Yeah it’s not a typo! You heard it right, saturated fat and cholesterol have nothing to do with your risk of developing heart disease!
In this article I’ll go on to show you examples of how people and even scientists will only believe what they want to believe, no matter how much evidence to the contrary exists. Here is a take on the popular notion that a low-fat diet low in saturated fats and cholesterol will reduce the incidence of CHD and related deaths.
Going through our education we were taught the basic science tenet that if a phenomenon occurs for a given set of conditions and if those set of conditions were to be replicated, the same phenomenon would occur. That was enough to establish causality (cause and effect). This basic tenet holds for any scientific investigation. And if what you thought was the ‘condition’ that made a certain phenomenon happen in certain cases and made the exact opposite phenomenon happen in other cases, then you would abandon the ‘condition’ as being the cause of that phenomenon…unless of course that ‘condition’ happens to be high cholesterol and the phenomenon happens to be coronary heart disease. Then, for some reason, the rules of science don’t apply!
So, any guesses as to what a CHD preventive diet should be? If you guessed a low-fat vegetarian diet, then you are in majority by a huge margin and you should be in power (after all we live in a democracy, right?). But too bad, science and democracy (or majority consensus) have nothing in common. If they did then the earth would still be flat and the sun would still be revolving around the earth.
If anyone has popularized a low-fat vegetarian diet like no one else, I would give the credit to Dr. Dean Ornish. A quick search on Google will show you that he is one of the most influential opinion leaders on dietary intervention for prevention of CHD. If you want to read more about his accolades and recognition, I suggest going to http://www.pmri.org/dean_ornish.html since his accolades are longer than what I am prepared to write in this article.
Before we jump into all the lifestyle intervention studies that have been done to prevent CHD lets have primer on the statistics behind clinical trials. Actually these principles are used in every realm of science like process control, manufacturing control and various testing methodologies and to a much more stringent level than used in clinical trials (thank the heavens!). Here are a few terms to get used to:
Sample size: This is the number of people tested. Its best to have the largest possible sample size since it randomizes for variation in lifestyle (smoking habits, alcohol consumption etc.), regional/cultural differences or other such confounding factors. Obviously it’s hard to study a large sample size due to cost/resource constraints so the experimenter has to choose from a small sub-set of the representative population. Furthermore a multi-center trail is better suited for generalization to a large population.
Factorial Design: When two or more different treatments are evaluated in single study this type of design is used to evaluate the effect of each treatment, independent of the other treatment. If two different factors are lumped into one treatment then no conclusion can be made about the effect of any one factor. It’s easy to see why this is the case because you can’t un-couple the effect that each factor has on the treatment. So it’s impossible to establish causality to any one factor. The best you can infer is that both factors have an effect on the treatment, but what percentage can be assigned to which factor will be unclear.
Blinding: The best way to remove bias from a trail is by making it blind. Blinding (masking) is a method of eliminating conscious or unconscious bias in how the experiment is conducted or how the data is analyzed or interpreted. It’s basically a way an experiment is conducted where the subject is not aware of which group is receiving the treatment (single blind) or in the best case even the test giver, investigator or the sponsor staff is unaware of which group receives which treatment. This includes anyone that is designing the test or is selecting the candidates for the test. Until such time that all opportunities for bias to affect the endpoint and data integrity is passed all involved parties are blind. This is maintained throughout the testing and analysis phase and when the data is cleaned of outliers to an acceptable level is when the appropriate authorities are un-blinded. This is the best and most objective way to conduct a clinical trail. Now realize that it’s not always possible to conduct a double blind trail especially in the case of lifestyle intervention trails, which is what we will be talking about.
Now that we got the basics down let’s look at the popular studies that have been done to assess the effect of lifestyle intervention on preventing CHD. Let’s look at the popular Ornish study also known as lifestyle heart trail  in which he claims that his particular diet regresses (meaning improves) the atherosclerosis in the blood vessels. Below is the abstract right from the publication:
In a prospective, randomised, controlled trial to determine whether comprehensive lifestyle changes affect coronary atherosclerosis after 1 year, 28 patients were assigned to an experimental group (low-fat vegetarian diet, stopping smoking, stress management training, and moderate exercise) and 20 to a usual-care control group. 195 coronary artery lesions were analysed by quantitative coronary angiography
And the conclusions stated (again from the publication):
The average percentage diameter stenosis regressed from 40.0 (SD 16.9)% to 37.8 (16.5)% in the experimental group yet progressed from 42.7 (15.5)% to 46.1 (18.5)% in the control group. When only lesions greater than 50% stenosed were analysed, the average percentage diameter stenosis regressed from 61.1 (8.8)% to 55.8 (11.0)% in the experimental group and progressed from 61.7 (9.5)% to 64.4 (16.3)% in the control group. Overall, 82% of experimental-group patients had an average change towards regression. Comprehensive lifestyle changes may be able to bring about regression of even severe coronary atherosclerosis after only 1 year, without use of lipid-lowering drugs.
