice and fruit diet, he refused to accept such anecdotal evidence as proof of success. He wanted objective measurements. The most famous were his "eyegrounds photographs," taken with a special camera that allowed one to visualize the back of the eye. In doing so, he proved diet can arrest the bleeding, oozing, and swelling you see in the back of the eye in people with severe kidney, hypertensive, or heart disease. Even more than that, he proved that diet could actually reverse it, something never thought possible.

In my video, Can Diabetic Retinopathy Be Reversed?, you can see before and after images of the back of patients' eyes. He found reversal to such a degree that even those who could no longer distinguish large objects were able to once again read fine print. Dr. Kempner had shown a reversal of blindness with diet.

The results were so dramatic that the head of the department of ophthalmology at Duke, where Kempner worked, was questioned as to whether they were somehow faked. He assured them they were not. In fact, he wrote in one person's chart, "This patient's eyegrounds are improved to an unbelievable degree." Not only had he never seen anything like it, he couldn't remember ever seeing a patient with such advanced disease even being alive 15 months later.

The magnitude of the improvements Kempner got--reversal of end-stage heart and kidney failure--was surprising, simply beyond belief. But as Kempner said as his closing sentence of a presentation before the American College of Physicians, "The important result is not that the change in the course of the disease has been achieved by the rice diet but that the course of the disease can be changed."

Now that we have high blood pressure drugs, we see less hypertensive retinopathy, but we still see a lot of diabetic retinopathy, now the leading cause of blindness in American adults. Even with intensive diabetes treatment--at least three insulin injections a day with the best modern technology has to offer--the best we can offer is usually just a slowing of the progression of the disease.

So, in the 21st century, we slow down your blindness. Yet a half century ago, Kempner proved we could reverse it. Kempner started out using his plant-based rice diet ultra-low in sodium, fat, cholesterol, and protein to reverse kidney and heart failure; he actually assumed the diet would make diabetes worse. He expected a 90% carbohydrate diet would increase insulin requirements, however, the opposite proved to be true. He took the next 100 patients with diabetes who walked through his door who went on the rice diet for at least three months and found their fasting blood sugars dropped despite a drop in the insulin they were taking. What really blew people away was this: Forty-four of the patients had diabetic retinopathy, and, in 30% of the cases, their eyes improved. That's not supposed to happen; diabetic retinopathy had been considered "a sign of irreversible destruction." What does this change mean in real life? Patients went from unable to even read headlines to normal vision.

The remarkable success Dr. Kempner had reversing some of the most dreaded complications of diabetes with his rice and fruit diet was not because of weight loss. The improvements occurred even in those patients who did not lose significant weight, so it must have been something specific about the diet. Maybe it was his total elimination of animal protein, animal fat, and cholesterol? Or perhaps it was his radical reduction in sodium, fat, and protein in general? We don't know.

How do we treat diabetic retinopathy these days? With steroids and other drugs injected straight into the eyeball. If that doesn't work, there's always pan-retinal laser photocoagulation, in which laser burns are etched over nearly the entire retina. Surgeons literally burn out the back of your eye. Why would they do that? The theory is that by killing off most of the retina, the little pieces you leave behind may get more blood flow.

When I see that, along with Kempner's work, I can't help but feel like history has been reversed. It seems as though it should have gone like, "Can you believe 50 years ago the best we had was this barbaric, burn-out-your-socket surgery? Thank goodness we've since learned that through dietary means alone, we can reverse the blindness." But instead of learning, medicine seems to have forgotten.

I documented the extraordinary Kempner story previously in Kempner Rice Diet: Whipping Us Into Shape and Drugs and the Demise of the Rice Diet. The reason I keep coming back to this is not to suggest people should go on such a diet (it is too extreme and potentially dangerous to do without strict medical supervision), but to show the power of dietary change to yield tremendous healing effects.

The best way to prevent diabetic blindness is to prevent or reverse diabetes in the first place. See, for example:

Why wouldn't a diet of white rice make diabetes worse? See If White Rice Is Linked to Diabetes, What About China?

For more on the nitty gritty on what is the actual cause of type 2 diabetes, see:

In health,

Michael Greger, M.D.

PS: If you haven't yet, you can subscribe to my free videos here and watch my live, year-in-review presentations:

Image Credit: Community Eye Health / Flickr. This image has been modified.

Original Link

Reversing Diabetic Blindness with Diet

Reversing Diabetic Blindness with Diet.jpeg

Though many reported feeling better on Dr. Walter Kempner's rice and fruit diet, he refused to accept such anecdotal evidence as proof of success. He wanted objective measurements. The most famous were his "eyegrounds photographs," taken with a special camera that allowed one to visualize the back of the eye. In doing so, he proved diet can arrest the bleeding, oozing, and swelling you see in the back of the eye in people with severe kidney, hypertensive, or heart disease. Even more than that, he proved that diet could actually reverse it, something never thought possible.

In my video, Can Diabetic Retinopathy Be Reversed?, you can see before and after images of the back of patients' eyes. He found reversal to such a degree that even those who could no longer distinguish large objects were able to once again read fine print. Dr. Kempner had shown a reversal of blindness with diet.

