How I Lost Over 100 Pounds and Gained a New Perspective on a Plant-Based Diet

In November 2016, I was miserable, hopeless, depressed, and desperate. I was well over 300 pounds, ashamed of myself, and 100 percent uncomfortable all the time. I could barely get out of the car without wheezing, and people would flinch... Read more

Original Link

Foods to Eat to Help Prevent Diabetes

Oct 26 Foods to Eat copy.jpeg

Why is meat consumption a risk factor for diabetes? Why does there appear to be a stepwise reduction in diabetes rates as meat consumption drops? Instead of avoiding something in meat, it may be that people are getting something protective from plants. Free radicals may be an important trigger for insulin resistance, and antioxidants in plant foods may help. Put people on a plant-based diet, and their antioxidant enzymes shoot up. So not only do plants provide antioxidants, but may boost our own anti-endogenous antioxidant defenses, whereas, on the conventional diabetic diet, they get worse.

In my video, How May Plants Protect Against Diabetes, I discuss how there are phytonutrients in plant foods that may help lower chronic disease prevalence by acting as antioxidants and anti-cancer agents, and by lowering cholesterol and blood sugar. Some, we're now theorizing, may even be lipotropes, which have the capacity to hasten the removal of fat from our liver and other organs, counteracting the inflammatory cascade believed to be directly initiated by saturated-fat-containing foods. Fat in the bloodstream--from the fat on our bodies or the fat we eat--not only causes insulin resistance, but also produces a low-grade inflammation that can contribute to heart disease and non-alcoholic fatty liver disease.

Fiber may also decrease insulin resistance. One of the ways it may do so is by helping to rid the body of excess estrogen. There is strong evidence for a direct role of estrogens in the cause of diabetes, and it's been demonstrated that certain gut bacteria can produce estrogens in our colon. High-fat, low-fiber diets appear to stimulate the metabolic activity of these estrogen-producing intestinal bacteria. This is a problem for men, too. Obesity is associated with low testosterone levels and marked elevations of estrogens produced not only by fat cells but also by some of the bacteria in our gut. Our intestinal bacteria may produce these so-called diabetogens (diabetes-causing compounds) from the fats we eat. By eating lots of fiber, though, we can flush this excess estrogen out of our bodies.

Vegetarian women, for example, excrete two to three times more estrogens in their stools than omnivorous women, which may be why omnivorous women have 50% higher estrogen blood levels. These differences in estrogen metabolism may help explain the lower incidence of diabetes in those eating more plant-based diets, as well as the lower incidence of breast cancer in vegetarian women, who get rid of twice as much estrogen because they get rid of twice as much daily waste in general.

Either way, "[m]eat consumption is consistently associated with diabetes risk. Dietary habits are readily modifiable, but individuals and clinicians will consider dietary changes only if they are aware of the potential benefits of doing so." The identification of meat consumption as a risk factor for diabetes provides helpful guidance that sets the stage for beneficial behavioral changes. Meat consumption is something doctors can easily ask about, and, once identified, at-risk individuals can then be encouraged to familiarize themselves with meatless options.


Plant foods may also protect against diabetes by replacing animal foods. Learn more with my Why Is Meat a Risk Factor for Diabetes? video.

What if your entire diet was filled with plants? See Plant-Based Diets and Diabetes. Find out which plants may be particularly protective with these videos: Amla Versus Diabetes, Flaxseed vs. Diabetes, and Diabetics Should Take Their Pulses.

Unfortunately, cinnamon has fallen out of favor. See my Update on Cinnamon for Blood Sugar Control.

I also have an ever-growing series on the science behind type 2 diabetes:

For more on the estrogen connection, see Relieving Yourself of Excess Estrogen and Breast Cancer and Constipation.

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:

Original Link

Foods to Eat to Help Prevent Diabetes

Oct 26 Foods to Eat copy.jpeg

Why is meat consumption a risk factor for diabetes? Why does there appear to be a stepwise reduction in diabetes rates as meat consumption drops? Instead of avoiding something in meat, it may be that people are getting something protective from plants. Free radicals may be an important trigger for insulin resistance, and antioxidants in plant foods may help. Put people on a plant-based diet, and their antioxidant enzymes shoot up. So not only do plants provide antioxidants, but may boost our own anti-endogenous antioxidant defenses, whereas, on the conventional diabetic diet, they get worse.

