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

The 3 Vitamins that Prevent Brain Loss

The 3 Vitamins that Prevent Brain Loss.jpeg

By our seventies, one in five of us will suffer from cognitive impairment. Within five years, half of those cognitively impaired will progress to dementia and death. The earlier we can slow or stop this process, the better.

Although an effective treatment for Alzheimer's disease is unavailable, interventions just to control risk factors could prevent millions of cases. An immense effort has been spent on identifying such risk factors for Alzheimer's and developing treatments to reduce them.

In 1990, a small study of 22 Alzheimer's patients reported high concentrations of homocysteine in their blood. The homocysteine story goes back to 1969 when a Harvard pathologist reported two cases of children, one dating back to 1933, whose brains had turned to mush. They both suffered from extremely rare genetic mutations that led to abnormally high levels of homocysteine in their bodies. Is it possible, he asked, that homocysteine could cause brain damage even in people without genetic defects?

Here we are in the 21st century, and homocysteine is considered "a strong, independent risk factor for the development of dementia and Alzheimer's disease." Having a blood level over 14 (µmol/L) may double our risk. In the Framingham Study, researchers estimate that as many as one in six Alzheimer's cases may be attributable to elevated homocysteine in the blood, which is now thought to play a role in brain damage and cognitive and memory decline. Our body can detoxify homocysteine, though, using three vitamins: folate, vitamin B12, and vitamin B6. So why don't we put them to the test? No matter how many studies find an association between high homocysteinea and cognitive decline, dementia, or Alzheimer's disease, a cause-and-effect role can only be confirmed by interventional studies.

Initially, the results were disappointing. Vitamin supplementation did not seem to work, but the studies were tracking neuropsychological assessments, which are more subjective compared to structural neuroimaging--that is, actually seeing what's happening to the brain. A double-blind randomized controlled trial found that homocysteine-lowering by B vitamins can slow the rate of accelerated brain atrophy in people with mild cognitive impairment. As we age, our brains slowly atrophy, but the shrinking is much accelerated in patients suffering from Alzheimer's disease. An intermediate rate of shrinkage is found in people with mild cognitive impairment. The thinking is if we could slow the rate of brain loss, we may be able to slow the conversion to Alzheimer's disease. Researchers tried giving people B vitamins for two years and found it markedly slowed the rate of brain shrinkage. The rate of atrophy in those with high homocysteine levels was cut in half. A simple, safe treatment can slow the accelerated rate of brain loss.

A follow-up study went further by demonstrating that B-vitamin treatment reduces, by as much as seven-fold, the brain atrophy in the regions specifically vulnerable to the Alzheimer's disease process. You can see the amount of brain atrophy over a two-year period in the placebo group versus the B-vitamin group in my Preventing Brain Loss with B Vitamins? video.

The beneficial effect of B vitamins was confined to those with high homocysteine, indicating a relative deficiency in one of those three vitamins. Wouldn't it be better to not become deficient in the first place? Most people get enough B12 and B6. The reason these folks were stuck at a homocysteine of 11 µmoles per liter is that they probably weren't getting enough folate, which is found concentrated in beans and greens. Ninety-six percent of Americans don't even make the minimum recommended amount of dark green leafy vegetables, which is the same pitiful number who don't eat the minimum recommendation for beans.

If we put people on a healthy diet--a plant-based diet--we can drop their homocysteine levels by 20% in just one week, from around 11 mmoles per liter down to 9 mmoles per liter. The fact that they showed rapid and significant homocysteine lowering without any pills or supplements implies that multiple mechanisms may have been at work. The researchers suggest it may be because of the fiber. Every gram of daily fiber consumption may increase folate levels in the blood nearly 2%, perhaps by boosting vitamin production in the colon by all our friendly gut bacteria. It also could be from the decreased methionine intake.

