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

Brown Fat: Losing Weight Through Thermogenesis

Sept 21 Brown Fat Thermo copy.jpeg

During World War I, it was discovered that many of the chemicals for new explosives had toxic or even lethal effects on the workers in the munitions factories. Chemicals such as di-nitro-phenol (DNP) can boost metabolism so much that workers were too often found wandering along the road after work, covered in sweat with temperatures of 106 to 109 degrees Fahrenheit before they died. Even after death, their temperatures kept going up, as if they were having a total body meltdown. At subacute doses, however, workers claimed to have grown thin to a notable extent after several months working with the chemical.

That got some Stanford pharmacologists excited about the "promising metabolic applications" of DNP. Our resting metabolic rate jumps up 30% after one dose of DNP, and therefore, it becomes an actual fat-burning drug. People started losing weight, as you can see in my video Brown Fat: Losing Weight Through Thermogenesis, with no apparent side effects. They felt great... and then thousands of people started going blind and users started dropping dead from hyperpyrexia, fatal fever due to the heat created by the burning fat. Of course, it continued to be sold. Ad copy read:

"Here, at last, is a [weight] reducing remedy that will bring you a figure men admire and women envy, without danger to your health or change in your regular mode of living....No diet, no exercise!"

It did work, but the therapeutic index--the difference between the effective dose and the deadly dose--was razor thin. It was not until thousands suffered irreversible harm that it got pulled from the market and remained unavailable. Unavailable, that is, until it was brought back by the internet for those dying to be thin.

There is, however, a way our body naturally burns fat to create heat. When we're born, we go from a nice tropical 98.6 in our mother's womb straight to room temperature, just when we're still all wet and slimy. As an adaptive mechanism to maintain warmth, the appearance of a unique organ around 150 million years ago allowed mammals to maintain our high body temperatures.

That unique organ is called brown adipose tissue, or BAT, and its role is to consume fat calories by generating heat in response to cold exposure. The white fat in our bellies stores fat, but the brown fat, located up between our shoulder blades, burns fat. BAT is essential for thermogenesis, the creation of heat in newborns, but has been considered unnecessary in adults who have higher metabolic rates and increased muscle mass for shivering to warm us up when we get chilled. We used to think brown tissue just shrank away when we grew up, but, if it was there, then it could potentially make a big difference for how many calories we burn every day.

When PET scans were invented to detect metabolically active tissues like cancer, oncologists kept finding hot spots in the neck and shoulder regions that on CT scans turned out not to be cancer, just fat. Then, some observant radiologists noticed they appeared in patients mostly during the cold winter months. When they looked closer at tissue samples taken from people who had undergone neck surgery, they found it: brown fat in adults.

The common message from a number of studies is that BAT is present and active in adults, and the more we have and the more active it is, the thinner we are. And we can rapidly activate our fat-burning brown fat by exposure to cold temperatures. For example, if you hang out in a cold room for two hours in your undies and put your legs on a block of ice for four minutes every five minutes, you can elicit a marked increase in energy expenditure, thanks to brown fat activation. So, the studies point to a potential "natural" intervention to stimulate energy expenditure: Turn down the heat to burn calories (and reduce the carbon footprint in the process).

Thankfully, for those of us who would rather not lay our bare legs on blocks of ice, our brown fat can also be activated by some food ingredients such as those that are covered in my Boosting Brown Fat Through Diet video.


I briefly touch on the role cold temperatures can play in weight loss in The Ice Diet and talk more about calories in (Nutrient-Dense Approach to Weight Management) and calories out (How Much Exercise to Sustain Weight Loss).

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

Brown Fat: Losing Weight Through Thermogenesis

Sept 21 Brown Fat Thermo copy.jpeg

During World War I, it was discovered that many of the chemicals for new explosives had toxic or even lethal effects on the workers in the munitions factories. Chemicals such as di-nitro-phenol (DNP) can boost metabolism so much that workers were too often found wandering along the road after work, covered in sweat with temperatures of 106 to 109 degrees Fahrenheit before they died. Even after death, their temperatures kept going up, as if they were having a total body meltdown. At subacute doses, however, workers claimed to have grown thin to a notable extent after several months working with the chemical.

That got some Stanford pharmacologists excited about the "promising metabolic applications" of DNP. Our resting metabolic rate jumps up 30% after one dose of DNP, and therefore, it becomes an actual fat-burning drug. People started losing weight, as you can see in my video Brown Fat: Losing Weight Through Thermogenesis, with no apparent side effects. They felt great... and then thousands of people started going blind and users started dropping dead from hyperpyrexia, fatal fever due to the heat created by the burning fat. Of course, it continued to be sold. Ad copy read:

"Here, at last, is a [weight] reducing remedy that will bring you a figure men admire and women envy, without danger to your health or change in your regular mode of living....No diet, no exercise!"

