Many of you have probably already heard of this trial that just got published, an energy-unrestricted Mediterranean diet supplemented with either extra-virgin olive oil or nuts that resulted in an absolute risk reduction of approximately 3 major cardiovascular events per 1000 person-years, for a relative risk reduction of approximately 30%, among high risk persons who were initially free of cardiovascular disease, as compared to a control group consuming a typical low fat diet.

But you may not have heard Dr. Esselstyn's response. Dr Esselstyn is a successful surgeon (featured in video above) and author of “Prevent and Reverse Heart Disease: The Revolutionary, Scientifically Proven, Nutrition-Based Cure,” who promotes a low fat vegan diet that does not allow olive oil, dismissed the new study. Those in the Mediterranean diet study, he expained, still had heart attacks and strokes! So all the study showed was that “the Mediterranean diet and the horrible control diet were able to create disease in people who otherwise did not have it.”

This logic is absolutely absurd and needs to be addressed. The study population consisted of men and women with an average age of 67 (ranging from 55-80) with no cardiovascular disease at enrollment, who had "either type 2 diabetes mellitus or at least three of the following major risk factors: smoking, hypertension, elevated low-density lipoprotein cholesterol levels, low high-density lipoprotein cholesterol levels, overweight or obesity, or a family history of premature coronary heart disease." 

In other words they were elderly patients followed for a median of 4.8 years, who were by definition at high risk to have a heart attack.  So according to Dr. Esselstyn's logic, the patients would have been heart disease free during these 5 years had they not been enrolled in to this study and succumbed to the toxic effects of the mediterranean and "horrible control" diets that were able to actually "create disease" in the study subjects.

If this were true, then every randomized clinical trial in the history of medicine would be invalid, and ongoing trials must be stopped immediately due to ethical reasons and impending harm. A certain percentage of patients assigned to take a placebo in a drug trial will almost certainly develop the disease in question, as will many in the experimental group of even the most successful drug trials in history. Does this mean that the drug or placebo caused the diseases observed? Of course not. A successful drug would have prevented more disease or death than the placebo, but the disease still occurs in both groups.

And what was this "horrible control diet" he speaks of? Subjects in the control group were encouraged to eat low-fat dairy products, bread, potatoes, pasta, rice, fresh fruits, vegetables, lean fish and seafood, while avoiding foods such as vegetable oils, fried snacks, red meat, fatty fish, and visible fats in soups. Also known as the government recommended, low fat high carbohydrate diet.

As Gina Kolata reports in the New York Times, "The magnitude of the diet’s benefits startled experts. The study ended early, after almost five years, because the results were so clear it was considered unethical to continue."
Mrs. Kolata also says that  these published findings were based on the first major clinical trial to measure the Mediterranean diet’s effect on heart risks. However, this is untrue. This result and early termination is almost identical to the last time the Mediterranean diet was tested to prevent heart disease, published in 1994 out of France.

The Lyon Diet Heart Study, which tested the benefits of a Mediterranean-type diet on the recurrence of heart attacks in 605 subjects, was originally planned for five years but was ended prematurely due to the intervention diet’s dramatic cardio-protective effects.  After 27 months, the risk of cardiac death or non-fatal MI was 73% lower in the experimental group compared to the controls (RR= 0.27, 95% CI: 0.12-0.59, p=0.0001) and overall mortality was 70% lower (RR=0.30, 95% CI: 0.11-0.82, p=0.02).

The benefits of the Mediterranean diet occurred despite no differences in serum LDL or total cholesterol levels between exposure groups, suggesting that diet’s influence on CVD risk extends further than the current, overly simplistic explanation that ties the mechanism to serum cholesterol elevations caused by excessive Saturated fat  intake.  At the four-year follow up, a 47% lower risk of CHD was experienced by the experimental group compared to the control group (RR=0.53, 95%CI: 0.38-0.74). There was a 72% decreased risk (RR=0.28, 95% CI: 0.15-0.53) of cardiac death and nonfatal MIs (14 events in the experimental group vs. 44 in the control, p=0.0001), and a 67% reduced risk (RR=0.33, 95% CI: 0.21-0.52) of secondary endpoints - unstable angina, stroke, heart failure, and pulmonary or peripheral embolism (27 events vs. 90, p=0.0001) - associated with the Mediterranean diet compared to the control diet.

Published in the Lancet in 1994, the Lyon study was originally rejected by the New England Journal of Medicine specifically because the intervention diet induced no changes in serum lipids, demonstrating how firmly held the diet-heart hypothesis was at the time, that somehow it was impossible to reduce heart disease without reducing total or LDL cholesterol. 

When someone is confronted with inconvenient, overwhelming evidence contrary to their livelihood, it is understandably very difficult to concede. However, when the two most dramatic reductions in cardiovascular disease ever seen in clinical trial history are breathing down your neck, denial is the only possible escape.

Listen to Dr. Thomas Dayspring explain the best predictors of heart disease, lipid physiology, blood tests, and how your triglycerides, HDL, and LDL are affected by the foods you eat. An engaging, entertaining, and fascinating discussion. Dr. Dayspring has given over 4000 lectures in all 50 states, including over 500 Continuing Medical Education programs at hospital and medical school grand rounds.

