Have you ever watched a movie that had a surprise ending, say, The Sixth Sense, for example, then watched it again? Once you know the ending, you see all kinds of things that make the ending obvious that you didn’t see the first time through.

When you have a movie (or a novelistic) experience like this, it makes you appreciate the talent of the creative people who make the movie (or write the novel). If these folks had just sprung the surprise ending on you without cleverly concealing all the clues, you would feel cheated.

It’s kind of the same with scientific research. Researchers uncover scientific knowledge bit by painstaking bit–sometimes over years–until a piece of the scientific puzzle is clarified. Once this piece is known, you can roam back through the scientific literature and find all the papers that lead to its clarification. Just as you would feel cheated if you watched The Sixth Sense a second time and didn’t see all the evidence of what was going on (which is really obvious once you know the ending) and were just slapped in the face with the surprise ending, you should find something amiss if practically the entire scientific establishment touts something as a fact and you can’t go back and find the evidence that leads to this conclusion.

I’ve been making this quest back through scientific time to look for the clues that lead to the conclusion (the surprise ending) that diet causes cholesterol to go up and that diet causes heart disease. So far, I haven’t found the clues. In fact, I’ve found clues that deny the conclusion.

Let’s start early on with some of the first evidence that came before even Ancel Keys published his discredited Seven Countries Study that kicked off the whole low-fat debacle. Let’s look at data from the venerable Framingham study that was so inconclusive that it wasn’t even published in a peer-reviewed journal.

For those who don’t know the Framingham Heart Study was kicked off back in the late 1940s in Framingham, MA. under the direction of the National Heart Institute (now known as the National Heart, Lung, and Blood Institute) According to their website

The objective of the Framingham Heart Study was to identify the common factors or characteristics that contribute to CVD by following its development over a long period of time in a large group of participants who had not yet developed overt symptoms of CVD or suffered a heart attack or stroke.

A large number of residents of Framingham were recruited into this longitudinal study that is still going on today. There are children (and probably grandchildren) of the original Framingham participants enrolled in the study currently. Researchers are monitoring diet, medication history, and a host of other parameters, and have generated God only knows how many papers using this data that has been collected over the past almost 60 years.

One of the first ideas that the researchers had was to look at how diet related to cholesterol levels and how diet related to the development of heart disease. I’ll give you the surprise ending right up front: there wasn’t any correlation. What’s interesting about this part of the study, however, is that the researchers didn’t publish it at the conclusion of the study, so it never really saw the light of day. You’ve probably heard the old saying that doctors bury their mistakes. Well, researchers often bury outcomes they don’t expect and don’t welcome.

In the case of this part of the Framingham study, ten years after the work was completed a statistician gathered the data and put it into typewritten form with a blue binding and disseminated it to the academic community under the name of the then director of the project Dr. Willam Kannel. As the statistician, Tavia Gordan, put it in the editorial note at the beginning

This report is based on a selection from a large body of tabular material prepared since the completion of data collection for the Framingham Diet Study. Unfortunately, these data were never incorporated into a definitive report by the original investigators and a large amount of very careful and thoughtful work has lain unused in the Framingham files. [my italics]

Once I learned of the existence of this report, I got hot on its trail.

Fram book web
I found the beaten up copy shown above through the Internet. It set me back a little over $80. When I got my hands on it, I was at first a little disappointed because I had expected a lot more information for my 80+ bucks.

Then I flipped through it and struck gold inside the back cover. Before we get to that, however, let’s look at what this report shows.

The project was undertaken between the years 1957-1960 and involved a sample of around 1000 participants who were to be studied over the following 36 months to

test the hypothesis that “The regulation of the level of serum cholesterol and the development of coronary heart disease are related to
1. The caloric balance
2. Level of animal fat intake
3. Level of vegetable fat intake
4. Level of protein intake
5. Level of cholesterol intake…”

The dietary studies were performed using a couple of techniques described here and here (both are large PDF files). Basically, researchers interviewed the subjects multiple times over the study period using a fairly complex Food Frequency Questionnaire (FFQ). (From a previous post you should know that I’m not a big fan of FFQs, but in this case with the kind of attention to detail the interviewers used, the FFQ has some value.

