How to Prevent a Heart Attack

How to Prevent a Heart Attack.jpeg

In my video Arterial Acne, I described atherosclerotic plaques as inflamed pockets of pus. Our coronary arteries start out healthy, but then the saturated fat, trans fat, and cholesterol in the standard American diet increases the cholesterol in our blood, which accumulates in the artery wall. This triggers an inflammatory response. This so-called fatty streak can then grow into an atherosclerotic plaque, which has the potential to rupture into our artery. If that happens, a blood clot forms, shutting off blood flow to a part of our heart, which can then die off and ultimately kill us.

What causes that final step, the rupture of the plaque? Ten years ago, researchers at Michigan State proposed a mechanism. They noted that when you look at ruptured plaques from autopsies of people who died from heart attacks, they were filled with cholesterol crystals protruding out from the plaque. So, the researchers wondered if maybe all that cholesterol in the plaque gets so supersaturated that it reaches a point where it crystallizes like sugar water forming rock candy. The growing crystals may then burst the plaque open.

To test out this theory they first made a supersaturated solution of cholesterol in a test tube to see if it expanded when it crystallized, and indeed it did-just like how water expands when it crystallizes into ice. In my video Cholesterol Crystals May Tear Through Our Artery Lining, you can see a massive cholesterol crystal shooting out the top of a test tube. Under a microscope, the tips of the cholesterol crystals were sharp jagged needles.

The researchers tried placing a thin membrane over the top of the test tube to see if the cholesterol needles would poke through, and indeed the sharp tips of the cholesterol crystals cut through the membrane. This suggested that the crystallization of supersaturated cholesterol in atherosclerotic plaques could indeed induce the rupture that kills us.

A test tube is one thing, but can you actually see crystals poking out in autopsy specimens? Yes, cholesterol crystals piercing the arterial plaque were found in patients who died with heart attacks, with extensive protrusions of cholesterol crystals into the middle of the artery.

What makes us think it was the crystals that actually burst the plaque? All those studied who died of acute heart attacks had perforating cholesterol crystals sticking out of their plaques, but no crystals were found perforating the arteries of people who had severe atherosclerosis, but died first of other, non-cardiac causes.

This can explain why dramatically lowering cholesterol levels with diet (and drugs, if necessary) can reduce the risk of fatal heart attack, by pulling cholesterol out of the artery wall, and decreasing the risk of crystallizing these cholesterol needles that may pop your plaque.

Given the powerful visuals, my Cholesterol Crystals May Tear Through Our Artery Lining video might be a good one to share with those in your life with heart disease, in hopes that they might reconsider eating artery-clogging diets.

Blocking the First Step of Heart Disease involves keeping our LDL cholesterol low by decreasing our intake of Trans Fat, Saturated Fat, and Cholesterol: Tolerable Upper Intake of Zero. Swapping red meat for white won't do it: Switching From Beef to Chicken and Fish May Not Lower Cholesterol

Does it matter if LDL cholesterol in our blood is small and dense or large and fluffy? See my video Does Cholesterol Size Matter?

In health,

Michael Greger, M.D.

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

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

Original Link

The Five Most Important Dietary Tweaks

The Five Most Important Dietary Tweaks.jpeg

Generally, adherence to healthy lifestyle patterns has decreased during the last 18 years. Obesity is up, exercise is down, and the number of people eating just five servings of fruits and veggies a day dropped like a rock. And we didn't start out that great to begin with.

Only 3% of Americans at the turn of the 21st century had the following four healthy lifestyle characteristics: not smoking, not overweight, five daily servings of fruits and vegetables, and exercising a half hour a day at least five days a week. Whether people were wealthy or college-educated didn't matter; no sub-group even remotely met clinical or public health recommendations.

Where are people falling down the most? You can see in my video What Percent of Americans Lead Healthy Lifestyles?. If you look at heart disease risk factors, for example, most people don't smoke and about half are exercising. But if we look at the healthy diet score-which is based on things like drinking less than four cups of soda a week-a scale of zero to five, only about 1% of Americans score a four or five. The American Heart Association's aggressive 2020 target to improve that by 20% would bring us up to 1.2%.

Since we've known for decades that advanced coronary artery disease may be present by age 20--with atherosclerosis often even present in young children--it is particularly disturbing that healthy lifestyle choices are declining rather than improving in the U.S.

In terms of life expectancy, the U.S. is down around 27 or 28 out of the 34 OECD free-market democracies. The people of Slovenia live a year longer than citizens of the United States. Why? According to the most rigorous analysis of risk factors ever published, the number one cause of death and disability in the United States is our diet.