Methionine is where homocysteine comes from. Homocysteine is a breakdown product of methionine, which comes mostly from animal protein. If we give someone bacon and eggs for breakfast and a steak for dinner, we can get spikes of homocysteine levels in the blood. Thus, decreased methionine intake on a plant-based diet may be another factor contributing to lower, safer homocysteine levels.

The irony is that those who eat plant-based diets long-term, not just at a health spa for a week, have terrible homocysteine levels. Meat-eaters are up at 11 µmoles per liter, but vegetarians at nearly 14 µmoles per liter and vegans at 16 µmoles per liter. Why? The vegetarians and vegans were getting more fiber and folate, but not enough vitamin B12. Most vegans were at risk for suffering from hyperhomocysteinaemia (too much homocysteine in the blood) because most vegans in the study were not supplementing with vitamin B12 or eating vitamin B12-fortified foods, which is critical for anyone eating a plant-based diet. If you take vegans and give them B12, their homocysteine levels can drop down below 5. Why not down to just 11? The reason meat-eaters were stuck up at 11 is presumably because they weren't getting enough folate. Once vegans got enough B12, they could finally fully exploit the benefits of their plant-based diets and come out with the lowest levels of all.

This is very similar to the findings in my video Vitamin B12 Necessary for Arterial Health.

For more details on ensuring a regular reliable source of vitamin B12:

There are more benefits to lowering your methionine intake. Check out Methionine Restriction as a Life Extension Strategy and Starving Cancer with Methionine Restriction.

For more on brain health in general, see these videos:

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: Thomas Hawk / Flickr. This image has been modified.

Original Link

The 3 Vitamins that Prevent Brain Loss

The 3 Vitamins that Prevent Brain Loss.jpeg

By our seventies, one in five of us will suffer from cognitive impairment. Within five years, half of those cognitively impaired will progress to dementia and death. The earlier we can slow or stop this process, the better.

Although an effective treatment for Alzheimer's disease is unavailable, interventions just to control risk factors could prevent millions of cases. An immense effort has been spent on identifying such risk factors for Alzheimer's and developing treatments to reduce them.

In 1990, a small study of 22 Alzheimer's patients reported high concentrations of homocysteine in their blood. The homocysteine story goes back to 1969 when a Harvard pathologist reported two cases of children, one dating back to 1933, whose brains had turned to mush. They both suffered from extremely rare genetic mutations that led to abnormally high levels of homocysteine in their bodies. Is it possible, he asked, that homocysteine could cause brain damage even in people without genetic defects?

Here we are in the 21st century, and homocysteine is considered "a strong, independent risk factor for the development of dementia and Alzheimer's disease." Having a blood level over 14 (µmol/L) may double our risk. In the Framingham Study, researchers estimate that as many as one in six Alzheimer's cases may be attributable to elevated homocysteine in the blood, which is now thought to play a role in brain damage and cognitive and memory decline. Our body can detoxify homocysteine, though, using three vitamins: folate, vitamin B12, and vitamin B6. So why don't we put them to the test? No matter how many studies find an association between high homocysteinea and cognitive decline, dementia, or Alzheimer's disease, a cause-and-effect role can only be confirmed by interventional studies.

Initially, the results were disappointing. Vitamin supplementation did not seem to work, but the studies were tracking neuropsychological assessments, which are more subjective compared to structural neuroimaging--that is, actually seeing what's happening to the brain. A double-blind randomized controlled trial found that homocysteine-lowering by B vitamins can slow the rate of accelerated brain atrophy in people with mild cognitive impairment. As we age, our brains slowly atrophy, but the shrinking is much accelerated in patients suffering from Alzheimer's disease. An intermediate rate of shrinkage is found in people with mild cognitive impairment. The thinking is if we could slow the rate of brain loss, we may be able to slow the conversion to Alzheimer's disease. Researchers tried giving people B vitamins for two years and found it markedly slowed the rate of brain shrinkage. The rate of atrophy in those with high homocysteine levels was cut in half. A simple, safe treatment can slow the accelerated rate of brain loss.