What did they find?

In terms of caloric balance vis a vis serum cholesterol they discovered that

calories per day showed a slight negative association with serum cholesterol (over all age groups) in men but no association in women.

In other words the more calories the men consumed, the lower were their serum cholesterol levels. Obviously, this wasn’t what the researchers expected to find.

This finding is somewhat puzzling and it is reasonable to inquire if this is related in some way to the level of physical activity.

Typical research thinking: if we don’t get the data that is consistent with our hypothesis, we must have overlooked something. It seems that the idea that maybe the hypothesis is wrong never crosses their minds.

In this case, they were banking on the idea that perhaps those subjects who ate more may have been more physically active and thus have lower cholesterol levels than those who ate less but were sedentary. After fiddling around with the different levels of activity of the subjects, the data fesses up:

Men in the same physical activity class tend to have higher serum cholesterol levels at lower caloric intake. This finding is contrary to expectation. [I’ll bet it was.]

In other words, even after correcting for differing levels of physical activity, the correlation remains the same: those subjects with lower caloric intake tended to have higher levels of cholesterol and vice versa.
What about fat intake?

Paralleling the findings for total calories there is a slight negative association between daily intake of total fat (and also of animal fat) with serum cholesterol level, in men but not in women. This parallel is not surprising given the high correlation between fat intake and total caloric intake. No association between percent of calories from fat and serum cholesterol level was shown; nor between ratio of plant fat to animal fat intake and serum cholesterol level.

How about protein?

There was a trivial negative correlation between daily protein intake (in grams) and serum cholesterol level.

Dietary cholesterol?

There is no indication of a relationship between dietary cholesterol and serum cholesterol level. If the intake on animal fat is held constant there is still no relation of cholesterol intake to serum cholesterol level. If (further) a multiple regression is calculated [using animal fat and dietary cholesterol] there is also little suggestion of an association between this pair of variables and serum cholesterol level.

The researchers weren’t going to give up easily.

The failure to turn up any positive association between food intake and serum cholesterol level in the Framingham Diet Study led to the exploration of a large number of variant analyses. [In other words, maybe if we torture the data unmercifully, it will confess to anything. Alas, for them, this wasn’t the case.] These were uniformly unsuccessful in finding expected relationships. Only a fraction of these explorations are included in this report.

When it comes to diet and coronary heart disease, nothing changes.

In undertaking the diet study at Framingham the primary interest was, of course, in the relation of diet to the development of coronary heart disease (CHD). It was felt, however, that any such relationship would be an indirect one, diet influencing serum cholesterol level and serum cholesterol level influencing the risk of CHD. However, no relationship could be discerned within the study cohort between food intake and serum cholesterol level.

In the period between the taking of the diet interviews and the end of the 16-year follow-up, 47 cases of de novo CHD developed in the Diet Study group. The means for all the diet variables measured were practically the same for these cases as for the original cohort at risk. There is, in short, no suggestion of any relation between diet and the subsequent development of CHD in the study group…

The study conclusions:

With one exception there was no discernible association between reported diet intake and serum cholesterol level in the Framingham Diet Study Group. The one exception was a weak negative association between caloric intake and serum cholesterol level in men. [As to] coronary heart disease–was it related prospectively to diet. No relationship was found.

So, I would say that the results of this study were pretty clear. These guys tried as hard as they could to show a correlation between diet and serum cholesterol and between diet and the incidence of coronary heart disease, but failed. The data conclusively demonstrated no such correlations.

What did they do with their data?

They certainly didn’t publish it in any scientific journals, though just about any journal in print would have accepted a paper from them.  No, they couldn’t let these results get out, so they basically threw them in a desk drawer.

Years later, Tavia Gordan, the statistician for the study, thought these findings should see the light of day, so he pushed through the private publication of a handful of copies of a monograph to be distributed privately.

