By William R. Ware, Ph.D :Aside from the indication that it is beneficial to replace saturated fat with unsaturated fat, the cohort and intervention studies fail to provide much guidance. It is instructive to turn to the relationship between fat consumption and serum (blood) cholesterol levels. It appears to be an uncontested fact that the consumption of saturated fat increases the levels of low-density lipoprotein (LDL) cholesterol, which is regarded as the bad lipoprotein.
However, life is never simple, since saturated fat also increases the high- density lipoprotein (HDL) cholesterol fraction as well, and HDL is considered very beneficial. The extent to which this results in a draw, so to speak, is not clear, but the conventional wisdom ignores the increase in HDL, focuses on the increase in LDL, and thus concludes that saturated fat as bad. However, if an individual had a normal level of LDL and a low level of HDL, raising the HDL might on balance be beneficial even if the LDL level also went up. The percentage decrease in risk is 3% for every 1% increase in HDL, whereas there is only a 1% increase in risk for each 1% increase in LDL (8). The changes in both LDL and HDL with the ingestion of saturated fat will depend on the nature of the fat, that is, the actual saturated fats involved, and as well, will depend on the individual, since there is considerable variation. Perhaps it is because of the combination of good and bad effects of saturated fats, coupled with individual variation, that the studies discussed above provided no definitive guidance as to the question of saturated fat increasing the risk of CHD, but only inconsistent findings.
Both monounsaturated fats (olive oil is high in monounsaturates) and polyunsaturated fats turn out to be beneficial in the context of cholesterol levels. They raise HDL and lower LDL. The interplay between diet and HDL, LDL, total cholesterol, and the other important blood lipids, the triglycerides, merits further discussion, not only since it relates the "bad" label attached to saturated fat and the "good" label associated with the mono- and polyunsaturates, but also because it relates to the question of high vs. low fat diets which can modify these blood lipid levels.
Studies far too numerous to list have established, probably beyond reasonable doubt, that high levels of total cholesterol and LDL cholesterol present a risk for the development of CHD. Since LDL cholesterol represents typically more than 50% of the total cholesterol, this total is considered a surrogate for LDL. Thus the studies that measured only total cholesterol remain valid today and are part of the case for high serum cholesterol being a risk factor. Four quite different and more or less independent approaches to lowering both total cholesterol and LDL produce reduced risk of CHD (surgery, sequesterant drugs, statin drugs and diet). This is one of the cornerstones of the argument that LDL is bad and that lowering it represents a beneficial intervention. There is also considerable literature indicating that low HDL carries added risk for CHD and that raising HDL decreases the risk (9-12).
However, there are some disturbing aspects to this picture. In fact, Ravnskov (4,7) and a few others have been very vocal critics of the hypothesis connecting cholesterol, fat and CHD, but their views are perhaps a bit extreme. Nevertheless, as any doctor involved with heart patients will tell you, something like 50% of all heart attacks occur in individuals who have a normal blood lipid profile, i.e. LDL is not elevated and HDL is not low. In addition, there is frequently no correlation between the extent of LDL lowering and the decrease in risk, and the decrease in risk in some studies is independent of the level of risk in the subjects studied (13,14). This latter phenomenon is also seen in the diet intervention studies, as discussed above. In addition, a significant decrease in CHD risk is found by lowering LDL in individuals that are already at low risk as judged by their blood lipid profile (15,16).
It does not help that the details of the mechanism of the adverse action of LDL is poorly understood, as is the overall mechanism of the formation of atherosclerotic plaques, from their beginnings as fatty streaks in arteries to large, unstable plaques, the rupture of which is thought to be related to heart attacks. In fact, the conventional wisdom that atherosclerosis is caused by high cholesterol has recently been challenged by Ravnskov in the Quarterly Journal of Medicine. He documents the following points (17):
* Serum cholesterol does not predict the degree of atherosclerosis at autopsy.
* Serum cholesterol does not correlate with the degree of coronary atherosclerosis on angiography.
* Serum cholesterol does not correlate with the degree of coronary calcification.
* Serum cholesterol does not correlate with the degree of peripheral atherosclerosis.
* Changes in serum cholesterol concentrations are not followed by parallel changes in atherosclerosis growth–i.e. there is no exposure response.