In my video, How May Plants Protect Against Diabetes, I discuss how there are phytonutrients in plant foods that may help lower chronic disease prevalence by acting as antioxidants and anti-cancer agents, and by lowering cholesterol and blood sugar. Some, we're now theorizing, may even be lipotropes, which have the capacity to hasten the removal of fat from our liver and other organs, counteracting the inflammatory cascade believed to be directly initiated by saturated-fat-containing foods. Fat in the bloodstream--from the fat on our bodies or the fat we eat--not only causes insulin resistance, but also produces a low-grade inflammation that can contribute to heart disease and non-alcoholic fatty liver disease.

Fiber may also decrease insulin resistance. One of the ways it may do so is by helping to rid the body of excess estrogen. There is strong evidence for a direct role of estrogens in the cause of diabetes, and it's been demonstrated that certain gut bacteria can produce estrogens in our colon. High-fat, low-fiber diets appear to stimulate the metabolic activity of these estrogen-producing intestinal bacteria. This is a problem for men, too. Obesity is associated with low testosterone levels and marked elevations of estrogens produced not only by fat cells but also by some of the bacteria in our gut. Our intestinal bacteria may produce these so-called diabetogens (diabetes-causing compounds) from the fats we eat. By eating lots of fiber, though, we can flush this excess estrogen out of our bodies.

Vegetarian women, for example, excrete two to three times more estrogens in their stools than omnivorous women, which may be why omnivorous women have 50% higher estrogen blood levels. These differences in estrogen metabolism may help explain the lower incidence of diabetes in those eating more plant-based diets, as well as the lower incidence of breast cancer in vegetarian women, who get rid of twice as much estrogen because they get rid of twice as much daily waste in general.

Either way, "[m]eat consumption is consistently associated with diabetes risk. Dietary habits are readily modifiable, but individuals and clinicians will consider dietary changes only if they are aware of the potential benefits of doing so." The identification of meat consumption as a risk factor for diabetes provides helpful guidance that sets the stage for beneficial behavioral changes. Meat consumption is something doctors can easily ask about, and, once identified, at-risk individuals can then be encouraged to familiarize themselves with meatless options.


Plant foods may also protect against diabetes by replacing animal foods. Learn more with my Why Is Meat a Risk Factor for Diabetes? video.

What if your entire diet was filled with plants? See Plant-Based Diets and Diabetes. Find out which plants may be particularly protective with these videos: Amla Versus Diabetes, Flaxseed vs. Diabetes, and Diabetics Should Take Their Pulses.

Unfortunately, cinnamon has fallen out of favor. See my Update on Cinnamon for Blood Sugar Control.

I also have an ever-growing series on the science behind type 2 diabetes:

For more on the estrogen connection, see Relieving Yourself of Excess Estrogen and Breast Cancer and Constipation.

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:

Original Link

Foods to Avoid to Help Prevent Diabetes

Oct 24 Foods to Avoid copy.jpeg

We've known that being overweight and obese are important risk factors for type 2 diabetes, but, until recently, not much attention has been paid to the role of specific foods. I discuss this issue in my video, Why Is Meat a Risk Factor for Diabetes?

A 2013 meta-analysis of all the cohorts looking at the connection between meat and diabetes found a significantly higher risk associated with total meat consumption--especially consumption of processed meat, particularly poultry. But why? There's a whole list of potential culprits in meat: saturated fat, animal fat, trans fats naturally found in meat, cholesterol, or animal protein. It could be the heme iron found in meat, which can lead to free radicals and iron-induced oxidative stress that may lead to chronic inflammation and type 2 diabetes, or advanced glycation end (AGE) products, which promote oxidative stress and inflammation. Food analyses show that the highest levels of these so-called glycotoxins are found in meat--particularly roasted, fried, or broiled meat, though any foods from animal sources (and even high fat and protein plant foods such as nuts) exposed to high dry temperatures can be potent sources of these pro-oxidant chemicals.

In another study, researchers fed diabetics glycotoxin-packed foods, like chicken, fish, and eggs, and their inflammatory markers--tumor necrosis factor, C-reactive protein, and vascular adhesion molecules--shot up. "Thus, in diabetes, environmental (dietary) AGEs promote inflammatory mediators, leading to tissue injury." The good news is that restriction of these kinds of foods may suppress these inflammatory effects. Appropriate measures to limit AGE intake, such as eliminating meat or using only steaming and boiling as methods for cooking it, "may greatly reduce the already heavy burden of these toxins in the diabetic patient." These glycotoxins may be the missing link between the increased consumption of animal fat and meats and the development of type 2 diabetes.