The results were so dramatic that the head of the department of ophthalmology at Duke, where Kempner worked, was questioned as to whether they were somehow faked. He assured them they were not. In fact, he wrote in one person's chart, "This patient's eyegrounds are improved to an unbelievable degree." Not only had he never seen anything like it, he couldn't remember ever seeing a patient with such advanced disease even being alive 15 months later.

The magnitude of the improvements Kempner got--reversal of end-stage heart and kidney failure--was surprising, simply beyond belief. But as Kempner said as his closing sentence of a presentation before the American College of Physicians, "The important result is not that the change in the course of the disease has been achieved by the rice diet but that the course of the disease can be changed."

Now that we have high blood pressure drugs, we see less hypertensive retinopathy, but we still see a lot of diabetic retinopathy, now the leading cause of blindness in American adults. Even with intensive diabetes treatment--at least three insulin injections a day with the best modern technology has to offer--the best we can offer is usually just a slowing of the progression of the disease.

So, in the 21st century, we slow down your blindness. Yet a half century ago, Kempner proved we could reverse it. Kempner started out using his plant-based rice diet ultra-low in sodium, fat, cholesterol, and protein to reverse kidney and heart failure; he actually assumed the diet would make diabetes worse. He expected a 90% carbohydrate diet would increase insulin requirements, however, the opposite proved to be true. He took the next 100 patients with diabetes who walked through his door who went on the rice diet for at least three months and found their fasting blood sugars dropped despite a drop in the insulin they were taking. What really blew people away was this: Forty-four of the patients had diabetic retinopathy, and, in 30% of the cases, their eyes improved. That's not supposed to happen; diabetic retinopathy had been considered "a sign of irreversible destruction." What does this change mean in real life? Patients went from unable to even read headlines to normal vision.

The remarkable success Dr. Kempner had reversing some of the most dreaded complications of diabetes with his rice and fruit diet was not because of weight loss. The improvements occurred even in those patients who did not lose significant weight, so it must have been something specific about the diet. Maybe it was his total elimination of animal protein, animal fat, and cholesterol? Or perhaps it was his radical reduction in sodium, fat, and protein in general? We don't know.

How do we treat diabetic retinopathy these days? With steroids and other drugs injected straight into the eyeball. If that doesn't work, there's always pan-retinal laser photocoagulation, in which laser burns are etched over nearly the entire retina. Surgeons literally burn out the back of your eye. Why would they do that? The theory is that by killing off most of the retina, the little pieces you leave behind may get more blood flow.

When I see that, along with Kempner's work, I can't help but feel like history has been reversed. It seems as though it should have gone like, "Can you believe 50 years ago the best we had was this barbaric, burn-out-your-socket surgery? Thank goodness we've since learned that through dietary means alone, we can reverse the blindness." But instead of learning, medicine seems to have forgotten.

I documented the extraordinary Kempner story previously in Kempner Rice Diet: Whipping Us Into Shape and Drugs and the Demise of the Rice Diet. The reason I keep coming back to this is not to suggest people should go on such a diet (it is too extreme and potentially dangerous to do without strict medical supervision), but to show the power of dietary change to yield tremendous healing effects.

The best way to prevent diabetic blindness is to prevent or reverse diabetes in the first place. See, for example:

Why wouldn't a diet of white rice make diabetes worse? See If White Rice Is Linked to Diabetes, What About China?

For more on the nitty gritty on what is the actual cause of type 2 diabetes, see:

In health,

Michael Greger, M.D.

PS: If you haven't yet, you can subscribe to my free videos here and watch my live, year-in-review presentations:

Image Credit: Community Eye Health / Flickr. This image has been modified.

Original Link

What Causes Diabetes?

What Causes Diabetes?.jpeg

After about age 20, we may have all the insulin-producing beta cells we're ever going to get. So if we lose them, we may lose them for good. Autopsy studies show that by the time type 2 diabetes is diagnosed, we may have already killed off half of our beta cells.

You can kill pancreatic cells right in a petri dish. If you expose the insulin-producing beta cells in our pancreas to fat, they suck it up and then start dying off. Fat breakdown products can interfere with the function of these cells and ultimately lead to their death. A chronic increase in blood fat levels can be harmful to our pancreas.

It's not just any fat; it's saturated fat. As you can see in my video, What Causes Diabetes?, predominant fat in olives, nuts, and avocados gives a tiny bump in death protein 5, but saturated fat really elevates this contributor to beta cell death. Therefore, saturated fats are harmful to beta cells. Cholesterol is, too. The uptake of bad cholesterol (LDL) can cause beta cell death as a result of free radical formation.

Diets rich in saturated fats not only cause obesity and insulin resistance, but the increased levels of circulating free fats in the blood (non-esterified fatty acids, or NEFAs) may also cause beta cell death and may thus contribute to the progressive beta cell loss we see in type 2 diabetes. These findings aren't just based on test tube studies. If researchers have infused fat into people's blood streams, they can show it directly impairing pancreatic beta cell function. The same occurs when we ingest it.

