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

How to Design a Misleading Study to Show Diet Doesn’t Work

How to Design a Misleading Study to Show Diet Doesn't Work.jpeg

A study out of the University of North Carolina found no association between dietary fiber intake and diverticulosis. They compared those who ate the highest amount of fiber, 25 grams, to those who ate the smallest amount, which was three times lower at only 8 grams. Finding no difference in disease rates, researchers concluded that a low-fiber diet was not associated with diverticulosis.

The university sent out a press release entitled: "Diets high in fiber won't protect against diverticulosis." The media picked it up and ran headlines such as "High-fiber diet may not protect against diverticulosis, study finds." It went all over the paleo blogs and even medical journals, publishing such statements as an "important and provocative paper...calls into question" the fiber theory of the development of diverticulosis. Other editorials, though, caught the study's critical flaw. To understand this, let's turn to another dietary deficiency disease: scurvy.

Medical experiments on prisoners at Iowa State Penitentiary showed that clinical signs of scurvy start appearing after just 29 days without vitamin C. Experiments on pacifists during World War II showed that it takes about 10 mg of vitamin C a day to prevent scurvy. Imagine going back a few centuries when they were still trying to figure scurvy out. Dr. James Linde had this radical theory that citrus fruits could cure scurvy. What if an experiment was designed to test this crazy theory, in which sailors were given the juice of either one wedge of lemon or three wedges of lemon each day? If a month later on the high seas there was no difference in scurvy rates, one might see headlines from printing presses touting that a low-vitamin C diet is not associated with scurvy.

Well, a wedge of lemon only yields about 2 mg of vitamin C, and it takes 10 mg to prevent scurvy. They would have been comparing one vitamin C-deficient dose to another vitamin C-deficient dose. No wonder there would be no difference in scurvy rates. We evolved eating so many plants that we likely averaged around 600 mg of vitamin C a day. That's what our bodies are biologically used to getting.

What about fiber? How much fiber are we used to getting? More than 100 grams a day! The highest fiber intake group in the North Carolina study was only eating 25 grams, which is less than the minimum recommended daily allowance of about 32 grams. The subjects didn't even make the minimum! The study compared one fiber-deficient diet to another fiber-deficient diet--no wonder there was no difference in diverticulosis rates.

The African populations with essentially no diverticulosis ate diets consisting in part of very large platefuls of leafy vegetables--similar, perhaps, to what we were eating a few million years ago. They were eating plant-based diets containing 70 to 90 grams of fiber a day. Most vegetarians don't even eat that many whole plant foods, although some do. At least vegetarians tend to hit the minimum mark, and they have less diverticulosis to show for it. A study of 47,000 people confirmed that "[c]onsuming a vegetarian diet and a high intake of dietary fiber were both associated with a lower risk of admission to hospital or death from diverticular disease." They had enough people to tease it out. As you'll see in my video Does Fiber Really Prevent Diverticulosis?, compared to people eating a single serving of meat a day or more, those who ate less than half a serving appeared to have a 16% lower risk and pescatarians (eating no meat except fish) had a risk down around 23%. Both of these results weren't in and of themselves statistically significant, but eating vegetarian was. Vegetarians had 35% lower risk, and those eating strictly plant-based appeared to be at 78% lower risk.

As with all lifestyle interventions, it only works if you do it. High-fiber diets only work if they're actually high in fiber.

There's more great information in my video Diverticulosis: When Our Most Common Gut Disorder Hardly Existed.

This reminds me of an ancient video I did: Flawed Study Interpretation.

People commonly ask Do Vegetarians Get Enough Protein?, but maybe they should be more concerned where everyone else is getting their fiber. Ninety-seven percent of Americans don't even reach the recommended daily minimum.

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: Yoshihide Nomura / Flickr. This image has been modified.

Original Link

How to Design a Misleading Study to Show Diet Doesn’t Work

How to Design a Misleading Study to Show Diet Doesn't Work.jpeg

A study out of the University of North Carolina found no association between dietary fiber intake and diverticulosis. They compared those who ate the highest amount of fiber, 25 grams, to those who ate the smallest amount, which was three times lower at only 8 grams. Finding no difference in disease rates, researchers concluded that a low-fiber diet was not associated with diverticulosis.

