Clostridium difficile in the Food Supply

Clostridium difficile in the Food Supply.jpeg

Clostridium difficile is one of our most urgent bacterial threats, sickening a quarter million Americans every year, and killing thousands at the cost of a billion dollars a year. And it's on the rise.

As shown in C. difficile Superbugs in Meat, uncomplicated cases have been traditionally managed with powerful antibiotics, but recent reports suggest that hypervirulent strains are increasingly resistant to medical management. There's been a rise in the percentage of cases that end up under the knife, which could be a marker of the emergence of these hypervirulent strains. Surgeons may need to remove our colon entirely to save our lives, although the surgery is so risky that the operation alone may kill us half the time.

Historically, most cases appeared in hospitals, but a landmark study published in the New England Journal of Medicine found that only about a third of cases could be linked to contact with an infected patient.

Another potential source is our food supply.

In the US, the frequency of contamination of retail chicken with these superbugs has been documented to be up to one in six packages off of store shelves. Pig-derived C. diff, however, have garnered the greatest attention from public health personnel, because the same human strain that's increasingly emerging in the community outside of hospitals is the major strain among pigs.

Since the turn of the century, C. diff is increasingly being reported as a major cause of intestinal infections in piglets. C. diff is now one of the most common causes of intestinal infections in baby piglets in the US. Particular attention has been paid to pigs because of high rates of C. diff shedding into their waste, which can lead to the contamination of retail pork. The U.S. has the highest levels of C. diff meat contamination tested so far anywhere in the world.

Carcass contamination by gut contents at slaughter probably contributes most to the presence of C. diff in meat and meat products. But why is the situation so much worst in the US? Slaughter techniques differ from country-to-country, with those in the United States evidently being more of the "quick and dirty" variety.

Colonization or contamination of pigs by superbugs such as C. difficile and MRSA at the farm production level may be more important than at the slaughterhouse level, though. One of the reasons sows and their piglets may have such high rates of C. diff is because of cross-contamination of feces in the farrowing crate, which are narrow metal cages that mother pigs are kept in while their piglets are nursing.

Can't you just follow food safety guidelines and cook the meat through? Unfortunately, current food safety guidelines are ineffective against C. difficile. To date, most food safety guidelines recommend cooking to an internal temperature as low as 63o C-the official USDA recommendation for pork-but recent studies show that C. diff spores can survive extended heating at 71o. Therefore, the guidelines should be raised to take this potentially killer infection into account.

One of the problems is that sources of C. diff food contamination might include not only fecal contamination on the surface of the meat, but transfer of spores from the gut into the actual muscles of the animal, inside the meat. Clostridia bacteria like C. diff comprise one of the main groups of bacteria involved in natural carcass degradation, and so by colonizing muscle tissue before death, C. diff can not only transmit to new hosts that eat the muscles, like us, but give them a head start on carcass break-down.

Never heard of C. diff? That's the Toxic Megacolon Superbug I've talked about before.

Another foodborne illness tied to pork industry practices is yersiniosis. See Yersinia in Pork.

MRSA (Methicillin-resistant Staph aureus) is another so-called superbug in the meat supply:

More on the scourge of antibiotic resistance and what can be done about it:

How is it even legal to sell foods with such pathogens? See Salmonella in Chicken & Turkey: Deadly But Not Illegal and Chicken Salmonella Thanks to Meat Industry Lawsuit.

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: USDA / Flickr. This image has been modified.

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White Meat May Be as Cholesterol-Raising as Red

White Meat May Be as Cholesterol-Raising as Red.jpeg

In light of recommendations for heart healthy eating from national professional organizations encouraging Americans to limit their intake of meat, the beef industry commissioned and co-wrote a review of randomized controlled trials comparing the effects of beef versus chicken and fish on cholesterol levels published over the last 60 years. They found that the impact of beef consumption on the cholesterol profile of humans is similar to that of fish and/or poultry--meaning that switching from red meat to white meat likely wouldn't make any difference. And that's really no surprise, given how fat we've genetically manipulated chickens to be these days, up to ten times more fat than they had a century ago (see Does Eating Obesity Cause Obesity?).

