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

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

What Is the Cause of ALS?

What Is the Cause of ALS?.jpeg

Lou Gehrig's disease, known as amyotrophic lateral sclerosis or ALS, strikes healthy, middle-aged people seemingly at random. Of the major neurodegenerative diseases, it has the least hope for treatment and survival. Although mental capabilities stay intact, ALS paralyzes people, often from the outside in, and most patients die within three years when they can no longer breathe or swallow. At any given time, an estimated 30,000 are fighting for their life with it in this country. We each have about a 1 in 400 chance of developing this dreaded disease.

ALS is more common than generally recognized, with an incidence rate now close to that of multiple sclerosis. What causes it? 50 years ago scientists found that the rate of ALS among the indigenous peoples on the island of Guam was 100 times that found in the rest of the world, potentially offering a clue into the cause of the disease. So instead of 1 in 400, in some villages in Guam, 1 in 3 adults died of the disease!

Cycad trees were suspected, since the powdered seeds were a dietary staple of the natives and there were reports of livestock showing neurological disease after eating from it. And indeed, a new neurotoxin was found in the seeds, called BMAA. Maybe that's what was causing such high levels of ALS? But the amount of BMAA in the seeds people ate was so small that it was calculated that people would have to eat a thousand kilograms a day to get a toxic dose--that's around a ton of seeds daily. So, the whole cycad theory was thrown out and the trail went cold.

But then famed neurologist Oliver Sachs and colleagues had an idea. Cycad seeds were not all the natives ate. They also ate fruit bats (also known as flying foxes) who ate Cycad tree seeds. So maybe this is a case of biomagnification up the food chain, as about a "tons" worth of BMAA does accumulate in the flesh of flying foxes.

The final nail in the coffin was the detection of high levels of BMMA in the brains of six out of six native victims of the disease on autopsy, but not in control brains of healthy people that died. So with the final puzzle piece apparently in place, the solution was found to this mysterious cluster on some exotic tropical isle of ALS/PDC, so-called because the form of ALS attacking people in Guam also had signs of Parkinson's disease and dementia, so they called it ALS parkinsonism dementia complex. So when the researchers were choosing a comparison group control brains, they also included two cases of Alzheimer's disease. But these brains had BMAA in their brains too. And not only that, but these were Alzheimer's victims in Canada, on the opposite side of the globe. So the researchers ran more autopsies and found no BMAA in the control brains, but BMAA detected in all the Canadian Alzheimer's victims tested.

Canadians don't eat fruit bats. What was going on? Well, the neurotoxin isn't made by the bat, it's made by the trees, although Canadians don't eat cycad trees either. It turns out that cycad trees don't make the neurotoxin either; it's actually a blue-green algae that grows in the roots of the cycad trees which makes the BMAA that gets in the seeds, which gets in the bats, that finally gets into the people. And it's not just this specific type of blue-green algae, but nearly all types of blue-green algae found all over the world produce BMAA. Up until only about a decade ago we thought this neurotoxin was confined to this one weird tropical tree, but now we know the neurotoxin is created by algae throughout the world; from Europe to the U.S., Australia, the Middle East, and elsewhere.

If these neurotoxin-producing blue-green algae are ubiquitous throughout the world, maybe BMAA is a cause of progressive neurodegenerative diseases including ALS worldwide. Researchers in Miami put it to the test and found BMAA in the brains of Floridians who died from sporadic Alzheimer's disease and ALS, but not in the brains of those that died of a different neurodegenerative disease called Huntington's, which we know is caused by a genetic mutation, not some neurotoxin. They found significant levels of BMAA in 49 out of 50 samples from 12 Alzheimer's patients and 13 ALS patients. The results (shown in the my video ALS: Fishing for Answers) for American Alzheimer's and ALS patients from the Atlantic southeast and from Canadian Alzheimer's patients from the Pacific Northwest suggested that exposure to BMAA was widespread. The same thing was then found in the brains of those dying from Parkinson's disease. You can apparently even pick up more BMAA in the hair of live ALS patients compared to controls.

So is BMAA present in Florida seafood? Yes, in freshwater fish and shellfish, like oysters and bass, and out in the ocean as well. Some of the fish, shrimp, and crabs had levels of BMAA comparable to those found in the fruit bats of Guam.

