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

Can You Eat Too Much Fruit?

Can You Eat Too Much Fruit?.jpeg

In my video If Fructose is Bad, What About Fruit?, I explored how adding berries to our meals can actually blunt the detrimental effects of high glycemic foods, but how many berries? The purpose of one study out of Finland was to determine the minimum level of blueberry consumption at which a consumer may realistically expect to receive antioxidant benefits after eating blueberries with a sugary breakfast cereal. If we eat a bowl of corn flakes with no berries, within two hours, so many free radicals are created that it puts us into oxidative debt. The antioxidant power of our bloodstream drops below where we started from before breakfast, as the antioxidants in our bodies get used up dealing with such a crappy breakfast. As you can see in How Much Fruit is Too Much? video, a quarter cup of blueberries didn't seem to help much, but a half cup of blueberries did.

What about fruit for diabetics? Most guidelines recommend eating a diet with a high intake of fiber-rich food, including fruit, because they're so healthy--antioxidants, anti-inflammatory, improving artery function, and reducing cancer risk. However, some health professionals have concerns about the sugar content of fruit and therefore recommend restricting the fruit intake. So let's put it to the test! In a study from Denmark, diabetics were randomized into two groups: one told to eat at least two pieces of fruit a day, and the other told at most, two fruits a day. The reduce fruit group indeed reduce their fruit consumption, but it had no effect on the control of their diabetes or weight, and so, the researchers concluded, the intake of fruit should not be restricted in patients with type 2 diabetes. An emerging literature has shown that low-dose fructose may actually benefit blood sugar control. Having a piece of fruit with each meal would be expected to lower, not raise the blood sugar response.

The threshold for toxicity of fructose may be around 50 grams. The problem is that's the current average adult fructose consumption. So, the levels of half of all adults are likely above the threshold for fructose toxicity, and adolescents currently average 75. Is that limit for added sugars or for all fructose? If we don't want more than 50 and there's about ten in a piece of fruit, should we not eat more than five fruit a day? Quoting from the Harvard Health Letter, "the nutritional problems of fructose and sugar come when they are added to foods. Fruit, on the other hand, is beneficial in almost any amount." What do they mean almost? Can we eat ten fruit a day? How about twenty fruit a day?

It's actually been put to the test.

Seventeen people were made to eat 20 servings a day of fruit. Despite the extraordinarily high fructose content of this diet, presumably about 200 g/d--eight cans of soda worth, the investigators reported no adverse effects (and possible benefit actually) for body weight, blood pressure, and insulin and lipid levels after three to six months. More recently, Jenkins and colleagues put people on about a 20 servings of fruit a day diet for a few weeks and found no adverse effects on weight or blood pressure or triglycerides, and an astounding 38 point drop in LDL cholesterol.

There was one side effect, though. Given the 44 servings of vegetables they had on top of all that fruit, they recorded the largest bowl movements apparently ever documented in a dietary intervention.


Cutting down on sugary foods may be easier said than done (see Are Sugary Foods Addictive?) but it's worth it. For more on the dangers of high levels of fructose in added sugars, see How Much Added Sugar Is Too Much?.

What's that about being in oxidative debt? See my three part series on how to pull yourself out of the red:

Ironically, fat may be more of a problem when it comes to diabetes than sugar, see:

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

Can You Eat Too Much Fruit?

Can You Eat Too Much Fruit?.jpeg

In my video If Fructose is Bad, What About Fruit?, I explored how adding berries to our meals can actually blunt the detrimental effects of high glycemic foods, but how many berries? The purpose of one study out of Finland was to determine the minimum level of blueberry consumption at which a consumer may realistically expect to receive antioxidant benefits after eating blueberries with a sugary breakfast cereal. If we eat a bowl of corn flakes with no berries, within two hours, so many free radicals are created that it puts us into oxidative debt. The antioxidant power of our bloodstream drops below where we started from before breakfast, as the antioxidants in our bodies get used up dealing with such a crappy breakfast. As you can see in How Much Fruit is Too Much? video, a quarter cup of blueberries didn't seem to help much, but a half cup of blueberries did.