There are a number of cuts of beef that have less cholesterol-raising saturated fat than chicken (see BOLD Indeed: Beef Lowers Cholesterol?), so it's not so surprising that white meat was found to be no better than red, but the beef industry researchers conclusion was that "therefore you can eat beef as part of a balanced diet to manage your cholesterol."

Think of the Coke versus Pepsi analogy. Coke has less sugar than Pepsi: 15 spoonfuls of sugar per bottle instead of 16. If studies on blood sugar found no difference between drinking Coke versus Pepsi, you wouldn't conclude that "Pepsi may be considered when recommending diets for the management of blood sugars," you'd say they're both equally as bad so we should ideally consume neither.

That's a standard drug industry trick. You don't compare your fancy new drug to the best out there, but to some miserable drug to make yours look better. Note they didn't compare beef to plant proteins, like in this study published in the American Journal of Clinical Nutrition. As I started reading it, though, I was surprised that they found no benefit of switching to a plant protein diet either. What were they eating? You can see the comparison in Switching from Beef to Chicken & Fish May Not Lower Cholesterol.

For breakfast, the plant group got a kidney bean and tomato casserole and a salad, instead of a burger. And for dinner, instead of another burger, the plant protein group just got some boring vegetables. So why was the cholesterol of the plant group as bad as the animal group? They had the plant protein group eating three tablespoons of beef tallow every day--three tablespoons of straight beef fat!

This was part of a series of studies that tried to figure out what was so cholesterol-raising about meat--was it the animal protein or was it the animal fat? So, researchers created fake meat products made to have the same amount of saturated fat and cholesterol by adding extracted animal fats and cholesterol. Who could they get to make such strange concoctions? The Ralston Purina dog food company.

But what's crazy is that even when keeping the saturated animal fat and cholesterol the same (by adding meat fats to the veggie burgers and making the plant group swallow cholesterol pills to equal it out), sometimes they still saw a cholesterol lowering advantage in the plant protein group.

If you switch people from meat to tofu, their cholesterol goes down, but what if you switch them from meat to tofu plus lard? Then their cholesterol may stay the same, though tofu and lard may indeed actually be better than meat, since it may result in less oxidized cholesterol. More on the role of oxidized cholesterol can be found in my videos Does Cholesterol Size Matter? and Arterial Acne.

Just swapping plant protein for animal protein may have advantages, but if you really want to maximize the power of diet to lower cholesterol, you may have to move entirely toward plants. The standard dietary advice to cut down on fatty meat, dairy, and eggs may lower cholesterol 5-10%, but flexitarian or vegetarian diets may drop our levels 10 to 15%, vegan diets 15 to 25%, and healthier vegan diets can cut up to 35%, as seen in this study out of Canada showing a whopping 61 point drop in LDL cholesterol within a matter of weeks.


You thought chicken was a low-fat food? It used to be a century ago, but not anymore. It may even be one of the reasons we're getting fatter as well: Chicken Big: Poultry and Obesity and Infectobesity: Adenovirus 36 and Childhood Obesity.

Isn't protein just protein? How does our body know if it's coming from a plant or an animal? How could it have different effects on cardiovascular risk? See Protein and Heart Disease, another reason why Plant Protein [is] Preferable.

Lowering cholesterol in your blood is as simple as reducing one's intake of three things: Trans Fat, Saturated Fat, and Cholesterol: Tolerable Upper Intake of Zero.

What about those news stories on the "vindication" of saturated fat? See the sneaky science in The Saturated Fat Studies: Buttering Up the Public and The Saturated Fat Studies: Set Up to Fail.

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: CDC/Debora Cartagena via Freestockphotos.biz. This image has been modified.

Original Link

White Meat May Be as Cholesterol-Raising as Red

White Meat May Be as Cholesterol-Raising as Red.jpeg

In light of recommendations for heart healthy eating from national professional organizations encouraging Americans to limit their intake of meat, the beef industry commissioned and co-wrote a review of randomized controlled trials comparing the effects of beef versus chicken and fish on cholesterol levels published over the last 60 years. They found that the impact of beef consumption on the cholesterol profile of humans is similar to that of fish and/or poultry--meaning that switching from red meat to white meat likely wouldn't make any difference. And that's really no surprise, given how fat we've genetically manipulated chickens to be these days, up to ten times more fat than they had a century ago (see Does Eating Obesity Cause Obesity?).