In the U.S., fish may be the fruit bats.

Maybe the ice bucket challenge should be to not serve seafood in them. See my video Diet and Amyotrophic Lateral Sclerosis (ALS) for more.

Diet may also play a role in other neurodegenerative disorders:

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: GraphicStock. This image has been modified.

Original Link

What Is the Cause of ALS?

What Is the Cause of ALS?.jpeg

Lou Gehrig's disease, known as amyotrophic lateral sclerosis or ALS, strikes healthy, middle-aged people seemingly at random. Of the major neurodegenerative diseases, it has the least hope for treatment and survival. Although mental capabilities stay intact, ALS paralyzes people, often from the outside in, and most patients die within three years when they can no longer breathe or swallow. At any given time, an estimated 30,000 are fighting for their life with it in this country. We each have about a 1 in 400 chance of developing this dreaded disease.

ALS is more common than generally recognized, with an incidence rate now close to that of multiple sclerosis. What causes it? 50 years ago scientists found that the rate of ALS among the indigenous peoples on the island of Guam was 100 times that found in the rest of the world, potentially offering a clue into the cause of the disease. So instead of 1 in 400, in some villages in Guam, 1 in 3 adults died of the disease!

Cycad trees were suspected, since the powdered seeds were a dietary staple of the natives and there were reports of livestock showing neurological disease after eating from it. And indeed, a new neurotoxin was found in the seeds, called BMAA. Maybe that's what was causing such high levels of ALS? But the amount of BMAA in the seeds people ate was so small that it was calculated that people would have to eat a thousand kilograms a day to get a toxic dose--that's around a ton of seeds daily. So, the whole cycad theory was thrown out and the trail went cold.

But then famed neurologist Oliver Sachs and colleagues had an idea. Cycad seeds were not all the natives ate. They also ate fruit bats (also known as flying foxes) who ate Cycad tree seeds. So maybe this is a case of biomagnification up the food chain, as about a "tons" worth of BMAA does accumulate in the flesh of flying foxes.

The final nail in the coffin was the detection of high levels of BMMA in the brains of six out of six native victims of the disease on autopsy, but not in control brains of healthy people that died. So with the final puzzle piece apparently in place, the solution was found to this mysterious cluster on some exotic tropical isle of ALS/PDC, so-called because the form of ALS attacking people in Guam also had signs of Parkinson's disease and dementia, so they called it ALS parkinsonism dementia complex. So when the researchers were choosing a comparison group control brains, they also included two cases of Alzheimer's disease. But these brains had BMAA in their brains too. And not only that, but these were Alzheimer's victims in Canada, on the opposite side of the globe. So the researchers ran more autopsies and found no BMAA in the control brains, but BMAA detected in all the Canadian Alzheimer's victims tested.

Canadians don't eat fruit bats. What was going on? Well, the neurotoxin isn't made by the bat, it's made by the trees, although Canadians don't eat cycad trees either. It turns out that cycad trees don't make the neurotoxin either; it's actually a blue-green algae that grows in the roots of the cycad trees which makes the BMAA that gets in the seeds, which gets in the bats, that finally gets into the people. And it's not just this specific type of blue-green algae, but nearly all types of blue-green algae found all over the world produce BMAA. Up until only about a decade ago we thought this neurotoxin was confined to this one weird tropical tree, but now we know the neurotoxin is created by algae throughout the world; from Europe to the U.S., Australia, the Middle East, and elsewhere.

If these neurotoxin-producing blue-green algae are ubiquitous throughout the world, maybe BMAA is a cause of progressive neurodegenerative diseases including ALS worldwide. Researchers in Miami put it to the test and found BMAA in the brains of Floridians who died from sporadic Alzheimer's disease and ALS, but not in the brains of those that died of a different neurodegenerative disease called Huntington's, which we know is caused by a genetic mutation, not some neurotoxin. They found significant levels of BMAA in 49 out of 50 samples from 12 Alzheimer's patients and 13 ALS patients. The results (shown in the my video ALS: Fishing for Answers) for American Alzheimer's and ALS patients from the Atlantic southeast and from Canadian Alzheimer's patients from the Pacific Northwest suggested that exposure to BMAA was widespread. The same thing was then found in the brains of those dying from Parkinson's disease. You can apparently even pick up more BMAA in the hair of live ALS patients compared to controls.