The university sent out a press release entitled: "Diets high in fiber won't protect against diverticulosis." The media picked it up and ran headlines such as "High-fiber diet may not protect against diverticulosis, study finds." It went all over the paleo blogs and even medical journals, publishing such statements as an "important and provocative paper...calls into question" the fiber theory of the development of diverticulosis. Other editorials, though, caught the study's critical flaw. To understand this, let's turn to another dietary deficiency disease: scurvy.

Medical experiments on prisoners at Iowa State Penitentiary showed that clinical signs of scurvy start appearing after just 29 days without vitamin C. Experiments on pacifists during World War II showed that it takes about 10 mg of vitamin C a day to prevent scurvy. Imagine going back a few centuries when they were still trying to figure scurvy out. Dr. James Linde had this radical theory that citrus fruits could cure scurvy. What if an experiment was designed to test this crazy theory, in which sailors were given the juice of either one wedge of lemon or three wedges of lemon each day? If a month later on the high seas there was no difference in scurvy rates, one might see headlines from printing presses touting that a low-vitamin C diet is not associated with scurvy.

Well, a wedge of lemon only yields about 2 mg of vitamin C, and it takes 10 mg to prevent scurvy. They would have been comparing one vitamin C-deficient dose to another vitamin C-deficient dose. No wonder there would be no difference in scurvy rates. We evolved eating so many plants that we likely averaged around 600 mg of vitamin C a day. That's what our bodies are biologically used to getting.

What about fiber? How much fiber are we used to getting? More than 100 grams a day! The highest fiber intake group in the North Carolina study was only eating 25 grams, which is less than the minimum recommended daily allowance of about 32 grams. The subjects didn't even make the minimum! The study compared one fiber-deficient diet to another fiber-deficient diet--no wonder there was no difference in diverticulosis rates.

The African populations with essentially no diverticulosis ate diets consisting in part of very large platefuls of leafy vegetables--similar, perhaps, to what we were eating a few million years ago. They were eating plant-based diets containing 70 to 90 grams of fiber a day. Most vegetarians don't even eat that many whole plant foods, although some do. At least vegetarians tend to hit the minimum mark, and they have less diverticulosis to show for it. A study of 47,000 people confirmed that "[c]onsuming a vegetarian diet and a high intake of dietary fiber were both associated with a lower risk of admission to hospital or death from diverticular disease." They had enough people to tease it out. As you'll see in my video Does Fiber Really Prevent Diverticulosis?, compared to people eating a single serving of meat a day or more, those who ate less than half a serving appeared to have a 16% lower risk and pescatarians (eating no meat except fish) had a risk down around 23%. Both of these results weren't in and of themselves statistically significant, but eating vegetarian was. Vegetarians had 35% lower risk, and those eating strictly plant-based appeared to be at 78% lower risk.

As with all lifestyle interventions, it only works if you do it. High-fiber diets only work if they're actually high in fiber.

There's more great information in my video Diverticulosis: When Our Most Common Gut Disorder Hardly Existed.

This reminds me of an ancient video I did: Flawed Study Interpretation.

People commonly ask Do Vegetarians Get Enough Protein?, but maybe they should be more concerned where everyone else is getting their fiber. Ninety-seven percent of Americans don't even reach the recommended daily minimum.

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: Yoshihide Nomura / Flickr. This image has been modified.

Original Link

How to Design a Misleading Study to Show Diet Doesn’t Work

How to Design a Misleading Study to Show Diet Doesn't Work.jpeg

A study out of the University of North Carolina found no association between dietary fiber intake and diverticulosis. They compared those who ate the highest amount of fiber, 25 grams, to those who ate the smallest amount, which was three times lower at only 8 grams. Finding no difference in disease rates, researchers concluded that a low-fiber diet was not associated with diverticulosis.

The university sent out a press release entitled: "Diets high in fiber won't protect against diverticulosis." The media picked it up and ran headlines such as "High-fiber diet may not protect against diverticulosis, study finds." It went all over the paleo blogs and even medical journals, publishing such statements as an "important and provocative paper...calls into question" the fiber theory of the development of diverticulosis. Other editorials, though, caught the study's critical flaw. To understand this, let's turn to another dietary deficiency disease: scurvy.