There are a number of cuts of beef that have less cholesterol-raising saturated fat than chicken (see BOLD Indeed: Beef Lowers Cholesterol?), so it's not so surprising that white meat was found to be no better than red, but the beef industry researchers conclusion was that "therefore you can eat beef as part of a balanced diet to manage your cholesterol."

Think of the Coke versus Pepsi analogy. Coke has less sugar than Pepsi: 15 spoonfuls of sugar per bottle instead of 16. If studies on blood sugar found no difference between drinking Coke versus Pepsi, you wouldn't conclude that "Pepsi may be considered when recommending diets for the management of blood sugars," you'd say they're both equally as bad so we should ideally consume neither.

That's a standard drug industry trick. You don't compare your fancy new drug to the best out there, but to some miserable drug to make yours look better. Note they didn't compare beef to plant proteins, like in this study published in the American Journal of Clinical Nutrition. As I started reading it, though, I was surprised that they found no benefit of switching to a plant protein diet either. What were they eating? You can see the comparison in Switching from Beef to Chicken & Fish May Not Lower Cholesterol.

For breakfast, the plant group got a kidney bean and tomato casserole and a salad, instead of a burger. And for dinner, instead of another burger, the plant protein group just got some boring vegetables. So why was the cholesterol of the plant group as bad as the animal group? They had the plant protein group eating three tablespoons of beef tallow every day--three tablespoons of straight beef fat!

This was part of a series of studies that tried to figure out what was so cholesterol-raising about meat--was it the animal protein or was it the animal fat? So, researchers created fake meat products made to have the same amount of saturated fat and cholesterol by adding extracted animal fats and cholesterol. Who could they get to make such strange concoctions? The Ralston Purina dog food company.

But what's crazy is that even when keeping the saturated animal fat and cholesterol the same (by adding meat fats to the veggie burgers and making the plant group swallow cholesterol pills to equal it out), sometimes they still saw a cholesterol lowering advantage in the plant protein group.

If you switch people from meat to tofu, their cholesterol goes down, but what if you switch them from meat to tofu plus lard? Then their cholesterol may stay the same, though tofu and lard may indeed actually be better than meat, since it may result in less oxidized cholesterol. More on the role of oxidized cholesterol can be found in my videos Does Cholesterol Size Matter? and Arterial Acne.

Just swapping plant protein for animal protein may have advantages, but if you really want to maximize the power of diet to lower cholesterol, you may have to move entirely toward plants. The standard dietary advice to cut down on fatty meat, dairy, and eggs may lower cholesterol 5-10%, but flexitarian or vegetarian diets may drop our levels 10 to 15%, vegan diets 15 to 25%, and healthier vegan diets can cut up to 35%, as seen in this study out of Canada showing a whopping 61 point drop in LDL cholesterol within a matter of weeks.


You thought chicken was a low-fat food? It used to be a century ago, but not anymore. It may even be one of the reasons we're getting fatter as well: Chicken Big: Poultry and Obesity and Infectobesity: Adenovirus 36 and Childhood Obesity.

Isn't protein just protein? How does our body know if it's coming from a plant or an animal? How could it have different effects on cardiovascular risk? See Protein and Heart Disease, another reason why Plant Protein [is] Preferable.

Lowering cholesterol in your blood is as simple as reducing one's intake of three things: Trans Fat, Saturated Fat, and Cholesterol: Tolerable Upper Intake of Zero.

What about those news stories on the "vindication" of saturated fat? See the sneaky science in The Saturated Fat Studies: Buttering Up the Public and The Saturated Fat Studies: Set Up to Fail.

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: CDC/Debora Cartagena via Freestockphotos.biz. 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

Reducing Glycotoxin Intake to Help Reduce Brain Loss

Reducing Glycotoxin Intake to Prevent Alzheimer's.jpg

Each of us has about six billion miles of DNA. How does our body keep it from getting all tangled up? There are special proteins called histones, which act like spools with DNA as the thread. Enzymes called sirtuins wrap the DNA around the histones and by doing so, silence whatever genes were in that stretch of DNA, hence their name SIRtuins, which stands for silencing information regulator.