Link to Video Here.

Dr. Dayspring reviews the methods of SpecialtyHealth's risk assessment and treatment of a 34-year old insulin resistant police officer. He went from incredibly high cardiovascular risk with insulin resistance to low risk in four months following SpecialtyHealth's model treatment program of a low carbohydrate diet, WWGF by Gary Taubes, and a statin. A must watch!

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Inconspicuously Absent Evidence

And what about these 14 clinical trials? How can the calorie unlimited, high fat diets keep producing more weight loss as compared to a low fat, calorie-restricted diet (at least in the short term), if they are characterized by high amounts of dietary fat, the vilified cause of obesity according to Dr. Ornish?

Even more striking is the fact that to our knowledge, a low-fat diet has NEVER in dietary clinical trial history produced more weight loss than a calorie unlimited, high fat diet. Many studies have shown no difference, but if it is true that a fat makes you fat, where are the clinical trials supporting this? 

If you can find a randomized control trial in which a calorie restricted low fat diet produces more weight loss than a calorie unlimited high fat diet, please e-mail it to us and we will post it: info@awlr.org.


Saturated Fat is Bad for you

Dr. Ornish says that "It’s not low carb or low fat," and then a few words later explains that an optimal diet is  "low in fat (especially saturated fats and trans fats) as well as in red meat and processed foods."

While we can definitely agree that trans fats and highly processed foods should be limited, the saturated fat argument is an archaic one that is not supported in the literature and has become an academic argument perpetuated by selective citation of supportive trials and variations in inclusion criteria. 

If we were to focus on the largest (i.e. > 100 subjects), randomized, most famous trials ever done lasting longer than 1 year, we are left with very few to assess that meet the following 2 criteria:

1) The only significant intervention involved a reduction in fat and saturated fat and an increase in polyunsaturated fats
2) They ask the question: does this diet reduce heart disease? (defined as heart attacks or death from heart disease)

Listed in reverse chronological order:
Women’s Health initiative (2006) – 48,835 women, 8 years, no significant difference between intervention and control.

Diet and Reinfarction trial (1989) – 2,033 men, 2 years, no significant difference between the groups given and not given fat and fiber advice. No significant differences in ischaemic heart disease between intervention and control (intervention was only advice in this trial)

Minnesota Coronary Survey* (1989) – 4,393 men and 4,664 women, double-blind, 4 years, no significant reduction in cardiovascular events or total deaths from the treatment diet

Finnish Mental Hospital (1972) – 12 years, physicians not blinded, significant decrease in coronary heart disease (CHD) death in men ( 5.7 deaths /1000 person-years vs 13 deaths /1000 person-years in the control. Non-significant decrease in CHD in women. (Not randomized, although included here because this is main experiment cited in support of diet-heart hypothesis)

Los Angeles Veteran’s Trial* (1969) –  846 subjects, up to 8 years, non significant difference in primary endpoints –  sudden cardiac death or myocardial infarction. More non-cardiac deaths in experimental group, resulting in near identical rates of total mortality

Oslo Heart Study (1968) – 412 men, 5 year, slight decrease in CHD with intervention. Many dietary interventions accompanied the low saturated fat diet. When stratified by age, the results were significant only in subjects younger than 60.

* Double blind

A full list of all the trials done supporting and refuting the saturated fat-heart-disease relationship, and a more in depth description of each, can be found here. 

Meta-analyses
If we instead focus on the recent meta-analyses of clinical trials testing this relationship, the majority have failed to elucidate a benefit associated with a low saturated fat diet:

• In 2010, Ramsden et al. published a meta-analysis of randomized clinical trials, including trials where polyunsaturated fats (PUFAs) were increased in place of saturated fats (SFAs) and/or trans fatty acids (TFA), and non-fatal heart attacks, coronary heart disease related deaths, and/or total deaths were reported.  In the nine studies included, there was a non-significant increased pooled risk of 13% for n-6 PUFA intake (RR=1.13, CI: 0.84, 1.53) and a decreased risk of 22% (RR=0.78, CI: 0.65, 0.93) for mixed n-3/n-6 PUFA diets. In other words, increasing polyunsaturated fats in the diet provides no benefit, and may be harmful according to this study.        

• Also in 2010, Mozaffarian et al published a systematic review and meta-analysis of randomized clinical trials investigating the effects of increasing PUFAs in place of other nutrients.  Among the seven studies included, an overall pooled risk reduction of 19% (RR= 0.81, CI=0.83-0.97) was observed for each 5% of energy of increased PUFA in the diet.      

• In 2009, Mente et al. published a systematic review of the randomized clinical trial (RCT) evidence that supports a causal link between various dietary factors and coronary heart disease.  The pooled analysis from 43 RCTs showed that increased consumption of marine omega-3 fatty acids (RR=0.77; 95% CI: 0.62-0.91) and a Mediterranean diet pattern (RR=0.32, 95% CI: 0.15-0.48) were each associated with a significantly lower risk of CHD. Higher intake of polyunsaturated fatty acids or total fats were not significantly associated with CHD, and the link between saturated fats and CHD received a Bradford Hill score of only 2 (out of a maximum score of 4), signifying weak evidence of a causal relationship.