What about fruit for diabetics? Most guidelines recommend eating a diet with a high intake of fiber-rich food, including fruit, because they're so healthy--antioxidants, anti-inflammatory, improving artery function, and reducing cancer risk. However, some health professionals have concerns about the sugar content of fruit and therefore recommend restricting the fruit intake. So let's put it to the test! In a study from Denmark, diabetics were randomized into two groups: one told to eat at least two pieces of fruit a day, and the other told at most, two fruits a day. The reduce fruit group indeed reduce their fruit consumption, but it had no effect on the control of their diabetes or weight, and so, the researchers concluded, the intake of fruit should not be restricted in patients with type 2 diabetes. An emerging literature has shown that low-dose fructose may actually benefit blood sugar control. Having a piece of fruit with each meal would be expected to lower, not raise the blood sugar response.

The threshold for toxicity of fructose may be around 50 grams. The problem is that's the current average adult fructose consumption. So, the levels of half of all adults are likely above the threshold for fructose toxicity, and adolescents currently average 75. Is that limit for added sugars or for all fructose? If we don't want more than 50 and there's about ten in a piece of fruit, should we not eat more than five fruit a day? Quoting from the Harvard Health Letter, "the nutritional problems of fructose and sugar come when they are added to foods. Fruit, on the other hand, is beneficial in almost any amount." What do they mean almost? Can we eat ten fruit a day? How about twenty fruit a day?

It's actually been put to the test.

Seventeen people were made to eat 20 servings a day of fruit. Despite the extraordinarily high fructose content of this diet, presumably about 200 g/d--eight cans of soda worth, the investigators reported no adverse effects (and possible benefit actually) for body weight, blood pressure, and insulin and lipid levels after three to six months. More recently, Jenkins and colleagues put people on about a 20 servings of fruit a day diet for a few weeks and found no adverse effects on weight or blood pressure or triglycerides, and an astounding 38 point drop in LDL cholesterol.

There was one side effect, though. Given the 44 servings of vegetables they had on top of all that fruit, they recorded the largest bowl movements apparently ever documented in a dietary intervention.


Cutting down on sugary foods may be easier said than done (see Are Sugary Foods Addictive?) but it's worth it. For more on the dangers of high levels of fructose in added sugars, see How Much Added Sugar Is Too Much?.

What's that about being in oxidative debt? See my three part series on how to pull yourself out of the red:

Ironically, fat may be more of a problem when it comes to diabetes than sugar, see:

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’s the Optimal Cholesterol Level?

Optimal Cholesterol Level.jpg

No matter where we live, how old we are or what we look like, health researchers from the Institute of Circulatory and Respiratory Health have discovered that 90% of the chance of having a first heart attack "can be attributed to nine modifiable risk factors." The nine factors that could save our lives include: smoking, too much bad cholesterol, high blood pressure, diabetes, abdominal obesity, stress, a lack of daily fruit and veggie consumption, as well as a lack of daily exercise.

Dr. William Clifford Roberts, Executive Director of Baylor Heart and Vascular Institute and long-time Editor in Chief of the American Journal of Cardiology, is convinced, however, that atherosclerosis has a single cause--namely cholesterol--and that the other so-called atherosclerotic risk factors are only contributory at most. In other words, we could be stressed, overweight, smoking, diabetic couch potatoes, but if our cholesterol is low enough, there may just not be enough cholesterol in our blood stream to infiltrate our artery walls and trigger the disease. Thus, the only absolute prerequisite for a fatal or nonfatal atherosclerotic event like a heart attack is an elevated cholesterol level.