Although they were discovered only about a decade ago, the study of sirtuins "has become one of the most promising areas of biomedicine," since they appear to be involved in promoting healthy aging and longevity. Suppression of this key host defense is considered a central feature of Alzheimer's disease, as shown in Reducing Glycotoxin Intake to Prevent Alzheimer's.

Autopsies of Alzheimer's victims reveal that loss of sirtuin activity is closely associated with the accumulation of the plaques and tangles in the brain that are characteristic of Alzheimer's disease. Sirtuin appears to activate pathways that steer the brain away from the formation of plaque and tangle proteins. "Because a decrease in sirtuin activity can clearly have deleterious effects" on nerve health, researchers are trying to come up with drugs to increase sirtuin activity, but why not just prevent its suppression in the first place?

Glycotoxins in our food suppress sirtuin activity, also known as advanced glycation end products, or AGE's. Our modern diet includes excessive AGE's, which can be neurotoxic. High levels in the blood may predict cognitive decline over time. If you measure the urine levels of glycotoxins flowing through the bodies of older adults, those with the highest levels went on to suffer the greatest cognitive decline over the subsequent nine years.

As we age, our brain literally shrinks. In our 60's and 70's, we lose an average of five cubic centimeters of total brain tissue volume every year, but some people lose more than others. Brain atrophy may be reduced in very healthy individuals, and a few people don't lose any brain at all. Normally we lose about 2% of brain volume every year, but that's just the average. Although the average brain loss for folks in their 70's and 80's was 2.1%, some lost more, some lost less, and some men and women lost none at all over a period of four years.

Researchers in Australia provided the first evidence linking AGEs with this kind of cerebral brain loss. So, limiting one's consumption of these compounds may end up having significant public health benefits. Because sirtuin deficiency is both preventable and reversible by dietary AGE reduction, a therapeutic strategy that includes eating less AGE's may offer a new strategy to combat the epidemic of Alzheimer's.

Some glycotoxins are produced internally, particularly in diabetics, but anyone can get them from smoking and eating, particularly foods high in fat and protein cooked at high temperatures. In my video, Avoiding a Sugary Grave, I listed the 15 foods most contaminated with glycotoxins; mostly chicken, but also pork, beef, and fish, which may help explain why those that eat the most meat may have triple the risk of getting dementia compared to long-time vegetarians. Note there are some relatively high fat and protein plant foods such as nuts and soy products, so I no longer recommend toasting nuts and would steer clear from roasted tofu.

I've covered advanced glycation end-products in Glycotoxins, Bacon, Eggs, and Gestational Diabetes During Pregnancy, and Why is Meat a Risk Factor for Diabetes?.

More on slowing brain aging in How to Slow Brain Aging By Two Years.

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: lightwise © 123RF.com. This image has been modified.

Original Link

Reducing Glycotoxin Intake to Help Reduce Brain Loss

Reducing Glycotoxin Intake to Prevent Alzheimer's.jpg

Each of us has about six billion miles of DNA. How does our body keep it from getting all tangled up? There are special proteins called histones, which act like spools with DNA as the thread. Enzymes called sirtuins wrap the DNA around the histones and by doing so, silence whatever genes were in that stretch of DNA, hence their name SIRtuins, which stands for silencing information regulator.

Although they were discovered only about a decade ago, the study of sirtuins "has become one of the most promising areas of biomedicine," since they appear to be involved in promoting healthy aging and longevity. Suppression of this key host defense is considered a central feature of Alzheimer's disease, as shown in Reducing Glycotoxin Intake to Prevent Alzheimer's.

Autopsies of Alzheimer's victims reveal that loss of sirtuin activity is closely associated with the accumulation of the plaques and tangles in the brain that are characteristic of Alzheimer's disease. Sirtuin appears to activate pathways that steer the brain away from the formation of plaque and tangle proteins. "Because a decrease in sirtuin activity can clearly have deleterious effects" on nerve health, researchers are trying to come up with drugs to increase sirtuin activity, but why not just prevent its suppression in the first place?