Type 2 diabetes is characterized by "defects in both insulin secretion and insulin action," and saturated fat appears to impair both. Researchers showed saturated fat ingestion reduces insulin sensitivity within hours. The subjects were non-diabetics, so their pancreases should have been able to boost insulin secretion to match the drop in sensitivity. But no, "insulin secretion failed to compensate for insulin resistance in subjects who ingested [the saturated fat]." This implies saturated fat impaired beta cell function as well, again just within hours after going into our mouth. "[I]ncreased consumption of [saturated fats] has a powerful short- and long-term effect on insulin action," contributing to the dysfunction and death of pancreatic beta cells in diabetes.

Saturated fat isn't just toxic to the pancreas. The fats found predominantly in meat and dairy--chicken and cheese are the two main sources in the American diet--are considered nearly "universally toxic." In contrast, the fats found in olives, nuts, and avocados are not. Saturated fat has been found to be particularly toxic to liver cells, contributing to the formation of fatty liver disease. If you expose human liver cells to plant fat, though, nothing happens. If you expose our liver cells to animal fat, a third of them die. This may explain why higher intake of saturated fat and cholesterol are associated with non-alcoholic fatty liver disease.

By cutting down on saturated fat consumption, we may be able to help interrupt these processes. Decreasing saturated fat intake can help bring down the need for all that excess insulin. So either being fat or eating saturated fat can both cause excess insulin in the blood. The effect of reducing dietary saturated fat intake on insulin levels is substantial, regardless of how much belly fat we have. It's not just that by eating fat we may be more likely to store it as fat. Saturated fats, independently of any role they have in making us fat, "may contribute to the development of insulin resistance and its clinical consequences." After controlling for weight, alcohol, smoking, exercise, and family history, diabetes incidence was significantly associated with the proportion of saturated fat in our blood.

So what causes diabetes? The consumption of too many calories rich in saturated fats. Just like everyone who smokes doesn't develop lung cancer, everyone who eats a lot of saturated fat doesn't develop diabetes--there is a genetic component. But just like smoking can be said to cause lung cancer, high-calorie diets rich in saturated fats are currently considered the cause of type 2 diabetes.

I have a lot of videos on diabetes, including:

Preventing the disease:

And treating it:

In health,

Michael Greger, M.D.

PS: If you haven't yet, you can subscribe to my free videos here and watch my live, year-in-review presentations:

Image Credit: Sally Plank. This image has been modified.

Original Link

What Causes Diabetes?

What Causes Diabetes?.jpeg

After about age 20, we may have all the insulin-producing beta cells we're ever going to get. So if we lose them, we may lose them for good. Autopsy studies show that by the time type 2 diabetes is diagnosed, we may have already killed off half of our beta cells.

You can kill pancreatic cells right in a petri dish. If you expose the insulin-producing beta cells in our pancreas to fat, they suck it up and then start dying off. Fat breakdown products can interfere with the function of these cells and ultimately lead to their death. A chronic increase in blood fat levels can be harmful to our pancreas.

It's not just any fat; it's saturated fat. As you can see in my video, What Causes Diabetes?, predominant fat in olives, nuts, and avocados gives a tiny bump in death protein 5, but saturated fat really elevates this contributor to beta cell death. Therefore, saturated fats are harmful to beta cells. Cholesterol is, too. The uptake of bad cholesterol (LDL) can cause beta cell death as a result of free radical formation.

Diets rich in saturated fats not only cause obesity and insulin resistance, but the increased levels of circulating free fats in the blood (non-esterified fatty acids, or NEFAs) may also cause beta cell death and may thus contribute to the progressive beta cell loss we see in type 2 diabetes. These findings aren't just based on test tube studies. If researchers have infused fat into people's blood streams, they can show it directly impairing pancreatic beta cell function. The same occurs when we ingest it.

Type 2 diabetes is characterized by "defects in both insulin secretion and insulin action," and saturated fat appears to impair both. Researchers showed saturated fat ingestion reduces insulin sensitivity within hours. The subjects were non-diabetics, so their pancreases should have been able to boost insulin secretion to match the drop in sensitivity. But no, "insulin secretion failed to compensate for insulin resistance in subjects who ingested [the saturated fat]." This implies saturated fat impaired beta cell function as well, again just within hours after going into our mouth. "[I]ncreased consumption of [saturated fats] has a powerful short- and long-term effect on insulin action," contributing to the dysfunction and death of pancreatic beta cells in diabetes.

Saturated fat isn't just toxic to the pancreas. The fats found predominantly in meat and dairy--chicken and cheese are the two main sources in the American diet--are considered nearly "universally toxic." In contrast, the fats found in olives, nuts, and avocados are not. Saturated fat has been found to be particularly toxic to liver cells, contributing to the formation of fatty liver disease. If you expose human liver cells to plant fat, though, nothing happens. If you expose our liver cells to animal fat, a third of them die. This may explain why higher intake of saturated fat and cholesterol are associated with non-alcoholic fatty liver disease.