Since the 2013 meta-analysis was published, another study came out in which approximately 17,000 people were followed for about a dozen years. Researchers found an 8% increased risk for every 50 grams of daily meat consumption. Just one quarter of a chicken breast's worth of meat for the entire day may significantly increase the risk of diabetes. Yes, we know there are many possible culprits: the glycotoxins or trans fat in meat, saturated fat, or the heme iron (which could actually promote the formation of carcinogens called nitrosamines, though they could also just be produced in the cooking process itself). However, we did learn something new: There also appears to be a greater incidence of diabetes among those who handle meat for a living. Maybe there are some diabetes-causing zoonotic infectious agents--such as viruses--present in fresh cuts of meat, including poultry.

A "crucial factor underlying the diabetes epidemic" may be the overstimulation of the aging enzyme TOR pathway by excess food consumption--but not by the consumption of just any food: Animal proteins not only stimulate the cancer-promoting hormone insulin growth factor-1 but also provide high amounts of leucine, which stimulates TOR activation and appears to contribute to the burning out of the insulin-producing beta cells in the pancreas, contributing to type 2 diabetes. So, it's not just the high fat and added sugars that are implicated; critical attention must be paid to the daily intake of animal proteins as well.

According to a study, "[i]n general, lower leucine levels are only reached by restriction of animal proteins." To reach the leucine intake provided by dairy or meat, we'd have to eat 9 pounds of cabbage or 100 apples to take an extreme example. That just exemplifies the extreme differences in leucine amounts provided by a more standard diet in comparison with a more plant-based diet.

I reviewed the role endocrine-disrupting industrial pollutants in the food supply may play in a three-part video series: Fish and Diabetes, Diabetes and Dioxins, and Pollutants in Salmon and Our Own Fat. Clearly, the standard America diet and lifestyle contribute to the epidemic of diabetes and obesity, but the contribution of these industrial pollutants can no longer be ignored. We now have experimental evidence that exposure to industrial toxins alone induces weight gain and insulin resistance, and, therefore, may be an underappreciated cause of obesity and diabetes. Consider what's happening to our infants: Obesity in a six-month-old is obviously not related to diet or lack of exercise. They're now exposed to hundreds of chemicals from their moms, straight through the umbilical cord, some of which may be obesogenic (that is, obesity-generating).

The millions of pounds of chemicals and heavy metals released every year into our environment should make us all stop and think about how we live and the choices we make every day in the foods we eat. A 2014 review of the evidence on pollutants and diabetes noted that we can be exposed through toxic spills, but "most of the human exposure nowadays is from the ingestion of contaminated food as a result of bioaccumulation up the food chain. The main source (around 95%) of [persistent pollutant] intake is through dietary intake of animal fats."


For more on the information mentioned here, see the following videos that take a closer look at these major topics:

AGEs: Glycotoxins, Avoiding a Sugary Grave, and Reducing Glycotoxin Intake to Prevent Alzheimer's.

TOR: Why Do We Age?, Caloric Restriction vs. Animal Protein Restriction, Prevent Cancer From Going on TOR, and Saving Lives By Treating Acne With Diet

Viruses: Infectobesity: Adenovirus 36 and Childhood Obesity

Poultry workers: Poultry Exposure and Neurological Disease, Poultry Exposure Tied to Liver and Pancreatic Cancer, and Eating Outside Our Kingdom

Industrial pollutants: Obesity-Causing Pollutants in Food, Fish and Diabetes, Diabetes and Dioxins, and Pollutants in Salmon and Our Own Fat

The link between meat and diabetes may also be due to a lack of sufficient protective components of plants in the diet, which is discussed in my videos How May Plants Protect Against Diabetes?, Plant-Based Diets for Diabetes, Plant-Based Diets and Diabetes, and 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:

Original Link

Foods to Avoid to Help Prevent Diabetes

Oct 24 Foods to Avoid copy.jpeg

We've known that being overweight and obese are important risk factors for type 2 diabetes, but, until recently, not much attention has been paid to the role of specific foods. I discuss this issue in my video, Why Is Meat a Risk Factor for Diabetes?