Glycotoxins in our food suppress sirtuin activity, also known as advanced glycation end products, or AGE's. Our modern diet includes excessive AGE's, which can be neurotoxic. High levels in the blood may predict cognitive decline over time. If you measure the urine levels of glycotoxins flowing through the bodies of older adults, those with the highest levels went on to suffer the greatest cognitive decline over the subsequent nine years.

As we age, our brain literally shrinks. In our 60's and 70's, we lose an average of five cubic centimeters of total brain tissue volume every year, but some people lose more than others. Brain atrophy may be reduced in very healthy individuals, and a few people don't lose any brain at all. Normally we lose about 2% of brain volume every year, but that's just the average. Although the average brain loss for folks in their 70's and 80's was 2.1%, some lost more, some lost less, and some men and women lost none at all over a period of four years.

Researchers in Australia provided the first evidence linking AGEs with this kind of cerebral brain loss. So, limiting one's consumption of these compounds may end up having significant public health benefits. Because sirtuin deficiency is both preventable and reversible by dietary AGE reduction, a therapeutic strategy that includes eating less AGE's may offer a new strategy to combat the epidemic of Alzheimer's.

Some glycotoxins are produced internally, particularly in diabetics, but anyone can get them from smoking and eating, particularly foods high in fat and protein cooked at high temperatures. In my video, Avoiding a Sugary Grave, I listed the 15 foods most contaminated with glycotoxins; mostly chicken, but also pork, beef, and fish, which may help explain why those that eat the most meat may have triple the risk of getting dementia compared to long-time vegetarians. Note there are some relatively high fat and protein plant foods such as nuts and soy products, so I no longer recommend toasting nuts and would steer clear from roasted tofu.

I've covered advanced glycation end-products in Glycotoxins, Bacon, Eggs, and Gestational Diabetes During Pregnancy, and Why is Meat a Risk Factor for Diabetes?.

More on slowing brain aging in How to Slow Brain Aging By Two Years.

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: lightwise © 123RF.com. This image has been modified.

Original Link

The Natural Human Diet

NF-Nov15 The Problem with the Paleo Diet Argument copy.jpg

Our epidemics of dietary disease have prompted a great deal of research into what humans are meant to eat for optimal health. In 1985, an influential article highlighted in my video The Problem With the Paleo Diet Argument was published proposing that our chronic diseases stem from a disconnect between what our bodies ate while evolving during the Stone Age (about 2 million years ago) and what we're stuffing our face with today. The proposal advocated for a return towards a hunter-gatherer type diet of lean meat, fruits, vegetables, and nuts.

It's reasonable to assume our nutritional requirements were established in the prehistoric past. However, the question of which prehistoric past we should emulate remains. Why just the last 2 million? We've been evolving for about 20 million years since our last common great ape ancestor, during which our nutrient requirements and digestive physiology were set down. Therefore our hunter-gatherer days at the tail end probably had little effect. What were we eating for the first 90% of our evolution? What the rest of the great apes ended up eating--95 percent or more plants.

This may explain why we're so susceptible to heart disease. For most of human evolution, cholesterol may have been virtually absent from the diet. No bacon, butter, or trans fats; and massive amounts of fiber, which pulls cholesterol from the body. This could have been a problem since our body needs a certain amount of cholesterol, but our bodies evolve not only to make cholesterol, but also to preserve it and recycle it.

If we think of the human body as a cholesterol-conserving machine, then plop it into the modern world of bacon, eggs, cheese, chicken, pork, and pastry; it's no wonder artery-clogging heart disease is our #1 cause of death. What used to be adaptive for 90% of our evolution--holding on to cholesterol at all costs since we weren't getting much in our diet--is today maladaptive, a liability leading to the clogging of our arteries. Our bodies just can't handle it.

As the editor-in-chief of the American Journal of Cardiology noted 25 years ago, no matter how much fat and cholesterol carnivores eat, they do not develop atherosclerosis. We can feed a dog 500 eggs worth of cholesterol and they just wag their tail; a dog's body is used to eating and getting rid of excess cholesterol. Conversely, within months a fraction of that cholesterol can start clogging the arteries of animals adapted to eating a more plant-based diet.