By cutting down on saturated fat consumption, we may be able to help interrupt these processes. Decreasing saturated fat intake can help bring down the need for all that excess insulin. So either being fat or eating saturated fat can both cause excess insulin in the blood. The effect of reducing dietary saturated fat intake on insulin levels is substantial, regardless of how much belly fat we have. It's not just that by eating fat we may be more likely to store it as fat. Saturated fats, independently of any role they have in making us fat, "may contribute to the development of insulin resistance and its clinical consequences." After controlling for weight, alcohol, smoking, exercise, and family history, diabetes incidence was significantly associated with the proportion of saturated fat in our blood.

So what causes diabetes? The consumption of too many calories rich in saturated fats. Just like everyone who smokes doesn't develop lung cancer, everyone who eats a lot of saturated fat doesn't develop diabetes--there is a genetic component. But just like smoking can be said to cause lung cancer, high-calorie diets rich in saturated fats are currently considered the cause of type 2 diabetes.

I have a lot of videos on diabetes, including:

Preventing the disease:

And treating it:

In health,

Michael Greger, M.D.

PS: If you haven't yet, you can subscribe to my free videos here and watch my live, year-in-review presentations:

Image Credit: Sally Plank. This image has been modified.

Original Link

How Exactly Does Type 2 Diabetes Develop?

How Exactly Does Type 2 Diabetes Develop.jpeg

Insulin resistance is the cause of both prediabetes and type 2 diabetes. OkK, so what is the cause of insulin resistance? Insulin resistance is now accepted to be closely associated with the accumulation of fat within our muscle cells. This fat toxicity inside of our muscles is a major factor in the cause of insulin resistance and type 2 diabetes, as it interferes with the action of insulin. I've explored how fat makes our muscles insulin resistant (see What Causes Insulin Resistance?), how that fat can come from the fat we eat or the fat we wear (see The Spillover Effect Links Obesity to Diabetes), and how not all fats are the same (see Lipotoxicity: How Saturated Fat Raises Blood Sugar). It's the type of fat found predominantly in animal fats, relative to plant fats, that appears to be especially deleterious with respect to fat-induced insulin insensitivity. But this insulin resistance in our muscles starts years before diabetes is diagnosed.

In my video, Diabetes as a Disease of Fat Toxicity, you can see that insulin resistance starts over a decade before diabetes is actually diagnosed, as blood sugar levels slowly start creeping up. And then, all of the sudden, the pancreas conks out, and blood sugars skyrocket. What could underlie this relatively rapid failure of insulin secretion?

At first, the pancreas pumps out more and more insulin, trying to overcome the fat-induced insulin resistance in the muscles, and high insulin levels can lead to the accumulation of fat in the liver, called fatty liver disease. Before diagnosis of type 2 diabetes, there is a long silent scream from the liver. As fat builds up in our liver, it also becomes resistant to insulin.

Normally, the liver is constantly producing blood sugar to keep our brain alive between meals. As soon as we eat breakfast, though, the insulin released to deal with the meal normally turns off liver glucose production, which makes sense since we don't need it anymore. But when our liver is filled with fat, it becomes insulin resistant like our muscles, and doesn't respond to the breakfast signal; it keeps pumping out blood sugar all day long on top of whatever we eat. Then the pancreas pumps out even more insulin to deal with the high sugars, and our liver gets fatter and fatter. That's one of the twin vicious cycles of diabetes. Fatty muscles, in the context of too many calories, leads to a fatty liver, which leads to an even fattier liver. This is all still before we have diabetes.

Fatty liver can be deadly. The liver starts trying to offload the fat by dumping it back into the bloodstream in the form of something called VLDL, and that starts building up in the cells in the pancreas that produce the insulin in the first place. Now we know how diabetes develops: fatty muscles lead to a fatty liver, which leads to a fatty pancreas. It is now clear that type 2 diabetes is a condition of excess fat inside our organs, whether we're obese or not.

The only thing that was keeping us from diabetes-unchecked skyrocketing blood sugars-is that the pancreas was working overtime pumping out extra insulin to overcome insulin resistance. But as the so-called islet or Beta cells in the pancreas are killed off by the fatty buildup, insulin production starts to fail, and we're left with the worst of both worlds: insulin resistance combined with a failing pancreas. Unable to then overcome the resistance, blood sugar levels go up and up, and boom: type 2 diabetes.

This has implications for cancer as well. Obesity leads to insulin resistance and our blood sugars start to go up, so our pancreas starts pumping out more insulin to try to force more sugar into our muscles, and eventually the fat spills over into the pancreas, killing off the insulin-producing cells. Then we develop diabetes, in which case we may have to start injecting insulin at high levels to overcome the insulin-resistance, and these high insulin levels promote cancer. That's one of the reasons we think obese women get more breast cancer. It all traces back to fat getting into our muscle cells, causing insulin resistance: fat from our stomach (obesity) or fat going into our stomach (saturated fats in our diet).

Now it should make sense why the American Diabetes Association recommends reduced intake of dietary fat as a strategy for reducing the risk for developing diabetes.


The reason I'm going into all this detail is that I'm hoping to empower both those suffering from the disease and those treating sufferers so as to better understand dietary interventions to prevent and treat the epidemic.

Here are some videos on prevention:

And here are some on treatment:

In health,
Michael Greger, M.D.

