What a Single Fatty Meal Can Do to Our Arteries

Oct12 Fatty Meal copy.jpeg

The phenomenon of postprandial angina was described more than 200 years ago: chest pain that occurs after a meal, even if you're just sitting down and resting. This could be intuitively attributed to redistribution of blood flow away from the heart to the gut during digestion. However, such a mechanism could not be demonstrated experimentally.

The problem appears to be within the coronary arteries themselves. The clue came in 1955 when researchers found they could induce angina in people with heart disease just by having them drink fat. My video Fatty Meals May Impair Artery Function includes a fascinating graph of so-called lactescence, or milkiness, over time. It shows how their blood became increasingly milky with fat over the next five hours, and each of the ten attacks of angina was found to occur about four-and-a-half to five hours after the fatty meal, right when blood milkiness was at or near its peak. After a nonfat meal with the same bulk and calories, but made out of starch, sugar, and protein, no anginal pain was elicited in any of the patients.

To understand how the mere presence of fat in the blood can affect blood flow to the heart, we need to understand the endothelium, the inner lining of all of our blood vessels. Our arteries are not just rigid pipes; they are living, breathing organs that actively dilate or constrict, thinning or thickening the blood and releasing hormones, depending on what's needed. This is all controlled by the single inner layer, the endothelium, which makes it the body's largest endocrine (hormone-secreting) organ. When it's all gathered up, the endothelium weighs a total of three pounds and has a combined surface area of 700 square yards.

We used to think the endothelium was just an inert layer lining our vascular tree, but now we know better:

Researchers found that low-fat meals tend to improve endothelial function, whereas high-fat meals tend to worsen it. This goes for animal fat, as well as isolated plant fats, such as sunflower oil. But, maybe it's just the digestion of fat rather than the fat itself? Our body can detect the presence of fat in the digestive tract and release a special group of hormones and enzymes. Researchers tried feeding people fake fat and found that the real fat deprived the heart of blood while the fake fat didn't. Is our body really smart enough to tell the difference?

A follow-up study settled the issue. Researchers tried infusing fat directly into people's bloodstream through an IV to sneak it past your mouth and brain. Within hours, their arteries stiffened, significantly crippling their ability to relax and dilate normally. So it was the fat after all! This decrease in the ability to vasodilate coronary arteries after a fatty meal, just when you need it, could explain the phenomenon of after-meal angina in patients with known coronary artery disease.


This effect could certainly help explain the findings in Low Carb Diets and Coronary Blood Flow. My video Olive Oil and Artery Function addresses less refined fats like extra virgin olive oil,.

For more on angina, see the beginning of my 2014 annual talk--From Table to Able: Combating Disabling Diseases with Food--and How Not to Die from Heart Disease.

Another consequence of endothelial dysfunction is lack of blood flow to other organs. Check out Survival of the Firmest: Erectile Dysfunction and Death and Atkins Diet: Trouble Keeping It Up.

Fat in the bloodstream can also impair our ability to control blood sugar levels. Learn more with What Causes Insulin Resistance?, The Spillover Effect Links Obesity to Diabetes, and Lipotoxicity: How Saturated Fat Raises Blood Sugar.

Finally, for more on how diet affects our arteries, check out Tea and Artery Function, Vinegar and Artery Function, and Plant-Based Diets and Artery Function.

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

What a Single Fatty Meal Can Do to Our Arteries

Oct12 Fatty Meal copy.jpeg

The phenomenon of postprandial angina was described more than 200 years ago: chest pain that occurs after a meal, even if you're just sitting down and resting. This could be intuitively attributed to redistribution of blood flow away from the heart to the gut during digestion. However, such a mechanism could not be demonstrated experimentally.

The problem appears to be within the coronary arteries themselves. The clue came in 1955 when researchers found they could induce angina in people with heart disease just by having them drink fat. My video Fatty Meals May Impair Artery Function includes a fascinating graph of so-called lactescence, or milkiness, over time. It shows how their blood became increasingly milky with fat over the next five hours, and each of the ten attacks of angina was found to occur about four-and-a-half to five hours after the fatty meal, right when blood milkiness was at or near its peak. After a nonfat meal with the same bulk and calories, but made out of starch, sugar, and protein, no anginal pain was elicited in any of the patients.