• Also in 2009, the Cochrane Collaboration, an international not-for-profit organization, published a meta-analysis of clinical trials that either reduced or modified dietary fat for preventing cardiovascular disease. Twenty-seven studies met the inclusion criteria, and no significant effect on total mortality (RR = 0.98, 95% CI: 0.86-1.12) or cardiovascular mortality (RR = 0.91, 95% CI: 0.77-1.07) was found between the intervention and control groups 

The only study above showing a benefit to replacing saturated fats with polyunsaturated fats was the Mozaffarian meta-analysis. The authors of the study claim to have only included randomized clinical trials in their meta-analysis. Surprisingly, the Finnish Mental Hospital Study was included twice – split into separate analytical pools of male and female subjects. It is unclear why this study was even included to begin with, since it was not randomized and contained a disproportionate number of control subjects who were taking cardio-toxic medications and consuming higher levels of trans fats than the experimental group. 

Inclusion of male and female Finnish data separately further raises concern since it clearly exaggerates the apparent cardio-protective effect of PUFAs demonstrated in this meta-analysis. Excluding the Finnish data from their pooled analysis would diminish the observed results and elicit a null finding, since all other included studies apart from the Oslo heart study (RR=0.75, CI 0.57-0.99) were null:    

Closing Thoughts

In medical school we are taught how to take an HPI (History of present illness) whenever we see a new patient. The importance of this history is stressed in every class, because of how important the patient's story is, and how helpful it can be in coming up with the diagnosis. 

Yet when it comes to figuring out why people are gaining weight, we don't listen. We are absolutely sure that the patient is at fault and we are correct: Just Eat less. 

We don't listen to the fact that people are universally hungry on a calorie-restricted diet. Eat 500 less calories a day than you normally would, then run for an hour each day, then ignore your most basic physiological drive to eat when you get hungry. And repeat this for the rest of your life and our obesity problems will be solved.

What if instead there was a way of eating in which people ate when they were hungry, and stopped when they were satisfied. A way of eating which didn't force you to count calories. A way of eating that, based on our most rigourous scientific data available, produces the most weight loss, reduces triglycerides and increases HDL. 

This way of eating exists, vilified by the medical community as "The Atkins diet", and relegated to a fringe movement and diet fad by the media as the "Caveman diet."

Yet when it comes down to which diet we should eat, the media, physicians and dietitians can make their case, but the final vote should be given to the patient. To the person actually eating the diet. If these patients from all over the world say they are no longer hungry, then maybe we should listen. 


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In Los Angeles in the 1960s, the Veteran's hospital would be the place of arguably the most rigorous clinical trial ever done, testing the potential benefits of a low saturated fat diet. Only three such trials took place in controlled hospital environments, enabling investigators to feed study subjects meals in which saturated fats were replaced with polyunsaturated fats while keeping the rest of the diet relatively unchanged, and this Veterans study was particularly well done. It was a double blind, randomized trial involving 846 subjects for up to 8 years. The subjects were former veterans, living in a domilicary unit. Half ate a control diet, similar to the American diet, and half ate the experimental diet. All meals were served in the cafeteria.

Dietary Intervention
Subjects were given meal tickets of a certain color, corresponding to a particular diet unknown to them. The control diet was 40% calories from fat, “mostly of animal origin,” and the experimental diet involved substitution of vegetable oils for 2/3 of the animal fat, incorporated into the diet in the form of milk, ice cream, margarine, and cheeses. In this trial the low saturated fat experimental diet produced a 13% reduction in serum cholesterol compared to the control group throughout the trial, objectively confirming the experimental group’s adherence to the low saturated fat diet.  

Outcome
After eight years of participation, there was no significant difference in heart disease rates, the primary endpoint, manifested as sudden cardiac death or heart attacks (78 events in 65 men in the control group vs. 60 events in 52 men in the experimental). However, when pooled with the data for cerebral infarction and "other secondary end points," the difference in total cardiovascular disease reached statistical significance, with 119 major events occurring in 96 subjects in the control group and 85 events in 66 subjects in the experimental group (p=0.01). 

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This clinical trial is all too often cited as supporting the diet-heart hypothesis. By reading the abstract, it seems reasonable, until you track down what these "secondary endpoints" happen to be. Which turned out to be quite difficult. After requesting an interlibrary loan from Pittsburgh, I eventually tracked down the ~80 page tome describing the study in vivid detail. And here are the secondary endpoints:

• ruptured aneurysms
• limb amputations due to peripheral vascular disease
• and “miscellaneous” events, such as occlusion of the mesenteric arteries
  

To say limb amputation and occlusion of arteries supplying your intestines is related to saturated fat intake would be a bit of a stretch. Extremity amputation was required if the dorsal pedal pulse and the posterior tibial pulse on the affected foot were absent or extremely faint. 