Even if our bodies were designed by natural selection to eat mostly fruit, greens and seeds for 90% of our evolution, why didn't we better adapt to meat-eating in the last 10%, during the Paleolithic? We've had nearly 2 million years to get used to all that extra saturated fat and cholesterol. If a lifetime of eating like that clogs up nearly everyone's arteries, why didn't the genes of those who got heart attacks die off and get replaced by those that could live to a ripe old age with clean arteries regardless of what they ate? Because most didn't survive into old age.

Most prehistoric peoples didn't live long enough to get heart attacks. When the average life expectancy is 25 years old, then the genes that get passed along are those that can live to reproductive age by any means necessary, and that means not dying of starvation. The more calories in food, the better. Eating lots of bone marrow and brains, human or otherwise, would have a selective advantage (as would discovering a time machine stash of Twinkies for that matter!). If we only have to live long enough to get our kids to puberty to pass along our genes, then we don't have to evolve any protections against the ravages of chronic disease.

To find a population nearly free of chronic disease in old age, we don't have to go back a million years. In the 20th century, networks of missionary hospitals in rural Africa found coronary artery disease virtually absent, and not just heart disease, but high blood pressure, stroke, diabetes, common cancers, and more. In a sense, these populations in rural China and Africa were eating the type of diet we've been eating for 90% of the last 20 million years, a diet almost exclusively of plant foods.

How do we know it was their diet and not something else? In the 25 year update to their original paleo paper, the authors tried to clarify that they did not then and do not now propose that people adopt a particular diet just based on what our ancient ancestors ate. Dietary recommendations must be put to the test. That's why the pioneering research from Pritikin, Ornish, and Esselstyn is so important, showing that plant-based diets can not only stop heart disease but have been proven to reverse it in the majority of patients. Indeed, it's the only diet that ever has.

For more on the absence of Western diseases in plant-based rural populations, see for example:

I've touched on "paleo" diets in the past:

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: Nathan Rupert / Flickr

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The Natural Human Diet

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Our epidemics of dietary disease have prompted a great deal of research into what humans are meant to eat for optimal health. In 1985, an influential article highlighted in my video The Problem With the Paleo Diet Argument was published proposing that our chronic diseases stem from a disconnect between what our bodies ate while evolving during the Stone Age (about 2 million years ago) and what we're stuffing our face with today. The proposal advocated for a return towards a hunter-gatherer type diet of lean meat, fruits, vegetables, and nuts.

It's reasonable to assume our nutritional requirements were established in the prehistoric past. However, the question of which prehistoric past we should emulate remains. Why just the last 2 million? We've been evolving for about 20 million years since our last common great ape ancestor, during which our nutrient requirements and digestive physiology were set down. Therefore our hunter-gatherer days at the tail end probably had little effect. What were we eating for the first 90% of our evolution? What the rest of the great apes ended up eating--95 percent or more plants.

This may explain why we're so susceptible to heart disease. For most of human evolution, cholesterol may have been virtually absent from the diet. No bacon, butter, or trans fats; and massive amounts of fiber, which pulls cholesterol from the body. This could have been a problem since our body needs a certain amount of cholesterol, but our bodies evolve not only to make cholesterol, but also to preserve it and recycle it.

If we think of the human body as a cholesterol-conserving machine, then plop it into the modern world of bacon, eggs, cheese, chicken, pork, and pastry; it's no wonder artery-clogging heart disease is our #1 cause of death. What used to be adaptive for 90% of our evolution--holding on to cholesterol at all costs since we weren't getting much in our diet--is today maladaptive, a liability leading to the clogging of our arteries. Our bodies just can't handle it.

As the editor-in-chief of the American Journal of Cardiology noted 25 years ago, no matter how much fat and cholesterol carnivores eat, they do not develop atherosclerosis. We can feed a dog 500 eggs worth of cholesterol and they just wag their tail; a dog's body is used to eating and getting rid of excess cholesterol. Conversely, within months a fraction of that cholesterol can start clogging the arteries of animals adapted to eating a more plant-based diet.