Imagine my surprise when I discovered the yellowed news clipping shown below taped into the back of my $80 booklet. This clipping, from the Framingham newspaper dated October 30, 1970, is worth the $80 all by itself.

Apparently, despite all the supporting evidence, Dr. Kannel, the director of the study and the guy listed as lead author, wasn’t buying into all this nonsense about there being no correlation. He felt the need to ‘clarify’ the already crystal clear findings.  Even though the information in this monograph wasn’t widely distributed, Kannel wanted to make sure no one might draw the wrong conclusion from his data.

The clipping begins:

Although there is no discernible relationship between reported diet intake and serum cholesterol levels in the Framingham Diet Study group, “it is incorrect to interpret this finding to mean that diet has no connection with blood cholesterol,” Dr. William B. Kannel, director of the Framingham Heart Study has stated.

Clarification, indeed.

Hmmm, I guess Dr. Kannel didn’t enjoy the surprise ending of that movie, so decided to change it on the fly. I think the rest of this remarkable clipping is legible, so read it and laugh. It’s a grand example of what I’ve written about before: scientists who present their conclusions one way in a scientific paper that other scientists will look at and call them on if they are incorrect and a totally different way to the press that reports to the population at large.

(Click on the image to enlarge if you have trouble reading it.)
Framingham article on the Framingham study


  1. very interesting. I wonder, did the studies see any correlation between serum cholesterol levels themselves and heart disease and/or CAD? Or did they only try to tie diet to serum cholesterol and assume the cholesterol–CVD connection needed no investigation?
    Hi Lisa–
    The way they did the studies was kind of weird. They divided the groups at the beginning into those who had very high cholesterol levels and those who had very low cholesterol levels. The ones who had the high cholesterol levels developed more heart disease over the course of the study, but that doesn’t really tell us a lot. Was their high cholesterol a marker for something else, i.e., insulin resistance? Even those with high cholesterol going in didn’t change their levels as a function of diet. Nor did those with low cholesterol.
    Hope this helps.

  2. Dr. Eades-
    I wish I had time to go back and read all of your archived stuff right now. Yours is fast becoming my favorite blog.
    I have been aware for some time about the true interpretation of the Framingham study, but it was great to get even more details.
    Only one problem, I couldn’t read the clipping! Any other way to view it?
    Daniel Chong
    Hi Daniel–
    Right click on the image and save it to another file. Then open and enlarge with your image viewing software.
    Good luck.

  3. Looks like they checked for a relationship between everything *but* dietary CHO and cholesterol/heart disease?
    Hi Peggyjo–
    Indeed. They actually mentioned in the paper that there may be other food components than the ones they tested that may have a relation to the development on CHD. They didn’t name any suspects, though.

  4. Hi Mike,
    Nice find. For those that can’t read the newspaper clipping, I suggest they could right click on the item in your blog, “save as” to somewhere accessible, and then open the file in whatever picture viewer they use (I grudgingly admit the Windows one is fine for this!) Then it is easy to zoom in to read the fine print.
    One thing that always confuses me about the dietary cholesterol debate is that Keys himself made it so clear that there was no relationship way back in 1953 when as I recall the first of his ‘Countries’ studies was published – where he explains that experiments on human subjects and animals (apart from herbivores like rabbits) showed massive doses of cholesterol only had a transient effect on blood readings.
    How come he was ignored when he was right, and championed when he was oh so wrong?!
    Hi Malcolm–
    Thanks for the tip on viewing the image. I put it up on the post.
    The Key’s history will be dealt with at length in Gary Taubes’ new book. It shows the strength of the bias that even a hero of the anti-fat, anti-cholesterol brigade can be ignored when his advice doesn’t fit their paradigm.”
    In my opinion, the reason the push was (and still is) on to show a correlation with cholesterol is because cholesterol is found only in foods of animal origin. With the strong vegetarian bias behind many low-fat, low-cholesterol proponents, it’s easy to see that they would love to come upon evidence that showed cholesterol to somehow be dangerous.