A 2013 meta-analysis of all the cohorts looking at the connection between meat and diabetes found a significantly higher risk associated with total meat consumption--especially consumption of processed meat, particularly poultry. But why? There's a whole list of potential culprits in meat: saturated fat, animal fat, trans fats naturally found in meat, cholesterol, or animal protein. It could be the heme iron found in meat, which can lead to free radicals and iron-induced oxidative stress that may lead to chronic inflammation and type 2 diabetes, or advanced glycation end (AGE) products, which promote oxidative stress and inflammation. Food analyses show that the highest levels of these so-called glycotoxins are found in meat--particularly roasted, fried, or broiled meat, though any foods from animal sources (and even high fat and protein plant foods such as nuts) exposed to high dry temperatures can be potent sources of these pro-oxidant chemicals.

In another study, researchers fed diabetics glycotoxin-packed foods, like chicken, fish, and eggs, and their inflammatory markers--tumor necrosis factor, C-reactive protein, and vascular adhesion molecules--shot up. "Thus, in diabetes, environmental (dietary) AGEs promote inflammatory mediators, leading to tissue injury." The good news is that restriction of these kinds of foods may suppress these inflammatory effects. Appropriate measures to limit AGE intake, such as eliminating meat or using only steaming and boiling as methods for cooking it, "may greatly reduce the already heavy burden of these toxins in the diabetic patient." These glycotoxins may be the missing link between the increased consumption of animal fat and meats and the development of type 2 diabetes.

Since the 2013 meta-analysis was published, another study came out in which approximately 17,000 people were followed for about a dozen years. Researchers found an 8% increased risk for every 50 grams of daily meat consumption. Just one quarter of a chicken breast's worth of meat for the entire day may significantly increase the risk of diabetes. Yes, we know there are many possible culprits: the glycotoxins or trans fat in meat, saturated fat, or the heme iron (which could actually promote the formation of carcinogens called nitrosamines, though they could also just be produced in the cooking process itself). However, we did learn something new: There also appears to be a greater incidence of diabetes among those who handle meat for a living. Maybe there are some diabetes-causing zoonotic infectious agents--such as viruses--present in fresh cuts of meat, including poultry.

A "crucial factor underlying the diabetes epidemic" may be the overstimulation of the aging enzyme TOR pathway by excess food consumption--but not by the consumption of just any food: Animal proteins not only stimulate the cancer-promoting hormone insulin growth factor-1 but also provide high amounts of leucine, which stimulates TOR activation and appears to contribute to the burning out of the insulin-producing beta cells in the pancreas, contributing to type 2 diabetes. So, it's not just the high fat and added sugars that are implicated; critical attention must be paid to the daily intake of animal proteins as well.

According to a study, "[i]n general, lower leucine levels are only reached by restriction of animal proteins." To reach the leucine intake provided by dairy or meat, we'd have to eat 9 pounds of cabbage or 100 apples to take an extreme example. That just exemplifies the extreme differences in leucine amounts provided by a more standard diet in comparison with a more plant-based diet.

I reviewed the role endocrine-disrupting industrial pollutants in the food supply may play in a three-part video series: Fish and Diabetes, Diabetes and Dioxins, and Pollutants in Salmon and Our Own Fat. Clearly, the standard America diet and lifestyle contribute to the epidemic of diabetes and obesity, but the contribution of these industrial pollutants can no longer be ignored. We now have experimental evidence that exposure to industrial toxins alone induces weight gain and insulin resistance, and, therefore, may be an underappreciated cause of obesity and diabetes. Consider what's happening to our infants: Obesity in a six-month-old is obviously not related to diet or lack of exercise. They're now exposed to hundreds of chemicals from their moms, straight through the umbilical cord, some of which may be obesogenic (that is, obesity-generating).

The millions of pounds of chemicals and heavy metals released every year into our environment should make us all stop and think about how we live and the choices we make every day in the foods we eat. A 2014 review of the evidence on pollutants and diabetes noted that we can be exposed through toxic spills, but "most of the human exposure nowadays is from the ingestion of contaminated food as a result of bioaccumulation up the food chain. The main source (around 95%) of [persistent pollutant] intake is through dietary intake of animal fats."


For more on the information mentioned here, see the following videos that take a closer look at these major topics:

AGEs: Glycotoxins, Avoiding a Sugary Grave, and Reducing Glycotoxin Intake to Prevent Alzheimer's.