It was not appreciated until recently "that the average blood cholesterol level in the United States, the so-called normal level, was actually abnormal," accelerating the blockages in our arteries and putting a large fraction of the normal population at risk. That's cited as one of the reasons the cholesterol controversy lasted so long--an "unwillingness to accept the notion that a very large fraction of our population actually has an unhealthily high cholesterol level."

Normal cholesterol levels may be fatal cholesterol levels.

The optimal "bad cholesterol" (LDL) level is 50 to 70. Accumulating data from multiple lines of evidence consistently demonstrate that that's where a physiologically normal LDL level would be. That appears to be the threshold above which atherosclerosis and heart attacks develop. That's what we start out at birth with, that's what fellow primates have, and that's the level seen in populations free of the heart disease epidemic. One can also look at all the big randomized controlled cholesterol lowering trials.

In my video, Optimal Cholesterol Level, you can see graphing of the progression of atherosclerosis versus LDL cholesterol. More cholesterol means more atherosclerosis, but if we draw a line down through the points, we can estimate that the LDL level at which there is zero progression is around 70. We can do the same with the studies preventing heart attacks. Zero coronary heart disease events might be reached down around 55, and those who've already had a heart attack and are trying to prevent a second one might need to push LDL levels even lower.

Atherosclerosis is endemic in our population in part because the average person's LDL level is up around 130, approximately twice the normal physiologic level. The reason the federal government doesn't recommend everyone shoot for under 100 is that despite the lower risk accompanying more optimal cholesterol levels, the intensity of clinical intervention required to achieve such levels for everyone in the population would "financially overload the health care system. Drug usage would rise enormously." But, they're assuming drugs are the only way to get our LDL that low. Those eating really healthy plant-based diets may hit the optimal cholesterol target without even trying, naturally nailing under 70.

The reason given by the federal government for not advocating for what the science shows is best was that it might frustrate the public, "who would have difficulty maintaining a lower level," but maybe the public's greatest frustration would come from not being informed of the optimal diet for health.


It's imperative for everyone to understand Dr. Rose's sick population concept, which I introduced in When Low Risk Means High Risk.

What about large fluffy LDL cholesterol versus small and dense? See Does Cholesterol Size Matter?

More from the Framingham Heart Study can be found in Barriers to Heart Disease Prevention and Everything in Moderation? Even Heart Disease?.

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

What’s the Optimal Cholesterol Level?

Optimal Cholesterol Level.jpg

No matter where we live, how old we are or what we look like, health researchers from the Institute of Circulatory and Respiratory Health have discovered that 90% of the chance of having a first heart attack "can be attributed to nine modifiable risk factors." The nine factors that could save our lives include: smoking, too much bad cholesterol, high blood pressure, diabetes, abdominal obesity, stress, a lack of daily fruit and veggie consumption, as well as a lack of daily exercise.

Dr. William Clifford Roberts, Executive Director of Baylor Heart and Vascular Institute and long-time Editor in Chief of the American Journal of Cardiology, is convinced, however, that atherosclerosis has a single cause--namely cholesterol--and that the other so-called atherosclerotic risk factors are only contributory at most. In other words, we could be stressed, overweight, smoking, diabetic couch potatoes, but if our cholesterol is low enough, there may just not be enough cholesterol in our blood stream to infiltrate our artery walls and trigger the disease. Thus, the only absolute prerequisite for a fatal or nonfatal atherosclerotic event like a heart attack is an elevated cholesterol level.

It was not appreciated until recently "that the average blood cholesterol level in the United States, the so-called normal level, was actually abnormal," accelerating the blockages in our arteries and putting a large fraction of the normal population at risk. That's cited as one of the reasons the cholesterol controversy lasted so long--an "unwillingness to accept the notion that a very large fraction of our population actually has an unhealthily high cholesterol level."

Normal cholesterol levels may be fatal cholesterol levels.

The optimal "bad cholesterol" (LDL) level is 50 to 70. Accumulating data from multiple lines of evidence consistently demonstrate that that's where a physiologically normal LDL level would be. That appears to be the threshold above which atherosclerosis and heart attacks develop. That's what we start out at birth with, that's what fellow primates have, and that's the level seen in populations free of the heart disease epidemic. One can also look at all the big randomized controlled cholesterol lowering trials.