So is BMAA present in Florida seafood? Yes, in freshwater fish and shellfish, like oysters and bass, and out in the ocean as well. Some of the fish, shrimp, and crabs had levels of BMAA comparable to those found in the fruit bats of Guam.

In the U.S., fish may be the fruit bats.

Maybe the ice bucket challenge should be to not serve seafood in them. See my video Diet and Amyotrophic Lateral Sclerosis (ALS) for more.

Diet may also play a role in other neurodegenerative disorders:

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: GraphicStock. This image has been modified.

Original Link

What Not to Add to White Rice, Potatoes, or Pasta

What Not to Add to White Rice, Potatoes, or Pasta.jpeg

Rice currently feeds almost half the human population, making it the single most important staple food in the world, but a meta-analysis of seven cohort studies following 350,000 people for up to 20 years found that higher consumption of white rice was associated with a significantly increased risk of type 2 diabetes, especially in Asian populations. They estimated each serving per day of white rice was associated with an 11% increase in risk of diabetes. This could explain why China has almost the same diabetes rates as we do.

Diabetes rates in China are at about 10%; we're at about 11%, despite seven times less obesity in China. Japan has eight times less obesity than we do, yet may have a higher incidence of newly diagnosed diabetes cases than we do--nine per a thousand compared to our eight. They're skinnier and still may have more diabetes. Maybe it's because of all the white rice they eat.

Eating whole fruit is associated with lower risk of diabetes, whereas eating fruit processed into juice may not just be neutral, but actually increases diabetes risk. In the same way, eating whole grains, like whole wheat bread or brown rice is associated with lower risk of diabetes, whereas eating white rice, a processed grain, may not just be neutral, but actually increase diabetes risk.

White rice consumption does not appear to be associated with increased risk of heart attack or stroke, though, which is a relief after an earlier study in China suggested a connection with stroke. But do we want to eat a food that's just neutral regarding some of our leading causes of death, when we can eat whole foods that are associated with lower risk of diabetes, heart attack, stroke, and weight gain?

If the modern diabetes epidemic in China and Japan has been linked to white rice consumption, how can we reconcile that with low diabetes rates just a few decades ago when they ate even more rice? If you look at the Cornell-Oxford-China Project, rural plant-based diets centered around rice were associated with relatively low risk of the so-called diseases of affluence, which includes diabetes. Maybe Asians just genetically don't get the same blood sugar spike when they eat white rice? This is not the case; if anything people of Chinese ethnicity get higher blood sugar spikes.

The rise in these diseases of affluence in China over the last half century has been blamed in part on the tripling of the consumption of animal source foods. The upsurge in diabetes has been most dramatic, and it's mostly just happened over the last decade. That crazy 9.7% diabetes prevalence figure that rivals ours is new--they appeared to have one of the lowest diabetes rates in the world in the year 2000.

So what happened to their diets in the last 20 years or so? Oil consumption went up 20%, pork consumption went up 40%, and rice consumption dropped about 30%. As diabetes rates were skyrocketing, rice consumption was going down, so maybe it's the animal products and junk food that are the problem. Yes, brown rice is better than white rice, but to stop the mounting Asian epidemic, maybe we should focus on removing the cause--the toxic Western diet. That would be consistent with data showing animal protein and fat consumption associated with increased diabetes risk.

But that doesn't explain why the biggest recent studies in Japan and China associate white rice intake with diabetes. One possibility is that animal protein is making the rice worse. If you feed people mashed white potatoes, a high glycemic food like white rice, you can see in my video If White Rice is Linked to Diabetes, What About China? the level of insulin your pancreas has to pump out to keep your blood sugars in check. But what if you added some tuna fish? Tuna doesn't have any carbs, sugar, or starch so it shouldn't make a difference. Or maybe it would even lower the mashed potato spike by lowering the glycemic load of the whole meal? Instead you get twice the insulin spike. This also happens with white flour spaghetti versus white flour spaghetti with meat. The addition of animal protein makes the pancreas work twice as hard.