A follow-up study went further by demonstrating that B-vitamin treatment reduces, by as much as seven-fold, the brain atrophy in the regions specifically vulnerable to the Alzheimer's disease process. You can see the amount of brain atrophy over a two-year period in the placebo group versus the B-vitamin group in my Preventing Brain Loss with B Vitamins? video.

The beneficial effect of B vitamins was confined to those with high homocysteine, indicating a relative deficiency in one of those three vitamins. Wouldn't it be better to not become deficient in the first place? Most people get enough B12 and B6. The reason these folks were stuck at a homocysteine of 11 µmoles per liter is that they probably weren't getting enough folate, which is found concentrated in beans and greens. Ninety-six percent of Americans don't even make the minimum recommended amount of dark green leafy vegetables, which is the same pitiful number who don't eat the minimum recommendation for beans.

If we put people on a healthy diet--a plant-based diet--we can drop their homocysteine levels by 20% in just one week, from around 11 mmoles per liter down to 9 mmoles per liter. The fact that they showed rapid and significant homocysteine lowering without any pills or supplements implies that multiple mechanisms may have been at work. The researchers suggest it may be because of the fiber. Every gram of daily fiber consumption may increase folate levels in the blood nearly 2%, perhaps by boosting vitamin production in the colon by all our friendly gut bacteria. It also could be from the decreased methionine intake.

Methionine is where homocysteine comes from. Homocysteine is a breakdown product of methionine, which comes mostly from animal protein. If we give someone bacon and eggs for breakfast and a steak for dinner, we can get spikes of homocysteine levels in the blood. Thus, decreased methionine intake on a plant-based diet may be another factor contributing to lower, safer homocysteine levels.

The irony is that those who eat plant-based diets long-term, not just at a health spa for a week, have terrible homocysteine levels. Meat-eaters are up at 11 µmoles per liter, but vegetarians at nearly 14 µmoles per liter and vegans at 16 µmoles per liter. Why? The vegetarians and vegans were getting more fiber and folate, but not enough vitamin B12. Most vegans were at risk for suffering from hyperhomocysteinaemia (too much homocysteine in the blood) because most vegans in the study were not supplementing with vitamin B12 or eating vitamin B12-fortified foods, which is critical for anyone eating a plant-based diet. If you take vegans and give them B12, their homocysteine levels can drop down below 5. Why not down to just 11? The reason meat-eaters were stuck up at 11 is presumably because they weren't getting enough folate. Once vegans got enough B12, they could finally fully exploit the benefits of their plant-based diets and come out with the lowest levels of all.

This is very similar to the findings in my video Vitamin B12 Necessary for Arterial Health.

For more details on ensuring a regular reliable source of vitamin B12:

There are more benefits to lowering your methionine intake. Check out Methionine Restriction as a Life Extension Strategy and Starving Cancer with Methionine Restriction.

For more on brain health in general, see these videos:

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: Thomas Hawk / Flickr. This image has been modified.

Original Link

Can You Eat Too Much Fruit?

Can You Eat Too Much Fruit?.jpeg

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

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

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

It's actually been put to the test.

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

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


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

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

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

In health,
Michael Greger, M.D.

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

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

Original Link

Can You Eat Too Much Fruit?

Can You Eat Too Much Fruit?.jpeg

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

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

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

It's actually been put to the test.

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

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


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

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

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

In health,
Michael Greger, M.D.

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

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

Original Link

Why Is Milk Consumption Associated with More Bone Fractures?

Why Is Milk Consumption Associated with More Bone Fractures?.jpg

Milk is touted to build strong bones, but a compilation of all the best studies found no association between milk consumption and hip fracture risk, so drinking milk as an adult might not help bones, but what about in adolescence? Harvard researchers decided to put it to the test.