It's the food.

According to the Global Burden of Disease study, the worst five things about our diet are: we don't eat enough fruit, we don't eat enough nuts and seeds, we eat too much salt, too much processed meat, and not enough vegetables.

Studies that have looked at diet quality and chronic disease mortality risk found that those scoring higher (e.g. more whole plant foods), reduced the risk of dying prematurely from heart disease, cancer, and all causes of death combined. There is now an overwhelming body of clinical and epidemiological evidence illustrating the dramatic impact of a healthy lifestyle on reducing all-cause mortality and preventing chronic diseases such as coronary heart disease, stroke, diabetes, and cancer.

Why do we eat so poorly? Aren't we scared of dying from these horrible chronic diseases? It's almost as if we're eating as though our future didn't matter. And there's actually data to back that up, from a study entitled Death Row Nutrition.

The growing macabre fascination with speculating about one's ''last meal'' offers a window into one's true consumption desires when one's value of the future is discounted close to zero. In contrast to pop culture anecdotes, a group of Cornell researchers created a catalog of actual last meals-the final food requests of 247 individuals executed in the United States during a recent five-year period. Meat was the most common request. The researchers go out of their way to note that tofu never made the list, and no one asked for a vegetarian meal. In fact, if you compare the last meals to what Americans normally eat, there's not much difference.

If we continue to eat as though they were our last meals, eventually, they will be.


A few years ago I did a video called Nation's Diet in Crisis. It's sad that it doesn't seem like much has changed. How Many Meet the Simple Seven? is another video in which you can see how your own habits stack up.

For more on fruits and veggies and living longer, see Fruits and Longevity: How Many Minutes per Mouthful? Surprised that nuts made the longevity list? See Nuts May Help Prevent Death. What about legumes? See Increased Lifespan from Beans.

The reason public health professionals are so keen on measuring lifestyle characteristics is because modest improvements may have extraordinary effects. See, for example:

Didn't know the beginnings of heart disease may already be present in children? See my video Heart Disease Starts in Childhood. Think that's tragic? Check out Heart Disease May Start in the Womb. Is it too late if we've been eating poorly most of our lives? It's Never Too Late to Start Eating Healthier.

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 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

Benefits of Oatmeal for Fatty Liver Disease

Benefits of Oatmeal for Fatty Liver Disease.jpeg

If oatmeal is so powerful that it can clear up some of the ravages of chemotherapy just applied to the skin (see my video Oatmeal Lotion for Chemotherapy-Induced Rash), what might it do if we actually ate it? Oats are reported to possess varied drug-like activities like lowering blood cholesterol and blood sugar, boosting our immune system, anticancer, antioxidant, and anti-atherosclerosis activites, in addition to being a topical anti-inflammatory, and reprtedly may also be useful in controlling childhood asthma and body weight.

Whole-grain intake in general is associated with lower risk of type 2 diabetes, cardiovascular disease, and weight gain, as shown in my video Can Oatmeal Help Fatty Liver Disease?. All of the cohort studies on type 2 diabetes and heart disease show whole grain intake is associated with lower risk.

Researchers have observed the same for obesity--consistently less weight gain for those who consumed a few servings of whole grains every day. All the forward-looking population studies demonstrate that a higher intake of whole grains is associated with lower body mass index and body weight gain. However, these results do not clarify whether whole grain consumption is simply a marker of a healthier lifestyle or a factor favoring lower body weight.

For example, high whole grain consumers--those who eat whole wheat, brown rice, and oatmeal for breakfast--tend to be more physically active, smoke less, and consume more fruit, vegetables, and dietary fiber than those that instead reach for fruit loops. Statistically, one can control these factors, effectively comparing nonsmokers to nonsmokers with similar exercise and diet as most of the studies did, and they still found whole grains to be protective via a variety of mechanisms.

For example, in terms of helping with weight control, the soluble fiber of oatmeal forms a gel in the stomach, delaying stomach emptying, making one feel full for a longer period. It seems plausible that whole grain intake does indeed offer direct benefits, but only results of randomized controlled intervention studies can provide direct evidence of cause and effect. In other words, the evidence is clear that oatmeal consumers have lower rates of disease, but that's not the same as proving that if we start eating more oatmeal, our risk will drop. To know that, we need an interventional trial, ideally a blinded study where you give half the people oatmeal, and the other half fake placebo oatmeal that looks and tastes like oatmeal, to see if it actually works. And that's what we finally got--a double-blinded randomized trial of overweight and obese men and women. Almost 90% of the real oatmeal-treated subjects had reduced body weight, compared to no weight loss in the control group. They saw a slimmer waist on average, a 20 point drop in cholesterol, and an improvement in liver function.