So the authors concluded that the artery diameter stenosis (ADS) improved by 5.5% ([40-37.8]/40) in the experimental group (intervention group) while it deteriorated by 8% in the control group (no intervention). So apparently the intervention improved things by 13.5%. A pretty big number if you ask me. So now you tell me, OK its settled, so will you please give in, bow down, bow out, take a hike, buzz off and shut up and agree that a vegetarian diet low in cholesterol and saturated fat is the answer to preventing CHD. I’ll say wait a minute, but let’s look a little closer at the results.
A few points to note about this trial: The sample size is pretty small (48) so making a generalization based on this study would be premature because it couldn’t have possibly accounted for regional, cultural, dietary and other socio economic factors in the sample size. How could you possibly make dietary recommendations for people world over based on the 48 people you tested? You wouldn’t.
The second point I would like to bring forth is the measurement error in coronary angiography. The numbers reported are absolute, without any error bars. Any real instrument has repeatability and reproducibility errors. Also take a closer look at the standard deviation in the measurements (the % numbers in parenthesis). It’s in the range of 16%. A quick search on google for measurement errors in coronary angiography shows the error to be about 10% standard error (http://spo.escardio.org/eslides/view.aspx?eevtid=33&fp=3022). In light of this fact do you think the numbers reported in the research have any statistical significance? Absolutely not! The measurement variation reported is in the signal noise.
The third point I would like to bring out is that the study made an attempt to correlate the effect of 4 parameters (low-fat vegetarian diet, stopping smoking, stress management training, and moderate exercise) on ADS. So this study cannot isolate the individual contributions from any one parameter and its effect on ADS. So based on this study can we recommend that a vegetarian diet will lower your chances of developing arterial lesions? I bet you, even the most diehard vegan wouldn’t agree if someone made a claim like that based on this data. And yet this study is cited for recommending a vegetarian diet low in saturated fat as a preventive step to lower your risk of CHD. Hilarious isn’t it?
Now let’s look at the other side of the coin and see how many studies have failed to show a correlation between dietary lifestyle modification and the development of CHD. The most popular one that is cited over and over again is called MRFIT (Multiple Risk Factor Intervention Trial) . This one was special intervention (SI) program consisting of stepped-care treatment for hypertension, counseling for cigarette smoking, and dietary advice for lowering blood cholesterol levels for the treatment group and no intervention for the control group. Below figure 1 shows the results of this study in a snap shot.
Figure 1. MRFIT study parameters and results snapshot.
Quoting straight from the research paper:
The Multiple Risk Factor Intervention Trial was a randomized primary prevention trial to test the effect of a multifactor intervention program on mortality from coronary heart disease (CHD) in 12,866 high-risk men aged 35 to 57 years. Men were randomly assigned either to a special intervention (SI) program consisting of stepped-care treatment for hypertension, counseling for cigarette smoking, and dietary advice for lowering blood cholesterol levels, or to their usual sources of health care in the community (UC).
Here you can at least see that the study had a large enough sample size and went on for long enough to make some conclusions. Here again it was a multifactor intervention program where they modulated three parameters (smoking, cholesterol lowering diet and anti-hypertensive drugs) simultaneously and studied its effect on CHD. The primary end point was any MI event. The first thing that should stand out is that the control group had 132% more smokers than the treatment group. Now looking at the improvement area we can see that it reduced the coronary death events in the treatment group by 9 people. Now let’s look at people that died of other causes. Wait, the difference is not 5 from what it seems like from the first results line (265-260). All the first line states that 5 more people died in the treatment group than in the control group. So overall more people died in the treatment group then in the control group. Doing the math it seems like 150 people in the treatment group died from other causes and 136 people in the control group died of other causes. So, overall 14 more people died in the treatment group from other causes. Now would you call the intervention program successful? I wouldn’t call it successful. So would I call it unsuccessful? I wouldn’t conclude that either. Basically I couldn’t conclude anything from these results. I think the results were statistically insignificant and study was inconclusive. But wait here is what the authors concluded (drum roll please):
Over an average follow-up period of seven years, risk factor levels declined in both groups, but to a greater degree for the SI men. Mortality from CHD was 17.9 deaths per 1,000 in the SI group and 19.3 per 1,000 in the UC group, a statistically non-significant difference of 7.1% (90% confidence interval, -15% to 25). Total mortality rates were 41.2 per 1,000 (SI) and 40.4 per 1,000 (UC). Three possible explanations for these findings are considered: (1) the overall intervention program, under these circumstances, does not affect CHD mortality; (2) the intervention used does affect CHD mortality, but the benefit was not observed in this trial of seven years' average duration, with lower-than-expected mortality and with considerable risk factor change in the UC group; and (3) measures to reduce cigarette smoking and to lower blood cholesterol levels may have reduced CHD mortality within subgroups of the SI cohort, with a possibly unfavorable response to antihypertensive drug therapy in certain but not all hypertensive subjects. This last possibility was considered most likely, needs further investigation, and lends support to some preventive measures while requiring reassessment of others.