In other words, these "secondary endpoints" involved small arteries that supply the muscles on the top and bottom of your foot. 

Deaths due to non-atherosclerotic causes were higher in the experimental group (85 vs. 71 in control), resulting in near identical rates of total mortality (177 in control vs. 174 in experimental group). This study also raised an interesting question as to whether or not a diet high in unsaturated fat may contribute to death by other causes, since the experimental group had more non-cardiac deaths (specifically from cancer: 7 deaths in experimental, and 2 in control). However, these numbers are much too small to determine if this result was significant or not. Other such clinical trials have not supported this phenomenon. 

This study is another perfect example of how profoundly misleading an abstract can be, and how important it is to read each study in its entirety before making bold claims that this study supports the idea that eating a low saturated fat diet prevents heart disease. 

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In the 1960s and 70s, mental institutions offered dietary researchers an excellent opportunity to test various diets in a highly controlled setting for a long duration. At the time, long term mental hospital stays were common, and researchers used this to their advantage. This opportunity was famously utilized three separate times, in Los Angeles, Helsinki, and Minnesota. In each city, researchers tested the long term effects of eating a low saturated fat diet, and how it may be related to developing cardiovascular disease. The last post discussed the pitfalls involved in blinding a diet study, and the Minnesota Coronary Survey is an example of quite the contrary. 

This was a double-blind randomized control trial lasting 4.5 years in 6 Minnesota state mental hospitals and one nursing home involving 4,393 men and 4,664 women. It examined effects of a lipid lowering diet on heart disease. This was the largest study by far that tested the diet heart hypothesis, and they did so with arguably the most rigorous study design to date.

Each patient was randomly assigned to consume either the low saturated fat intervention diet (38% fat diet; 9% Saturated fat, 15% polyunsaturated fat, 14% monounsaturated, 166 mg cholesterol), or the control diet (39% fat diet; 18% saturated fat, 5% polyunsaturated fat, 16% monounsaturated fat, 446mg cholesterol). The difficult part then, is to create two different diets containing these macronutrient compositions that are not discernable by taste or smell. The next challenge is serving over 9,000 people their correct diet for years, based on which group they were randomly assigned to. Here is how they did it:

"Both diets were served in a single line. As a participant entered the line, he or she was handed a label bearing his or her name and a code number that was incomprehensible to the uninitiated but easily interpreted by the foodservers to determine which diet was to be served...The label also enabled the food service worker to serve the proper tray without compromising the blind design, and the labels remaining on the sheet provided the basis for the daily tally of missed meals. Each month the hospital technicians transferred the missing meals data to a "Port-o-Punch card." These cards were read by the computer and at the end provided a correlation between adherence and cholesterol response"

To compliment the rigorous study design, the cholesterol levels of the patients can be used as an objective marker throughout the study to make sure everything is going as planned. Since we know from feeding studies that when you replace saturated fats with polyunsaturated fats, total cholesterol levels decrease, researchers can use this phenomenon to measure adherence. Here is a graph of the cholesterol levels of the study subjects over the course of 4+ years on their respective diets:

Intervention group cholesterol levels decreased 14.5% and were stable for the entire study. The stability of these graphs is spectacular, offering an excellent test of the diet heart hypothesis. Those who kept their cholesterol levels 14.5% lower for 1-4 years should have less heart disease. However this was not the case.
After 4.5 years, no reduction in cardiovascular events or total deaths from the treatment diet. In fact there was a non-significant trend towards a benefit to a high saturated fat diet:

Although the trial laster 4.5 years, not everyone consumed the diet that long. The main criticism of this study was the average length of time on the diet, which was 384 days. However, the number of person years observed was 9,538, with 5,903 of these years continuously for more than 2 years and 2,495 for more than 4 years. 

The authors waited about 16 years before publishing this data. According to Gary Taubes in Good Calories, Bad Calories, when he asked Dr. Frantz, the principal investigator, why they waited so long to publish the study, he explained in an interview: "We were just disappointed in the way it came out."

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In 2004, PBS did a special entitled "Diet Wars," interviewing experts from all over the dietary advice spectrum, such as Dean Ornish and Gary Taubes. Below are selected exerts from one of the interviews. At first glance it may sound like Gary Taubes, but in fact it is Dr. Walter Willet, the chair of the department of nutrition in the School of Public Health at Harvard Medical School. 

Worth noting: early in the interview, Dr. Willet explains that  "farmers have known for thousands of years that you can make animals fat by feeding them grains, as long as you don't let them run around too much, and it turns out that applies to humans." Yet at the end of the interview, Dr. Willet states that at the base of the Harvard Food Pyramid (PDF) are exercise and whole grains. They have since updated their recommendations to the plate. It seems difficult to reconcile this advice. 

This low-fat dogma was incorporated into the USDA food guide pyramid in 1992?

