Published in Modern Dietary fat intakes in disease promotion. Nutr Health 2010, part 2, p 109-119
Uffe Ravnskov, MD, PhD
To-day a reduction of the intake of saturated fat is one of the cornerstones in dietary prevention of obesity, diabetes and cardiovascular disease. However, several recent trials have documented that the main argument for this advice, its alleged influence on blood cholesterol, is questionable. More disturbing is that a large number of epidemiological, clinical, pathological and experimental studies have falsified the idea that a high intake is harmful to human health and that a reduction may be beneficial; indeed, several observations point to the opposite.
For many years we have been taught that too much fat, in particular saturated fat in our diet may lead to overweight, diabetes and cardiovascular disease. According to a joint WHO/FAO Expert Consultation  “the relationship between dietary fats and CVD, especially coronary heart disease, has been extensively investigated, with strong and consistent associations emerging from a wide body of evidence”. This statement was followed by a reference to a consensus report from the Nutrition Committee of the American Heart Association . The only evidence presented in that paper or in other official documents for an atherogenic effect of saturated fat is its effect on the blood lipids and a single cohort study claimed to have shown that intake of saturated fat is associated with an increased risk of coronary disease . Most disturbing is that the numerous contradictory epidemiological, pathological and clinical observations as well as the unsupportive results from the dietary trials, the most important proof of causality, have been ignored by all guideline authors.
Any idea can be verified if one seeks for confirmation only, but a scientific hypothesis demands that it is able to present predictions that can be falsified. According to Karl Popper´s principle the assumption that a high intake of saturated fat may worsen human health is a true scientific hypothesis, because there are at least three major predictions that are open for falsification:
1. Obesity, diabetes, atherosclerosis and cardiovascular disease should be more common in populations with a high intake of saturated fat.
2. People with these maladies should have had a higher intake of saturated fat than healthy people of the same age and sex
3. A reduction of the intake of saturated fat should lower the risk.
These three logical assumptions have been falsified by many researchers, however. Consequently, objections against the vilification of saturated fat have been put forward [4-9], but they have made little impact on the official health policy. Since then even more contradictory findings have been published. This paper is an attempt to present a review of the full range of studies that in various ways have tested the mentioned predictions. As almost all of them contradict the current view and as some of them even point to a beneficial effect of saturated fat, the only possible conclusion of the accumulated evidence is that the hypothesis has been falsified effectively.
The influence of saturated fat on the blood lipids
The allegation that a high intake of saturated fat raises cholesterol is indirect evidence. Therefore, even if it were not true this finding cannot be used as a falsification of the hypothesis. However, it seems relevant to analyse this question as well because of its major role in the WHO guidelines. The idea was questioned by Reiser already in 1973. In a thorough review of 40 trials he pointed at several types of methodological and interpretational errors . Instead of natural saturated fat many authors had used vegetable oils saturated by hydro- genation, and effects on cholesterol were attributed to saturated fat when it could be due to polyunsaturated fat as well. In spite of these flaws several authors maintain that saturated fat raises cholesterol, whereas monounsaturated and in particular polyunsaturated fat lower it, and some saturated fatty acids my be neutral [11-15]. These conclusions have been based mainly on mathematical formulas using data from a large number of trials. But as almost all trial directors have made similar errors as those reviewed by Keys by changing the intake of several fats at the same time without controlling for intake of trans fat it is obviously difficult to rule out the effect of each type of fat.
Even if saturated fat is hypercholesterolaemic the effect must be small. In a review of eight trials where the intake was reduced by 30-40 % the net reduction of cholesterol was only 0-4 % , and other studies have shown no effect at all. In experiments for instance, where carbohydrates were substituted with saturated fat, not even intakes between 20 % and 50 % of calories influenced total or LDL-cholesterol (table 1) [17-26].
Table 1. Changes of blood lipids after a low-carbohydrate diet rich in saturated fat in
In the abovementioned low-carbohydrate trials (table 1) a high intake of saturated fat had no adverse effects on other lipids either. On the contrary HDL-cholesterol remained unchanged or went up and triglycerides went down significantly (table 1) [18-27] whereas a reduction of the intake had the opposite effects [37-39]. As cardiovascular disease is stronger associated with small-size LDL than with other lipid fractions it is also contradictory that high intakes of saturated fat are followed by an increase of LDL size [37,40,41].
Effects of saturated fat on the blood lipids is surrogate outcome, however. The crucial question is whether a high intake of saturated fat is deleterious to health and whether a reduction of the intake is beneficial.
There is little evidence from epidemiological studies that high intakes of saturated fat leads to cardiovascular disease. Ancel Keys introduced the idea that dietary fat plays a pathogenic role in heart disease. His main argument was a strong, curvilinear correlation between heart mortality and the total amount of fat available for consumption in six countries . However, Keys had selected his data. At that time figures for fat consumption and heart mortality were obtainable from 22 countries and if all of them were included the association became trivial , and an analysis based on the totality of more recent data that included 35 countries found an inverse association .
