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

Using a Smell Test to Diagnose Alzheimer’s Disease

Using a Smell Test to Diagnose Alzheimer's Disease.jpeg

Alzheimer's disease (AD) pathology appears to start in the part of the brain that handles smell before subsequently spreading to additional brain regions and then, ultimately, taking over much of the rest of the brain. This led some to speculate that Alzheimer's disease may begin in the nose. Perhaps there's some environmental agent that might enter the brain through some portal in the nostrils?

This is the so-called olfactory vector hypothesis. The anatomy of the nose is well suited for the transfer of things directly into the brain, since the olfactory nerves that stick out into the nose project directly into the brain, bypassing the blood-brain barrier. The nose was actually a major infection route for the polio virus. Public health officials you started cauterizing the nasal passages of schoolchildren by spraying caustic chemicals up their noses in an effort to prevent the disease.

The concern is if people breathe in some ionized metals like aluminum dust, for example, it could be transported into the brain through these olfactory nerves at a rate of about 2 millimeters an hour, which is practically 2 inches a day. Doubt has been cast on this theory, however, by a case report of a woman born with a birth defect in which she had no smell nerves yet still developed Alzheimer's-like pathology. And so, to date, all the supporting evidence is really just circumstantial. It is clear, though, that changes in the sense of smell is among the first clinical signs of Alzheimer's, occurring during the preclinical phase--that is, before there's any noticeable cognitive decline. Could we use these changes to predict or diagnose the disease?

For years, researchers have been trying to find markers of brain illness hidden in people's ability to smell using all sorts of fancy gadgets. For example, functional MRI scans can detect differences in brain activation in response to an odor. In my video, Peanut Butter Smell Test for Alzheimer's, you can see the responses to lavender. You'll see a representation of a normal brain's responses to the odor versus an Alzheimer's brain. This unequivocally demonstrates that we can pick up changes in smell function due to Alzheimer's. But do we really need a million-dollar machine?

An ingenious group of researchers at the University of Florida discovered all we may need is some peanut butter and a ruler.

Considering that the left side of the brain primarily processes what we smell through our left nostril and the right side of our brain covers the right nostril, and understanding that Alzheimer's strikes the left side more than the right, what if you performed the following experiment: Close your eyes and mouth, breathe normally through the nose, then close one nostril, and hold a foot-long ruler out from the open nostril. Once your eyes, mouth, and one nostril are closed, open a container of peanut butter at the bottom of the ruler (one foot away from your open nostril). Move the peanut butter closer by 1 centimeter upon each exhale until you can detect the odor. Then repeat the whole procedure again using your other nostril.

This is exactly what the University of Florida researchers did with their subjects. What did they find? The normal elderly control subjects in the study smelled the peanut butter as soon as it came within an average of 18 centimeters (about 7 inches) from either nostril. It was about the same, roughly 7 inches, in the right nostrils of Alzheimer's patients. But in their left nostrils, it was a mere 2 inches! The peanut butter had to be only 2 inches away before the Alzheimer's patients could detect it through their left nostrils. This happened every single time. Indeed, the researchers found that a "left nostril impairment of odor detection was present in all the patients with probable AD." There was no left-right difference in the control group; they could smell the peanut butter when it was the same distance away from both their left and right nostrils. In the Alzheimer's group, however, there was a 12-centimeter difference.

The disparity was so great that we may be able to set a cutoff value for the diagnosis of Alzheimer's. The researchers reported that "[c]ompared to patients with other causes of dementia this nostril asymmetry of odor detection...was 100% sensitive and 100% specific for probable AD," meaning no false positives and no false negatives. Compared to healthy people, it was 100% sensitive in picking up cases of probable Alzheimer's and 92% specific. What exactly does that mean? In this study, if you had Alzheimer's, there was a 100% chance of having that wide left-right discrepancy. But, if you did have that discrepancy, the chance of having Alzheimer's was only 92%. This means there were some false positives.

The reason it's only "probable" Alzheimer's is because the only way we can really confirm someone has the disease is on autopsy. The current criteria for diagnosing Alzheimer's require an extensive evaluation, combined with fancy positron emission tomography (PET) scans and spinal taps. All of these tests are expensive and hard to get, can be invasive, and can have potential complications. On top of that, they are neither highly sensitive nor specific. The left-right nostril / peanut butter odor detection test, however, was fast, simple, non-invasive, and inexpensive. They concluded that may make peanut butter an ideal instrument for the early detection of Alzheimer's disease.