Medical experiments on prisoners at Iowa State Penitentiary showed that clinical signs of scurvy start appearing after just 29 days without vitamin C. Experiments on pacifists during World War II showed that it takes about 10 mg of vitamin C a day to prevent scurvy. Imagine going back a few centuries when they were still trying to figure scurvy out. Dr. James Linde had this radical theory that citrus fruits could cure scurvy. What if an experiment was designed to test this crazy theory, in which sailors were given the juice of either one wedge of lemon or three wedges of lemon each day? If a month later on the high seas there was no difference in scurvy rates, one might see headlines from printing presses touting that a low-vitamin C diet is not associated with scurvy.

Well, a wedge of lemon only yields about 2 mg of vitamin C, and it takes 10 mg to prevent scurvy. They would have been comparing one vitamin C-deficient dose to another vitamin C-deficient dose. No wonder there would be no difference in scurvy rates. We evolved eating so many plants that we likely averaged around 600 mg of vitamin C a day. That's what our bodies are biologically used to getting.

What about fiber? How much fiber are we used to getting? More than 100 grams a day! The highest fiber intake group in the North Carolina study was only eating 25 grams, which is less than the minimum recommended daily allowance of about 32 grams. The subjects didn't even make the minimum! The study compared one fiber-deficient diet to another fiber-deficient diet--no wonder there was no difference in diverticulosis rates.

The African populations with essentially no diverticulosis ate diets consisting in part of very large platefuls of leafy vegetables--similar, perhaps, to what we were eating a few million years ago. They were eating plant-based diets containing 70 to 90 grams of fiber a day. Most vegetarians don't even eat that many whole plant foods, although some do. At least vegetarians tend to hit the minimum mark, and they have less diverticulosis to show for it. A study of 47,000 people confirmed that "[c]onsuming a vegetarian diet and a high intake of dietary fiber were both associated with a lower risk of admission to hospital or death from diverticular disease." They had enough people to tease it out. As you'll see in my video Does Fiber Really Prevent Diverticulosis?, compared to people eating a single serving of meat a day or more, those who ate less than half a serving appeared to have a 16% lower risk and pescatarians (eating no meat except fish) had a risk down around 23%. Both of these results weren't in and of themselves statistically significant, but eating vegetarian was. Vegetarians had 35% lower risk, and those eating strictly plant-based appeared to be at 78% lower risk.

As with all lifestyle interventions, it only works if you do it. High-fiber diets only work if they're actually high in fiber.

There's more great information in my video Diverticulosis: When Our Most Common Gut Disorder Hardly Existed.

This reminds me of an ancient video I did: Flawed Study Interpretation.

People commonly ask Do Vegetarians Get Enough Protein?, but maybe they should be more concerned where everyone else is getting their fiber. Ninety-seven percent of Americans don't even reach the recommended daily minimum.

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: Yoshihide Nomura / Flickr. This image has been modified.

Original Link

9 out of 10 That Die From it Never Knew They Even Had This Preventable Disease

9 out of 10 That Die From it Never Knew They Even Had This Preventable Disease.jpeg

Diverticula are out-pouchings of our intestine. Doctors like using a tire analogy: high pressures within the gut can force the intestines to balloon out through weak spots in the intestinal wall like an inner tube poking out through a worn tire tread. You can see what they actually look like in my video, Diverticulosis: When Our Most Common Gut Disorder Hardly Existed. These pockets can become inflamed and infected, and, to carry the tire analogy further, can blow out and spill fecal matter into the abdomen, and lead to death. Symptoms can range from no symptoms at all, to a little cramping and bloating, to "incapacitating pain that is a medical emergency." Nine out of ten people who die from the disease never even knew they had it.

The good news is there may be a way to prevent the disease. Diverticular disease is the most common intestinal disorder, affecting up to 70% of people by age 60. If it's that common, though, is it just an inevitable consequence of aging? No, it's a new disease. In 1907, 25 cases had been reported in the medical literature. Not cases in 25% of people, but 25 cases period. And diverticular disease is kind of hard to miss on autopsy. A hundred years ago, in 1916, it didn't even merit mention in medical and surgical textbooks. The mystery wasn't solved until 1971.

How did a disease that was almost unknown become the most common affliction of the colon in the Western world within one lifespan? Surgeons Painter and Burkitt suggested diverticulosis was a deficiency disease--i.e., a disease caused by a deficiency of fiber. In the late 1800s, roller milling was introduced, further removing fiber from grain, and we started to fill up on other fiber-deficient foods like meat and sugar. A few decades of this and diverticulosis was rampant.