Let me put it in simple terms for you. The data screams that the intervention didn’t work! At least not to a statistical significance. But wait there is a possible explanation of why it didn’t work. The authors hypothesize (because data is telling otherwise) that the intervention may have worked within sub-groups of the intervention group but a possibly unfavorable response to antihypertensive drug therapy confounded the results and that the last possibility is considered most likely. And why is that? Let me tell you why? Because the authors don’t want to give up the original hypothesis (that the intervention works). So they already were expecting (AKA bias) which way the results should have gone even before testing the hypothesis. Wow, this is new age statistics for all of us! Old school taught us to start an experiment with the null hypothesis and if data disproves the null hypothesis then you take the alternate hypothesis. This new way of still holding on to the null hypothesis when experiment shows otherwise is called ad-hoc hypothesis and you will see many instances of this with respect to the cholesterol hypothesis. It’s a nifty way to explain away unfavorable results.
Ok so moving on now lets look at another one. This is the famous Helsinki Study  that was conducted in Poland. The primary intervention in this one was not only diet, smoking and exercise but also anti-hypertensive drugs and for all the cholesterol haters they also gave the preventive treatment group cholesterol lowering drugs. So it must have been a win-win for the treatment group and I feel sorry for the control group that didn’t receive any of the life saving miracle drugs or dietary advice or counseling. The primary end-point was mortality. Figure 2 is the snap shot of the test methodology and results.
Figure 2. The Helsinki heart study methodology and results
Looking at the snapshot of the results it seems like there were 8.5% more smokers in the control group. And lo and behold only one person from the control group died of a coronary even while 4 people in the treatment group died from coronary event. If it were the other way around you would be hearing things like “miracle drugs save your chance of heart attack by 75%” ([4-1]/4). But no such miracles happened and no wonder you don’t hear much about this study. Also note that 6 people in the treatment group died from other causes while only 4 in the control group died from other causes. Suddenly I don’t feel so bad for the people in the control group. The treatment group however…that’s another story.
During the next 18 years (Between 1974 and 1989) post trail mortality in the Helsinki Study was followed up and the results straight from the publication are:
the total number of deaths was 67 in the intervention group and 46 in the control group (relative risk [RR], 1.45; 95% confidence interval [CI], 1.01 to 2.08; P = .048); there were 34 and 14 cardiac deaths (RR, 2.42; 95% CI, 1.31 to 4.46; P = .001), two and four deaths due to other CVD (not significant), 13 and 21 deaths due to cancer (RR, 0.62; 95% CI, 0.31 to 1.22; P = .15), and 13 and one deaths due to violence (RR, 13.0; 95% CI, 1.70 to 98.7; P = .002), respectively. Multiple logistic regression analysis of treatments in the intervention group did not explain the 15-year excess cardiac mortality.
Well here again you see the researchers in denial as to why they got unexpected results. Even though they aren’t able to explain the high cardiac mortality in the treatment group they aren’t able to fathom the possibility that cholesterol has nothing to do with heart disease.
Let move on to the next study. This one was called the Finnish mental hospital study  which had 600 women aged 49 yrs av. The treatment intervention was cholesterol lowering diet low in saturated fats and increased polyunsaturated vegetable oils. The control group had no intervention. This was the only study that looked at dietary intervention alone. So anyone that understands anything about statistics should put the most faith in this study. And for all the saturated fat and cholesterol haters this is the basket you should be putting all your eggs (no pun intended) into.