In my video, Optimal Cholesterol Level, you can see graphing of the progression of atherosclerosis versus LDL cholesterol. More cholesterol means more atherosclerosis, but if we draw a line down through the points, we can estimate that the LDL level at which there is zero progression is around 70. We can do the same with the studies preventing heart attacks. Zero coronary heart disease events might be reached down around 55, and those who've already had a heart attack and are trying to prevent a second one might need to push LDL levels even lower.

Atherosclerosis is endemic in our population in part because the average person's LDL level is up around 130, approximately twice the normal physiologic level. The reason the federal government doesn't recommend everyone shoot for under 100 is that despite the lower risk accompanying more optimal cholesterol levels, the intensity of clinical intervention required to achieve such levels for everyone in the population would "financially overload the health care system. Drug usage would rise enormously." But, they're assuming drugs are the only way to get our LDL that low. Those eating really healthy plant-based diets may hit the optimal cholesterol target without even trying, naturally nailing under 70.

The reason given by the federal government for not advocating for what the science shows is best was that it might frustrate the public, "who would have difficulty maintaining a lower level," but maybe the public's greatest frustration would come from not being informed of the optimal diet for health.


It's imperative for everyone to understand Dr. Rose's sick population concept, which I introduced in When Low Risk Means High Risk.

What about large fluffy LDL cholesterol versus small and dense? See Does Cholesterol Size Matter?

More from the Framingham Heart Study can be found in Barriers to Heart Disease Prevention and Everything in Moderation? Even Heart Disease?.

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

How to Design Saturated Fat Studies to Hide the Truth

NF-Oct4 Saturated Fat Studies Set up to Fail.jpeg

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

Original Link

Paleo Diet May Undermine Benefit of CrossFit Exercise

NF-Sept6 Paleo Diets May Negate Benefits of Exercise.jpeg

Much of the low-carb and paleo reasoning revolves around insulin. To quote a paleo blogger, "carbohydrates increase insulin, the root of all evil when it comes to dieting and health." So the logic follows that because carbs increase insulin, we should stick mostly to meat, which is fat and protein with no carbs, so no increase in insulin, right?

Wrong.

We've known for half a century that if you give someone just a steak: no carbs, no sugar, no starch; their insulin goes up. Carbs make our insulin go up, but so does protein.

In 1997 an insulin index of foods was published, ranking 38 foods to determine which stimulates higher insulin levels. Researchers compared a large apple and all its sugar, a cup of oatmeal packed with carbs, a cup and a half of white flour pasta, a big bun-less burger with no carbs at all, to half of a salmon fillet. As you can see in the graph in my video Paleo Diets May Negate Benefits of Exercise, the meat produced the highest insulin levels.

Researchers only looked at beef and fish, but subsequent data showed that that there's no significant difference between the insulin spike from beef, chicken, or pork--they're all just as high. Thus, protein and fat rich foods may induce substantial insulin secretion. In fact, meat protein causes as much insulin release as pure sugar.

So, based on the insulin logic, if low-carbers and paleo folks really believed insulin to be the root of all evil, then they would be eating big bowls of spaghetti day in and day out before they would ever consume meat.

They are correct in believing that having hyperinsulinemia, high levels of insulin in the blood like type 2 diabetics have, is not a good thing, and may increase cancer risk. But if low-carb and paleo dieters stuck to their own insulin theory, then they would be out telling everyone to start eating plant-based. Vegetarians have significantly lower insulin levels even at the same weight as omnivores. This is true for ovo-lacto-vegetarians, lacto-vegetarians, and vegans. Meat-eaters have up to 50% higher insulin levels.