You can do it with straight sugar water too. If you do a glucose challenge test to test for diabetes, where you drink a certain amount of sugar and add some meat, you get a much bigger spike than without meat. And the more meat you add, the worse it gets. Just adding a little meat to carbs doesn't seem to do much, but once you get up to around a third of a chicken breast's worth, you can elicit a significantly increased surge of insulin. This may help explain why those eating plant-based have such low diabetes rates, because animal protein can markedly potentiate the insulin secretion triggered by carbohydrate ingestion.

The protein exacerbation of the effect of refined carbs could help explain the remarkable results achieved by Dr. Kempner with a don't-try-this-at-home diet composed of mostly white rice and sugar. See my video, Kempner Rice Diet: Whipping Us Into Shape.

Refined grains may also not be good for our blood pressure (see Whole Grains May Work As Well As Drugs).

What should we be eating to best decrease our risk of diabetes? See:

And check out my summary video, How Not to Die from Diabetes.

In health,
Michael Greger, M.D.

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

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

Original Link

What Not to Add to White Rice, Potatoes, or Pasta

What Not to Add to White Rice, Potatoes, or Pasta.jpeg

Rice currently feeds almost half the human population, making it the single most important staple food in the world, but a meta-analysis of seven cohort studies following 350,000 people for up to 20 years found that higher consumption of white rice was associated with a significantly increased risk of type 2 diabetes, especially in Asian populations. They estimated each serving per day of white rice was associated with an 11% increase in risk of diabetes. This could explain why China has almost the same diabetes rates as we do.

Diabetes rates in China are at about 10%; we're at about 11%, despite seven times less obesity in China. Japan has eight times less obesity than we do, yet may have a higher incidence of newly diagnosed diabetes cases than we do--nine per a thousand compared to our eight. They're skinnier and still may have more diabetes. Maybe it's because of all the white rice they eat.

Eating whole fruit is associated with lower risk of diabetes, whereas eating fruit processed into juice may not just be neutral, but actually increases diabetes risk. In the same way, eating whole grains, like whole wheat bread or brown rice is associated with lower risk of diabetes, whereas eating white rice, a processed grain, may not just be neutral, but actually increase diabetes risk.

White rice consumption does not appear to be associated with increased risk of heart attack or stroke, though, which is a relief after an earlier study in China suggested a connection with stroke. But do we want to eat a food that's just neutral regarding some of our leading causes of death, when we can eat whole foods that are associated with lower risk of diabetes, heart attack, stroke, and weight gain?

If the modern diabetes epidemic in China and Japan has been linked to white rice consumption, how can we reconcile that with low diabetes rates just a few decades ago when they ate even more rice? If you look at the Cornell-Oxford-China Project, rural plant-based diets centered around rice were associated with relatively low risk of the so-called diseases of affluence, which includes diabetes. Maybe Asians just genetically don't get the same blood sugar spike when they eat white rice? This is not the case; if anything people of Chinese ethnicity get higher blood sugar spikes.

The rise in these diseases of affluence in China over the last half century has been blamed in part on the tripling of the consumption of animal source foods. The upsurge in diabetes has been most dramatic, and it's mostly just happened over the last decade. That crazy 9.7% diabetes prevalence figure that rivals ours is new--they appeared to have one of the lowest diabetes rates in the world in the year 2000.

So what happened to their diets in the last 20 years or so? Oil consumption went up 20%, pork consumption went up 40%, and rice consumption dropped about 30%. As diabetes rates were skyrocketing, rice consumption was going down, so maybe it's the animal products and junk food that are the problem. Yes, brown rice is better than white rice, but to stop the mounting Asian epidemic, maybe we should focus on removing the cause--the toxic Western diet. That would be consistent with data showing animal protein and fat consumption associated with increased diabetes risk.