Well, there's a little bit of complexity. It's interesting. In the '70s and early '80s, while heart disease rates were going bad, we were not talking about low-fat diets. We were talking about replacing saturated fat with a healthy fat, polyunsaturated fat. But somewhere in the mid-1980s, we lost that message. It's perhaps partly because some nutritionists felt it was too complicated to talk about different types of fat, and developed the notion we should just reduce all types of fat across the board. That was really the beginning of the low-fat, high-carbohydrate crusade.

How is the simplification -- eat less fat -- manifest in this food guide pyramid?

Well, the food guide pyramid that was developed in 1991 really is based on the idea that all fat is bad. Therefore [if] fat is bad, and you have to eat something, carbohydrate must be wonderful. So the base of the pyramid is really emphasizing large amounts of starch in the diet. We're told we can eat up to 11 servings a day, and if that wasn't enough starch, the pyramid puts potatoes along with the vegetables, so you can have up to 13 servings a day. That's a huge amount of starch.

Where's fat?

Fat's up at the top of the pyramid, and where it says explicitly "fats and oils, use sparingly." It doesn't make any distinction about the type of fat, and it tells us to eat basically as little as possible.

From a public health standpoint, how would you characterize this pyramid?

Well, this pyramid is really not compatible with good scientific evidence, and it was really out of date from the day it was printed in 1991, because we knew, and we've known for 30 or 40 years that the type of fat is very important. That was totally neglected.

[What were the] unintended consequences? The food industry started using vegetable oils, but baking was difficult so they made a technical modification.

In some ways, we do have to credit the food industry with being responsive to what nutritionists were saying. They did believe or accepted the evidence that vegetable fats, vegetable oils, would be better than animal fats, and that really led to the development and promotion of the margarine industry and Crisco, baking fats that were made from vegetable oils. But they were made by a process called partial hydrogenation, which converts a liquid oil, say like soybean oil or corn oil, to something like margarine or vegetable shortening. As it turns out that was a very disastrous mistake, because in the process of partial hydrogenation, a totally new type of fat is formed called trans fat. The evidence has now become very clear that trans fat is far worse than saturated fat.

So when people were told to switch from butter to margarine?

Unfortunately, as a physician back in the 1980s, I was telling people that they should replace butter with margarine because it was cholesterol free, and professional organizations like the American Heart Association were telling us as physicians that we should be promoting this. In reality, there was never any evidence that these margarines, that were high in trans fat, were any better than butter, and as it turned out, they were actually far worse than butter.

People read on the label "cholesterol free."

Right. This is a good example where just focusing too much on one particular piece of the diet, one particular substance or nutrient, can really mislead us. It is true that these vegetable shortenings and margarines were cholesterol-free, and that was pushed. ... Even though these products were cholesterol-free, the trans fats in them raised our blood cholesterol much more than actual cholesterol in the margarines would have done.

"All fat is bad" led to many low-fat products, some of which had beneficial value. Talk about one example.

This campaign to reduce fat in the diet has had some pretty disastrous consequences. ... One of the most unfortunate unintended consequences of the fat-free crusade was the idea that if it wasn't fat, it wouldn't make you fat. I even had colleagues who were telling the public that you can't get fat eating carbohydrates. Actually, farmers have known for thousands of years that you can make animals fat by feeding them grains, as long as you don't let them run around too much, and it turns out that applies to humans [my emphasis]. We can very easily get fat from eating too many carbohydrates, and the public was really directed to only focus on fat calories, when we really have to keep an eye on calories no matter where they're coming from.

With more fat-free products than ever, Americans got fatter.

Right. The reality is that during this campaign for fat-free and reduced-fat products, actual fat consumption did go down, but Americans got much fatter during this period of time. Now of course lots of things were going on at the same period in time, but I think it's highly likely this focus only on fat calories to the neglect of carbohydrate calories has contributed to this epidemic of obesity.

Is it fair to blame the food pyramid when people don't follow it anyway?

The food guide pyramid has actually had a substantial impact on the diets of Americans. If we look back compared to 20 years ago, the percentage of calories from fat in the American diet is quite a bit lower compared to earlier days. Second, there're some important indirect impacts of the food guide pyramid, in that many tens of billions of dollars of federal food policies have to be compliant with the food guide pyramid. So many programs -- for example, what's fed to young children, to pregnant mothers, to low-income families -- have to be consistent with low-fat diets. So the impact really has been, overall, substantial.

Behind the food pyramid were a collection of constituencies. Were people receptive when you raised these criticisms in the '90s?

There was not much receptivity in the 1990s, when we raised these criticisms of the food guide pyramid. It was almost an accepted religious belief that fat was bad and carbohydrates were good. Then there were lots of economic interests behind the food pyramid as well. Clearly the dairy industry is extremely well represented in the food pyramid. The beef industry is there, and it's very convenient that beef is combined along with fish and poultry and nuts and legumes. So each one of those industries can say: It's healthy to have three servings a day of our product.

What makes it so difficult to study the relation between diet and health?

The relation between diet and health is unusually complicated to study, and that's probably why we don't have all the final answers even yet. In a trial of a drug, for example, you can randomly assign people, one group to a placebo and another [group] to the new drug, and see what happens to them. But obviously you can't do that with nutrients or a whole diet very easily.

