The Keys and Hegsted Equations were instrumental in describing a role for saturated fats in the diet, their ability to increase plasma cholesterol levels and consequential risk for coronary artery disease (CAD). This was further cemented by observations from the Framingham Heart Study and other large epidemiological studies specifically in the Western hemisphere examining the impact of diet on non communicable diseases (NCD). In the 50 odd years since these events were triggered, our understanding of the role of dietary fats and in particular saturated fats, in the overall etiology of CAD has undergone dramatic changes. This was precipitated by the landmark study in 1990 (Mensink & Katan), that set scientific directions towards the elimination of trans fatty acids from our food supply. There has since been overwhelming evidence for the negative health and nutritional endpoints that result from the consumption of trans fats. Scientific curiosity has prevailed – the isolation of trans as the dietary fat moiety that was most troublesome for health also allowed a better assessment of the role of saturated fats in NCD and in particular CAD.
The emerging evidence strongly fans the current scientific school of thought that saturated fats are no longer strongly correlated with CAD risk and mortality, yet such evidence is being opposed by many who wish to maintain the negative and adverse stigmas ascribed towards saturated fats. In a continuing saga of debates, the just published review in Advances in Nutrition (4; 294-302, 2013) by Glen D Lawrence, “Dietary Fats and Health: Dietary Recommendation in the Context of Scientific Evidence“, merits discussion.
Oxidation and Lipid Peroxidation Triggered by an Imbalance of Dietary Fatty Acids
Dr. Glen Lawrence rightly traces scientific developments that have leapfrogged from merely determining plasma cholesterol and association with fat (saturates – SAFA, polyunsaturates -PUFA, and mononunsaturates – MUFA) consumption to lipoprotein fractions (VLDL, LDL, HDL), lipoprotein particle sizes and a series of regulatory binding proteins that alter transcription of genes involved in lipid metabolism. Consequently, lipid or fatty acid oxidation which is a core physiological function must be responsive to the dietary fats we consume and needs to be regulated. Of the dietary fatty acids we consume, polyunsaturated linoleic (18:2 n-6) and linoleinic (18:3 n-3) acids make LDL most susceptible to lipid peroxidatiion. Oxidized fatty acid moieties are the components that ultimately become foam cells and block the arteries through arterial plaque formation and it would stand to reason that an imbalance between PUFAs, MUFAs and SAFAs could trigger oxidation. Oxidative stress and lipid peroxidation products have been implicated in heart disease, cancer and other chronic diseases. Since SAFAs are not susceptible to lipid peroxidation, they have been found to be not involved in these mechanisms and by reason should not provoke atherogenesis.
Saturated Fats Are Less Pro-Inflammatory than Polyunsaturated and Trans Fats
Saturated fats in our diet are associated with far less inflammation than diets rich in n-3 or n-6 PUFAs or trans. Scientific evidence suggests that dietary SAFA do not promote inflammation and it may be more prudent to advocate the minimization of n-6 PUFA rich sources (such as the seed oils) in our diet and consume reasonable levels of SAFA to minimize various inflammatory processes in our body. This concept however remains elusive since there have been relatively few studies along these lines due to biased and misguided concerns that all saturated fats may be detrimental to human health. Clearly there also appears a need to differentiate the role of saturated animal fats from those of vegetable oils such as coconut, palm kernel and palm oils that are higher in their SAFA content.
Low Fat, Low Saturated Fat Diets – Are they Healthier Choices?
Fat, quantity and quality, in our diet is an on-going heated debate that is often emotionally imbalanced. Global food industries have been quick off the mark to try and please the public by innovating new product streams that had hardly gone through the required scientific scrutiny. The most glaring of these modern day public health lapses was the anti-tropical oils campaign in the 1980s. A feverish response from industry in support of this campaign resulted in fat-rich products being reformulated with partially hydrogenated fats. Palm, coconut and palm kernel oils were removed from most food formulations. Nearly a decade later, this exaggerated trans consumption began to adversely shape non communicable disease outcomes. Researchers at the Harvard Medical School, led by Prof. Walter Willett, in an editorial, described the possibility that nearly 30,000 deaths in the United States alone were associated with such amplification of trans fats consumption. With overwhelming evidence from a battery of clinical and epidemiological studies, food industry has turned around and has mostly eliminated trans through structured use of natural fats including palm oil.
The pursuit of low fat, low saturated fat products however continues somewhat unabated with firm believes among industry and the consuming public that these are healthier than full fat products. We should remember that in our diets such fat substitution is usually accompanied by an inevitable increase in carbohydrate (starch) consumption. Lager amounts of sugar (mainly refined fructose) are generally added to low fat products to make them more palatable. The use of fructose in these products continues despite documented evidence for its adverse effects on serum triglycerides, uric acid (associated with gout and hypertension) and increased lipid oxidation and peroxidation. Hydrogenated fats that used in many of these low fat formulations were promoted as healthy and high in polyunsaturated fatty acids. The lay-consumer had insufficient knowledge to make the right choices. Even today there is evidence that such products linger on in the market place due to imprecise food labeling regulations that are based on portion sizes rather than absolute fat composition.
Substituting carbohydrates for SAFA in the diet has little effect on serum lipids. However, the excess carbohydrates consumed, if not utilized for energy metabolism will be synthesized and stored as body fat. Hence the possible prevalence of obesity in the population. Moreover, it has been observed that a low-fat, high carbohydrate diet causes increases in serum triglyceride and small dense LDL particles which are in turn strongly correlated with increased risk of CAD.
Dr. Glen Lawrence also alludes to the fact that the anti-tropical oils campaign in the 1980s overlooked an obvious fact that palm oil contains about as much MUFAs as SAFAs and has ample PUFAs to meet daily dietary requirements. Indeed, he quotes at least two studies that compared palm oil with olive oil which had no adverse effects in healthy volunteers. Another lipid curiosity that is often overlooked is the fact that diets rich in SAFA increase the beneficial HDL-cholesterol more than they increase the atherogenic LDL-cholesterol and often give a more favorable lipid profile relative to dietary carbohydrates. The shorter chain SAFAs also have beneficial health effects including an ability to lower Lp(a), an independent risk factor for CAD and plasminogen activator antigen.
Overall there have been a recent spate of publications that have revisited the role of SAFA and most seem to clearly disassociate from the previously held notions that SAFA are a causative or promoting factor in coronary artery disease. Indeed saturated fats are benign with regards to inflammatory effects and share this property with monounsaturated but not the polyunsaturated oils. In the end it would be timely to re-evaluate our current approaches to focus only on dietary recommendations towards lowering SAFA to lower plasma cholesterol. We should also not forget to adopt a more holistic dietary policy approach that includes different fatty acid components and their specific health effects.
Glen D. Lawrence. Dietary Fats and Health: Dietary Recommendations in the Context of Scientific Evidence. Advances in Nutrition, 2013, 4:294-302; doi:10.3945/an.113.003657
Article Credit: Dr. Kalyana Sundram, MPOC.
June 10, 2013