By William R. Ware, Ph.D :In the past 25 years, eggs have been held up as a prime example of fat, cholesterol and caloric excesses in the American diet. The widespread bad publicity resulted in almost a 50% drop in egg consumption. Eggs typically contain about 200 mg of cholesterol per egg, and are a major source of dietary cholesterol in Western diets. In addition, the egg contains many other nutrients including unsaturated fats, essential amino acids, folic acid and other B vitamins. Eggs are also low in saturated fat. The so-called omega-3 eggs from chickens fed on a diet that includes flax seed in addition have a high content n-3 polyunsaturates and in fact a very favorable ratio of n-3 to n-6 essential fatty acids. How deserving of blanket condemnation eggs really are has been addressed in a number of studies. They fall into two classes. First there are the studies that examine the relationship between dietary cholesterol and serum cholesterol. The other type of study actually examines the question of an association between egg consumption and heart disease and stroke. As regards cholesterol intake and serum levels, there have been a number of studies that find dietary cholesterol raises levels of total and LDL cholesterol, but the effects are very small, especially compared to the effects of saturated and trans-fatty acids (28). An interesting aspect of the cholesterol feeding studies is the observation that dietary cholesterol raises both LDL and HDL with little change in the LDL:HDL ratio. This provides another argument that dietary cholesterol is unimportant, except for the small minority who adversely respond to its ingestion (29). In fact there is a large variation in individual response of serum levels to dietary cholesterol, with many showing no change at all.
There have been 10 important prospective cohort studies of the effect of dietary cholesterol on the risk of heart disease. Only two provided a statistically significant indication that there was an increased risk, and these were not controlled for confounding from total energy or fiber (30). The two studies with corrections for confounding by total energy and fat or by total energy, fat and fiber both failed to provide a statistically significant indication of increased risk associated with an increment of 200 mg cholesterol per 1000 kcal caloric intake (about 400 to 500 mg/day). These two studies involved 37,851 men and 80,082 women. The study involving these two cohorts also looked at egg consumption in excess of one egg per day, and found no significant risk (28). Also, no risk associated with egg consumption was found for ischemic or hemorrhagic stroke. It is worth remarking that the eggs in these studies were not the new omega-3 eggs. These eggs are of recent origin and the studies in question involved a number of years of follow-up. In spite of these studies, the notion that eggs are associated with heart disease persists (31).
FAT AND CANCER
The above discussion makes it clear that it is hard to document a convincing case, in connection with heart disease, against any kind of fat other than trans-fat. But how about the notion that fat causes cancer? As mentioned at the beginning of this review, the same types of studies done twenty or thirty years ago that suggested a link between fat and heart disease also implicated fat with the incidence of cancer. These studies suffered from the same weaknesses as those that attempted to associate fat and heart disease. The conclusions from these early studies have not been confirmed by modern epidemiology. Unfortunately, the only extensive data relates to breast and colon cancer, although there is significant data concerning prostate cancer. Other sites have not been studied with the statistical power found in studies of cancer epidemiology of these three sites, so any discussion of diet and cancer is of necessity incomplete. As regards breast cancer, the clearest and most consistent finding is that high calorie intake, regardless of the food source, is far more important than dietary fat. In the Nurses’ Health Study, which involved a large cohort studied over a long period, there was no hint of an increase in breast cancer with higher dietary fat. In fact those with a very low intake of fat (less than 15% of total calories) had a significant increased risk of breast cancer (3,32,33).
The early studies connecting colon cancer and dietary fat have also not held up against modern studies. The only connection appears to be with red meat, but no one knows if it is something in the red meat or has to do with chemicals produced on cooking. There is on-going research that is looking at this connection, especially the degree of "doneness" associated with cooking or broiling red meat. Again, the strongest link is with too many calories in relation to the exercise level–the problem of a positive energy balance (3,24,32,33).
The situation with prostate cancer is complex. The incidence and mortality of prostate cancer shows remarkable variation across geographical and ethnic groups, and changes in risk seen among migrants has inspired a search for dietary factors that might influence the development of this common disease. Fat is one of the most extensively studied dietary factors in this context. The current status has been reviewed by Moyad (34), Schulman et al (35) and earlier by Kolonel et al (36). Moyad reviews eleven prospective cohort studies involving over 200,000 subjects. While three studies showed positive association with red meat, the association failed to reach statistical significance. The one study that found a statistically significant connection between high-fat foods and prostate cancer has been criticized for an inadequate questionnaire and for the absence of high intakes of milk and beef that prevented the comparison with low intakes.