TOR: Why Do We Age?, Caloric Restriction vs. Animal Protein Restriction, Prevent Cancer From Going on TOR, and Saving Lives By Treating Acne With Diet

Viruses: Infectobesity: Adenovirus 36 and Childhood Obesity

Poultry workers: Poultry Exposure and Neurological Disease, Poultry Exposure Tied to Liver and Pancreatic Cancer, and Eating Outside Our Kingdom

Industrial pollutants: Obesity-Causing Pollutants in Food, Fish and Diabetes, Diabetes and Dioxins, and Pollutants in Salmon and Our Own Fat

The link between meat and diabetes may also be due to a lack of sufficient protective components of plants in the diet, which is discussed in my videos How May Plants Protect Against Diabetes?, Plant-Based Diets for Diabetes, Plant-Based Diets and Diabetes, and 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:

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

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.

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Solving a Colon Cancer Mystery

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Colorectal cancer is the second leading cause of cancer death in the United States, after lung cancer. The rates of lung cancer around the world vary by a factor of 10. If there was nothing we could do to prevent lung cancer--if it just happened at random--we'd assume that the rates everywhere would be about the same. But since there's such a huge variation in rates, it seems like there's probably some external cause. Indeed, we now know smoking is responsible for 90% of lung cancer cases. If we don't want to die of the number-one cancer killer, we can throw 90% of our risk out the window just by not smoking.

There's an even bigger variation around the world for colon cancer. As discussed in Solving a Colon Cancer Mystery, it appears colon cancer doesn't just happen, something makes it happen. If our lungs can get filled with carcinogens from smoke, maybe our colons are getting filled with carcinogens from food. Researchers from the University of Pittsburgh and the University of Limpopo sought to answer the question, "Why do African Americans get more colon cancer than native Africans?" Why study Africans? Because colon cancer is extremely rare in native African populations, more than 50 times lower than rates of Americans, white or black.

It's the fiber, right? The first to describe the low rates of colon cancer in native Africans, Dr. Denis Burkitt ascribed it to their staple diet traditionally high in whole grains and, consequently, high in fiber content. We seem to get a 10% reduction in risk for every 10 grams of fiber we eat a day. If it's a 1% drop for each gram, and native Africans are eating upwards of 100 grams a day, it could explain why colon cancer is so rare in sub-Saharan Africa.

Wait a second. The modern African diet is highly processed and low in fiber, yet there has been no dramatic increase in colon cancer incidence. Their diet today has such a low fiber content because most populations now depend on commercially produced refined cornmeal. We're not just talking low fiber intake, we're talking United States of America low, down around half the recommended daily allowance. Yet colon disease in Africa is still about 50 times less common than in the United States.

Maybe it's because native Africans are thinner and exercise more? No, they're not, and no, they don't. If anything, their physical activity levels may now be even lower than Americans'. So if they're sedentary like us and eating mostly refined carbs, few whole plant foods, and little fiber like us, why do they have 50 times less colon cancer than we do? There is one difference. The diet of both African Americans and Caucasian Americans is rich in meat, whereas the native Africans' diet is so low in meat and saturated fat they have total cholesterol levels averaging 139 mg/dL, compared to over 200 mg/dL in the United States.

They may not get a lot of fiber anymore, but they continue to minimize meat and animal fat consumption, which supports other evidence indicating the most powerful determinants of colon cancer risk may be meat and animal fat intake levels. So why do Americans get more colon cancer than Africans? Maybe the rarity of colon cancer in Africans is not the fiber, but their low animal product consumption.

Although opinions diverge as to whether cholesterol, animal fat, or animal protein is most responsible for the increased colon cancer risk, given that all three have been proven to have carcinogenic properties, it may not really matter which component is worse, as a diet laden in one is usually laden in the others.

I've previously suggested phytates may play a critical role as well (Phytates for the Prevention of Cancer). Resistant starch may be another player. Since native Africans cool down their corn porridge, some of the starch can crystallize and effectively turn into fiber. (This is the same reason pasta salad and potato salad better feed our gut bacteria than starchy dishes served hot.) I touch on it briefly in Bowel Wars: Hydrogen Sulfide vs. Butyrate. Resistant starch may also help explain Beans and the Second Meal Effect. And for even more, see Resistant Starch & Colon Cancer and Getting Starch to Take the Path of Most Resistance.

Fiber may just be a marker for healthier eating since it's only found concentrated in unprocessed plant foods. So the apparent protection afforded by high fiber diets may derive from whole food plant-based nutrition rather than the fiber itself (so fiber supplements would not be expected to provide the same protection). Here are some videos that found protective associations with higher fiber diets:

What might be in animal products that can raise cancer risk? Here's a smattering:

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: Department of Foreign Affairs and Trade / Flickr. This image has been modified.

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