PS: If you haven't yet, you can subscribe to my free videos here and watch my live, year-in-review presentations:

Image Credit: Nephron. This image has been modified.

Original Link

How Exactly Does Type 2 Diabetes Develop?

How Exactly Does Type 2 Diabetes Develop.jpeg

Insulin resistance is the cause of both prediabetes and type 2 diabetes. OkK, so what is the cause of insulin resistance? Insulin resistance is now accepted to be closely associated with the accumulation of fat within our muscle cells. This fat toxicity inside of our muscles is a major factor in the cause of insulin resistance and type 2 diabetes, as it interferes with the action of insulin. I've explored how fat makes our muscles insulin resistant (see What Causes Insulin Resistance?), how that fat can come from the fat we eat or the fat we wear (see The Spillover Effect Links Obesity to Diabetes), and how not all fats are the same (see Lipotoxicity: How Saturated Fat Raises Blood Sugar). It's the type of fat found predominantly in animal fats, relative to plant fats, that appears to be especially deleterious with respect to fat-induced insulin insensitivity. But this insulin resistance in our muscles starts years before diabetes is diagnosed.

In my video, Diabetes as a Disease of Fat Toxicity, you can see that insulin resistance starts over a decade before diabetes is actually diagnosed, as blood sugar levels slowly start creeping up. And then, all of the sudden, the pancreas conks out, and blood sugars skyrocket. What could underlie this relatively rapid failure of insulin secretion?

At first, the pancreas pumps out more and more insulin, trying to overcome the fat-induced insulin resistance in the muscles, and high insulin levels can lead to the accumulation of fat in the liver, called fatty liver disease. Before diagnosis of type 2 diabetes, there is a long silent scream from the liver. As fat builds up in our liver, it also becomes resistant to insulin.

Normally, the liver is constantly producing blood sugar to keep our brain alive between meals. As soon as we eat breakfast, though, the insulin released to deal with the meal normally turns off liver glucose production, which makes sense since we don't need it anymore. But when our liver is filled with fat, it becomes insulin resistant like our muscles, and doesn't respond to the breakfast signal; it keeps pumping out blood sugar all day long on top of whatever we eat. Then the pancreas pumps out even more insulin to deal with the high sugars, and our liver gets fatter and fatter. That's one of the twin vicious cycles of diabetes. Fatty muscles, in the context of too many calories, leads to a fatty liver, which leads to an even fattier liver. This is all still before we have diabetes.

Fatty liver can be deadly. The liver starts trying to offload the fat by dumping it back into the bloodstream in the form of something called VLDL, and that starts building up in the cells in the pancreas that produce the insulin in the first place. Now we know how diabetes develops: fatty muscles lead to a fatty liver, which leads to a fatty pancreas. It is now clear that type 2 diabetes is a condition of excess fat inside our organs, whether we're obese or not.

The only thing that was keeping us from diabetes-unchecked skyrocketing blood sugars-is that the pancreas was working overtime pumping out extra insulin to overcome insulin resistance. But as the so-called islet or Beta cells in the pancreas are killed off by the fatty buildup, insulin production starts to fail, and we're left with the worst of both worlds: insulin resistance combined with a failing pancreas. Unable to then overcome the resistance, blood sugar levels go up and up, and boom: type 2 diabetes.

This has implications for cancer as well. Obesity leads to insulin resistance and our blood sugars start to go up, so our pancreas starts pumping out more insulin to try to force more sugar into our muscles, and eventually the fat spills over into the pancreas, killing off the insulin-producing cells. Then we develop diabetes, in which case we may have to start injecting insulin at high levels to overcome the insulin-resistance, and these high insulin levels promote cancer. That's one of the reasons we think obese women get more breast cancer. It all traces back to fat getting into our muscle cells, causing insulin resistance: fat from our stomach (obesity) or fat going into our stomach (saturated fats in our diet).

Now it should make sense why the American Diabetes Association recommends reduced intake of dietary fat as a strategy for reducing the risk for developing diabetes.


The reason I'm going into all this detail is that I'm hoping to empower both those suffering from the disease and those treating sufferers so as to better understand dietary interventions to prevent and treat the epidemic.

Here are some videos on prevention:

And here are some on treatment:

In health,
Michael Greger, M.D.

PS: If you haven't yet, you can subscribe to my free videos here and watch my live, year-in-review presentations:

Image Credit: Nephron. This image has been modified.

Original Link

Can You Eat Too Much Fruit?

Can You Eat Too Much Fruit?.jpeg

In my video If Fructose is Bad, What About Fruit?, I explored how adding berries to our meals can actually blunt the detrimental effects of high glycemic foods, but how many berries? The purpose of one study out of Finland was to determine the minimum level of blueberry consumption at which a consumer may realistically expect to receive antioxidant benefits after eating blueberries with a sugary breakfast cereal. If we eat a bowl of corn flakes with no berries, within two hours, so many free radicals are created that it puts us into oxidative debt. The antioxidant power of our bloodstream drops below where we started from before breakfast, as the antioxidants in our bodies get used up dealing with such a crappy breakfast. As you can see in How Much Fruit is Too Much? video, a quarter cup of blueberries didn't seem to help much, but a half cup of blueberries did.