To understand how the mere presence of fat in the blood can affect blood flow to the heart, we need to understand the endothelium, the inner lining of all of our blood vessels. Our arteries are not just rigid pipes; they are living, breathing organs that actively dilate or constrict, thinning or thickening the blood and releasing hormones, depending on what's needed. This is all controlled by the single inner layer, the endothelium, which makes it the body's largest endocrine (hormone-secreting) organ. When it's all gathered up, the endothelium weighs a total of three pounds and has a combined surface area of 700 square yards.

We used to think the endothelium was just an inert layer lining our vascular tree, but now we know better:

Researchers found that low-fat meals tend to improve endothelial function, whereas high-fat meals tend to worsen it. This goes for animal fat, as well as isolated plant fats, such as sunflower oil. But, maybe it's just the digestion of fat rather than the fat itself? Our body can detect the presence of fat in the digestive tract and release a special group of hormones and enzymes. Researchers tried feeding people fake fat and found that the real fat deprived the heart of blood while the fake fat didn't. Is our body really smart enough to tell the difference?

A follow-up study settled the issue. Researchers tried infusing fat directly into people's bloodstream through an IV to sneak it past your mouth and brain. Within hours, their arteries stiffened, significantly crippling their ability to relax and dilate normally. So it was the fat after all! This decrease in the ability to vasodilate coronary arteries after a fatty meal, just when you need it, could explain the phenomenon of after-meal angina in patients with known coronary artery disease.


This effect could certainly help explain the findings in Low Carb Diets and Coronary Blood Flow. My video Olive Oil and Artery Function addresses less refined fats like extra virgin olive oil,.

For more on angina, see the beginning of my 2014 annual talk--From Table to Able: Combating Disabling Diseases with Food--and How Not to Die from Heart Disease.

Another consequence of endothelial dysfunction is lack of blood flow to other organs. Check out Survival of the Firmest: Erectile Dysfunction and Death and Atkins Diet: Trouble Keeping It Up.

Fat in the bloodstream can also impair our ability to control blood sugar levels. Learn more with What Causes Insulin Resistance?, The Spillover Effect Links Obesity to Diabetes, and Lipotoxicity: How Saturated Fat Raises Blood Sugar.

Finally, for more on how diet affects our arteries, check out Tea and Artery Function, Vinegar and Artery Function, and Plant-Based Diets and Artery Function.

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

Fish Consumption and Suicide

Sept 12 Fish Consumption copy.jpeg

Depression is a serious and common mental disorder responsible for the majority of suicides. As I've covered in Antioxidants & Depression, intake of fruits, vegetables, and naturally occurring antioxidants have been found to be protectively associated with depression. Therefore, researchers have considered that "it may be possible to prevent depression or to lessen its negative effects through dietary intervention."

But not so fast. Cross-sectional studies are snapshots in time, so we don't know "whether a poor dietary pattern precedes the development of depression or if depression causes poor dietary intake." Depression and even treatments for depression can affect appetite and dietary intake. Maybe people who feel crappier just eat crappier, instead of the other way around.

What we need is a prospective study (a study performed over time) where we start out with people who are not depressed and follow them for several years. In 2012, we got just such a study, which ran over six years. As you'll see in my video Fish Consumption and Suicide, those with higher carotenoid levels in their bloodstream, which is considered a good indicator of fruit and vegetable intake, had a 28% lower risk of becoming depressed within that time. The researchers conclude that having low blood levels of those healthy phytonutrients may predict the development of new depressive symptoms. What about suicide?

Worldwide, a million people kill themselves every year. Of all European countries, Greece appears to have the lowest rates of suicide. It may be the balmy weather, but it may also have something to do with their diet. Ten thousand people were followed for years, and those following a more Mediterranean diet pattern were less likely to be diagnosed with depression. What was it about the diet that was protective? It wasn't the red wine or fish; it was the fruit, nuts, beans, and effectively higher plant to animal fat ratio that appeared protective. Conversely, significant adverse trends were observed for dairy and meat consumption.

A similar protective dietary pattern was found in Japan. A high intake of vegetables, fruits, mushrooms, and soy products was associated with a decreased prevalence of depressive symptoms. The healthy dietary pattern was not characterized by a high intake of seafood. Similar results were found in a study of 100,000 Japanese men and women followed for up to 10 years. There was no evidence of a protective role of higher fish consumption or the long-chain omega 3s EPA and DHA against suicide. In fact, they found a significantly increased risk of suicide among male nondrinkers with high seafood omega 3 intake. This may have been by chance, but a similar result was found in the Mediterranean. High baseline fish consumption with an increase in consumption were associated with an increased risk of mental disorders.