Does all this sound a bit too good to be true? It may be. A University of Pennsylvania research team was unable to replicate the results. Click here to read their paper. So at this point, the data are mixed. I'll do another post once more studies are published and we have a better handle on whether it's useful or not.

Of course, it's better to prevent Alzheimer's in the first place. Check out these videos for more information.

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

Original Link

Using a Smell Test to Diagnose Alzheimer’s Disease

Using a Smell Test to Diagnose Alzheimer's Disease.jpeg

Alzheimer's disease (AD) pathology appears to start in the part of the brain that handles smell before subsequently spreading to additional brain regions and then, ultimately, taking over much of the rest of the brain. This led some to speculate that Alzheimer's disease may begin in the nose. Perhaps there's some environmental agent that might enter the brain through some portal in the nostrils?

This is the so-called olfactory vector hypothesis. The anatomy of the nose is well suited for the transfer of things directly into the brain, since the olfactory nerves that stick out into the nose project directly into the brain, bypassing the blood-brain barrier. The nose was actually a major infection route for the polio virus. Public health officials you started cauterizing the nasal passages of schoolchildren by spraying caustic chemicals up their noses in an effort to prevent the disease.

The concern is if people breathe in some ionized metals like aluminum dust, for example, it could be transported into the brain through these olfactory nerves at a rate of about 2 millimeters an hour, which is practically 2 inches a day. Doubt has been cast on this theory, however, by a case report of a woman born with a birth defect in which she had no smell nerves yet still developed Alzheimer's-like pathology. And so, to date, all the supporting evidence is really just circumstantial. It is clear, though, that changes in the sense of smell is among the first clinical signs of Alzheimer's, occurring during the preclinical phase--that is, before there's any noticeable cognitive decline. Could we use these changes to predict or diagnose the disease?

For years, researchers have been trying to find markers of brain illness hidden in people's ability to smell using all sorts of fancy gadgets. For example, functional MRI scans can detect differences in brain activation in response to an odor. In my video, Peanut Butter Smell Test for Alzheimer's, you can see the responses to lavender. You'll see a representation of a normal brain's responses to the odor versus an Alzheimer's brain. This unequivocally demonstrates that we can pick up changes in smell function due to Alzheimer's. But do we really need a million-dollar machine?

An ingenious group of researchers at the University of Florida discovered all we may need is some peanut butter and a ruler.

Considering that the left side of the brain primarily processes what we smell through our left nostril and the right side of our brain covers the right nostril, and understanding that Alzheimer's strikes the left side more than the right, what if you performed the following experiment: Close your eyes and mouth, breathe normally through the nose, then close one nostril, and hold a foot-long ruler out from the open nostril. Once your eyes, mouth, and one nostril are closed, open a container of peanut butter at the bottom of the ruler (one foot away from your open nostril). Move the peanut butter closer by 1 centimeter upon each exhale until you can detect the odor. Then repeat the whole procedure again using your other nostril.

This is exactly what the University of Florida researchers did with their subjects. What did they find? The normal elderly control subjects in the study smelled the peanut butter as soon as it came within an average of 18 centimeters (about 7 inches) from either nostril. It was about the same, roughly 7 inches, in the right nostrils of Alzheimer's patients. But in their left nostrils, it was a mere 2 inches! The peanut butter had to be only 2 inches away before the Alzheimer's patients could detect it through their left nostrils. This happened every single time. Indeed, the researchers found that a "left nostril impairment of odor detection was present in all the patients with probable AD." There was no left-right difference in the control group; they could smell the peanut butter when it was the same distance away from both their left and right nostrils. In the Alzheimer's group, however, there was a 12-centimeter difference.

The disparity was so great that we may be able to set a cutoff value for the diagnosis of Alzheimer's. The researchers reported that "[c]ompared to patients with other causes of dementia this nostril asymmetry of odor detection...was 100% sensitive and 100% specific for probable AD," meaning no false positives and no false negatives. Compared to healthy people, it was 100% sensitive in picking up cases of probable Alzheimer's and 92% specific. What exactly does that mean? In this study, if you had Alzheimer's, there was a 100% chance of having that wide left-right discrepancy. But, if you did have that discrepancy, the chance of having Alzheimer's was only 92%. This means there were some false positives.