What about fruit for diabetics? Most guidelines recommend eating a diet with a high intake of fiber-rich food, including fruit, because they're so healthy--antioxidants, anti-inflammatory, improving artery function, and reducing cancer risk. However, some health professionals have concerns about the sugar content of fruit and therefore recommend restricting the fruit intake. So let's put it to the test! In a study from Denmark, diabetics were randomized into two groups: one told to eat at least two pieces of fruit a day, and the other told at most, two fruits a day. The reduce fruit group indeed reduce their fruit consumption, but it had no effect on the control of their diabetes or weight, and so, the researchers concluded, the intake of fruit should not be restricted in patients with type 2 diabetes. An emerging literature has shown that low-dose fructose may actually benefit blood sugar control. Having a piece of fruit with each meal would be expected to lower, not raise the blood sugar response.

The threshold for toxicity of fructose may be around 50 grams. The problem is that's the current average adult fructose consumption. So, the levels of half of all adults are likely above the threshold for fructose toxicity, and adolescents currently average 75. Is that limit for added sugars or for all fructose? If we don't want more than 50 and there's about ten in a piece of fruit, should we not eat more than five fruit a day? Quoting from the Harvard Health Letter, "the nutritional problems of fructose and sugar come when they are added to foods. Fruit, on the other hand, is beneficial in almost any amount." What do they mean almost? Can we eat ten fruit a day? How about twenty fruit a day?

It's actually been put to the test.

Seventeen people were made to eat 20 servings a day of fruit. Despite the extraordinarily high fructose content of this diet, presumably about 200 g/d--eight cans of soda worth, the investigators reported no adverse effects (and possible benefit actually) for body weight, blood pressure, and insulin and lipid levels after three to six months. More recently, Jenkins and colleagues put people on about a 20 servings of fruit a day diet for a few weeks and found no adverse effects on weight or blood pressure or triglycerides, and an astounding 38 point drop in LDL cholesterol.

There was one side effect, though. Given the 44 servings of vegetables they had on top of all that fruit, they recorded the largest bowl movements apparently ever documented in a dietary intervention.


Cutting down on sugary foods may be easier said than done (see Are Sugary Foods Addictive?) but it's worth it. For more on the dangers of high levels of fructose in added sugars, see How Much Added Sugar Is Too Much?.

What's that about being in oxidative debt? See my three part series on how to pull yourself out of the red:

Ironically, fat may be more of a problem when it comes to diabetes than sugar, see:

In health,
Michael Greger, M.D.

PS: If you haven't yet, you can subscribe to my free videos here and watch my live, year-in-review presentations:

Image Credit: Sally Plank / Flickr. This image has been modified.

Original Link

Can You Eat Too Much Fruit?

Can You Eat Too Much Fruit?.jpeg

In my video If Fructose is Bad, What About Fruit?, I explored how adding berries to our meals can actually blunt the detrimental effects of high glycemic foods, but how many berries? The purpose of one study out of Finland was to determine the minimum level of blueberry consumption at which a consumer may realistically expect to receive antioxidant benefits after eating blueberries with a sugary breakfast cereal. If we eat a bowl of corn flakes with no berries, within two hours, so many free radicals are created that it puts us into oxidative debt. The antioxidant power of our bloodstream drops below where we started from before breakfast, as the antioxidants in our bodies get used up dealing with such a crappy breakfast. As you can see in How Much Fruit is Too Much? video, a quarter cup of blueberries didn't seem to help much, but a half cup of blueberries did.

What about fruit for diabetics? Most guidelines recommend eating a diet with a high intake of fiber-rich food, including fruit, because they're so healthy--antioxidants, anti-inflammatory, improving artery function, and reducing cancer risk. However, some health professionals have concerns about the sugar content of fruit and therefore recommend restricting the fruit intake. So let's put it to the test! In a study from Denmark, diabetics were randomized into two groups: one told to eat at least two pieces of fruit a day, and the other told at most, two fruits a day. The reduce fruit group indeed reduce their fruit consumption, but it had no effect on the control of their diabetes or weight, and so, the researchers concluded, the intake of fruit should not be restricted in patients with type 2 diabetes. An emerging literature has shown that low-dose fructose may actually benefit blood sugar control. Having a piece of fruit with each meal would be expected to lower, not raise the blood sugar response.

The threshold for toxicity of fructose may be around 50 grams. The problem is that's the current average adult fructose consumption. So, the levels of half of all adults are likely above the threshold for fructose toxicity, and adolescents currently average 75. Is that limit for added sugars or for all fructose? If we don't want more than 50 and there's about ten in a piece of fruit, should we not eat more than five fruit a day? Quoting from the Harvard Health Letter, "the nutritional problems of fructose and sugar come when they are added to foods. Fruit, on the other hand, is beneficial in almost any amount." What do they mean almost? Can we eat ten fruit a day? How about twenty fruit a day?

It's actually been put to the test.

