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

Original Link

Egg Consumption and LDL Cholesterol Size

NF-Apr26 Does Cholesterol Size Matter.jpeg

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

Original Link

Four Brazil Nuts Once a Month…

NF-Mar29 Four Nuts Once a Month.jpeg

One of the craziest studies I read all year involved feeding people a single serving of Brazil nuts to see what it would do to the cholesterol levels of healthy volunteers. They gave ten men and women a single meal containing zero, one, four, or eight Brazil nuts, and found that the ingestion of just that single serving almost immediately improved cholesterol levels. LDL, so-called "bad" cholesterol levels in the blood, was significantly lower starting just nine hours after the ingestion of nuts, and by no insignificant amount, nearly 20 points within a day. Even drugs don't work that fast. It takes statins around four days to have a significant effect.

But that's not even the crazy part.

The researchers went back and measured their cholesterol five days later, and then 30 days later. Now keep in mind they weren't eating Brazil nuts this whole time. They just had that single serving of Brazil nuts a month before and their cholesterol was still down 30 days later. It went down and stayed down, after eating just four nuts... That's nuts!

And no, the study was not funded by the Brazil nut industry.

Interestingly, four nuts actually seemed to work faster than the eight nuts to lower bad cholesterol and boost good cholesterol. These results suggest that eating just four nuts might be enough to improve the levels of LDL and HDL for up to 30 days, and maybe longer--they didn't test past 30.

Now normally, when a study comes out in the medical literature showing some too-good-to-be-true result like this you want to wait to see the results replicated before you change your clinical practice, before you recommend something to your patients, particularly when the study is done on only ten people, and especially when the findings are literally just too incredible to be believed. But when the intervention is cheap, easy, harmless and healthy--eating four Brazil nuts a month--then, in my opinion, the burden of proof is kind of reversed. I think the reasonable default position is to do it until proven otherwise.

They concluded a single serving was sufficient "without producing liver and kidney toxicity." What they're referring to is the high selenium content of Brazil nuts--so high that four eaten every day may actually bump us up against the tolerable daily limit for selenium, but not something we have to worry about if we're just eating four once a month.

I'd be curious to hear if anyone experiences similar results. Even if the study was just a fluke, Nuts May Help Prevent Death by improving the function of our arteries (Walnuts and Artery Function) and fighting cancer (Which Nut Fights Cancer?) and inflammation (Fighting Inflammation in a Nut Shell).

Even eating nuts every day does not appear to result in expected weight gain (Nuts and Obesity: The Weight of Evidence), so enjoy!

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: CIFOR / Flickr

Original Link

Stopping Heart Disease in Childhood

NF-July15 Heart Disease Starts in Childhood.jpg

A landmark paper in 1953 radically changed our view about the development of heart disease forever. The study looked at a series of 300 autopsies performed on U.S. battle casualties of the Korean War. The average age was 22 years old, but 77% of the soldiers' hearts had gross evidence--meaning visible-to-the-eye evidence--of coronary atherosclerosis, hardening of their arteries. Some of them had vessels that were clogged off 90% or more. As an editorial in the Journal of the American Medical Association concluded, "This widely cited publication dramatically showed that atherosclerotic changes appear in the coronary arteries years and decades before the age at which coronary heart disease (CHD) becomes a clinically recognized problem." Follow-up studies on the hearts of thousands of more soldiers over the subsequent years confirmed their results.

How young does it go? Fatty streaks, the first stage of atherosclerosis, were found in the arteries of 100% of kids by age ten. What's accounting for this buildup of plaque even in childhood? In the '80s we got our first clue in the famous Bogalusa Heart Study. This looked at autopsies of those who died between the ages of 3 to 26 years old, and the #1 risk factor was cholesterol intake. There was a dramatic stepwise increase in the proportion of their arteries covered in fatty streaks as the level of bad cholesterol in the blood increased. As powerful as this was, the study only looked at 30 kids. So they decided to study 3000: three thousand accidental death victims, ages 15 through 34.

After thousands of autopsies, they were able to produce a scoring system that could predict the presence of advanced atherosclerotic lesions in the coronary arteries of young people. The higher our score, the higher the likelihood we have these lesions growing in the arteries that pump blood and oxygen to our heart. So if we're young and we smoke, our risk goes up by one point. If we have high blood pressure at such a young age, that's four points. If we're an obese male, that's six points, but high cholesterol was the worst of all. If our non-HDL cholesterol (meaning the total cholesterol minus the good cholesterol) is above 220 or so, our risk increased eight times more than if we smoked.

Let's say you're a woman with relatively high cholesterol, but you don't smoke, you're not overweight, your blood pressure and blood sugars are OK. At your sweet 16 there's just about a 1 in 30 (3%) chance you already have an advanced atherosclerotic lesion in your heart, but if you don't improve your diet, by your 30th birthday, it's closer to a one in five (20%) chance you have some serious heart disease, and if you have really high cholesterol it could be closer to one in three (33%).

In the video, Heart Disease Starts in Childhood, you can see what happens to our risk if we bring our cholesterol down to even just that of a lacto-ovo vegetarian, or if we exercise to boost our HDL, etc. It shows that even in 15 to 19-year-olds, atherosclerosis has begun in a substantial number of individuals, and this observation suggests beginning primary prevention at least by the late teenage years to ameliorate every stage of atherosclerosis and to prevent or retard progression to more advanced lesions.

If we start kids out on a low saturated fat diet, we may see a significant improvement in their arterial function by 11 years old. The study concluded, "Exposure to high serum cholesterol concentration even in childhood may accelerate the development of atherosclerosis. Consequently the long-term prevention of atherosclerosis might be most effective when initiated early in life." And by early in life they meant infancy.

Atherosclerosis, hardening of the arteries, begins in childhood. By age ten nearly all kids have fatty streaks, the first stage of the disease. Then the plaques start forming in our 20s, get worse in our 30s, and can start killing us off in middle age. In our hearts it's a heart attack, in our brains it's a stroke, in our extremities it can mean gangrene, and in our aorta, an aneurism.

For those of us older than ten years of age, the choice likely isn't whether or not to eat healthy to prevent heart disease, it's whether or not we want to reverse the heart disease we likely already have.

Drs. Dean Ornish and Caldwell Esselstyn Jr. proved that we can reverse heart disease with a plant-based diet, but we don't have to wait until our first heart attack to start unclogging our arteries. We can start reversing our heart disease right now. We can start reversing heart disease in our kids tonight.

The bottom line is that we have tremendous control over our medical destinies. How do we go about reversing our heart disease? I address that question in my latest live annual review presentation More Than an Apple a Day. Or, for shorter snippets:

Heart disease is a choice.

-Michael Greger, M.D.

PS: If you haven't yet, you can subscribe to my free videos here and watch my 2012 live year-in-review presentation Uprooting the Leading Causes of Death.

Image Credit: James MacDonald / Flickr

Original Link