  5. Thank you for tracking this down. Honestly my entire nutrition degree(’84) felt like something was just not right, that I would not be teaching the truth if I went on to get my RD. The research conclusions were part of the strangeness. Kinda ‘we didn’t find it, but we know somebody will so buck up and keep at it’. Also, why pay $ & spend time learning a profession with no significant positive outcomes.
    Hi Nean–
    I understand your frustration. Sometimes you have to go through the BS just to get the certification you want, then go ahead and practice the way you know is right.
    I’m sure that I would fail any nutritional exam given by any RD program because the people who write the exams are themselves not in possession of the facts.

  6. wow! Wow! WOW!!!!!
    I went to nursing school at Framingham, so these studies have always interested me. I graduated in 1976 and had a classmate who’s dad was enrolled in the study. We were also taught by the docs in the study.
    My classmate’s dad had heart disease, was on a special diet, but I don’t remember it specifically being low fat. I DO remember he was on 12 different meds….all for his heart. Yep, 12. I remember because he used the bottom of an egg carton to hold his pill bottles. He died very young, probably mid-50’s max.
    I also remember years (maybe 1992?)later running into one of my old docs. He was a cardiologist, but not involved in any of the studies. He was dismissive of the studies….didn’t really say much, just that changed the subject every time we tried to ask him about it. Would never clarify, but would never talk about the studies either.
    I was able to view the news article by pasting into Word and then viewing at higher resolution. I’m saving a copy (hope you don’t mind). There are several people I am planning on sending your post and the article to!!
    Hi Cindy–
    Thanks for the history. There is a reason the cardiologist didn’t want to talk about it–the study didn’t show what they all thought it was going to show. Instead of rethinking their hypothesis, they all just wrote the study off as a waste of time and money.
    As for the clipping, copy and send away. Be my guest.

  7. For those who got problems reading the small print of the newspaper, try to store the picture to your hard disk and open it seperately.
    For me it was way more readable this way.
    Hi Sam–
    Thanks for the info.

  8. Well doc, Ive read most of the reports issued be the folks doing the Framingham study, I’ve never seen them state that SFA or cholesterol was causative in anything, just that there was a correlation. Its their media and bandwagon jumpers who twist correlation into causation. Anecdotally, If you were to look at folks not eating a carb controlled diet, the folks who eat the most SFA and dietary Chol, would also be most likely to eat the most sugar, TransFA, the fewest vegetables, and exercise the least.
    Hi Kevin–
    In this case it is the head of the Fram study who is denying the correlation. Or at least saying that it is meaningless.
    You are absolutely right about the people eating non-carb controlled diets. Most eat a lot of sat fat, a lot of trans fat, a lot of sugar, and just a lot in general.

  9. Clinical Dietary Intervention Trials have COMPLETELT FAILED to lower the incidence of coronary heart disease mortality or overall mortality by the use of saturated fat restriction.
    There are 18 of them to date. All printed out in Colpo’s book “The Great Cholesterol Con”, results and all.
    Hi Razwell–
    There are probably more than those 18. And all fail to ‘prove’ a correlation.

  10. Simply amazing! Framingham has become the gift that keeps on giving. Someone needs to put this story into a book written for the general public. It is an astounding example of the manipulation of science for the sake of pride, prejudice and cold hard cash.
    Richard Morris
    Hi Richard–
    The ‘gift’ that keeps on giving indeed. What’s even more astounding than this little booklet are the Framingham guidelines for avoiding heart disease. Many of the recommendations are not borne out by their own studies. I plan to post on this issue again later and really get into the guidelines part.
    BTW, I love your site. Great job on the weight loss!

  11. Thanks Dr Eades
    I forgot to mention the 26 Prospective Trials regarding this. They also found NO benefit to saturated fat restriction. They are also all listed in Colpo’s book.
    You should team up with Dr Uffe Ravnskov and Anthony Colpo to form a strong coalition in exposing this sham.
    Hi Razwell–
    I guess that in a way we are teamed up. There ain’t all that many of us that will openly say that there is nothing wrong with saturated fat. Mary Enig is another.