One possible explanation could be the mercury content of fish. Could an accumulation of mercury compounds in the body increase the risk of depression? We know that mercury in fish can cause neurological damage, associated with increased risk of Alzheimer's disease, memory loss, and autism, but also depression. Therefore, "the increased risk of suicide among persons with a high fish intake might also be attributable to the harmful effects of mercury in fish."

Large Harvard University cohort studies found similar results. Hundreds of thousands were followed for up to 20 years, and no evidence was found that taking fish oil or eating fish lowered risk of suicide. There was even a trend towards higher suicide mortality.

What about fish consumption for the treatment of depression? When we put together all the trials done to date, neither the EPA nor DHA long-chain omega-3s appears more effective than sugar pills. We used to think omega-3 supplementation was useful, but several recent studies have tipped the balance the other way. It seems that "[n]early all of the treatment efficacy observed in the published literature may be attributable to publication bias," meaning the trials that showed no benefit tended not to get published at all. So, all doctors saw were a bunch of positive studies, but only because a bunch of the negative ones were buried.

This reminds me of my Is Fish Oil Just Snake Oil? video. Just like we thought omega-3 supplementation could help with mood, we also thought it could help with heart health, but the balance of evidence has decidedly shifted. I still recommend the consumption of pollutant-free sources of preformed long-chain omega 3s for cognitive health and explain my rationale in Should We Take DHA Supplements to Boost Brain Function? and Should Vegans Take DHA to Preserve Brain Function?


For more on the neurotoxic nature of mercury-contaminated seafood, see:

What can we do to help our mood? See:

What about antidepressant drugs? Sometimes they can be absolutely life-saving, but other times they may actually do more harm than good. See my controversial video Do Antidepressant Drugs Really Work?.

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

Fish Consumption and Suicide

Sept 12 Fish Consumption copy.jpeg

Depression is a serious and common mental disorder responsible for the majority of suicides. As I've covered in Antioxidants & Depression, intake of fruits, vegetables, and naturally occurring antioxidants have been found to be protectively associated with depression. Therefore, researchers have considered that "it may be possible to prevent depression or to lessen its negative effects through dietary intervention."

But not so fast. Cross-sectional studies are snapshots in time, so we don't know "whether a poor dietary pattern precedes the development of depression or if depression causes poor dietary intake." Depression and even treatments for depression can affect appetite and dietary intake. Maybe people who feel crappier just eat crappier, instead of the other way around.

What we need is a prospective study (a study performed over time) where we start out with people who are not depressed and follow them for several years. In 2012, we got just such a study, which ran over six years. As you'll see in my video Fish Consumption and Suicide, those with higher carotenoid levels in their bloodstream, which is considered a good indicator of fruit and vegetable intake, had a 28% lower risk of becoming depressed within that time. The researchers conclude that having low blood levels of those healthy phytonutrients may predict the development of new depressive symptoms. What about suicide?

Worldwide, a million people kill themselves every year. Of all European countries, Greece appears to have the lowest rates of suicide. It may be the balmy weather, but it may also have something to do with their diet. Ten thousand people were followed for years, and those following a more Mediterranean diet pattern were less likely to be diagnosed with depression. What was it about the diet that was protective? It wasn't the red wine or fish; it was the fruit, nuts, beans, and effectively higher plant to animal fat ratio that appeared protective. Conversely, significant adverse trends were observed for dairy and meat consumption.

A similar protective dietary pattern was found in Japan. A high intake of vegetables, fruits, mushrooms, and soy products was associated with a decreased prevalence of depressive symptoms. The healthy dietary pattern was not characterized by a high intake of seafood. Similar results were found in a study of 100,000 Japanese men and women followed for up to 10 years. There was no evidence of a protective role of higher fish consumption or the long-chain omega 3s EPA and DHA against suicide. In fact, they found a significantly increased risk of suicide among male nondrinkers with high seafood omega 3 intake. This may have been by chance, but a similar result was found in the Mediterranean. High baseline fish consumption with an increase in consumption were associated with an increased risk of mental disorders.