But that doesn't explain why the biggest recent studies in Japan and China associate white rice intake with diabetes. One possibility is that animal protein is making the rice worse. If you feed people mashed white potatoes, a high glycemic food like white rice, you can see in my video If White Rice is Linked to Diabetes, What About China? the level of insulin your pancreas has to pump out to keep your blood sugars in check. But what if you added some tuna fish? Tuna doesn't have any carbs, sugar, or starch so it shouldn't make a difference. Or maybe it would even lower the mashed potato spike by lowering the glycemic load of the whole meal? Instead you get twice the insulin spike. This also happens with white flour spaghetti versus white flour spaghetti with meat. The addition of animal protein makes the pancreas work twice as hard.

You can do it with straight sugar water too. If you do a glucose challenge test to test for diabetes, where you drink a certain amount of sugar and add some meat, you get a much bigger spike than without meat. And the more meat you add, the worse it gets. Just adding a little meat to carbs doesn't seem to do much, but once you get up to around a third of a chicken breast's worth, you can elicit a significantly increased surge of insulin. This may help explain why those eating plant-based have such low diabetes rates, because animal protein can markedly potentiate the insulin secretion triggered by carbohydrate ingestion.

The protein exacerbation of the effect of refined carbs could help explain the remarkable results achieved by Dr. Kempner with a don't-try-this-at-home diet composed of mostly white rice and sugar. See my video, Kempner Rice Diet: Whipping Us Into Shape.

Refined grains may also not be good for our blood pressure (see Whole Grains May Work As Well As Drugs).

What should we be eating to best decrease our risk of diabetes? See:

And check out my summary video, How Not to Die from Diabetes.

In health,
Michael Greger, M.D.

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

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

Original Link

What Do All the Blue Zones Have in Common?

Do Flexitarians Live Longer.jpg

What accounts for the benefits of a Mediterranean-style diet? An anatomy of health effects was published, and the single most important component was the high consumption of plant foods. In contrast, fish and seafood consumption, the only animal foods promoted in the Mediterranean diet, did not seem to help.

If you look at four of the major dietary quality scoring systems, which have all been associated with extending lifespan and lowering heart disease and cancer mortality, they all share only four things in common: more fruit, more vegetables, more whole grains and more nuts and beans. They are all built on a common core of a diet rich in plant foods, whereas opposite food patterns, rich in animal foods and poor in plant-based foods (in other words, the Western diet), is associated with higher risks. So we need to optimize the food environment to support whole grains, vegetables, fruit and plant-based proteins.

That's one of the things all the so-called Blue Zones have in common: the longest living populations have not only social support and engagement and daily exercise, but nutritionally they all center their diets around plant foods, reserving meat mostly for special occasions. In fact, the population with perhaps the highest life-expectancy in the world, the California Adventist vegetarians, doesn't eat any meat at all.

So if the primary benefits of the Mediterranean diet are due to all the whole plant foods, what if you went back to the famous PREDIMED study and created a "provegetarian" scoring system? We know vegetarians live longer, but because a pure vegetarian diet might not easily be embraced by many individuals, maybe it would be easier to swallow if we just tell people more plant-based foods and less animal-based foods. But would just moving along the spectrum towards more plants actually enable people to live longer? Researchers thought of this food pattern as a "gentle approach" to vegetarianism, figuring that if it improved survival it would be an easily understandable message for health promotion: more plant foods, less animal foods.

On this scoring system, you get points for eating fruit, vegetables, nuts, grains, beans, olive oil and potatoes, but get docked points for any animal fats, eggs, fish, dairy or any type of meat or meat products. Of course that means you get a higher score the more potato chips and French fries you eat. That's why I prefer the term "whole-food, plant-based diet" since it's defined by what you eat, not by what you don't eat. When I taught at Cornell I had "vegan" students who apparently were trying to live off French fries and beer; vegan does not necessarily mean health-promoting.

But did the provegetarian scoring system work? Regardless of healthy versus unhealthy, if you give points to people for any kind of plant food, processed or not, and detract points for any kind of animal product consumption, people with higher scores live longer. The maximum provegetarian score is 60, but even just scoring 40 or more was associated with a 40 percent drop in mortality. In fact, there were so few deaths in the highest category of adherence to the provegetarian diet, they had to merge the two upper categories for their analysis. This is evidence that simple advice to increase the consumption of plant-derived foods with reductions in the consumption of foods from animal sources confers a survival advantage. You can view the graph in my video Do Flexitarians Live Longer?