The reason it's only "probable" Alzheimer's is because the only way we can really confirm someone has the disease is on autopsy. The current criteria for diagnosing Alzheimer's require an extensive evaluation, combined with fancy positron emission tomography (PET) scans and spinal taps. All of these tests are expensive and hard to get, can be invasive, and can have potential complications. On top of that, they are neither highly sensitive nor specific. The left-right nostril / peanut butter odor detection test, however, was fast, simple, non-invasive, and inexpensive. They concluded that may make peanut butter an ideal instrument for the early detection of Alzheimer's disease.

Does all this sound a bit too good to be true? It may be. A University of Pennsylvania research team was unable to replicate the results. Click here to read their paper. So at this point, the data are mixed. I'll do another post once more studies are published and we have a better handle on whether it's useful or not.

Of course, it's better to prevent Alzheimer's in the first place. Check out these videos for more information.

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

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The Food Safety Risk of Organic versus Conventional

The Food Safety Risk of Organic versus Conventional.jpeg

The stated principles of organic agriculture are "health, ecology, fairness, and care," but if you ask people why they buy organic, the strongest predictor is concern for their own health. People appear to spend more for organic foods for selfish reasons, rather than altruistic motives. Although organic foods may not have more nutrients per dollar (see my video Are Organic Foods More Nutritious?), consumption of organic foods may reduce exposure to pesticide residues and antibiotic-resistant bacteria.

Food safety-wise, researchers found no difference in the risk for contamination with food poisoning bacteria in general. Both organic and conventional animal products have been found to be commonly contaminated with Salmonella and Campylobacter, for example. Most chicken samples (organic and inorganic), were found to be contaminated with Campylobacter, and about a third with Salmonella, but the risk of exposure to multidrug-resistant bacteria was lower with the organic meat. They both may carry the same risk of making us sick, but food poisoning from organic meat may be easier for doctors to treat.

What about the pesticides? There is a large body of evidence on the relation between exposure to pesticides and elevated rate of chronic diseases such as different types of cancers, diabetes, neurodegenerative disorders like Parkinson's, Alzheimer's, and ALS, as well as birth defects and reproductive disorders--but these studies were largely on people who live or work around pesticides.

Take Salinas Valley California, for example, where they spray a half million pounds of the stuff. Daring to be pregnant in an agricultural community like that may impair childhood brain development, such that pregnant women with the highest levels running through their bodies (as measured in their urine) gave birth to children with an average deficit of about seven IQ points. Twenty-six out of 27 studies showed negative effects of pesticides on brain development in children. These included attention problems, developmental disorders, and short-term memory difficulties.

Even in urban areas, if you compare kids born with higher levels of a common insecticide in their umbilical cord blood, those who were exposed to higher levels are born with brain anomalies. And these were city kids, so presumably this was from residential pesticide use.

Using insecticides inside your house may also be a contributing risk factor for childhood leukemia. Pregnant farmworkers may be doubling the odds of their child getting leukemia and increase their risk of getting a brain tumor. This has lead to authorities advocating that awareness of the potentially negative health outcome for children be increased among populations occupationally exposed to pesticides, though I don't imagine most farmworkers have much of a choice.

Conventional produce may be bad for the pregnant women who pick them, but what about our own family when we eat them?

Just because we spray pesticides on our food in the fields doesn't necessarily mean it ends up in our bodies when we eat it, or at least we didn't know that until a study was published in 2006. Researchers measured the levels of two pesticides running through children's bodies by measuring specific pesticide breakdown products in their urine. In my video, Are Organic Foods Safer?, you can see the levels of pesticides flowing through the bodies of three to 11-year olds during a few days on a conventional diet. The kids then went on an organic diet for five days and then back to the conventional diet. As you can see, eating organic provides a dramatic and immediate protective effect against exposures to pesticides commonly used in agricultural production. The study was subsequently extended. It's clear by looking at the subsequent graph in the video when the kids were eating organic versus conventional. What about adults, though? We didn't know... until now.