Seventeen people were made to eat 20 servings a day of fruit. Despite the extraordinarily high fructose content of this diet, presumably about 200 g/d--eight cans of soda worth, the investigators reported no adverse effects (and possible benefit actually) for body weight, blood pressure, and insulin and lipid levels after three to six months. More recently, Jenkins and colleagues put people on about a 20 servings of fruit a day diet for a few weeks and found no adverse effects on weight or blood pressure or triglycerides, and an astounding 38 point drop in LDL cholesterol.

There was one side effect, though. Given the 44 servings of vegetables they had on top of all that fruit, they recorded the largest bowl movements apparently ever documented in a dietary intervention.


Cutting down on sugary foods may be easier said than done (see Are Sugary Foods Addictive?) but it's worth it. For more on the dangers of high levels of fructose in added sugars, see How Much Added Sugar Is Too Much?.

What's that about being in oxidative debt? See my three part series on how to pull yourself out of the red:

Ironically, fat may be more of a problem when it comes to diabetes than sugar, see:

In health,
Michael Greger, M.D.

PS: If you haven't yet, you can subscribe to my free videos here and watch my live, year-in-review presentations:

Image Credit: Sally Plank / Flickr. This image has been modified.

Original Link

What Not to Add to White Rice, Potatoes, or Pasta

What Not to Add to White Rice, Potatoes, or Pasta.jpeg

Rice currently feeds almost half the human population, making it the single most important staple food in the world, but a meta-analysis of seven cohort studies following 350,000 people for up to 20 years found that higher consumption of white rice was associated with a significantly increased risk of type 2 diabetes, especially in Asian populations. They estimated each serving per day of white rice was associated with an 11% increase in risk of diabetes. This could explain why China has almost the same diabetes rates as we do.

Diabetes rates in China are at about 10%; we're at about 11%, despite seven times less obesity in China. Japan has eight times less obesity than we do, yet may have a higher incidence of newly diagnosed diabetes cases than we do--nine per a thousand compared to our eight. They're skinnier and still may have more diabetes. Maybe it's because of all the white rice they eat.

Eating whole fruit is associated with lower risk of diabetes, whereas eating fruit processed into juice may not just be neutral, but actually increases diabetes risk. In the same way, eating whole grains, like whole wheat bread or brown rice is associated with lower risk of diabetes, whereas eating white rice, a processed grain, may not just be neutral, but actually increase diabetes risk.

White rice consumption does not appear to be associated with increased risk of heart attack or stroke, though, which is a relief after an earlier study in China suggested a connection with stroke. But do we want to eat a food that's just neutral regarding some of our leading causes of death, when we can eat whole foods that are associated with lower risk of diabetes, heart attack, stroke, and weight gain?

If the modern diabetes epidemic in China and Japan has been linked to white rice consumption, how can we reconcile that with low diabetes rates just a few decades ago when they ate even more rice? If you look at the Cornell-Oxford-China Project, rural plant-based diets centered around rice were associated with relatively low risk of the so-called diseases of affluence, which includes diabetes. Maybe Asians just genetically don't get the same blood sugar spike when they eat white rice? This is not the case; if anything people of Chinese ethnicity get higher blood sugar spikes.

The rise in these diseases of affluence in China over the last half century has been blamed in part on the tripling of the consumption of animal source foods. The upsurge in diabetes has been most dramatic, and it's mostly just happened over the last decade. That crazy 9.7% diabetes prevalence figure that rivals ours is new--they appeared to have one of the lowest diabetes rates in the world in the year 2000.

So what happened to their diets in the last 20 years or so? Oil consumption went up 20%, pork consumption went up 40%, and rice consumption dropped about 30%. As diabetes rates were skyrocketing, rice consumption was going down, so maybe it's the animal products and junk food that are the problem. Yes, brown rice is better than white rice, but to stop the mounting Asian epidemic, maybe we should focus on removing the cause--the toxic Western diet. That would be consistent with data showing animal protein and fat consumption associated with increased diabetes risk.

But that doesn't explain why the biggest recent studies in Japan and China associate white rice intake with diabetes. One possibility is that animal protein is making the rice worse. If you feed people mashed white potatoes, a high glycemic food like white rice, you can see in my video If White Rice is Linked to Diabetes, What About China? the level of insulin your pancreas has to pump out to keep your blood sugars in check. But what if you added some tuna fish? Tuna doesn't have any carbs, sugar, or starch so it shouldn't make a difference. Or maybe it would even lower the mashed potato spike by lowering the glycemic load of the whole meal? Instead you get twice the insulin spike. This also happens with white flour spaghetti versus white flour spaghetti with meat. The addition of animal protein makes the pancreas work twice as hard.

You can do it with straight sugar water too. If you do a glucose challenge test to test for diabetes, where you drink a certain amount of sugar and add some meat, you get a much bigger spike than without meat. And the more meat you add, the worse it gets. Just adding a little meat to carbs doesn't seem to do much, but once you get up to around a third of a chicken breast's worth, you can elicit a significantly increased surge of insulin. This may help explain why those eating plant-based have such low diabetes rates, because animal protein can markedly potentiate the insulin secretion triggered by carbohydrate ingestion.

The protein exacerbation of the effect of refined carbs could help explain the remarkable results achieved by Dr. Kempner with a don't-try-this-at-home diet composed of mostly white rice and sugar. See my video, Kempner Rice Diet: Whipping Us Into Shape.