Researchers from the University of Memphis put a variety of people on a vegan diet (men, women, younger folks, older folks, skinny and fat) and their insulin levels dropped significantly within just three weeks. And then, just by adding egg whites back to their diet, their insulin production rose 60% within four days.

In a study out of MIT, researchers doubled participants' carbohydrate intake, and their insulin levels went down. Why? Because the researchers weren't feeding people jellybeans and sugar cookies, they were feeding people whole, plant foods, lots of whole grains, beans, fruits, and vegetables.

What if we put someone on a very-low carb diet, like an Atkins diet? Low carb advocates such as Dr. Westman assumed that it would lower insulin levels. Dr. Westman is the author of the new Atkins books, after Dr. Atkins died obese with, according to the medical examiner, a history of heart attack, congestive heart failure, and hypertension. But, Dr. Westman was wrong in his assumption. There are no significant drop in insulin levels on very low-carb diets. Instead, there is a significant rise in LDL cholesterol levels, the number one risk factor for our number one killer, heart disease.

Atkins is an easy target though. No matter how many "new" Atkins diets that come out, it's still old news. What about the paleo diet? The paleo movement gets a lot of things right. They tell people to ditch dairy and doughnuts, eat lots of fruits, nuts, and vegetables, and cut out a lot of processed junk food. But a new study published in the International Journal of Exercise Science is pretty concerning. Researchers took young healthy people, put them on a Paleolithic diet along with a CrossFit-based, high-intensity circuit training exercise program.

If you lose enough weight exercising, you can temporarily drop our cholesterol levels no matter what you eat. You can see that with stomach stapling surgery, tuberculosis, chemotherapy, a cocaine habit, etc. Just losing weight by any means can lower cholesterol, which makes the results of the Paleo/Crossfit study all the more troubling. After ten weeks of hardcore workouts and weight loss, the participants' LDL cholesterol still went up. And it was even worse for those who started out the healthiest. Those starting out with excellent LDL's (under 70), had a 20% elevation in LDL cholesterol, and their HDL dropped. Exercise is supposed to boost our good cholesterol, not lower it.

The paleo diet's deleterious impact on blood fats was not only significant, but substantial enough to counteract the improvements commonly seen with improved fitness and body composition. Exercise is supposed to make things better.

On the other hand, if we put people instead on a plant-based diet and a modest exercise program, mostly just walking-based; within three weeks their bad cholesterol can drop 20% and their insulin levels 30%, despite a 75-80% carbohydrate diet, whereas the paleo diets appeared to "negate the positive effects of exercise."

I touched on paleo diets before in Paleolithic Lessons, and I featured a guest blog on the subject: Will The Real Paleo Diet Please Stand Up?

but my favorite paleo videos are probably The Problem With the Paleo Diet Argument and Lose Two Pounds in One Sitting: Taking the Mioscenic Route.

I wrote a book on low carb diets in general (now available free full-text online) and touched on it in Atkins Diet: Trouble Keeping It Up and Low Carb Diets and Coronary Blood Flow.

And if you're thinking, but what about the size of the cholesterol, small and dense versus large and fluffy? Please 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--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: Vincent Lit / Flickr

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Egg Consumption and LDL Cholesterol Size

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Maria Fernandez has received nearly a half million dollars from the egg industry and writes papers like "Rethinking dietary cholesterol." She admits that eggs can raise LDL cholesterol, bad cholesterol, but argues that HDL, so-called "good cholesterol," also rises, thereby maintaining the ratio of bad to good. To support this assertion, she cites one study that she performed with Egg Board money that involved 42 people.

If we look at a meta-analysis, a measure of the balance of evidence, the rise in bad is much more than the rise in good with increasing cholesterol intake. The analysis of 17 different studies showed that dietary cholesterol increases the ratio of total to HDL cholesterol, suggesting that the favorable rise in HDL fails to compensate for the adverse rise in total and LDL cholesterol. Therefore, increased intake of dietary cholesterol from eggs may indeed raise the risk of coronary heart disease.