Second, we have to follow people for many years to learn all the consequences of diet, and perhaps even almost a lifetime, because some of the effects of diet may be operating during childhood and not be manifested until adult life. So there's no one simple kind of study that will give us all the truth about how diet influences our health, and we need to combine the results of many different studies to have the best and most complete picture.

One [kind] of study, for example, involves feeding small groups of people very controlled diets for short periods of time, and seeing what happens, for example, to their blood cholesterol levels. But blood cholesterol levels are only part of the picture, so we are also conducting very large studies where we enroll tens of thousands of people and follow them for many years, all the way along, finding out what they're eating, and then what happens to them in terms of their risk of heart attacks, cancers, and other conditions. And of course in those studies we need to control for many factors, like whether they smoke, how much exercise they have, their family history of various diseases. It's really only when we put those kinds of studies together with the more detailed metabolic, biochemical studies that we can have the best information about the effects of diet.

So you find out what they eat, rule out the bad things they do, and look for associations?

Right. What we do is find out what people eat through very detailed, structured questionnaires, observe what happens to them in terms of disease rates -- heart attacks and cancers, for example -- and then put these together, controlling for other aspects of lifestyle like diet and activity.

What did you notice that seemed to clash with the low-fat dogma?

When we began our studies back in the late 1970s, we expected that we would find a relationship between, say, fat intake and breast cancer, because that was almost an accepted relationship. But as the data started coming in over the years, we just did not find any higher risk of breast cancer among women who consume more fat in the diet. And the same was true for colon cancer and for heart attacks and risk of type 2 diabetes. In fact, the percentage of calories from fat in a diet has not been related to any important health outcome.

Amount of fat has no relationship to coronary heart disease?

The amount of fat had no relationship to risk of coronary heart disease, but the type of fat was extremely important.

So the advice we were getting was not just misleading but dangerous?

Right. The evidence that we accrued really suggested not only that the type of advice that people were getting was not useful, but it actually could be dangerous, because some people were eliminating the very healthy types of fat that actually reduce heart disease rates.

Certain fatty acids can dramatically reduce the incidence of cardiac arrhythmia?

One of the important findings, not just from our studies but several trials conducted by other people in Europe and also some careful animal studies, have very clearly indicated that some types of fatty acids in the diet, in particular the omega-3 fatty acids, can actually reduce the heart arrhythmias that really cause people to drop dead in the street. We call that sudden death. And that's very important because some people were eliminating those critically important fatty acids from their diet because they were told that all fat is bad. ...

Traditionally people think of carbohydrates as made up of simple sugars and complex starches. What's wrong about that?

Right. The thinking in nutrition about carbohydrates really had broken them down into two classes: sugars and so-called complex carbohydrates, which are mostly starches. ... The idea has been pushed that all forms of so-called complex carbohydrates are really the poster child of nutrients, and we should be eating them in large amounts. That's what the pyramid tells us to do. But in fact, these kinds of starches -- white bread, white rice, potatoes -- are starches that are very rapidly converted to glucose, really pure sugar, and almost instantly absorbed into the bloodstream. And these are the kinds of carbohydrates that we really should be minimizing in our diets.

A sugar rush from a potato?

Actually, careful studies have shown, demonstrated that you get a bigger rise in blood sugar after eating potatoes, a baked potato, say, than you do from eating pure table sugar.

Really!

Really.

That seems pretty extreme. Why is that?

... There are several problems with these rapid rises in blood glucose after you ingest large amounts of a rapidly digested form of carbohydrate. First of all, when the blood sugar goes skyrocketing up, the body wants to bring it back down. So our pancreas pumps out a big blast of insulin, and as a result, the blood sugar comes crashing down rapidly. In fact, in many people, after three and four hours, it overshoots and actually become a little hypoglycemic, and that rapid crashing down of blood glucose and insulin stimulates hunger. That would be no problem, except that it's often all too easy to go in the refrigerator or find a snack, and if we do that frequently throughout the day, that can add up to too many calories over weeks and months and years, and contribute to obesity.

Second, these high rises in blood glucose and insulin have a bad metabolic effect on the blood cholesterol fractions. Specifically the HDL, the good cholesterol, is driven down, and triglycerides, another type of fat in the blood that leads to heart attacks, goes up.

Third, after many years of demand for high amounts of insulin, the pancreas tends to give out. And at that point in time, we've got type 2 diabetes.

[What is the role of insulin?]

The role of insulin is to transport glucose from the blood into the cells, like into muscle or into fat cells.

What can go wrong with this system?

Well, the problem really comes about when we develop insulin resistance. And that means that the cells, like the muscle cells, become more resistant to the action of insulin transporting the glucose inside the cell. And we can become insulin-resistant in several different ways. There's some genetic component, and as it turns our, for example, many Asians tend to have more insulin resistance. Also if we have overweight or low levels of physical activity, we'll be more insulin resistant.

Many people argue the virtues of Asian diets, with a lot of white rice.