The researchers conclude, "this modest change is realistic, affordable, and achievable because a sizable proportion of their population was already eating that way. So one can get significant survival benefit without a radical shift to the exclusive consumption of plant foods, a more gradual and gentle approach which is more easily translatable into public policy." A 41 percent drop in mortality rates in the United States would mean saving the lives of hundreds of thousands of Americans every year.

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

I've done a few videos on the health of so-called semi-vegetarians or flexitarians ("flexible" vegetarians). See how they rate in:

The Provegetarian Score reminds me of the animal to vegetable protein ratio in Prostate Cancer Survival: The A/V Ratio. My favorite dietary quality index is the one in Calculate Your Healthy Eating Score. How do you rate? Even the healthiest among us may be able to continue to push the envelope.

In health,

Michael Greger, M.D.

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

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

Original Link

What Do All the Blue Zones Have in Common?

Do Flexitarians Live Longer.jpg

What accounts for the benefits of a Mediterranean-style diet? An anatomy of health effects was published, and the single most important component was the high consumption of plant foods. In contrast, fish and seafood consumption, the only animal foods promoted in the Mediterranean diet, did not seem to help.

If you look at four of the major dietary quality scoring systems, which have all been associated with extending lifespan and lowering heart disease and cancer mortality, they all share only four things in common: more fruit, more vegetables, more whole grains and more nuts and beans. They are all built on a common core of a diet rich in plant foods, whereas opposite food patterns, rich in animal foods and poor in plant-based foods (in other words, the Western diet), is associated with higher risks. So we need to optimize the food environment to support whole grains, vegetables, fruit and plant-based proteins.

That's one of the things all the so-called Blue Zones have in common: the longest living populations have not only social support and engagement and daily exercise, but nutritionally they all center their diets around plant foods, reserving meat mostly for special occasions. In fact, the population with perhaps the highest life-expectancy in the world, the California Adventist vegetarians, doesn't eat any meat at all.

So if the primary benefits of the Mediterranean diet are due to all the whole plant foods, what if you went back to the famous PREDIMED study and created a "provegetarian" scoring system? We know vegetarians live longer, but because a pure vegetarian diet might not easily be embraced by many individuals, maybe it would be easier to swallow if we just tell people more plant-based foods and less animal-based foods. But would just moving along the spectrum towards more plants actually enable people to live longer? Researchers thought of this food pattern as a "gentle approach" to vegetarianism, figuring that if it improved survival it would be an easily understandable message for health promotion: more plant foods, less animal foods.

On this scoring system, you get points for eating fruit, vegetables, nuts, grains, beans, olive oil and potatoes, but get docked points for any animal fats, eggs, fish, dairy or any type of meat or meat products. Of course that means you get a higher score the more potato chips and French fries you eat. That's why I prefer the term "whole-food, plant-based diet" since it's defined by what you eat, not by what you don't eat. When I taught at Cornell I had "vegan" students who apparently were trying to live off French fries and beer; vegan does not necessarily mean health-promoting.

But did the provegetarian scoring system work? Regardless of healthy versus unhealthy, if you give points to people for any kind of plant food, processed or not, and detract points for any kind of animal product consumption, people with higher scores live longer. The maximum provegetarian score is 60, but even just scoring 40 or more was associated with a 40 percent drop in mortality. In fact, there were so few deaths in the highest category of adherence to the provegetarian diet, they had to merge the two upper categories for their analysis. This is evidence that simple advice to increase the consumption of plant-derived foods with reductions in the consumption of foods from animal sources confers a survival advantage. You can view the graph in my video Do Flexitarians Live Longer?

The researchers conclude, "this modest change is realistic, affordable, and achievable because a sizable proportion of their population was already eating that way. So one can get significant survival benefit without a radical shift to the exclusive consumption of plant foods, a more gradual and gentle approach which is more easily translatable into public policy." A 41 percent drop in mortality rates in the United States would mean saving the lives of hundreds of thousands of Americans every year.