One possible explanation could be the mercury content of fish. Could an accumulation of mercury compounds in the body increase the risk of depression? We know that mercury in fish can cause neurological damage, associated with increased risk of Alzheimer's disease, memory loss, and autism, but also depression. Therefore, "the increased risk of suicide among persons with a high fish intake might also be attributable to the harmful effects of mercury in fish."

Large Harvard University cohort studies found similar results. Hundreds of thousands were followed for up to 20 years, and no evidence was found that taking fish oil or eating fish lowered risk of suicide. There was even a trend towards higher suicide mortality.

What about fish consumption for the treatment of depression? When we put together all the trials done to date, neither the EPA nor DHA long-chain omega-3s appears more effective than sugar pills. We used to think omega-3 supplementation was useful, but several recent studies have tipped the balance the other way. It seems that "[n]early all of the treatment efficacy observed in the published literature may be attributable to publication bias," meaning the trials that showed no benefit tended not to get published at all. So, all doctors saw were a bunch of positive studies, but only because a bunch of the negative ones were buried.

This reminds me of my Is Fish Oil Just Snake Oil? video. Just like we thought omega-3 supplementation could help with mood, we also thought it could help with heart health, but the balance of evidence has decidedly shifted. I still recommend the consumption of pollutant-free sources of preformed long-chain omega 3s for cognitive health and explain my rationale in Should We Take DHA Supplements to Boost Brain Function? and Should Vegans Take DHA to Preserve Brain Function?


For more on the neurotoxic nature of mercury-contaminated seafood, see:

What can we do to help our mood? See:

What about antidepressant drugs? Sometimes they can be absolutely life-saving, but other times they may actually do more harm than good. See my controversial video Do Antidepressant Drugs Really Work?.

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

Fish Consumption and Suicide

Sept 12 Fish Consumption copy.jpeg

Depression is a serious and common mental disorder responsible for the majority of suicides. As I've covered in Antioxidants & Depression, intake of fruits, vegetables, and naturally occurring antioxidants have been found to be protectively associated with depression. Therefore, researchers have considered that "it may be possible to prevent depression or to lessen its negative effects through dietary intervention."

But not so fast. Cross-sectional studies are snapshots in time, so we don't know "whether a poor dietary pattern precedes the development of depression or if depression causes poor dietary intake." Depression and even treatments for depression can affect appetite and dietary intake. Maybe people who feel crappier just eat crappier, instead of the other way around.

What we need is a prospective study (a study performed over time) where we start out with people who are not depressed and follow them for several years. In 2012, we got just such a study, which ran over six years. As you'll see in my video Fish Consumption and Suicide, those with higher carotenoid levels in their bloodstream, which is considered a good indicator of fruit and vegetable intake, had a 28% lower risk of becoming depressed within that time. The researchers conclude that having low blood levels of those healthy phytonutrients may predict the development of new depressive symptoms. What about suicide?

Worldwide, a million people kill themselves every year. Of all European countries, Greece appears to have the lowest rates of suicide. It may be the balmy weather, but it may also have something to do with their diet. Ten thousand people were followed for years, and those following a more Mediterranean diet pattern were less likely to be diagnosed with depression. What was it about the diet that was protective? It wasn't the red wine or fish; it was the fruit, nuts, beans, and effectively higher plant to animal fat ratio that appeared protective. Conversely, significant adverse trends were observed for dairy and meat consumption.

A similar protective dietary pattern was found in Japan. A high intake of vegetables, fruits, mushrooms, and soy products was associated with a decreased prevalence of depressive symptoms. The healthy dietary pattern was not characterized by a high intake of seafood. Similar results were found in a study of 100,000 Japanese men and women followed for up to 10 years. There was no evidence of a protective role of higher fish consumption or the long-chain omega 3s EPA and DHA against suicide. In fact, they found a significantly increased risk of suicide among male nondrinkers with high seafood omega 3 intake. This may have been by chance, but a similar result was found in the Mediterranean. High baseline fish consumption with an increase in consumption were associated with an increased risk of mental disorders.

One possible explanation could be the mercury content of fish. Could an accumulation of mercury compounds in the body increase the risk of depression? We know that mercury in fish can cause neurological damage, associated with increased risk of Alzheimer's disease, memory loss, and autism, but also depression. Therefore, "the increased risk of suicide among persons with a high fish intake might also be attributable to the harmful effects of mercury in fish."