It did work, but the therapeutic index--the difference between the effective dose and the deadly dose--was razor thin. It was not until thousands suffered irreversible harm that it got pulled from the market and remained unavailable. Unavailable, that is, until it was brought back by the internet for those dying to be thin.

There is, however, a way our body naturally burns fat to create heat. When we're born, we go from a nice tropical 98.6 in our mother's womb straight to room temperature, just when we're still all wet and slimy. As an adaptive mechanism to maintain warmth, the appearance of a unique organ around 150 million years ago allowed mammals to maintain our high body temperatures.

That unique organ is called brown adipose tissue, or BAT, and its role is to consume fat calories by generating heat in response to cold exposure. The white fat in our bellies stores fat, but the brown fat, located up between our shoulder blades, burns fat. BAT is essential for thermogenesis, the creation of heat in newborns, but has been considered unnecessary in adults who have higher metabolic rates and increased muscle mass for shivering to warm us up when we get chilled. We used to think brown tissue just shrank away when we grew up, but, if it was there, then it could potentially make a big difference for how many calories we burn every day.

When PET scans were invented to detect metabolically active tissues like cancer, oncologists kept finding hot spots in the neck and shoulder regions that on CT scans turned out not to be cancer, just fat. Then, some observant radiologists noticed they appeared in patients mostly during the cold winter months. When they looked closer at tissue samples taken from people who had undergone neck surgery, they found it: brown fat in adults.

The common message from a number of studies is that BAT is present and active in adults, and the more we have and the more active it is, the thinner we are. And we can rapidly activate our fat-burning brown fat by exposure to cold temperatures. For example, if you hang out in a cold room for two hours in your undies and put your legs on a block of ice for four minutes every five minutes, you can elicit a marked increase in energy expenditure, thanks to brown fat activation. So, the studies point to a potential "natural" intervention to stimulate energy expenditure: Turn down the heat to burn calories (and reduce the carbon footprint in the process).

Thankfully, for those of us who would rather not lay our bare legs on blocks of ice, our brown fat can also be activated by some food ingredients such as those that are covered in my Boosting Brown Fat Through Diet video.


I briefly touch on the role cold temperatures can play in weight loss in The Ice Diet and talk more about calories in (Nutrient-Dense Approach to Weight Management) and calories out (How Much Exercise to Sustain Weight Loss).

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.

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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

Foods that Affect Testosterone Levels

Foods that Affect Testosterone Levels.jpeg

A number of studies suggest that exposure to industrial pollutants may affect sexual function, for example, loss of libido, sexual dysfunction, and impotence. This may be due to effects on testosterone levels. In a study of men who ate a lot of contaminated fish, an elevation in PCB levels in the blood was associated with a lower concentration of testosterone levels. These pollutants are found predominantly in fish, but also meat and dairy. The lowest levels are found in plants (see Dietary Pollutants May Affect Testosterone Levels).

Testosterone doesn't just play a role in the determination of secondary sex characteristics like facial hair at puberty. It also regulates normal sexual functioning and the overall physical and psychological well-being of adult men. Abnormally low levels of testosterone can lead to decreased physical endurance and memory capacity, loss of libido, drop in sperm count, loss of bone density, obesity, and depression.

Endocrine-disrupting compounds that build up in fish may be able to mimic or block hormone receptors, or alter rates of synthesis or breakdown of sex steroid hormones. In children, these pollutants may actually impair sexual development. Boys who are exposed may grow up with smaller penises (although only by about two-thirds of an inch shorter at most). Researchers have tried exposing cells from aborted fetal human penises to these kinds of dietary pollutants, and gene expression related to genital development is indeed affected at real-life exposure levels. We're not sure if the effects on penis length are due to the pro-estrogenic effects of the toxins, though, or the anti-testosterone effects.

You've heard of save the whales? Well, male reproductive organs may be at risk from environmental hazards as well.

I previously addressed how we discovered the endocrine disruptor phenomenon in Alkylphenol Endocrine Disruptors and Allergies, as well as where they're found (Dietary Sources of Alkylphenol Endocrine Disruptors).

For more on sustaining male virility, see Male Fertility and Diet, The Role of Diet in Declining Sperm Counts, and Dairy Estrogen and Male Fertility.

I've talked about the role a plastics chemical may play in male sexual functioning (BPA Plastic and Male Sexual Dysfunction). But it's not just toxins, it's the total diet (Survival of the Firmest: Erectile Dysfunction and Death), and not only in men (Cholesterol and Female Sexual Dysfunction). My latest on the topic is Best Foods to Improve Sexual 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:

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

Original Link