This is what Painter and Burkitt thought was going on: Just as it would be easy to squeeze a lump of butter through a bicycle tube, it's easy to move large, soft, and moist intestinal contents through the gut. In contrast, try squeezing through a lump of tar. When we eat fiber-deficient diets, our feces can become small and firm, and our intestines have to really squeeze down hard to move them along. This buildup of pressure may force out those bulges. Eventually, a low-fiber diet can sometimes lead to the colon literally rupturing itself.

If this theory is true, then populations eating high­-fiber diets would have low rates of diverticulosis. That's exactly what's been found. More than 50% of African Americans in their 50s were found to have diverticulosis, compared to less than 1% in African Africans eating traditional plant-based diets. By less than 1%, we're talking zero out of a series of 2,000 autopsies in South Africa and two out of 4,000 in Uganda. That's about one thousand times lower prevalence.

What, then, do we make of a new study concluding that a low-fiber diet was not associated with diverticulosis. I cover that in my video Does Fiber Really Prevent Diverticulosis?

For more on bowel health, see:

What if your doctor says you shouldn't eat healthy foods like nuts and popcorn because of your diverticulosis? Share with them my Diverticulosis & Nuts video.

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: Sean T Evans / Flickr. This image has been modified.

Original Link

9 out of 10 That Die From it Never Knew They Even Had This Preventable Disease

9 out of 10 That Die From it Never Knew They Even Had This Preventable Disease.jpeg

Diverticula are out-pouchings of our intestine. Doctors like using a tire analogy: high pressures within the gut can force the intestines to balloon out through weak spots in the intestinal wall like an inner tube poking out through a worn tire tread. You can see what they actually look like in my video, Diverticulosis: When Our Most Common Gut Disorder Hardly Existed. These pockets can become inflamed and infected, and, to carry the tire analogy further, can blow out and spill fecal matter into the abdomen, and lead to death. Symptoms can range from no symptoms at all, to a little cramping and bloating, to "incapacitating pain that is a medical emergency." Nine out of ten people who die from the disease never even knew they had it.

The good news is there may be a way to prevent the disease. Diverticular disease is the most common intestinal disorder, affecting up to 70% of people by age 60. If it's that common, though, is it just an inevitable consequence of aging? No, it's a new disease. In 1907, 25 cases had been reported in the medical literature. Not cases in 25% of people, but 25 cases period. And diverticular disease is kind of hard to miss on autopsy. A hundred years ago, in 1916, it didn't even merit mention in medical and surgical textbooks. The mystery wasn't solved until 1971.

How did a disease that was almost unknown become the most common affliction of the colon in the Western world within one lifespan? Surgeons Painter and Burkitt suggested diverticulosis was a deficiency disease--i.e., a disease caused by a deficiency of fiber. In the late 1800s, roller milling was introduced, further removing fiber from grain, and we started to fill up on other fiber-deficient foods like meat and sugar. A few decades of this and diverticulosis was rampant.

This is what Painter and Burkitt thought was going on: Just as it would be easy to squeeze a lump of butter through a bicycle tube, it's easy to move large, soft, and moist intestinal contents through the gut. In contrast, try squeezing through a lump of tar. When we eat fiber-deficient diets, our feces can become small and firm, and our intestines have to really squeeze down hard to move them along. This buildup of pressure may force out those bulges. Eventually, a low-fiber diet can sometimes lead to the colon literally rupturing itself.

If this theory is true, then populations eating high­-fiber diets would have low rates of diverticulosis. That's exactly what's been found. More than 50% of African Americans in their 50s were found to have diverticulosis, compared to less than 1% in African Africans eating traditional plant-based diets. By less than 1%, we're talking zero out of a series of 2,000 autopsies in South Africa and two out of 4,000 in Uganda. That's about one thousand times lower prevalence.

What, then, do we make of a new study concluding that a low-fiber diet was not associated with diverticulosis. I cover that in my video Does Fiber Really Prevent Diverticulosis?

For more on bowel health, see:

What if your doctor says you shouldn't eat healthy foods like nuts and popcorn because of your diverticulosis? Share with them my Diverticulosis & Nuts video.

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: Sean T Evans / 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

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