Studies have shown that greater milk consumption during childhood and adolescence contributes to peak bone mass, and is therefore expected to help avoid osteoporosis and bone fractures in later life. But that's not what researchers have found (as you can see in my video Is Milk Good for Our Bones?). Milk consumption during teenage years was not associated with a lower risk of hip fracture, and if anything, milk consumption was associated with a borderline increase in fracture risk in men.

It appears that the extra boost in total body bone mineral density from getting extra calcium is lost within a few years; even if you keep the calcium supplementation up. This suggests a partial explanation for the long-standing enigma that hip fracture rates are highest in populations with the greatest milk consumption. This may be an explanation for why they're not lower, but why would they be higher?

This enigma irked a Swedish research team, puzzled because studies again and again had shown a tendency of a higher risk of fracture with a higher intake of milk. Well, there is a rare birth defect called galactosemia, where babies are born without the enzymes needed to detoxify the galactose found in milk, so they end up with elevated levels of galactose in their blood, which can causes bone loss even as kids. So maybe, the Swedish researchers figured, even in normal people that can detoxify the stuff, it might not be good for the bones to be drinking it every day.

And galactose doesn't just hurt the bones. Galactose is what scientists use to cause premature aging in lab animals--it can shorten their lifespan, cause oxidative stress, inflammation, and brain degeneration--just with the equivalent of like one to two glasses of milk's worth of galactose a day. We're not rats, though. But given the high amount of galactose in milk, recommendations to increase milk intake for prevention of fractures could be a conceivable contradiction. So, the researchers decided to put it to the test, looking at milk intake and mortality as well as fracture risk to test their theory.

A hundred thousand men and women were followed for up to 20 years. Researchers found that milk-drinking women had higher rates of death, more heart disease, and significantly more cancer for each glass of milk. Three glasses a day was associated with nearly twice the risk of premature death, and they had significantly more bone and hip fractures. More milk, more fractures.

Men in a separate study also had a higher rate of death with higher milk consumption, but at least they didn't have higher fracture rates. So, the researchers found a dose dependent higher rate of both mortality and fracture in women, and a higher rate of mortality in men with milk intake, but the opposite for other dairy products like soured milk and yogurt, which would go along with the galactose theory, since bacteria can ferment away some of the lactose. To prove it though, we need a randomized controlled trial to examine the effect of milk intake on mortality and fractures. As the accompanying editorial pointed out, we better find this out soon since milk consumption is on the rise around the world.

What can we do for our bones, then? Weight-bearing exercise such as jumping, weight-lifting, and walking with a weighted vest or backpack may help, along with getting enough calcium (Alkaline Diets, Animal Protein, & Calcium Loss) and vitamin D (Resolving the Vitamin D-Bate). Eating beans (Phytates for the Prevention of Osteoporosis) and avoiding phosphate additives (Phosphate Additives in Meat Purge and Cola) may also help.

Maybe the galactose angle can help explain the findings on prostate cancer (Prostate Cancer and Organic Milk vs. Almond Milk) and Parkinson's disease (Preventing Parkinson's Disease With Diet).

Galactose is a milk sugar. There's also concern about milk proteins (see my casomorphin series) and fats (The Saturated Fat Studies: Buttering Up the Public and Trans Fat in Meat and Dairy) as well as the hormones (Dairy Estrogen and Male Fertility, Estrogen in Meat, Dairy, and Eggs and Why Do Vegan Women Have 5x Fewer Twins?).

Milk might also play a role in diabetes (Does Casein in Milk Trigger Type 1 Diabetes, Does Bovine Insulin in Milk Trigger Type 1 Diabetes?) and breast cancer (Is Bovine Leukemia in Milk Infectious?, The Role of Bovine Leukemia Virus in Breast Cancer, and Industry Response to Bovine Leukemia Virus in Breast Cancer).

In health,

Michael Greger, M.D.

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

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

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Why Is Milk Consumption Associated with More Bone Fractures?