Large Harvard University cohort studies found similar results. Hundreds of thousands were followed for up to 20 years, and no evidence was found that taking fish oil or eating fish lowered risk of suicide. There was even a trend towards higher suicide mortality.

What about fish consumption for the treatment of depression? When we put together all the trials done to date, neither the EPA nor DHA long-chain omega-3s appears more effective than sugar pills. We used to think omega-3 supplementation was useful, but several recent studies have tipped the balance the other way. It seems that "[n]early all of the treatment efficacy observed in the published literature may be attributable to publication bias," meaning the trials that showed no benefit tended not to get published at all. So, all doctors saw were a bunch of positive studies, but only because a bunch of the negative ones were buried.

This reminds me of my Is Fish Oil Just Snake Oil? video. Just like we thought omega-3 supplementation could help with mood, we also thought it could help with heart health, but the balance of evidence has decidedly shifted. I still recommend the consumption of pollutant-free sources of preformed long-chain omega 3s for cognitive health and explain my rationale in Should We Take DHA Supplements to Boost Brain Function? and Should Vegans Take DHA to Preserve Brain Function?


For more on the neurotoxic nature of mercury-contaminated seafood, see:

What can we do to help our mood? See:

What about antidepressant drugs? Sometimes they can be absolutely life-saving, but other times they may actually do more harm than good. See my controversial video Do Antidepressant Drugs Really Work?.

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

Comparing Pollutant Levels Between Different Diets

Comparing Pollutant Levels Between Different Diets.jpeg

The results of the CHAMACOS (Center for the Health Assessment of Mothers and Children of Salinas) study were published recently. This study of a California birth cohort investigated the relationship between exposure to flame retardant chemical pollutants in pregnancy and childhood, and subsequent neurobehavioral development. Why California? Because California children's exposures to these endocrine disruptors and neurotoxins are among the highest in the world.

What did they find? The researchers concluded that both prenatal and childhood exposures to these chemicals "were associated with poorer attention, fine motor coordination, and cognition" (particularly verbal comprehension) by the time the children reached school age. "This study, the largest to date, contributes to growing evidence suggesting that PBDEs [polybrominated diphenyl ethers, flame retardant chemicals] have adverse impacts on child neurobehavioral development." The effects may extend into adolescence, again affecting motor function as well as thyroid gland function. The effect on our thyroid glands may even extend into adulthood.

These chemicals get into moms, then into the amniotic fluid, and then into the breast milk. The more that's in the milk, the worse the infants' mental development may be. Breast milk is still best, but how did these women get exposed in the first place?

The question has been: Are we exposed mostly from diet or dust? Researchers in Boston collected breast milk samples from 46 first-time moms, vacuumed up samples of dust from their homes, and questioned them about their diets. The researchers found that both were likely to blame. Diet-wise, a number of animal products were implicated. This is consistent with what's been found worldwide. For example, in Europe, these flame retardant chemical pollutants are found mostly in meat, including fish, and other animal products. It's similar to what we see with dioxins--they are mostly found in fish and other fatty foods, with a plant-based diet offering the lowest exposure.

If that's the case, do vegetarians have lower levels of flame retardant chemical pollutants circulating in their bloodstreams? Yes. Vegetarians may have about 25% lower levels. Poultry appears to be the largest contributor of PBDEs. USDA researchers compared the levels in different meats, and the highest levels of these pollutants were found in chicken and turkey, with less in pork and even less in beef. California poultry had the highest, consistent with strict furniture flammability codes. But it's not like chickens are pecking at the sofa. Chickens and turkeys may be exposed indirectly through the application of sewer sludge to fields where feed crops are raised, contamination of water supplies, the use of flame-retarded materials in poultry housing, or the inadvertent incorporation of fire-retardant material into the birds' bedding or feed ingredients.

Fish have been shown to have the highest levels overall, but Americans don't eat a lot of fish so they don't contribute as much to the total body burden in the United States. Researchers have compared the level of PBDEs found in meat-eaters and vegetarians. The amount found in the bloodstream of vegetarians is noticeably lower, as you can see in my video Flame Retardant Pollutants and Child Development. Just to give you a sense of the contribution of chicken, higher than average poultry eaters have higher levels than omnivores as a whole, and lower than average poultry eaters have levels lower than omnivores.