Right. The Asian diet as it's traditionally been used raises some very interesting issues in nutrition, in fact, some of the most important findings during the last several years. What we've come to realize is that if we have a higher degree of insulin resistance, then we much less well tolerate a high-carbohydrate diet.

Interestingly, in traditional Asian societies, people were very lean, very active, and therefore had low insulin resistance. They could eat large amounts of rice, even white rice, in the diet and have low heart attack rates and have low rates of type 2 diabetes. But if you take that same person, and they [now] may be living in Beijing and driving a car and watching a television, and they put on a few pounds, they're going to have much more insulin resistance. So if you take that same diet, high in carbohydrate and white rice, they will have a much worse metabolic response and much higher rates of type 2 diabetes.

If you're American and overweight, won't you be put on a low-fat diet?

If you're overweight and living in the United States, and you go to a hospital and see a dietician, almost for sure, you're going to be put on a low-fat, high-carbohydrate diet.

What's your view of that?

The problem is that that's really the wrong diet for an overweight person. Because the person is overweight, in general they're going to have quite a bit more insulin resistance and much less well able to tolerate low-fat, high-carbohydrate diet.

But fats have twice the amount of calories per gram as carbohydrates. Doesn't it make sense to push the low-calorie diet and therefore a diet low in fat?

There's been a very simplistic idea: Just because fats have more calories per ounce than carbohydrates, we should be eliminating fats or reducing fats to control our total caloric intake, in other words, to help control our weight. What's really important though is how satisfying a diet is, because we have very complex mechanisms that control our total intake of calories, and it's become pretty apparent that if we have a high-carbohydrate diet, particularly high refined carbohydrate, it makes it much more difficult to control our total caloric intake. That's probably because when we eat refined carbohydrates, we get these swings in blood glucose and insulin that lead to hunger between meals; whereas if we have a diet that's somewhat higher in fat, we tend to be more satisfied over the long run.

Is this what Dr. Atkins was saying 30 years ago?

Dr. Atkins was saying as much as 30 years ago, that if we reduce our carbohydrate intake to quite low levels, that will make it easier to control our caloric intake and thus promote weight loss. As it turns out, there is a strong element of truth in that. A number of studies in the last year have looked in a very careful way, comparing low-fat, high-carbohydrate diets with reduced-carbohydrate diets, and in general people have done better on the reduced-carbohydrate diets in terms of their weight.

Even though each ounce of fat has twice as many calories, you eat fewer calories because they're more satisfying?

Yeah. Well, first of all, this idea of how many calories per gram of fat versus how many calories per gram of carbohydrate is a little simplistic, because we almost never eat foods that are pure fat and pure carbohydrate. They come in foods as mixes, and often with a lot of fiber and a lot of water, and all of those things make a difference as well. But what is really important in the long run is how satisfying a food will be. And as it turns out, that many high-fat foods -- sometimes like meat, but even think of a handful of nuts -- are often very satisfying even though the physical amount is not very great.

One of the interesting observations in the recent studies that have compared high-fat diets with high-carbohydrate diets is that there are a lot of differences between people; that it's not that everybody loses a certain amount of weight on a reduced carbohydrate diet. Some people lose a lot of weight. Other people hardly lose any, so one of the things we have to come to understand better is the reasons why there's such a difference in response to these diets.

Talk about your food pyramid.

We've tried to put together an alternative food guide pyramid that would be based on the best available science. And of course it is a little bit challenging to boil down a tremendous amount of complex science to a simple graphic, and you really have to focus on the things that are well established and important.

Right at the bottom, we put weight control and regular physical activity, because overweight is the number one nutrition problem in the United States. Almost everyone is going to need to exercise on a regular basis if they want to control their weight over the long run. And this also is a message that all forms of calories are important.

On the next level, we put healthy forms of carbohydrate, meaning whole-grain carbohydrates and healthy forms of fat, meaning from vegetable oils, in the recognition that in most people's diet, most calories are going to be coming from some source of carbohydrate and fat. And what's really important is that those both be healthy sources.

Some of those fats have come right from the top of the other pyramid.

Right. What we've done is, we've brought some of those fats from the top of the pyramid down to the base, because healthy fats are an important part of a healthy diet.

The rest of the pyramid?

Our alternative pyramid, like the USDA pyramid, does emphasize plenty of fruits and vegetables, but we've taken potatoes out of the vegetable group. We've put legumes and nuts as a layer. If you want to be a vegetarian, those are good protein sources. But moderate amounts of poultry, fish, and nuts can also make a diet be a non-vegetarian diet and still very healthy. And up at the top we've put red meat and dairy products, dairy fat, because those are high in saturated fat. ... At the top of the pyramid, we've put foods like white bread, white rice, white pasta, and sweets as those that should be used sparingly. And that was really the base of the USDA pyramid.

Some nutritionists have criticized your pyramid as "floating on a lake of olive oil."

The formal studies that had compared a more moderate fat intake as we've suggested, with low-fat diets, have actually consistently shown that people did as well or better controlling their weight on a moderate-fat diet compared to a high-carbohydrate, low-fat diet.