Why Is Milk Consumption Associated with More Bone Fractures?.jpg

Milk is touted to build strong bones, but a compilation of all the best studies found no association between milk consumption and hip fracture risk, so drinking milk as an adult might not help bones, but what about in adolescence? Harvard researchers decided to put it to the test.

Studies have shown that greater milk consumption during childhood and adolescence contributes to peak bone mass, and is therefore expected to help avoid osteoporosis and bone fractures in later life. But that's not what researchers have found (as you can see in my video Is Milk Good for Our Bones?). Milk consumption during teenage years was not associated with a lower risk of hip fracture, and if anything, milk consumption was associated with a borderline increase in fracture risk in men.

It appears that the extra boost in total body bone mineral density from getting extra calcium is lost within a few years; even if you keep the calcium supplementation up. This suggests a partial explanation for the long-standing enigma that hip fracture rates are highest in populations with the greatest milk consumption. This may be an explanation for why they're not lower, but why would they be higher?

This enigma irked a Swedish research team, puzzled because studies again and again had shown a tendency of a higher risk of fracture with a higher intake of milk. Well, there is a rare birth defect called galactosemia, where babies are born without the enzymes needed to detoxify the galactose found in milk, so they end up with elevated levels of galactose in their blood, which can causes bone loss even as kids. So maybe, the Swedish researchers figured, even in normal people that can detoxify the stuff, it might not be good for the bones to be drinking it every day.

And galactose doesn't just hurt the bones. Galactose is what scientists use to cause premature aging in lab animals--it can shorten their lifespan, cause oxidative stress, inflammation, and brain degeneration--just with the equivalent of like one to two glasses of milk's worth of galactose a day. We're not rats, though. But given the high amount of galactose in milk, recommendations to increase milk intake for prevention of fractures could be a conceivable contradiction. So, the researchers decided to put it to the test, looking at milk intake and mortality as well as fracture risk to test their theory.

A hundred thousand men and women were followed for up to 20 years. Researchers found that milk-drinking women had higher rates of death, more heart disease, and significantly more cancer for each glass of milk. Three glasses a day was associated with nearly twice the risk of premature death, and they had significantly more bone and hip fractures. More milk, more fractures.

Men in a separate study also had a higher rate of death with higher milk consumption, but at least they didn't have higher fracture rates. So, the researchers found a dose dependent higher rate of both mortality and fracture in women, and a higher rate of mortality in men with milk intake, but the opposite for other dairy products like soured milk and yogurt, which would go along with the galactose theory, since bacteria can ferment away some of the lactose. To prove it though, we need a randomized controlled trial to examine the effect of milk intake on mortality and fractures. As the accompanying editorial pointed out, we better find this out soon since milk consumption is on the rise around the world.

What can we do for our bones, then? Weight-bearing exercise such as jumping, weight-lifting, and walking with a weighted vest or backpack may help, along with getting enough calcium (Alkaline Diets, Animal Protein, & Calcium Loss) and vitamin D (Resolving the Vitamin D-Bate). Eating beans (Phytates for the Prevention of Osteoporosis) and avoiding phosphate additives (Phosphate Additives in Meat Purge and Cola) may also help.

Maybe the galactose angle can help explain the findings on prostate cancer (Prostate Cancer and Organic Milk vs. Almond Milk) and Parkinson's disease (Preventing Parkinson's Disease With Diet).

Galactose is a milk sugar. There's also concern about milk proteins (see my casomorphin series) and fats (The Saturated Fat Studies: Buttering Up the Public and Trans Fat in Meat and Dairy) as well as the hormones (Dairy Estrogen and Male Fertility, Estrogen in Meat, Dairy, and Eggs and Why Do Vegan Women Have 5x Fewer Twins?).

Milk might also play a role in diabetes (Does Casein in Milk Trigger Type 1 Diabetes, Does Bovine Insulin in Milk Trigger Type 1 Diabetes?) and breast cancer (Is Bovine Leukemia in Milk Infectious?, The Role of Bovine Leukemia Virus in Breast Cancer, and Industry Response to Bovine Leukemia Virus in Breast Cancer).