Case-control studies, on the other hand, have shown a connection between fat or fat-type food as well as alpha-linolenic acid and the incidence of prostate cancer. However, these studies are viewed as suspect because of recall bias and confounding. Also, prospective studies fail to confirm the positive risk connection with alpha-linolenic acid. Thus it seems clear that the association between dietary fat and the incidence of prostate cancer is very weak if not totally absent. However there is a positive association with red meat and dairy products and prostate cancer in individuals who have metastatic disease (37-40). In what appears to be the most recent large prospective study in this context, intakes of red meat and dairy products were not associated with total or advanced cancer (stage A2, B, C), but consumers of red meat had a significantly elevated risk of metastatic prostate cancer (stage D and fatal). A high intake of dairy products was also associated with an increased risk of metastatic disease, but the investigators were able to explain this association by known confounders (38). This study involved over 51,000 men followed for over 10 years. However, it is not clear if the connection with red meat is due to the meat per se or something in the meat or something associated with the cooking process. The association of prostate cancer with dairy products is thought to be confounded by the positive association with calcium intake observed is some studies of this disease (39,41). There does not appear to be any link with prostate cancer and vegetable fats (33).
With regard to other cancer sites, there is no significant evidence that there is a link between fat and cancer, but the data is very sparse (33,42).
Thus, if there is a relationship between dietary fat and cancer, it is very weak, and appears to be limited to animal fat and red meat. Limiting red meat and animal fat consumption (but not eliminating it) is part of many prudent diets, since replacing saturated fat with unsaturated fat in order to reduce the risk of CHD would normally involve decreasing the consumption of red meat and animal fat. Because red meat does in fact turn up in studies as a possible risk factor for both colon and prostate cancer, it may indeed be wise to limit consumption of this type of food until more definitive information is available. Willett holds to the view that the important factors in the relationship between diet and cancer appear to be a positive energy balance, reflected in part in early height and weight gain, early onset of menstruation for women and weight gain as an adult (24).
FAT IS BAD BECAUSE FAT MAKES YOU FAT
This is a popular concept that has a strong logical appeal to the layman. However, it appears to be an oversimplification of a complex subject. Viewed in its most general form, there is of course an element of truth in the statement that eating fat makes one fat. Total energy intake is related to the consumption of fat, protein and carbohydrate, and fat being more energy dense, can contribute to an energy imbalance where excess macronutrients are stored as fat. But this is not an argument for low-fat diets. One of the highest profile opponents of the fat makes you fat dogma is Harvard’s Walter Willett. He points out that there has been a significant decline in the percentage of energy obtained from fat in the US population in the past two decades, as would be expected from the success of the anti-fat movement. However, at the same time there has been a significant increase in obesity. In short-term dietary intervention trials, individuals who are assigned to a diet that had a lower percentage of energy from fat generally had a modest reduction in weight. However, compensatory mechanisms appear to come into play, since in trials lasting over a year with fat consumption in the range of 18-40% (a very wide range indeed) of total energy, there appears to be little if any effect on the ultimate degree of fatness. Thus the available evidence points to the fact that diets high in fat do not appear to be the primary cause of the high degree of excess body fat in the US population, and reductions in fat will not be the solution (24,43).
If we turn to anecdotal evidence, the most successful long-term weight loss programs in North America, if not worldwide, appear to involve diets that are not low in fat but low or very low in carbohydrates, especially carbohydrates that are rapidly digested with concomitant adverse swings in both serum glucose and insulin. The diet programs with the highest profile include those of Atkins (44), the Eades (45), the Hellers (46), and Sears (22). Atkins pioneered the low-carbohydrate diet. While his anecdotal evidence is extensive with over 60,000 patients treated in his Manhattan clinic, nutritional scientists simply do not like anecdotal evidence, even when it is supported by thousands of case histories from other advocates of the same protocol. But progress is being made on this front. There are now two papers presented at national meetings that provide scientific evidence for the effectiveness and safety of the Atkin’s type diet (47,48). There is also one study in the context of adolescent obesity (49). The Atkins’ and other low-carbohydrate diets provide a counter argument to the fat makes you fat view since these are diets that have a higher percentage of fat than is common in North American diets, and patients are losing weight, not gaining it, without, for most individuals, adverse effects on blood lipid profiles.
Obviously, weight gain and obesity are complex subjects. However, there seems little doubt that there is a strong relationship with carbohydrate metabolism, blood levels of glucose and insulin, and the development of insulin resistance, which frequently accompanies obesity or the state of being overweight (18). To focus on fat alone would appear to be a serious mistake.
WHAT DO THE EXPERTS RECOMMEND?
Expert Panel on the Identification, Evaluation and Treatment of Overweight and Obesity in Adults (50)
In the context of strategies for weight loss and weight maintenance, they comment:
"Reducing the percentage of dietary fat alone will not produce weight loss unless total energy intake is also reduced. Isoenergetic replacement of fat with carbohydrates will reduce the energy fraction from fat but will not cause weight loss. Reducing intake of dietary fat, along with reducing dietary carbohydrate, usually will be needed to produce the energy deficit needed for an acceptable weight loss. When fat intake is reduced, priority should be given to reducing saturated fat to enhance lowering of LDL-C levels." Note: In this note, LDL-C is LDL.