Even if our bodies were designed by natural selection to eat mostly fruit, greens and seeds for 90% of our evolution, why didn't we better adapt to meat-eating in the last 10%, during the Paleolithic? We've had nearly 2 million years to get used to all that extra saturated fat and cholesterol. If a lifetime of eating like that clogs up nearly everyone's arteries, why didn't the genes of those who got heart attacks die off and get replaced by those that could live to a ripe old age with clean arteries regardless of what they ate? Because most didn't survive into old age.

Most prehistoric peoples didn't live long enough to get heart attacks. When the average life expectancy is 25 years old, then the genes that get passed along are those that can live to reproductive age by any means necessary, and that means not dying of starvation. The more calories in food, the better. Eating lots of bone marrow and brains, human or otherwise, would have a selective advantage (as would discovering a time machine stash of Twinkies for that matter!). If we only have to live long enough to get our kids to puberty to pass along our genes, then we don't have to evolve any protections against the ravages of chronic disease.

To find a population nearly free of chronic disease in old age, we don't have to go back a million years. In the 20th century, networks of missionary hospitals in rural Africa found coronary artery disease virtually absent, and not just heart disease, but high blood pressure, stroke, diabetes, common cancers, and more. In a sense, these populations in rural China and Africa were eating the type of diet we've been eating for 90% of the last 20 million years, a diet almost exclusively of plant foods.

How do we know it was their diet and not something else? In the 25 year update to their original paleo paper, the authors tried to clarify that they did not then and do not now propose that people adopt a particular diet just based on what our ancient ancestors ate. Dietary recommendations must be put to the test. That's why the pioneering research from Pritikin, Ornish, and Esselstyn is so important, showing that plant-based diets can not only stop heart disease but have been proven to reverse it in the majority of patients. Indeed, it's the only diet that ever has.

For more on the absence of Western diseases in plant-based rural populations, see for example:

I've touched on "paleo" diets in the past:

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: Nathan Rupert / Flickr

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How to Design Saturated Fat Studies to Hide the Truth

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Where do the international consensus guidelines to dramatically lower saturated fat consumption come from? (I show the list in my video, The Saturated Fat Studies: Buttering Up the Public). They came from literally hundreds of metabolic ward experiments, which means you don't just ask people to change their diets, you essentially lock them in a room--for weeks if necessary--and have total control over their diet. You can then experimentally change the level of saturated fat consumed by subjects however you want to, and see the corresponding change in their cholesterol levels. And the results are so consistent that you can create an equation, the famous Hegsted Equation, where you can predict how much their cholesterol will go up based on how much saturated fat you give them. So if you want your LDL cholesterol to go up 50 points, all you have to do is eat something like 30% of your calories in saturated fat. When you plug the numbers in, the change in cholesterol shoots up as predicted. The experiments match the predictions. You can do it at home with one of those home cholesterol testing kits, eat a stick of butter every day, and watch your cholesterol climb.

These ward experiments were done in 1965; meaning we've known for 50 years that even if you keep calorie intake the same, increases in saturated fat intake are associated with highly significant increases in LDL bad cholesterol. Your good cholesterol goes up a bit too, but that increase is smaller than the increase in bad, which would translate into increased heart disease risk.

So if you feed vegetarians meat even just once a day, their cholesterol jumps nearly 20% within a month. To prevent heart disease, we need a total cholesterol under 150, which these vegetarians were, but then even just eating meat once a day, and their cholesterol shot up 19%. The good news is that within just two weeks of returning to their meat-free diet, their cholesterol dropped back down into the safe range. Note that their HDL good cholesterol hardly moved at all, so their ratio went from low risk of heart attack to high risk in a matter of weeks with just one meat-containing meal a day. And indeed randomized clinical trials show that dietary saturated fat reduction doesn't just appear to reduce cholesterol levels, but also reduces the risk of subsequent cardiovascular events like heart attacks.