These studies concerned total fat, but similar data for saturated fat are contradictory as well, as appears best from dynamic population studies. Several authors of such studies have used concurrent trends of saturated fat consumption and coronary mortality in a single country as an argument for causality. Parallel changes may occur by chance, however, clearly demonstrated by a review of 103 time periods in 35 countries. Here, consumption of saturated fat increased in 63 periods; in 33 of these periods heart mortality increased as well, but in ten periods it was unchanged and in 23 it went down .
In a review of cross-sectional studies of the association between intake of saturated fat and coronary heart disease (CHD) an association was found in a few only, whereas more than 30 studies were partly or totally contradictive [4,44]. A few of the most contradictory observations are worth mentioning.
In seven studies of American Indians coronary mortality was only 10-50 % of the mortality of white Americans and degree of atherosclerosis was much smaller although their intake of saturated fat was similar or higher .
A study of Japanese emigrants in the US apparently was in support and is often used as an argument because after migration their low cholesterol rose to American levels, as did their risk of dying from CHD. However, the determining factor was not the diet or their cholesterol but their way of living. Those who maintained their cultural traditions were protected against CHD although their cholesterol went up. Even more striking was that immigrants who became accustomed to the American way of life, but preferred the lean Japanese food had CHD twice as often as those who maintained Japanese traditions, but preferred high-fat American food .
In a five-year follow-up study of more than 1 million male employees of the Indian railways Malhotra found that the lowest and highest rates of coronary mortality were seen in Punjab and Madras, 20 and 135 per 100,000 employees, respectively, and the mean age at death was 12 years lower in Madras than in Punjab. But in Punjab people ate about 17 times more fat than in Madras, the main part of which was of animal origin. In addition more people smoked in that area .
In a study considered as the strongest argument for the diet-heart idea Keys selected 16 cohorts in seven countries and found an association between intake of saturated fat and the prevalence and 5-year incidence of coronary mortality . But within each country there was little or no association at all although all risk factors including the intake of saturated fat were similar. Coronary mortality for instance was more than twice as high in Crevalcore, Italy than in Montegiorgio, five times higher in Karelia than in West Finland and 16-17 times higher on Corfu than on Crete. In addition, no association was seen between intake of saturated fat and major ECG abnormalities at entry. The latter finding has more importance considering that the ECGs were analysed by specialists in the American centre, whereas the cause of death was determined by local doctors with varying competence.
Cohort and case-control studies of saturated fat intake
The diet of coronary patients and healthy individuals has been compared in numerous cohort and case-control studies. In a previous review of 28 cohorts in 21 studies patients with CHD had eaten significantly more saturated fat than the controls in three cohorts, but the differences were trivial, in one cohort they had eaten significantly less and in the other 24 cohorts no differences were seen . No difference was seen either in two recent, large cohort studies [48-49], or in the study referred to by the WHO guideline authors; in the latter the statistical significance disappeared after controlling for other dietary factors .
No difference in fat intake was seen either in three case control studies between patients with CHD and control individuals of the same age and sex [50-52]. It can be argued that case control studies may be confounded by changes in the diet after the diagnosis of heart disease, but the mentioned studies were performed between 1958 and 1968 before dietary advices had become standard treatment.
Even more contradictory are the findings in stroke patients. In ten prospective cohort studies of healthy people the authors compared the intake of saturated fat in those who had stroke at follow-up with the intake of the others [53-62] . With one exception  all studies found that stroke patients had eaten less saturated fat than had the non-stroke individuals; in six of the studies the difference was statistically significant (table 2).
Table 2. Association between intake of saturated fat and stroke in ten cohort studies.
A relevant objection against such studies is that dietary information is inaccurate. A more reliable way to study previous intakes with disease is analyses of fat tissue, because intake of saturated fat during the last weeks or months is reflected by the levels of individual fatty acids in the fat tissue. The strongest associations are found between intake and concentrations of the short chain acids 12:0-15:0 [63-67], and of the total numbers [68-71], but weakly or not at all of the longer ones, probably because a high intake of simple carbohydrates stimulates endogenous synthesis of the long chain saturated fatty acids .
In three case-control studies of patients with myocardial infarction and healthy controlindividuals no difference was found as regards the content of the short-chain saturated fatty acids; in two studies it was even significantly lower in the patients (Table 3) [73-77]. These studies concerned only patients with first myocardial infarction [74-77] or patients who were not on a diet , and a diet bias is therefore unlikely.
Table 3.Five case-control studies of the content of short-chain saturated fatty acids
Saturated fat intake and atherosclerosis
If high intakes of saturated fat should lead to atherosclerosis, people with high intakes should be more atherosclerotic than people with low intakes. No such association has been found in any study. In the International Atherosclerosis Project, fifteen populations were ranked by raised atherosclerosis and by selected diet components. Degree of atherosclerosis was associated with the total fat intake, but not with the intake of saturated fat . In three cohort studies of healthy individuals followed for several years, post-mortems of those who had died at follow-up found no association either between intake of saturated fat and degree of atherosclerosis [79-81]. No association was found either between the content of 14:0 and 15:0 saturated fatty acids in the fat tissue and degree of atherosclerosis, determined either by autopsy  or by coronary angiography .