The Egg Board responded (as seen in my video, Does Cholesterol Size Matter?) by saying that the increased heart disease risk associated with eating eggs needs to be put in perspective relative to other risk factors, arguing that it's worse to be overweight than it is to eat eggs, to which the authors of the meta-analysis replied, "Be that as it may, many people do not find it a major hardship to cut back on egg intake, whereas most people find it impossible to lose weight permanently."

Fine, Fernandez admitted, eggs increase LDL, but she claims that the increase is in large LDL, arguing that large, fluffy LDL particles are not as bad as small, dense particles. Indeed, large LDL only raises heart disease risk of women by 44%, instead of 63% for small LDL. Light large buoyant LDL still significantly increases our risk of dying from our #1 killer. The difference is similar for men: large LDL only increases risk of heart attack or death by 31%, instead of 44%. As the latest review on the subject concluded, LDL cholesterol has "clearly been established as a causal agent in atherosclerosis ... Regardless of size, LDL particles are atherogenic." Yet Egg Board researcher, Fernandez, wrote that the formation of larger LDL from eggs is considered protective against heart disease, relative to small LDL. That's like saying getting stabbed with a knife is protective--relative to getting shot!

Health practitioners should bear in mind, she writes, that "restricting dietary cholesterol puts a burden on egg intake" and leads to the avoidance of a food that contains dietary components like carotenoids and choline. She wrote this in 2012, before the landmark 2013 study showing that choline from eggs appears to increase the risk of stroke, heart attack, and death, so she can be excused for that. But what about the carotenoids in eggs, like lutein and zeaxanthin, which are so important for protecting vision and reducing cholesterol oxidation? As I explored previously, the amounts of these phytonutrients in eggs are miniscule. One spoonful of spinach contains as much as nine eggs. Comparing the predictable effects on eye health of organic free-range eggs versus corn and spinach, the effect of eggs is tiny.

What about the effects of eggs on cholesterol oxidation? We've known for decades that LDL cholesterol is bad, but oxidized LDL is even worse. Therefore, according to Fernandez, since eggs have trace amounts of antioxidants, eggs may prevent cholesterol oxidation. But the science shows the exact opposite. Consumption of eggs increases the susceptibility of LDL cholesterol to oxidation. The researchers found that not only does eating eggs raise LDL levels, but also increases LDL oxidizability, in addition to the oxidizability of our entire bloodstream. This was published 18 years ago, yet Fernandez still tries to insinuate that eggs would reduce oxidation.

She acknowledges receiving funding from the American Egg Board, and then claims she has no conflicts of interest.

This is why a site like NutritionFacts.org can be so useful, because even when a paper is published in the peer-reviewed medical literature, it can misrepresent the science. But who has time to check the primary sources? I do! If you'd like to support this work, please consider making a tax-deductible donation.

Here are some other videos in which I contrast the available science with what the egg industry asserts:

Only the meat industry may be as bold: BOLD Indeed: Beef Lowers Cholesterol?

For more on the role of cholesterol, see:

In health,
Michael Greger, M.D.

PS: If you haven't yet, you can subscribe to my free videos here and watch my live year-in-review presentations Uprooting the Leading Causes of Death, More Than an Apple a Day, From Table to Able, and Food as Medicine.

Image Credit: Kool skatkat / Flickr

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How to Protect Our Telomeres with Diet

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In my video, Does Meditation Affect Cellular Aging?, I discussed how stress reduction through meditation might be able to lengthen telomeres, the protective caps at the tips of our chromosomes that tend to deplete as we age.

What about exercise? We can't always change our situation in life, but we can always go out for a walk. London researchers studied 2,400 twins, and those who exercised more may have pumped up their telomeres along with their muscles. Apparently it doesn't take much either. The "heavy" exercise group was only averaging about a half-hour a day.

These were mostly folks in their 40's, but does it still work in your 50's? Yes. A study out of South Korea found that people in their 50's who work out three hours a week had longer telomeres.