Figure 3. The Finnish Mental Hospital study methodology and results
Here is a description of the study conditions and methodology straight from the research article:
A controlled intervention trial, with the purpose of testing the hypothesis that the incidence of coronary heart disease (CHD) could be decreased by the use of a serum-cholesterol-lowering (SCL) diet, was carried out in two mental hospitals near Helsinki in 1959-71. The subjects were hospitalized middle-aged women. One of the hospitals received the SCL diet, ie a diet low in saturated fats and cholesterol and relatively high in poly-unsaturated fats, while the other served as the control with a normal hospital diet. Six years later the diets were reversed, and the trial was continued another six years. The use of the SCL diet was associated with markedly lowered serum cholesterol values. The incidence of CHD, as measured by the appearance of certain electrocardiographic patterns and by the occurrence of coronary deaths, was in both hospitals during the SCL-diet periods lower than during the normal-diet periods.
Please note that the SCL diet resulted in markedly lowered serum cholesterol values during both phases of the study, so there is no ambiguity about the cholesterol lowering capability of the intervention diet. So now you can’t wait to see the conclusions of this study. Well I won’t keep you holding your breath too much longer, so here are the conclusions, again, straight from the paper:
The differences, however, failed to reach statistical significance. An examination of a number of potential confounding variables indicated that the changes in them were small and failed to account for the reduction in the incidence of CHD. Although the results of this trial do not permit firm conclusions, they support the idea that also among female populations the SCL diet exerts a preventive effect on CHD.
Now wait a minute. I am jumping up and down! How did we come to this conclusion? Where did I see that this diet exerts a preventive effect on CHD when 50% ([10-5]/10) more people died in the intervention group of all causes, and 75% ([4-1]/4) more died of cardiac deaths compared to the untreated control group? Am I missing something here? Can someone please explain? I am dumbfounded, or maybe I am just plain dumb!
The next one was a better controlled study because the total fat intake was kept constant between the two groups but the composition of fat in terms of saturated, poly-unsaturated, mono-unsaturated and total cholesterol intake percentages were varied. This was the Minnesota Coronary study . The test design and administration, straight from the paper states:
The Minnesota Coronary Survey was a 4.5-year, open enrollment, single end-time double-blind, randomized clinical trial that was conducted in six Minnesota state mental hospitals and one nursing home. It involved 4393 institutionalized men and 4664 institutionalized women. The trial compared the effects of a 39% fat control diet (18% saturated fat, 5% polyunsaturated fat, 16% monounsaturated fat, 446 mg dietary cholesterol per day) with a 38% fat treatment diet (9% saturated fat, 15% polyunsaturated fat, 14% monounsaturated fat, 166 mg dietary cholesterol per day) on serum cholesterol levels and the incidence of myocardial infarctions, sudden deaths, and all-cause mortality. The mean duration of time on the diets was 384 days, with 1568 subjects consuming the diet for over 2 years. The mean serum cholesterol level in the pre-admission period was 207 mg/dl, falling to 175 mg/dl in the treatment group and 203 mg/dl in the control group.
So this intervention dropped the total cholesterol level for the intervention group to 175 mg/dl and didn’t change it for the control group (203 mg/dl). All good right? But when you look at the summary of results in figure 4 (below) it seems like coronary deaths were about 13% higher and deaths from cancer were 25% higher in the intervention group. All cause deaths and coronary events were insignificantly different. But the results quoted from the paper state:
For the entire study population, no differences between the treatment and control groups were observed for cardiovascular events, cardiovascular deaths, or total mortality. A favorable trend for all these end-points occurred in some younger age groups.
Now what does the term “A favorable trend occurred in some younger age groups” mean? Does it mean that younger people will benefit from the cholesterol lowering diet? And does it mean that by the time they get old this diet wouldn’t save them the first heart attack because they are not young anymore? I don’t know what it means but the results speak for themselves and no one in their right minds could argue with such glaring data.
Figure 4. The Minnesota Coronary study methodology and results
Now the next one is a study with a dietary intervention of changing total fat intake to below 20% of total calorie intake (from 32% or more before the intervention) and to include at least 5 servings of vegetables and fruits and 6 servings of grains. This would be an ideal textbook diet for the healthiest of them all. I am mean, vegetables and fruits and grains and fat less than 20% of total calories! Who can argue with the CHD preventive benefits of such a diet? No changes were made in the control group diet. This was the Women’s Health Initiative (WHI) low-fat study . Figure 5 shows the test summary snapshot below.
Here again the test description states that the objective of this study was:
To test the hypothesis that a dietary intervention, intended to be low in fat and high in vegetables, fruits, and grains to reduce cancer, would reduce CVD risk.