Executive Summary of the Third Report of the National Cholesterol Education Program (NCEP) Expert Panel on the Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III) (51)
"ATP III’s TLC (Therapeutic Lifestyle Changes) diet generally contains the recommendations embodied in the Dietary Guidelines for Americans 2000. One exception is that total fat is allowed to range from 25-35% of total calories provided saturated fats and trans fatty acids are kept low. A higher intake of total fat, mostly in the form of unsaturated fat, can help reduce triglycerides and raise HDL cholesterol in persons with the metabolic syndrome."
Note: The suggestion to increase fat intake is no doubt directed at the large population of individuals on low or very low fat diets that have high triglycerides and low HDL. Metabolic syndrome is also known as Syndrome-X.
Sense for Women. Your Plan for Natural Prevention and Treatment (52)
"Like many cardiologists, I used to recommend low-fat, high-carbohydrate foods to my cardiac patients. I was caught up in the low-fat, high-carbohydrate craze that swept the country ten years ago. Boy, was I off the mark! Many of my patients did initially lose weight on the no-fat, low-fat diets, but over time their HDL "good" cholesterol decreased and their triglycerides shot up, and they often regained weight."
Note: Stephen Sinatra, M.D., is Director of Medical Education at Manchester Memorial Hospital and Assistant clinical Professor of Medicine at the University of Connecticut School of Medicine. He is the author of several popular books.
Eat, Drink and Be Healthy. The Harvard Medical School Guide to Healthy Eating (24)
"PUTTING IT INTO PRACTICE:
* Remember that not all fats are bad–unsaturated fats protect against heart disease and other chronic conditions.
* Make decisions about dietary fats based on their proven impact on heart disease, not by their weak- -if any–connection with cancer.
* Limit the amount of saturated fat in your diet, as the American Heart Association, National Cholesterol Education Program and others recommend. But there is no good evidence that replacing saturated fat with carbohydrates will lower rates of heart disease, while there is solid proof that replacing saturated fat with unsaturated fat will.
* Reduce saturated fats by limiting the amount of full-fat diary products you eat and replace red meat with nuts, legumes, poultry and fish whenever possible.
* Use liquid vegetables oils in cooking and at the table.
* Eat one or more good sources of n-3 fatty acids every day–fish, walnuts, canola or soybean oil, ground flaxseeds or flaxseed oil."
Note: Walter C. Willet, M.D., Dr. PH. is one of the world’s leading nutritional epidemiologists. He is a professor of medicine at Harvard University and chairman of the Department of Nutrition, Harvard School of Public Health. He has co-directed or directed a number of large and highly significant studies on the relationship of diet and health. He is the author of the definitive textbook on this subject (3).
This discussion should have made it clear that conducting studies that yield clear-cut answers is not the norm in this area. In fact the attempts to examine the question of the link between fat and heart disease have been remarkably inconsistent, when viewed as a whole. There have been a very large number of studies, especially if one counts those dating back to the 50s, and yet if one searched for one word to characterize the whole lot, it would probably be "inconclusive." Also a recurrent observation is that prospective cohort studies are at odds with case-control studies. While it is suspected that this is due, in case-control studies, to recall bias and failure to correct for confounding factors, this explanation can hardly be considered well established. Even the dietary intervention studies that replaced saturated fat with unsaturated fat were in a sense inconclusive, since two variables were simultaneously changed, but in this case, the overall result was clear enough–in fact convincing enough to become a popular recommendation from many authorities. It should also be apparent that by selecting studies, it is possible to support practically any point of view. Unfortunately, this is not a totally unknown practice(53).
As was mentioned above, there are many puzzling features of the cholesterol–fat–CHD picture, especially in the context of the initiation and progression of atherosclerosis. The most important "new vista" that has opened up in the past decade associates inflammation with atherosclerosis and the risk of heart attacks (54). This has become an exceedingly active area of research, and inflammation may well push cholesterol off its long held position at center stage. Research now suggests some association of inflammation with the adverse aspects of hypertension, diabetes, obesity and abnormal blood lipid levels as they relate to heart disease (54). In fact, the leading researchers in the field of inflammation and CHD predict that quite soon the measurement of serum C-reactive protein will become as routine as cholesterol level measurements. There are also other markers of inflammation that are currently under investigation in connection with CHD, and in addition, a lot of attention is being given to the role of chronic infections (e.g. gingivitis, prostatitis, bronchitis, etc.) in the formation and acceleration of atherosclerotic lesions.
The flip-flops in dietary advice which are evident from this discussion of fat and heart disease could very well have an adverse effect on the future public willingness to accept or even listen to the nutritional experts or health care providers when it come to dietary advice. A widespread loss of confidence in studies of all types would be a natural response of the general public to what we are witnessing, not only in the field of nutrition, but also in many other health related areas. A recent example is the change in the view of mainstream medicine toward hormone replacement therapy, a flip-flop that has received extensive coverage in the media and generated great concern among women either taking or contemplating hormone replacement therapy. The general public will probably always have trouble dealing with flip-flops, which are unfortunately a natural phenomenon in scientific research, especially when it involves human subjects and human disease.
Emeritus Professor of Chemistry, University of Western Ontario, London, Ontario, Canada