In my video, Telomeres: Cap It All Off with Diet, you can see the telomere lengths of young healthy regular folk controls at around age 20, and then at age 50. As we'd expect, the older subjects' telomeres were significantly shorter. What about athletes? The young athletes started out in the same boat, with nice, long, young, healthy telomeres capping all their chromosomes. The older athletes, in contrast to the controls, appeared to still have the chromosomes of 20-year-olds. But these were marathon runners, triathletes running 50 miles a week for 35 years.

What was it about the Ornish intervention that so powerfully protected telomeres after just three months? We saw that stress management seems to help, but what about diet and exercise? Was it the plant-based diet, was it the walking 30 minutes a day, or was it just because of the weight loss? In 2013 a study was published that can help us anser just that question.

The researchers took about 400 women and randomized them into four groups: a portion-controlled diet group, an exercise group, a portion controlled diet and exercise group, and a control group for a full year. In the video, you can see a comparison of the length of each group's telomeres. After a year of doing nothing, there was essentially no change in the control group, which is what we'd expect. The exercise group was 45 minutes of moderate-to-vigorous exercise like jogging. After a year of that, they did no better. What about just weight loss? Nothing. The same thing for exercise and weight loss, no significant change either.

So as long as we're eating the same diet, it doesn't appear to matter how small our portions are, or how much weight we lose, or how hard we exercise. After a year, the subjects saw no benefit. On the other hand, the Ornish group on the plant-based diet, who lost the same amount of weight after just three months and exercised less than half as hard, saw significant telomere protection.

It wasn't the weight loss or the exercise: it was the food.

What aspects of a plant-based diet make it so protective? Studies have associated more vegetables and fruit, and less butter, with longer telomeres. From the latest review, foods high in fiber and vitamins are strongly related to longer telomeres. However, the key may be avoiding saturated fat. Swapping just 1% of saturated fat calories in our diet for anything else can add nearly a whole year of aging's worth of length onto our telomeres.

Saturated fats like palmitic acid, the primary saturated fat in salmon, and found in meat, eggs, and dairy in general, can be toxic to cells. This has been demonstrated in heart cells, bone marrow cells, pancreatic cells, and brain cells. The toxic effects on cell death rates happen right around what you'd see in the blood stream of people who eat a lot of animal products. It may not be the saturated fat itself, however, as saturated fat may just be a marker for the increased oxidative stress and inflammation associated with those foods.

With this link to saturated fat, it's no wonder that lifelong low cholesterol levels have been related to longer telomeres and a smaller proportion of short telomeres--in other words, markers of slower biological aging. In fact, there's a rare congenital birth defect called progeria syndrome, where children age 8-10 times faster than normal. It seems associated with a particular inability to handle animal fats.

The good news is that "despite past accumulated injury leading to shorter telomere lengths, current healthy behaviors might help to decrease a person's risk of some of the potential consequences like heart disease." Eating more fruit and vegetables and less meat, and having more support from friends and family, attenuate the association between shorter telomeres and the ravages of aging.

To summarize: inflammation, oxidation, damage and dysfunction are constantly hacking away at our telomeres. At the same time, our antioxidant defenses, healthy diet, exercise and stress reduction are constantly rebuilding them.


I've asked this diet versus exercise question in a few other contexts. See:

Though dietary change appears more impactful, I'm a big fan of walking. See Longer Life Within Walking Distance and for my personal favorite exercise, Standing Up for Your Health.

For more on the role saturated fat may play in disease, see, for example, my videos Heart Disease Starts in Childhood and Treating Multiple Sclerosis with the Swank MS Diet.

In health,
Michael Greger, M.D.

PS: If you haven't yet, you can subscribe to my free videos here and watch my live year-in-review presentations Uprooting the Leading Causes of Death, More Than an Apple a Day, From Table to Able, and Food as Medicine.

Image Credit: AJC ajcann.wordpress.com / Flickr

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