Nonalcoholic fatty liver disease, meaning a fatty liver caused by excess food rather than excess drink, is now the most common cause of liver disease in the United States, and can lead in rare cases to cirrhosis of the liver, cancer of the liver, and death. Theoretically, whole grains could help prevent and treat fatty liver disease, but this is the first time it had been put to the test. A follow-up study in 2014 confirmed these findings of a protective role of whole grains, but refined grains was associated with increased risk. So one would not expect to get such wonderful results from wonder bread.

How can you make your oatmeal even healthier? See Antioxidants in a Pinch.

Whole Grains May Work As Well As Drugs for hypertension, but refined grain intake may linked with high blood pressure and diseases like diabetes. But If White Rice is Linked to Diabetes, What About China?.

More on keeping the liver healthy in videos like:

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

Benefits of Oatmeal for Fatty Liver Disease

Benefits of Oatmeal for Fatty Liver Disease.jpeg

If oatmeal is so powerful that it can clear up some of the ravages of chemotherapy just applied to the skin (see my video Oatmeal Lotion for Chemotherapy-Induced Rash), what might it do if we actually ate it? Oats are reported to possess varied drug-like activities like lowering blood cholesterol and blood sugar, boosting our immune system, anticancer, antioxidant, and anti-atherosclerosis activites, in addition to being a topical anti-inflammatory, and reprtedly may also be useful in controlling childhood asthma and body weight.

Whole-grain intake in general is associated with lower risk of type 2 diabetes, cardiovascular disease, and weight gain, as shown in my video Can Oatmeal Help Fatty Liver Disease?. All of the cohort studies on type 2 diabetes and heart disease show whole grain intake is associated with lower risk.

Researchers have observed the same for obesity--consistently less weight gain for those who consumed a few servings of whole grains every day. All the forward-looking population studies demonstrate that a higher intake of whole grains is associated with lower body mass index and body weight gain. However, these results do not clarify whether whole grain consumption is simply a marker of a healthier lifestyle or a factor favoring lower body weight.

For example, high whole grain consumers--those who eat whole wheat, brown rice, and oatmeal for breakfast--tend to be more physically active, smoke less, and consume more fruit, vegetables, and dietary fiber than those that instead reach for fruit loops. Statistically, one can control these factors, effectively comparing nonsmokers to nonsmokers with similar exercise and diet as most of the studies did, and they still found whole grains to be protective via a variety of mechanisms.

For example, in terms of helping with weight control, the soluble fiber of oatmeal forms a gel in the stomach, delaying stomach emptying, making one feel full for a longer period. It seems plausible that whole grain intake does indeed offer direct benefits, but only results of randomized controlled intervention studies can provide direct evidence of cause and effect. In other words, the evidence is clear that oatmeal consumers have lower rates of disease, but that's not the same as proving that if we start eating more oatmeal, our risk will drop. To know that, we need an interventional trial, ideally a blinded study where you give half the people oatmeal, and the other half fake placebo oatmeal that looks and tastes like oatmeal, to see if it actually works. And that's what we finally got--a double-blinded randomized trial of overweight and obese men and women. Almost 90% of the real oatmeal-treated subjects had reduced body weight, compared to no weight loss in the control group. They saw a slimmer waist on average, a 20 point drop in cholesterol, and an improvement in liver function.

Nonalcoholic fatty liver disease, meaning a fatty liver caused by excess food rather than excess drink, is now the most common cause of liver disease in the United States, and can lead in rare cases to cirrhosis of the liver, cancer of the liver, and death. Theoretically, whole grains could help prevent and treat fatty liver disease, but this is the first time it had been put to the test. A follow-up study in 2014 confirmed these findings of a protective role of whole grains, but refined grains was associated with increased risk. So one would not expect to get such wonderful results from wonder bread.

How can you make your oatmeal even healthier? See Antioxidants in a Pinch.

Whole Grains May Work As Well As Drugs for hypertension, but refined grain intake may linked with high blood pressure and diseases like diabetes. But If White Rice is Linked to Diabetes, What About China?.

More on keeping the liver healthy in videos like:

In health,
Michael Greger, M.D.

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

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

Original Link

Why Is Milk Consumption Associated with More Bone Fractures?

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

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

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

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

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

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

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

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

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

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

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

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

In health,

Michael Greger, M.D.

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

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

Original Link

Why Is Milk Consumption Associated with More Bone Fractures?

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

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

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

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

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

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

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

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

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

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

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

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

In health,

Michael Greger, M.D.

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

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

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.

Original Link