Even good fats are more fattening than good carbs. So they think you're contributing to the obesity epidemic, or there's a risk of that. A tablespoon of olive oil is 14 grams of fat.

There are all kinds of beliefs about the amount of fat in a diet, tremendously strong opinions. What we really need is sound data, and the studies that have been done show that people actually end up controlling their weight at least as well, and usually better, on moderate-fat diets compared to low-fat, high-carbohydrate diets.

Is it okay to get more than 30 percent of your calories from fat?

The evidence is quite clear that it's perfectly fine to get more than 30 percent of your calories from fat, and probably, in fact, it's even better to be getting more than 30 percent of calories from fat, if it's the healthy form of fat. ...

When you look at the causes of obesity, what do you find?

The causes of obesity and the obesity epidemic in the United States are extremely complex. In fact, obesity is sort of a tip of the iceberg of tremendous social change that's been going on during the last few decades. First of all, our activity patterns have changed greatly. We have children and adults now watching on the average, about four hours of television per day, and in study after study, we've seen just the number of hours of television watching being the strongest predictor of obesity. When I was young and came home after school, we'd all go out and play, and our mothers would have to drag us in for dinner. That doesn't happen very often anymore. Often the mothers are not there. Kids are inside. The television is used as baby sitters. We've also made it dangerous and uninviting to walk to places, to walk to stores, to ride bikes in urban areas, and that's removed an important amount of physical activity from our lives as well.

So the physical activities pattern's changed, but the food environment has also changed. We have food available fast and very low-cost and very convenient, almost everywhere. The food industry has invested many tens of billions of dollars in making their products more attractive, more sweet, more salty, more sexy, more seductive in every way that they can, and we're vulnerable to that promotion, and we are eating more. So you put these two factors together -- reduction in activity, heavy promotion of food -- and you've got, not surprisingly, an epidemic of obesity.

Which we're exporting to the rest of the world.

Unfortunately, what we've created is now being exported to the rest of the world. And in almost every country, in Europe as well as Africa, Latin America and Asia, rates of obesity are climbing rapidly.

When you think about solutions, how can we proceed?

The causes of obesity are very complex, and therefore any response is going to have to be complicated and multi-faceted as well. There is no single solution to this, but we have to do many things to really solve this problem.

We've actually looked at this in a very detailed manner over the past two years in the New England states, and identified eight different areas that we have to really modify. For example, schools have to change what's served, what's promoted in schools. The healthcare providers -- physicians, nurses -- have to be providing much better and effective advice to their patients about controlling their weight. Work sites have to change. The whole food environment and what we promote to children has to be somehow modified, and we do have to protect children from these aggressive advertisements. We have to change the physical environment to make it more conducive, more attractive to bicycle to work, to destinations, not just drive places. Many other things need to be done if we're going to solve this problem, and it's time we really began.

The national obesity crisis, I mean, it's really severe. And to hear you talk about it, it sounds like it's hopeless to overcome it.

The crisis we're facing is severe, and it's getting worse. Interestingly, the full consequences won't be seen for another 30 or 40 years, because it takes that long a time for the risk of diabetes and the complication of diabetes to play out. But it's not hopeless, and I think that's the good news. There are places, if we look around the world, where people have been controlling their weight. For example, in Japan and in Sweden, women have really not been gaining weight as they've gone through midlife and gotten older, so we do need to learn more about how they're doing it.

Also in the U.S. there are many people who are controlling their weight successfully. Not everybody is going to be as successful, even if they do the same diet and do the same amount of physical activity, but many people are doing pretty well. And one piece of evidence we have is that upper-income groups actually only have about half the rate of obesity compared to lower-education groups. So it's not hopeless, but we are going to have to devote many more resources to doing this if, as a whole country, we're going to be successful. ...

The advice for so long was: Buy something that says "fat-free," or at least "low-fat" on it. All these [salad] dressings, fat free. But not necessarily a good idea?

In fact, a pretty bad idea, and that was really unfortunate that the crusade against fat really led the food industry to produce all these fat-free salad dressing products. The problem is that the fats that were in the salad dressings were the healthy fats, the ones you should be including in the diet. They were the unsaturated fats that reduce our blood cholesterol levels, and we've also seen that they reduce heart attack risk and type 2 diabetes, as well. So people were giving up these healthy fats, and what we've seen is actually an increase in risk of heart disease among people avoiding full-fat salad dressings.

Of course one of the important roles of a full-fat salad dressing is that it makes salads taste good, and we want people to be eating those vegetables. So it's not that we're telling people to gulp down bottles of salad dressing. We want them to use it on a salad and enjoy it. ...

[At] the base of your pyramid, after exercise: whole grains. Right?

Right. On the base of our pyramid, side-by-side, we put healthy fats and whole grains. And that's because we do see positive benefits in study after study, that there's lower risks of type 2 diabetes and heart disease, and probably better weight control as well, with some whole grains in the product. And that's because these carbohydrates are generally absorbed more slowly, they give less of a spike in blood glucose, and they come with a whole package of minerals, vitamins, and fiber that all have positive health benefits. ...

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