What are the PBDE levels in vegans? We know the intake of many other classes of pollutants is almost exclusively from the ingestion of animal fats in the diet. What if we take them all out of the diet? It works for dioxins. Vegan dioxin levels appear markedly lower than the general population. What about for the flame retardant chemicals? Vegans have levels lower than vegetarians, with those who've been vegan around 20 years having even lower concentrations. This tendency for chemical levels to decline the longer one eats plant-based suggests that food of animal origin contributes substantially. But note that levels never get down to zero, so diet is not the only source.

The USDA researchers note that there are currently no regulatory limits on the amount of flame retardant chemical contamination in U.S. foods, "but reducing the levels of unnecessary, persistent, toxic compounds in our diet is certainly desirable."

I've previously talked about this class of chemicals in Food Sources of Flame Retardant Chemicals. The same foods seem to accumulate a variety of pollutants:

Many of these chemicals have hormone- or endocrine-disrupting effects. See, for example:

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: Mitchell Haindfield / Flickr. This image has been modified.

Original Link

Comparing Pollutant Levels Between Different Diets

Comparing Pollutant Levels Between Different Diets.jpeg

The results of the CHAMACOS (Center for the Health Assessment of Mothers and Children of Salinas) study were published recently. This study of a California birth cohort investigated the relationship between exposure to flame retardant chemical pollutants in pregnancy and childhood, and subsequent neurobehavioral development. Why California? Because California children's exposures to these endocrine disruptors and neurotoxins are among the highest in the world.

What did they find? The researchers concluded that both prenatal and childhood exposures to these chemicals "were associated with poorer attention, fine motor coordination, and cognition" (particularly verbal comprehension) by the time the children reached school age. "This study, the largest to date, contributes to growing evidence suggesting that PBDEs [polybrominated diphenyl ethers, flame retardant chemicals] have adverse impacts on child neurobehavioral development." The effects may extend into adolescence, again affecting motor function as well as thyroid gland function. The effect on our thyroid glands may even extend into adulthood.

These chemicals get into moms, then into the amniotic fluid, and then into the breast milk. The more that's in the milk, the worse the infants' mental development may be. Breast milk is still best, but how did these women get exposed in the first place?

The question has been: Are we exposed mostly from diet or dust? Researchers in Boston collected breast milk samples from 46 first-time moms, vacuumed up samples of dust from their homes, and questioned them about their diets. The researchers found that both were likely to blame. Diet-wise, a number of animal products were implicated. This is consistent with what's been found worldwide. For example, in Europe, these flame retardant chemical pollutants are found mostly in meat, including fish, and other animal products. It's similar to what we see with dioxins--they are mostly found in fish and other fatty foods, with a plant-based diet offering the lowest exposure.

If that's the case, do vegetarians have lower levels of flame retardant chemical pollutants circulating in their bloodstreams? Yes. Vegetarians may have about 25% lower levels. Poultry appears to be the largest contributor of PBDEs. USDA researchers compared the levels in different meats, and the highest levels of these pollutants were found in chicken and turkey, with less in pork and even less in beef. California poultry had the highest, consistent with strict furniture flammability codes. But it's not like chickens are pecking at the sofa. Chickens and turkeys may be exposed indirectly through the application of sewer sludge to fields where feed crops are raised, contamination of water supplies, the use of flame-retarded materials in poultry housing, or the inadvertent incorporation of fire-retardant material into the birds' bedding or feed ingredients.

Fish have been shown to have the highest levels overall, but Americans don't eat a lot of fish so they don't contribute as much to the total body burden in the United States. Researchers have compared the level of PBDEs found in meat-eaters and vegetarians. The amount found in the bloodstream of vegetarians is noticeably lower, as you can see in my video Flame Retardant Pollutants and Child Development. Just to give you a sense of the contribution of chicken, higher than average poultry eaters have higher levels than omnivores as a whole, and lower than average poultry eaters have levels lower than omnivores.

What are the PBDE levels in vegans? We know the intake of many other classes of pollutants is almost exclusively from the ingestion of animal fats in the diet. What if we take them all out of the diet? It works for dioxins. Vegan dioxin levels appear markedly lower than the general population. What about for the flame retardant chemicals? Vegans have levels lower than vegetarians, with those who've been vegan around 20 years having even lower concentrations. This tendency for chemical levels to decline the longer one eats plant-based suggests that food of animal origin contributes substantially. But note that levels never get down to zero, so diet is not the only source.