Thirteen men and women consumed a diet of at least 80% organic or conventional food for seven days and then switched. No surprise, during the mostly organic week, pesticide exposure was significantly reduced by a nearly 90% drop.

If it can be concluded that consumption of organic foods provides protection against pesticides, does that also mean protection against disease? We don't know. The studies just haven't been done. Nevertheless, in the meantime, the consumption of organic food provides a logical precautionary approach.

For more on organic foods:

For more on the infectious disease implications of organic versus conventional, see Superbugs in Conventional vs. Organic Chicken. Organic produce may be safer too. See Norovirus Food Poisoning from Pesticides. Organic eggs may also have lower Salmonella risk, which is an egg-borne epidemic every year in the US. See my video Who Says Eggs Aren't Healthy or Safe?

More on Parkinson's and pesticides in Preventing Parkinson's Disease With Diet.

Those surprised by the California data might have missed my video California Children Are Contaminated.

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: IFPRI -IMAGES / Flickr. This image has been modified.

Original Link

The Food Safety Risk of Organic versus Conventional

The Food Safety Risk of Organic versus Conventional.jpeg

The stated principles of organic agriculture are "health, ecology, fairness, and care," but if you ask people why they buy organic, the strongest predictor is concern for their own health. People appear to spend more for organic foods for selfish reasons, rather than altruistic motives. Although organic foods may not have more nutrients per dollar (see my video Are Organic Foods More Nutritious?), consumption of organic foods may reduce exposure to pesticide residues and antibiotic-resistant bacteria.

Food safety-wise, researchers found no difference in the risk for contamination with food poisoning bacteria in general. Both organic and conventional animal products have been found to be commonly contaminated with Salmonella and Campylobacter, for example. Most chicken samples (organic and inorganic), were found to be contaminated with Campylobacter, and about a third with Salmonella, but the risk of exposure to multidrug-resistant bacteria was lower with the organic meat. They both may carry the same risk of making us sick, but food poisoning from organic meat may be easier for doctors to treat.

What about the pesticides? There is a large body of evidence on the relation between exposure to pesticides and elevated rate of chronic diseases such as different types of cancers, diabetes, neurodegenerative disorders like Parkinson's, Alzheimer's, and ALS, as well as birth defects and reproductive disorders--but these studies were largely on people who live or work around pesticides.

Take Salinas Valley California, for example, where they spray a half million pounds of the stuff. Daring to be pregnant in an agricultural community like that may impair childhood brain development, such that pregnant women with the highest levels running through their bodies (as measured in their urine) gave birth to children with an average deficit of about seven IQ points. Twenty-six out of 27 studies showed negative effects of pesticides on brain development in children. These included attention problems, developmental disorders, and short-term memory difficulties.

Even in urban areas, if you compare kids born with higher levels of a common insecticide in their umbilical cord blood, those who were exposed to higher levels are born with brain anomalies. And these were city kids, so presumably this was from residential pesticide use.

Using insecticides inside your house may also be a contributing risk factor for childhood leukemia. Pregnant farmworkers may be doubling the odds of their child getting leukemia and increase their risk of getting a brain tumor. This has lead to authorities advocating that awareness of the potentially negative health outcome for children be increased among populations occupationally exposed to pesticides, though I don't imagine most farmworkers have much of a choice.

Conventional produce may be bad for the pregnant women who pick them, but what about our own family when we eat them?

Just because we spray pesticides on our food in the fields doesn't necessarily mean it ends up in our bodies when we eat it, or at least we didn't know that until a study was published in 2006. Researchers measured the levels of two pesticides running through children's bodies by measuring specific pesticide breakdown products in their urine. In my video, Are Organic Foods Safer?, you can see the levels of pesticides flowing through the bodies of three to 11-year olds during a few days on a conventional diet. The kids then went on an organic diet for five days and then back to the conventional diet. As you can see, eating organic provides a dramatic and immediate protective effect against exposures to pesticides commonly used in agricultural production. The study was subsequently extended. It's clear by looking at the subsequent graph in the video when the kids were eating organic versus conventional. What about adults, though? We didn't know... until now.

Thirteen men and women consumed a diet of at least 80% organic or conventional food for seven days and then switched. No surprise, during the mostly organic week, pesticide exposure was significantly reduced by a nearly 90% drop.