And the test itself was:
Randomized controlled trial of 48,835 postmenopausal women aged 50 to 79 years, of diverse backgrounds and ethnicities, who participated in the Women's Health Initiative Dietary Modification Trial. Women were randomly assigned to an intervention (19,541 [40%]) or comparison group (29,294 [60%]) in a free-living setting. Study enrollment occurred between 1993 and 1998 in 40 US clinical centers; mean follow-up in this analysis was 8.1 years.
I love this study for three reasons. One that the sample size was huge and the participants were from a diverse background so the results would be applicable to the general population. Second, the diet was an ideal text-book diet that we have grown-up believing was beneficial to heart health and third that the mean follow-up period was pretty long (8.1 years). Looking at the summary of results in figure 5 we can see that the risk reduction for heart disease was insignificant even with this textbook perfect diet. Quoting the authors straight from the paper:
Over a mean of 8.1 years, a dietary intervention that reduced total fat intake and increased intakes of vegetables, fruits, and grains did not significantly reduce the risk of CHD, stroke, or CVD in postmenopausal women and achieved only modest effects on CVD risk factors, suggesting that more focused diet and lifestyle interventions may be needed to improve risk factors and reduce CVD risk.
Figure 5. WHI low-fat study test methodology and results.
So it seems like the textbook perfect low-fat diet with fruits and vegetables and grains didn’t do squat in reducing the risk for heart disease. The authors still had a back-alleyway for explaining away the unfavorable results by saying that the lifestyle intervention wasn’t focused enough and there was more room for improvement. Seems like ad-hoc-hypothesis land to me!
There are many more studies that failed to show a direct correlation between fat or cholesterol intake and the risk of developing CHD no matter how hard the cholesterol haters have tried. I have yet to find a single one that succeeded to show a correlation. And if someone can find that one elusive study that we all have chased for the last half a century then please let me know. I am sure the researchers would also love to hear about it. By now it should be fairly clear that diet has nothing to do with your risk for developing CHD. So eat what you want and you will not develop heart disease just because of a certain type of food in your diet, be it saturated fat or cholesterol. And in fact I have reasons to believe that a low-fat high carb diet will pre-dispose you to developing CHD not directly but by impairing your body’s insulin response and making you type II diabetic, because the correlation between a high carb diet and developing type II diabetes has been shown in studies after studies. And studies have also shown that having type II diabetes predisposes you to developing CHD. Now that data is un-ambiguous and incontrovertible. Smoking and stress are the two other significant risk factors for developing CHD.
So eat all the saturated fat and cholesterol you like and you won’t develop heart disease just because of that. There are of course merits to eating a diet rich in vegetables and fruits (for preventing cancer, type II diabetes etc) but not for reasons of preventing heart disease. Heart disease is a completely different animal that is caused due to reasons other than diet. In fact in the coming series of articles I will even show that a lower lipid cholesterol increases your risk of dying of other causes after a certain age (47 yrs to be precise) than having a higher level of cholesterol in your blood.
Why, then you ask, is cholesterol and fat made out to be such a toxin if there are no studies that show a correlation between lipid cholesterol levels and CHD? For that you have to understand the relation between the expert opinion leaders in the medical community and the pharmaceutical industry that sell the cholesterol lowering drugs and the American Heart Association (AHA) that makes hundreds of millions of dollars endorsing low-fat products with the famous AHA logo shown below.
But this is a topic for another article. For now I will just say that cholesterol hypothesis is based on pseudoscience or consensus science or what I like to call as ‘puppet science’. Just as puppets can seem to defy the laws of physics because of the attached strings, cholesterol science can be made to defy the laws of real science because of the attached ‘strings’ that make us ‘see’ something that doesn’t exist. Noble laureate Richard Feynmann had an interesting take on pseudoscience that he called Cargo Cult science (http://www.physics.brocku.ca/etc/cargo_cult_science.php).
More to come, but in the mean time enjoy that piece of steak that you have been avoiding because your doctor told you so. And if your doctor has a problem with it please direct him to this blogJ
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4) Miettinen M, Turpeinen O, Karvonen MJ, Pekkarinen M, Paavilainen E, Elosuo R. Dietary prevention of coronary heart disease in women: the Finnish mental hospital study. Int J Epidemiol 1983;12:17-25
5) Frantz ID Jr, Dawson EA, Ashman PL, Gatewood LC, Bartsch GE, Kuba K, Brewer ER. Test of effect of lipid lowering by diet on cardiovascular risk. The Minnesota Coronary Survey. Arteriosclerosis 1989;9:129-35
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