  12. Correct me if I’m wrong but I noticed that all English speaking countries seems to have the same problem with their official perception of intake saturated fat being related to their heart problems, and official recommendations are the same too eg. Malaysia with about half the populations considered fat.
    Hi Antnagir–
    That appears to be the case.

  13. Hi Dr Eades. I am late to the party and wondered if I could have your permission to link to this fine article from my own web-site. I have also transcribed the newspaper clipping and wondered if you would you like a copy?
    Kind regards,
    Jeff Cable
    Hi Jeff–
    Be my guest.  Link to any of the posts you would like.

  14. Thank you very much… 🙂 herewith the transcription…

    Page 36 The News, Framingham-Natick, Friday October 30th 1970
    Findings of the Framingham Diet Study Clarified
    Framingham – Although there is no discernible relationship between reported diet intake and serum cholesterol levels in the Framingham Diet study group, “it is incorrect to interpret this finding to mean that diet has no connection with blood cholesterol” Dr William B Kannel, director of the Framingham heart study has stated.
    “It has been repeatedly demonstrated that blood cholesterol levels can be altered by changes in diet; and dietary alteration is still the most acceptable form of medical management for persons with elevated blood lipids” Dr. Kannel said.
    “The available evidence indicates that coronary heart disease appears to result from a combination of contributing factors and that no single factor capable of producing the disease by itself has been convincingly demonstrated”, he stated.
    “However”, he added, “if any common denominator does exist through which such multiple, inter-related factors operate to produce athersclerotic lesions, then some aberration of blood lipids is certainly the chief contender. It appears to be the thread running through the web of circumstances leading to coronary heart disease.”
    A number of blood lipids have been implicated in coronary disease, Dr. Kannel Said, but none more substantially than the blood cholesterol content. That blood cholesterol is somehow intimately related to coronary atherosclerosis is no longer subject to reasonable doubt because of massive evidence that:
    – diseases associated with hypercholesterolemia are also associated with premature atherosclerosis.
    – persons with inborn errors of cholesterol metabolism develop extremely precocious atherosclerotic disease
    – persons with high cholesterol levels in epidemiological study populations have been observed to develop coronary heart disease with greater frequency than those with low cholesterol levels, the risk being proportional to the degree of elevation of the blood cholesterol.
    – countries with high average cholesterol values among their citizens report high coronary death rates; those with low average cholesterol values report low coronary death rates.
    – atherosclerotic deposits are usually loaded with cholesterol and the movement of cholesterol from the blood into the deposits has been amply demonstrated.
    – producing high cholesterol values in animals produces atherosclerotic deposits that can be made to regress by lowering blood cholesterol.
    “Moreover”, Dr Kannel said, “the evidence incriminating diet in producing elevated serum cholesterol is quite substantial; for example,
    – areas in which the population exhibits high cholesterol values characteristically have diets different from those where low values are characteristic.
    – migrants from ‘low cholesterol’ areas to ‘high cholesterol’ areas are often subsequently found to have higher cholesterol levels and to have changed their dietary pattern.
    – manipulation of diet can alter serum cholesterol values in a predictable fashion in humans and, in animals, can produce atherosclerotic deposits or cause established deposits to regress”.
    “The reason for the high cholesterol values frequently found in free-living population groups is not always apparent and the details of the mechanism involved, the role of inheritance, regulatory mechanisms, and what constitutes the ‘normal range’ of cholesterol values are not completely understood.” Dr Kannel said.
    Hi Jeff–
    Thanks for the transcription.  I appreciate it.