If it can be concluded that consumption of organic foods provides protection against pesticides, does that also mean protection against disease? We don't know. The studies just haven't been done. Nevertheless, in the meantime, the consumption of organic food provides a logical precautionary approach.

For more on organic foods:

For more on the infectious disease implications of organic versus conventional, see Superbugs in Conventional vs. Organic Chicken. Organic produce may be safer too. See Norovirus Food Poisoning from Pesticides. Organic eggs may also have lower Salmonella risk, which is an egg-borne epidemic every year in the US. See my video Who Says Eggs Aren't Healthy or Safe?

More on Parkinson's and pesticides in Preventing Parkinson's Disease With Diet.

Those surprised by the California data might have missed my video California Children Are Contaminated.

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: IFPRI -IMAGES / Flickr. This image has been modified.

Original Link

Foods Linked to ALS

Foods Linked to ALS.jpeg

As explored in my video ALS (Lou Gehrig's Disease): Fishing for Answers, there may be a link in the consumption of the neurotoxin BMAA, produced by algae blooms, and increased risk of ALS. It now appears that BMAA could be found in high concentrations in aquatic animals in many areas of the world.

This could explain ALS clustering around lakes in New Hampshire--up to 25 times the expected rate of ALS with some families eating fish several times a week. Or in Wisconsin, where the most significant ALS risk factor was the past consumption of fish out of Lake Michigan. Or clustering in Finland's Lakeland district, or seafood eaters in France, or around the Baltic sea, building up particularly in fish, mussels and oysters.

When I think of algae blooms I think of the Chesapeake bay near where I live, that gets choked off thanks in part to the poultry industry pollution. And indeed there was a recent report linking BMAA exposure to ALS in Maryland. The ALS victims, all of whom ate Chesapeake Bay blue crabs every week, lived within a half mile of each other, which raised some eyebrows at the Hopkins ALS center. And so researchers tested a few crabs, and two out of three tested positive for BMAA, indicating that the neurotoxin is present in the aquatic food chain of the Chesapeake Bay and is a potential route for human exposure.

To bring the story full circle, things in Guam, where the link between BMAA consumption and ALS was first discovered, are looking up. The ALS epidemic there may have been triggered by their acquisition of guns. Now though, the epidemic appears to be over thanks to near-extinction of the fruit bats they were eating due to over-hunting. But while the rates decline in Guam, neurodegenerative diseases like ALS around the rest of the world are on the rise.

It's plausible that humans have been exposed to some level of BMAA throughout their evolutionary history, but the increase in algae blooms as a result of human activities is probably increasing this exposure. There is a general consensus that harmful algal blooms are increasing worldwide thanks in part to industrialized agriculture (as shown in my video Diet & Amyotrophic Lateral Sclerosis-ALS). More people means more sewage, fertilizer, and manure, which can mean more algae, which may mean more exposure to this neurotoxin, leading to a possible increased incidence of neurodegenerative diseases such as Alzheimer's, Parkinson's, and ALS.

BMAA is considered a strong contender as the cause of, or at least a major contributor to the cause of both endemic and sporadic ALS and Alzheimer's disease, and possibly conferring risk for Parkinson's diseases as well. The ramifications of this discovery are enormous.

As researchers from Australia stated, "With substantial and ever growing evidence that BMAA does play a role in the onset and progression of neurodegenerative diseases, the most important question is, what mode of activity does BMAA exert?" Huh? That's not the most important question we should be asking. The most important question is "How can we reduce our risk?"

We know that the presence of BMAA in aquatic food chains could be a significant human health hazard. There may even be a synergistic toxicity between mercury and BMAA, making certain fish even riskier. Until more is known about the possible link of BMAA to Alzheimer's and ALS, it may be prudent to limit exposure of BMAA in the human diet.

For other neurotoxins found in the food supply, see Amnesic Seafood Poisoning, Essential Tremor and Diet, Ciguatera Poisoning & Chronic Fatigue Syndrome.

Other toxic substances can also build up in the aquatic food chain, for example:

In health,
Michael Greger, M.D.

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

Image Credit: Peter Miller / Flickr. This image has been modified.

Original Link