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

I've done a few videos on the health of so-called semi-vegetarians or flexitarians ("flexible" vegetarians). See how they rate in:

The Provegetarian Score reminds me of the animal to vegetable protein ratio in Prostate Cancer Survival: The A/V Ratio. My favorite dietary quality index is the one in Calculate Your Healthy Eating Score. How do you rate? Even the healthiest among us may be able to continue to push the envelope.

In health,

Michael Greger, M.D.

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

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

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Ciguatera Poisoning & Chronic Fatigue Syndrome

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Ciguatera is one of the most common forms of food poisoning, which occurs after the consumption of fish contaminated with neurotoxins produced by certain microalgae that build up the food chain. Just a few bites can be sufficient to induce the condition. Disturbingly, affected fish looks, smells, and tastes normal, and ciguatoxins are resistant to all forms of cooking. So, there is no straightforward method to predict whether a seafood meal can turn into a ciguatera nightmare.

It literally can cause nightmares; about one in six may experience signs of hallucinatory poisoning: lack of coordination, hallucinations, depression, and nightmares. Most suffer some kind of neurological symptoms such as tingling, numbness, and a burning cold sensation. Sometimes a reversal of temperature sensation occurs, where cold objects feel hot and vice versa. For instance, ciguatera sufferers have reported that a refreshing dive in the ocean actually caused burning pain, or that drinking cool beer felt like too hot coffee.

The toxin may also be apparently sexually transmitted, or as one of my favorite public health bloggers put it, "when hot sex turns cold and painful, blame it on dinner."

As seen in my video Ciguatera Poisoning & Chronic Fatigue Syndrome, the symptoms can persist for months or even years. Ongoing research has shown that people with chronic fatigue syndrome may actually be suffering the long-term effects of this fish food poisoning or a condition called polymyositis, which causes diffuse muscle aches, pains, and inflammation. Some individuals intoxicated by fish consumption 25 years previously experience a recurrence of the main neurological disturbances during periods of overwork, fatigue, or stress. You can still find the toxins stuck in your body decades later.

Recent outbreaks in New York City have drawn attention to the problem. For example, a man ate grouper at a Manhattan restaurant and went from swimming two miles a day to having difficulty walking that lasted for months. But these aren't just rare anecdotes. Ciguatera fish poisoning affects an estimated 15,000 Americans every year, causing hundreds of hospitalizations and even a few deaths. Because the toxins are colorless, odorless, tasteless, and not destroyed by cooking, CDC scientists suggest "education aimed at the prevention of seafood intoxication by avoidance of high-risk fish altogether."

The AMA put out a similar advisory, suggesting that the only way to prevent it is to avoid eating fish like red snapper or grouper, but the problem is that a third of fish sold in the United States is mislabeled, so we don't know what we're getting. Some suggest first feeding a portion of the fish meal to a cat, treating them like a court tester, and if they're okay six hours later, we can dig in -- but this was considered inhumane. But if it's inhumane to feed it to your cat, how is it not inhumane to feed it to other members of the family?

Many more are killed by more conventional food poisoning bugs (Chicken Salmonella Thanks to Meat Industry Lawsuit), but how scary that you can get these toxins stuck in you and ruin your life? Reminds me of my Amnesic Seafood Poisoning video.

Other neurotoxin videos include Preventing Parkinson's Disease With Diet and Essential Tremor and Diet.

In health,
Michael Greger, M.D.

PS: If you haven't yet, you can subscribe to my free videos here and watch my live, year-in-review presentations--2013: Uprooting the Leading Causes of Death, More Than an Apple a Day, 2014: From Table to Able: Combating Disabling Diseases with Food, 2015: Food as Medicine: Preventing and Treating the Most Dreaded Diseases with Diet, and my latest, 2016: How Not To Die: The Role of Diet in Preventing, Arresting, and Reversing Our Top 15 Killers.

Image Credit: Pen Waggener / Flickr

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How to Reduce Your Dietary Cadmium Absorption

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Cadmium is known as a highly toxic metal that represents a major hazard to human health. It sticks around in our body for decades because our body has no efficient way to get rid of it and may contribute to a variety of illnesses, including heart disease, cancer, and diabetes.