Refined grains may also not be good for our blood pressure (see Whole Grains May Work As Well As Drugs).

What should we be eating to best decrease our risk of diabetes? See:

And check out my summary video, How Not to Die from Diabetes.

In health,
Michael Greger, M.D.

PS: If you haven't yet, you can subscribe to my free videos here and watch my live, year-in-review presentations:

Image Credit: Sally Plank / Flickr. This image has been modified.

Original Link

What Not to Add to White Rice, Potatoes, or Pasta

What Not to Add to White Rice, Potatoes, or Pasta.jpeg

Rice currently feeds almost half the human population, making it the single most important staple food in the world, but a meta-analysis of seven cohort studies following 350,000 people for up to 20 years found that higher consumption of white rice was associated with a significantly increased risk of type 2 diabetes, especially in Asian populations. They estimated each serving per day of white rice was associated with an 11% increase in risk of diabetes. This could explain why China has almost the same diabetes rates as we do.

Diabetes rates in China are at about 10%; we're at about 11%, despite seven times less obesity in China. Japan has eight times less obesity than we do, yet may have a higher incidence of newly diagnosed diabetes cases than we do--nine per a thousand compared to our eight. They're skinnier and still may have more diabetes. Maybe it's because of all the white rice they eat.

Eating whole fruit is associated with lower risk of diabetes, whereas eating fruit processed into juice may not just be neutral, but actually increases diabetes risk. In the same way, eating whole grains, like whole wheat bread or brown rice is associated with lower risk of diabetes, whereas eating white rice, a processed grain, may not just be neutral, but actually increase diabetes risk.

White rice consumption does not appear to be associated with increased risk of heart attack or stroke, though, which is a relief after an earlier study in China suggested a connection with stroke. But do we want to eat a food that's just neutral regarding some of our leading causes of death, when we can eat whole foods that are associated with lower risk of diabetes, heart attack, stroke, and weight gain?

If the modern diabetes epidemic in China and Japan has been linked to white rice consumption, how can we reconcile that with low diabetes rates just a few decades ago when they ate even more rice? If you look at the Cornell-Oxford-China Project, rural plant-based diets centered around rice were associated with relatively low risk of the so-called diseases of affluence, which includes diabetes. Maybe Asians just genetically don't get the same blood sugar spike when they eat white rice? This is not the case; if anything people of Chinese ethnicity get higher blood sugar spikes.

The rise in these diseases of affluence in China over the last half century has been blamed in part on the tripling of the consumption of animal source foods. The upsurge in diabetes has been most dramatic, and it's mostly just happened over the last decade. That crazy 9.7% diabetes prevalence figure that rivals ours is new--they appeared to have one of the lowest diabetes rates in the world in the year 2000.

So what happened to their diets in the last 20 years or so? Oil consumption went up 20%, pork consumption went up 40%, and rice consumption dropped about 30%. As diabetes rates were skyrocketing, rice consumption was going down, so maybe it's the animal products and junk food that are the problem. Yes, brown rice is better than white rice, but to stop the mounting Asian epidemic, maybe we should focus on removing the cause--the toxic Western diet. That would be consistent with data showing animal protein and fat consumption associated with increased diabetes risk.

But that doesn't explain why the biggest recent studies in Japan and China associate white rice intake with diabetes. One possibility is that animal protein is making the rice worse. If you feed people mashed white potatoes, a high glycemic food like white rice, you can see in my video If White Rice is Linked to Diabetes, What About China? the level of insulin your pancreas has to pump out to keep your blood sugars in check. But what if you added some tuna fish? Tuna doesn't have any carbs, sugar, or starch so it shouldn't make a difference. Or maybe it would even lower the mashed potato spike by lowering the glycemic load of the whole meal? Instead you get twice the insulin spike. This also happens with white flour spaghetti versus white flour spaghetti with meat. The addition of animal protein makes the pancreas work twice as hard.

You can do it with straight sugar water too. If you do a glucose challenge test to test for diabetes, where you drink a certain amount of sugar and add some meat, you get a much bigger spike than without meat. And the more meat you add, the worse it gets. Just adding a little meat to carbs doesn't seem to do much, but once you get up to around a third of a chicken breast's worth, you can elicit a significantly increased surge of insulin. This may help explain why those eating plant-based have such low diabetes rates, because animal protein can markedly potentiate the insulin secretion triggered by carbohydrate ingestion.

The protein exacerbation of the effect of refined carbs could help explain the remarkable results achieved by Dr. Kempner with a don't-try-this-at-home diet composed of mostly white rice and sugar. See my video, Kempner Rice Diet: Whipping Us Into Shape.

Refined grains may also not be good for our blood pressure (see Whole Grains May Work As Well As Drugs).

What should we be eating to best decrease our risk of diabetes? See:

And check out my summary video, How Not to Die from Diabetes.

In health,
Michael Greger, M.D.

PS: If you haven't yet, you can subscribe to my free videos here and watch my live, year-in-review presentations:

Image Credit: Sally Plank / Flickr. This image has been modified.

Original Link