Angiographic follow-up studies have given disparate results. In a trial including 50 men with CHD, where a low-fat diet was compared with usual care, progress of the angiographic changes over 39 months was associated with intakes of palmitic and stearic acids . However, the group that ate the low-fat diet was also instructed to increase their intake of fish, fruit and vegetables, and intake of such food have been found inversely associated with the risk of CHD in almost all studies.
In the MARGARIN study 81 hypercholesterolaemic individuals were followed for two years after having received dietary advice . At follow-up associations between the changes of intima-media thickness of the coronary and femoral arteries, measured by ultrasound, and intake of saturated fat were not significant in multivariate regression analyses. When the patients were grouped into quintiles of change of saturated fat intake, a weak association was seen with the changes of the femoral, but not with the changes of the coronary arteries. However, a similar bias was introduced in that study also, because vascular changes were inversely associated with intake of fruit. As the effect of a reduced intake of saturated fat is said to be due to a lowering of LDL cholesterol it is also contradictory that LDL cholesterol was lowest in those whose intake of saturated fat had increased during the study period. In contrast, a highly significant inverse association was found between intake of saturated fat and progress of angiographic lesions in a 3-year follow-up study of 235 postmenopausal women with CHD .
Saturated fat and type 2 diabetes
Epidemiological studies have found a high intake of saturated fat to be associated with higher fasting blood glucose and a greater risk of developing type 2 diabetes, and several such studies are cited in the WHO guidelines. The associations were weak, however and in the largest study that included more than 50,000 individuals the association disappeared after correction for other factors. The authors concluded that an incomplete control of physical activity and other dietary factors might have influenced the results in the previous studies . That a high intake of saturated fat should predispose for type 2 diabetes is contradicted by experiments with diets poor in carbohydrates and rich in saturated fat. No worsening of the diabetic condition were seen in these experiments; on the contrary most of them showed an improvement of insulin sensitivity, a lowering of HbA1C and some of the patients were able to stop or lower their antidiabetic treatment [18,20,21,24,25,27,88].
Saturated fat and body weight
Fat has more calories per weight unit than have carbohydrates and protein. This is one of the main arguments for the advise to obese patients to exchange dietary fat with carbohydrates, although there is no evidence that fat per ingested calorie is more fattening than carbohydrates. The increase of mean body weight seen in many Western countries since the introduction of the low-fat diet rather points at the opposite. Meta-analyses of controlled trials of calorie restriction by fat reduction have found that this regime may lead to weight loss, but the effect is trivial and is not sustainable. Willett and Leibel have pointed at serious errors in most of these studies; many of them were not randomised, there were multiple reports from the same trial, fat reduction was combined with increased physical activity and other weight-reducing measures and long-term studies were excluded. Their most serious objection is that the fat reduction and control groups did not receive a comparable intensity of dietary instruction and motivation . A strong argument against the idea that a high intake of animal fat is more fattening than a low-fat diet is that in all trials mentioned in table 1 a greater weight loss was seen in those who were instructed to follow a high-fat diet than in those on a low-fat diet.
In many populations a major contribution of saturated fat comes from dairy products and all authoritative guidelines recommend a restriction of such food. However, in a meta-analysis of ten cohort studies including more than 400,000 individuals Elwood et al. found that compared with low-consumers the risks of myocardial infarction, ischaemic stroke and all cardiovascular events in high-consumers were 0.87 (0.74-1.03), 0.83 (0.77-0.90) and 0.84 (0.78-0.90) respectively . In a thorough review of the associations between dairy products and cardiovascular disease Tolstrup found no strong evidence in support either . Besides, in a study of adolescents the low-chain fatty acids 4:0-10:0, 12:0 and 14:0, that closely reflected the intake of milk  were inversely associated with serum cholesterol . The studies of fat tissue fatty acids mentioned above are contradictive as well.
The dietary trials
The most important argument for causality is improvement or disappearance of the disease after decrease or discontinuation of the exposure to the suspected causal factor. To-day relevant data have been published from nine randomised, controlled trials where the only intervention was a change of dietary fat. Two meta-analyses of these trials found no significant effect, neither on cardiovascular or total mortality [4,93,94], and as mentioned above, most trials comparing high-carbohydrate-low-saturated fat diets with low-carbohydrate-high-saturated fat have found a better outcome as regards body weight an metabolic control in the latter ones.
The idea that too much saturated fat in the diet is harmful to human health has no support from ecological, dynamic population, or case-control studies of the association between dietary saturated fat, or tissue saturated fatty acids, and cardiovascular disease, nor from meta-analyses of randomised, controlled, unifactorial dietary trials. Even if the author of this review has studied the scientific literature on this issue meticulously for eighteen years, supportive studies may have been overlooked. However, a scientific hypothesis must be in accord with all observations; a few supportive studies cannot outweigh more than hundred studies that have falsified the hypothesis.…
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Is saturated fat bad?
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