Most recently, data suggests that cadmium exposure may impair cognitive performance even at levels once thought to be safe. Recent studies also suggest that cadmium exposure may produce other adverse health effects at lower exposure levels than previously predicted, including increased risk of hormonal cancers. For example, researchers on Long Island estimated that as much as a third of breast cancer in the U.S. might be associated with elevated cadmium levels.

Inhalation of cigarette smoke is one of the major routes for human exposure to cadmium. Seafood consumption is another route of human exposure. The highest levels, though, are found in organ meats. But how many horse kidneys do people eat? Since people eat so few organs, grains and vegetables actually end up contributing the largest amount to our collective diets.

However, don't drop the salad from the menu yet.

Whole grains and vegetables are among the major dietary sources of fiber, phytoestrogens, and antioxidants that may protect against breast cancer. Indeed, even though the risk of breast cancer goes up as women consume more and more cadmium, and even though on paper most cadmium comes from grains and vegetables, breast cancer risk goes down the more and more whole grains and vegetables women eat. So are animal sources of cadmium somehow worse, or do the benefits of plant foods just overwhelm any adverse effects of the cadmium?

A study out of the Journal of the Medical Association of Thailand highlighted in my video, Cadmium and Cancer: Plant vs. Animal Foods, may have helped solve the mystery. It's not what we eat, it's what we absorb.

Cadmium bioavailability from animal-based foods may be higher than that from vegetable-based foods. There appears to be something in plants that inhibits cadmium absorption. In fact, researchers found when they added kale to boiled pig kidneys, they could cut down on the toxic exposure. Just one tablespoon of pig kidney, and we may exceed the daily safety limit--unless we add kale, in which case we could eat a whole quarter cup. The pronounced effects of the inhibitory factors in kale point out, as the researchers note, "the importance of vegetable foods in terms of prevention of health hazard from [cadmium] ingested as mixed diets in a real situation."

Reesearchers have concluded: "Even if a vegetarian diet contains more lead and cadmium than a mixed diet, it is not certain that it will give rise to higher uptake of the metals, because the absorption of lead and cadmium is inhibited by plant components such as fiber and phytate." Having whole grains in our stomach up to three hours before we swallow lead can eliminate 90% of absorption, thought to be due to phytates in whole grains, nuts, and beans grabbing onto it.

So vegetarians may have lower levels of lead and cadmium even though they have higher intakes.

In fact, there is a significant decrease in the hair concentrations of lead and cadmium after the change from an omnivorous to a vegetarian diet, indicating a lower absorption of the metals. Researchers took folks eating a standard Swedish diet and put them on a vegetarian diet. The vegetarians were encouraged to eat lots of whole, unrefined plant foods, with no meat, poultry, fish, and eggs. Junk food was also discouraged. Within three months on a vegetarian diet, their levels significantly dropped, and stayed down for the rest of the year-long experiment. The researchers came back three years later, three years after the subjects stopped eating vegetarian, and found that their levels of mercury, cadmium, and lead had shot back up.

Since the cadmium in plants is based on the cadmium in soil, plant-eaters that live in a really polluted area like Slovakia, which has some of the highest levels thanks to the chemical and smelting industries, can indeed build up higher cadmium levels, especially if they eat lots of plants. It's interesting that, "in spite of the significantly higher blood cadmium concentration as a consequence of a greater cadmium intake from polluted plants, all the antioxidants in those same plants were found to help inhibit the harmful effects of higher free radical production caused by the cadmium exposure." Still, though, in highly polluted areas it might be an especially good idea not to smoke or eat too much seafood or organ meats. But even if we live in the Slovak Republic's "black triangle of pollution," the benefits of whole plant foods would outweigh the risks. For people in highly polluted areas, zinc supplements may decrease cadmium absorption, but I'd recommend against multi-mineral supplements, as they have been found to be contaminated with cadmium itself.

There are other toxins in cigarette smoke also found in food. See:

Toxic metals have also been found in dietary supplements. See for example, Get the Lead Out and Heavy Metals in Protein Powder Supplements.

Mercury is also a serious problem. See:

More on pollution in seafood can be found in:

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 Uprooting the Leading Causes of Death, More Than an Apple a Day, From Table to Able, and Food as Medicine.

Image Credit: Julie / Flickr

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