So we have randomized clinical trials, controlled interventional experiments--our most robust forms of evidence--no wonder there's a scientific consensus to decrease saturated fat intake! You'll note, though, that the Y-axis in these studies seen in my video The Saturated Fat Studies: Set Up to Fail is not cholesterol, but change in cholesterol. That's because everyone's set-point is different. Two people eating the same diet with the same amount of saturated fat can have very different cholesterol levels. One person can eat ten chicken nuggets a day and have an LDL cholesterol of 90; another person eating ten a day could start out with an LDL of 120. It depends on your genes. But while our genetics may be different, our biology is the same, meaning the rise and drop in cholesterol is the same for everyone. So if both folks cut out the nuggets, the 90 might drop to 85, whereas the 120 would drop to 115. Wherever we start, we can lower our cholesterol by eating less saturated fat, but if I just know your saturated fat intake--how many nuggets you eat, I can't tell you what your starting cholesterol is. All I can say with certainty is that if you eat less, your cholesterol will likely improve.

But because of this extreme "interindividual variation"--this wide variability in baseline cholesterol levels for any given saturated fat intake--if you take a cross-section of the population, you can find no statistical correlation between saturated fat intake and cholesterol levels, because it's not like everyone who eats a certain set amount of saturated fat is going to have over a certain cholesterol. So there are three ways you could study diet and cholesterol levels: controlled feeding experiments, free-living dietary change experiments, or cross-sectional observations of large populations. As we know, there is a clear and strong relationship between change in diet and change in serum cholesterol in the interventional designs, but because of that individual variability, in cross-sectional designs, you can get zero correlation. In fact, if you do the math, that's what you'd expect you'd get. In statistical parlance, one would say that a cross-sectional study doesn't have the power for detecting such a relationship. Thus because of that variability, these kinds of observational studies would seem an inappropriate method to study this particular relationship. So since diet and serum cholesterol have a zero correlation cross-sectionally, an observational study of the relationship between diet and coronary heart disease incidence will suffer from the same difficulties. So again, if you do the math, observational studies would unavoidably show nearly no correlation between saturated fat and heart disease. These prospective studies can be valuable for other diseases, but the appropriate design demonstrating or refuting the role of diet and coronary heart disease is a dietary change experiment.

And those dietary change experiments have been done; they implicate saturated fat, hence the lower saturated guidelines from basically every major medical authority. In fact, if we lower saturated fat enough, we may be able to reverse heart disease, opening up arteries without drugs or surgery. So with this knowledge, how would the meat and dairy industry prove otherwise? They use the observational studies that mathematically would be unable to show any correlation.

All they need now is a friendly researcher, such as Ronald M. Krauss, who has been funded by the National Dairy Council since 1989, also the National Cattleman's Beef Association, as well as the Atkins Foundation. Then they just combine all the observational studies that don't have the power to provide significant evidence, and not surprisingly, as published in their 2010 meta-analysis, no significant evidence was found.

The 2010 meta-analysis was basically just repackaged for 2014, using the same and similar studies. As the Chair of Harvard's nutrition department put it, their conclusions regarding the type of fat being unimportant are seriously misleading and should be disregarded, going as far as suggesting the paper be retracted, even after the authors corrected a half dozen different errors.

It's not as though they falsified or fabricated data--they didn't have to. They knew beforehand the limitations of observational studies, they knew they'd get the "right" result and so they published it, helping to "neutralize the negative impact of milk and meat fat by regulators and medical professionals." And it's working, according to the dairy industry, as perceptions about saturated fat in the scientific community are changing. They even go so far to say this is a welcome message to consumers, who may be tired of hearing what they shouldn't eat. They don't need to convince consumers, just confuse them. Confusion can easily be misused by the food industry to promote their interests.

It's like that infamous tobacco industry memo that read, "Doubt is our product since it's the best means of competing with the body of fact that exist in the mind of the general public." They don't have to convince the public that smoking is healthy to get people to keep consuming their products. They just need to establish a controversy. Conflicting messages in nutrition cause people to become so frustrated and confused they may just throw their hands up in the air and eat whatever is put in front of them, which is exactly what saturated fat suppliers want, but at what cost to the public's health?


If that "Doubt is our product" memo sounded familiar, I also featured it in my Food Industry Funded Research Bias video. More on how industries can design deceptive studies in BOLD Indeed: Beef Lowers Cholesterol? and How the Egg Board Designs Misleading Studies.

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: Taryn / Flickr

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