In health,

Michael Greger, M.D.

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

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

Original Link

The Two Most Active Ingredients of the Mediterranean Diet

Which Parts of the Mediterranean Diet Extended Life.jpg

Olives and nuts are plant foods, and as such, are packed with antioxidants, raising the antioxidant level of our bloodstream resulting in lower fat oxidation and free radical DNA damage, but what's happening inside people's arteries?

Researchers measured the amount of atherosclerotic plaque in the neck arteries going to the brain in folks who for years were eating added nuts, added extra virgin olive oil or neither to their daily diets. In the control group, the plaque got worse, which is what happens when one continues to eat an artery-clogging diet, but there were no significant changes in the added extra virgin olive oil group, and the plaque in the added nut group appeared to get better. The nuts appeared to induce a regression of the disease, or at least a significant delay in the progression. The nut group was still suffering strokes, but only half as many, perhaps because the reduction in plaque height within the arteries on extra nuts was indicating a stabilization of the plaque, rendering them less likely to rupture. You can see these results in my video Which Parts of the Mediterranean Diet Extended Life?

Adding nuts to our diet may also improve endothelial function, boosting the ability of our arteries to dilate naturally by about 30 percent. If you look at the baseline adherence to Mediterranean diet principles and control for things like smoking and exercise, there were only two factors significantly associated with reduced heart attack and stroke risk: more vegetables and more nuts. No significant association with the olive oil, wine, fish or cutting back on soda and cookies. Among the individual components, only increased consumption of vegetables and nuts were related to reduced cardiovascular events.

On the one hand, cutting stroke risk in half just by eating a handful of nuts a day is pretty amazing, but those in the added nut group didn't appear to live any longer overall. This is in contrast to other studies that suggested that frequent nut consumption may extend life. For example, the Harvard health professionals studies, involving a whopping three million person-years of follow-up over decades, found nut consumption associated with fewer deaths from cancer, heart disease, respiratory disease and most importantly fewer deaths overall. This was confirmed by all the other big major prospective studies in a recent review.

So what's going on here with the study showing no longevity benefit from nuts? Did they just not wait long enough? Just because people were randomized to the nut group didn't mean they actually ate more nuts, and those randomized to the other groups didn't necessarily stay away.

If you re-analyze the data comparing the death rates of those who actually ate more nuts to those who actually didn't, nut consumption was indeed associated with significantly reduced risk of death. If you do the same kind of post hoc analysis with olive oil, even with the extra virgin, there is no benefit in terms of living longer. This is consistent with how Ancel Keys, the so-called Father of the Mediterranean diet, viewed olive oil. He thought of its benefit more as a way of just replacing animal fats; anything to get people to eat less lard and butter.

What is the best kind of nut? The greatest benefits were attributed to walnuts, particularly for preventing cancer deaths. Those eating more than three servings of walnuts a week appeared to cut their risk of dying from cancer in half.

Now it's just a matter of communicating the research to the public. All the major cancer groups emphasize a more plant-based diet, remarkably consistent with the World Health Organization guidelines for healthy eating. The far-reaching positive effects of a plant-based diet--including walnuts--may be the most critical message for the public.

Here are some of my previous videos on the Mediterranean diet:

Think the effects of adding a few nuts to one's daily diet are too good to believe? Check out my video Four Nuts Once a Month. For more on Walnuts and Artery Function check out the video, and for more on nuts and cancer prevention, see Which Nut Fights Cancer Better?

Nuts May Help Prevent Death and so may beans; see Increased Lifespan from Beans. What about Fruits and Longevity: How Many Minutes per Mouthful?

More on protecting ourselves from "brain attacks" in Preventing Strokes with Diet.

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: garlandcannon / Flickr. This image has been modified.

Original Link