  15. It’s utterly amazing and frustrating that people fall for whatever the television tells them. I have printed off lots of the truth about cholesterol and cannot even convince my own mother how flawed all the arguments about choloesterol leading to heart disease are.
    It is amusing that so many people will accuse the government and businesses of lying about this and that but when it comes to cholesterol (and radon, Splenda ..other pet peeves of mine), suddenly the news they get is accurate.
    My own cholesterol is considered high by the mainstream. Ha!, I say. I exercise, eat a variety of foods in moderation, don’t smoke, and drink a little. I’m not losing any sleep over my cholesterol numbers. I hate to see my eat her Lipitor poison to lower her numbers which is a total waste of money…and of health, too.
    It is amusing that people assume the government is either wrong or is out and out lying about virtually everything except for nutritional issues. On nutritional issues they say that it must be so because the government says it’s so.

  16. Did the Framingham study look at type of fats? If not, then it is certainly true that no correlation could exist between undifferentiated “fat” since some types of fat have positive correlations and some negative to blood cholesterol.
    Trans fats have very different relationship to cholesterol build-up than polyunsaturated fat.
    So while the results were not “expected” – I am not sure they understood that much about types of fats to expect anything that would be correct.
    There have been other studies besides Framingham that show no relationship of “fat consumption” to blood cholesterol – but there are studies on specific types of fats that do show positive correlations – that is, larger amounts correlate to higher, or lower, blood cholesterol, depending upon the type of fat.
    The current simplistic rules, however, might be ignoring beneficial foods with saturated fats – such as whole, raw milk. And maybe our current classification of four types of fats is not complete.
    As I recall (I didn’t go back and pull the papers) Framingham looked at saturated and unsaturated fats – not the specific fatty acids.

  17. For me, there is a definite correlation between dietary cholesterol consumption and serum cholesterol. When I stopped consuming cholesterol entirely, my serum cholesterol dropped from 240 to 180 in two months.
    Note also the findings of The China Study. In rural China, the animal protein intake was 7g/day while the American intake was 70g/day. The serum cholesterol ranges were 127 in China and 215 in America. At that time the death rate from CHD was 17 times greater in American men than rural Chinese men. Maybe that’s worth trying to understand.
    My guess is that, in the Framingham study, very few people ate plant based, whole foods, low protein, zero cholesterol diets.
    There is no question that reducing cholesterol in the diet can reduce cholesterol in the blood all other things being equal. But so what? Show me the studies showing that lowering cholesterol increases lifespan.
    Rural Chinese worked much physically harder than American men and consumed significantly fewer calories. But, despite all that, do rural Chinese live longer than Americans? The answer is no. Statins reduce the risk for heart disease but they simply replace that risk with something else because people who take statins don’t live longer than those who don’t. You’ve got to be careful in looking at evidence like this because what you want is to decrease all-cause mortality, i.e., have people live longer, not simply trade one risk factor for another.

  18. I suspect the reason is that the human body can manufacture cholesterol on its own. So it does not matter if it is in the diet or not. If you do not have it in the diet, you can use different molecules to make it. The experiment to do would be to take a bunch of volunteers and measure their cholesterol at baseline. then put them on a low cholesterol diet for a week and measure their cholesterol level. then put the same volunteers on a high cholesterol diet for one week. If the cholesterol level does not change significantly in each individual it would mean that the diet does not matter and that the cholesterol levels are set genetically. Each Volunteer would act as his/her own control.

  19. I got hooked into the Low Cholesterol / Low Fat etc nonsense back in the mid ’70’s when the doctors and white coats who know everything about health in Australia were adamant that diet did NOT lower Cholesterol or reduce arterial plaque. Interesting to read the report in 1970 in which the chief scientist says it did.
    Today I wonder whether Serum Cholesterol 1) is essential to health, especially the brain, 2) When it increases and stays high it is the body attempting to repair arterial damage from other causes.
    That is that Serum Cholesterol and Arterial Plaque are part of the repair process and NOT the CAUSE of the problem rather than part of the natural CURE process.

    1. Cholesterol is absolutely essential to health – without it you die. Since the brain is made primarily of cholesterol, it especially important there. But it can’t get into the brain via the blood, so the brain makes it itself. There are a whole host of reasons cholesterol levels may be high – repair is just one of those.
      Read here for more info on manipulating cholesterol.

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