The USDA researchers note that there are currently no regulatory limits on the amount of flame retardant chemical contamination in U.S. foods, "but reducing the levels of unnecessary, persistent, toxic compounds in our diet is certainly desirable."

I've previously talked about this class of chemicals in Food Sources of Flame Retardant Chemicals. The same foods seem to accumulate a variety of pollutants:

Many of these chemicals have hormone- or endocrine-disrupting effects. See, for example:

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: Mitchell Haindfield / 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.

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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

Big Sugar Takes on the World Health Organization

Big Sugar Takes on the World Health Organization.jpeg

The World Health Organization (WHO) recommends we reduce our consumption of salt, trans fats, saturated fats, and added sugars. Why? Because consumption of such foods is the cause of at least 14 million deaths every year from chronic diseases.

"Several decades ago, it was heresy to talk about an impending global pandemic of obesity." Today, we're seeing chronic disease rates skyrocket around the world. The Western diet has been exported to the far reaches of the planet, with white flour, sugar, fat, and animal-based foods replacing beans, peas, lentils, other vegetables, and whole grains.

In order to understand the reasons underlying this trend toward greater consumption of animal products, sugar, and oils, and reduced consumption of whole plant foods, we need to begin by understanding the purposeful economic manipulations that have occurred since World War II relating to agricultural policies around the world. For example, since early in the last century, the U.S. government "has supported food production through subsidies and other policies, resulting in large surpluses of food commodities, meat, and calories. In this artificial market, large food producers and corporations-Big Agriculture and Big Food-became very profitable." Their profitability may be part of the problem.

Dr. Margaret Chan, the Director-General of the World Health Organization, gave the opening address at the 8th Global Conference on Health Promotion. One of the biggest challenges facing health promotion worldwide, she said, is that the efforts to prevent our top killers "go against the business interests of powerful economic operators." It is not just Big Tobacco anymore. "Public health must also contend with Big Food, Big Soda, and Big Alcohol. All of these industries fear regulation and protect themselves by using the same tactics...front groups, lobbies, promises of self-regulation, lawsuits, and industry-funded research that confuses the evidence and keeps the public in doubt."

And the World Health Organization should know. In 2003, the organization released a draft report that outlined a global strategy to address issues of diet. Although many of the WHO's recommendations were rather tame, a remarkable series of events was spurred by six words in the report: "limit the intake of 'free' sugars" (added sugar). Within days, the sugar industry, through the Sugar Association, enlisted the support of officials high in the U.S. government and led a vigorous attack on both the report and the World Health Organization itself, culminating in a threat to get Congress to withdraw U.S. funding to the WHO. The WHO, the organization that "deals with AIDS, malnutrition, infectious disease, bioterrorism, and more, threatened because of its stance on sugar." At the same time, the U.S. went to bat for American tobacco companies and led the charge against the World Health Organization's Framework Convention on Tobacco Control.

As discussed in my video, Big Sugar Takes on the World Health Organization, the threat from the sugar industry was described by WHO insiders as worse than any pressure they ever got from the tobacco lobby. As revealed in an internal memo, the U.S. government apparently had a list of demands. These included deletion of all references to the science that WHO experts had compiled on the matter and the removal of all references to fat, oils, sugar, and salt.

The threats failed to make the WHO withdraw their report. Entitled "Diet, Nutrition and the Prevention of Chronic Disease," it "concluded that a diet low in saturated fat, sugar and salt and high in fruit and vegetables was required to tackle the epidemic rise in chronic diseases worldwide." They did end up watering it down, though. Gone was reference to the comprehensive scientific report, and gone was its call for its recommendations to be actually translated into national guidelines.

History has since repeated. At the last high-level United Nations meeting to address chronic diseases, representatives from some Western countries, including the United States, helped block a consensus on action after lobbying from the alcohol, food, tobacco, and drug industries. When asked why Michelle Obama's successful childhood obesity programs in the U.S. should not be modeled around the world, a U.S. official responded that they might harm American exports.

See also: How Much Added Sugar Is Too Much?

If sugar is bad, then what about all the sugar in fruit? See If Fructose Is Bad, What About Fruit? and How Much Fruit Is Too Much?.

For more on the corrupting political and economic influences in nutrition, see videos such as:

And because of that, check out a couple of my introductory videos: Why You Should Care about Nutrition and Taking Personal Responsibility for Your Health.

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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