Thus an important question: why does high cholesterol predict cardiovascular disease if LDL levels and changes in LDL do not correlate with the degree of atherosclerosis or with atherosclerosis growth? As Ravnskov points out, there can be many reasons for these observations. One is that high LDL or total cholesterol may be secondary to other factors that promote cardiovascular disease (17). On-going research will no doubt eventually produce a more satisfactory picture.
It seems clear that LDL is bad cholesterol and HDL is good cholesterol. Saturated fat consumption raises both and might be viewed as neutral. Eating mono- or polyunsaturated fat decreases LDL and raises HDL. From this one might conclude that it is pointless to worry about fat. However, to not worry about fat at all would be to ignore the apparently beneficial effects of the unsaturated fats and the studies that demonstrated a significant decrease in the risk of CHD when saturated fat is replaced with unsaturated fat– a benefit that does not appear to prove that the reduction of saturated fat was indeed beneficial, but that merely the combined action has merit. In this context, it is important to understand that if one merely increases the consumption of unsaturated fat and does not decrease the saturated component, there may be a risk of adversely disturbing the energy balance with an associated weight gain, unless other macronutrients such as protein or carbohydrate are decreased.
Once the "fat is bad" religion was firmly established and supported by the US government, the medical profession, the nutritionist community, the media, and, with great enthusiasm, the food industry, the so- called low-fat or very low-fat diet was a natural result. Since most people tend to maintain a certain level of caloric intake, low fat in fact meant a dietary change that involved replacing fat with carbohydrate. Protein in general was not viewed as a candidate since most common protein sources contained lots of fat. Carbohydrate has roughly half the calories per gram as compared to fat (4 vs. 9 kcal/gram), so the low fat diet was also a high carbohydrate diet, and this was embraced by millions as the path to health and longevity. Lack of knowledge among the general public as to the various types of carbohydrates and their relative effects on blood glucose, insulin, and the development of insulin resistance led to the indiscriminate consumption of increased amounts of carbohydrates, in many cases carbohydrates from sources such as potatoes, white rice, ordinary pasta, white bread, bagels, baked goods, sugar-rich deserts, non-diet soft drinks and juices, etc. Much of the carbohydrate that replaced fat was of the type that was rapidly digested to yield large increases in post-meal (called postprandial) blood glucose and insulin, which frequently leads to insulin resistance and eventually the so-called metabolic syndrome or Syndrome-X (18). Carbohydrate not needed for energy was turned into fat and stored–something the general public was probably not aware of, since the "fat is bad" religion did not include information on the metabolism of carbohydrates. The notion that eating fat made one fat, and avoiding fat therefore would result in weight stability or weight loss, was part of the conventional wisdom of the masses.
The replacement of fat with carbohydrate has been studied a great deal since the "fat is bad" religion became commonplace. In many individuals, such a change in diet results in a significant decrease in serum HDL, an equally significant increase in serum triglycerides, and eventually the development of insulin resistance, where the body requires larger and larger amounts of insulin to manage the load of serum glucose that arises from the heavy carbohydrate component of the diet. Insulin resistance frequently leads to type 2 diabetes, which in turn results in a whole host of serious health problems and a well documented huge increase in the risk of heart disease. Most diabetics in fact die of heart disease. The above-described changes in HDL and triglycerides also are in the direction of increasing the risk of CHD. It actually turns out to be difficult to separate the effects on CHD risk of high triglycerides and low HDL, since these two conditions frequently occur together, but there are studies that indicate that high triglycerides can be viewed as an independent risk factor (19). Suffice to say that there are a number of studies in the recent literature that indicate a very high level of increased risk when HDL is low and triglycerides are high (9-12). Interestingly enough, men with conventional risk factors for CHD actually have low risk if they have low triglycerides and high HDL (11). Some investigators think that in fact low HDL and high triglycerides can present a greater risk than either high total cholesterol or high LDL (8). In some individuals, low HDL and high triglycerides are accompanied by a change to smaller LDL particles. There is considerable evidence that these are more dangerous in the context of heart disease than large, less dense LDL particles (20). In fact, this is one of the frequently encountered arguments against the low-fat high-carbohydrate diet. However, not all studies find that CHD risk higher when the serum concentration of small, dense LDL particles predominates (21).
Emeritus Professor of Chemistry, University of Western Ontario, London, Ontario, Canada