Low Fat Diets: Dangers and Benefits
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Contents
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Several key studies published in 1995 and 1996 explain when a low-fat diet may work or fail. These studies showed that it is calories, not merely fat, that cause weight gain. Low fat diets can also cause EFA deficiency (EFAD). An important study by Dr. Schaefer et al showed that very low fat diets, unless accompanied by weight loss, lead to a decrease in HDL and an increase in total triglycerides. This study showed that low-fat diets low in EFAs, when used as maintenance diets, increased the risk factors for heart disease. See an exchange of letters, published in the J. of the American Medical Association, between Dr. Siguel and the authors of the study.
Low-fat diets may decrease the risk factors for heart disease when they cause weight loss. Siguel's research indicates that weight loss in patients who have plenty of EFAs may lead to a preferential loss of saturated fat over PUFA, thereby increasing the ratio of PUFA/NoPUFA in the blood.
A 1995 study showed that low fat diets do not lower plasma cholesterol levels in healthy men compared to high-fat diets of similar calories. Moreover, the low fat diets increased total TGs and reduced the linoleic acid content of the plasma, platelets, and red blood cells in these subjects. Contrary to previous assumptions, it is now well documented that high TGs increase the risk for CHD. Thus, substituting foods high in fat with foods having more calories from carbohydrates or protein is likely to increase the risk of heart disease.
Contrary to popular belief, substituting an approximate amount of calories from fat with calories from carbohydrates does not always lead to weight loss. These recent studies debunk the myth that low fat diets are the optimal treatment for abnormal cholesterol, and may explain why current nutrition policy has been a dismal failure. We must, however, distinguish some low fat vegetarian diets and programs, such as the one sponsored by Dr. Ornish, from low fat diets that are high in processed carbohydrates, as commonly interpreted by many physicians and patients.
Dr. Schaefer fed about 29 subjects diets low in fat for about 3 months. During the study, 2 out of the 29 subjects developed evidence of heart disease. One of the subjects had an infarct. This is a rate of about 25% per year. It is a gigantic rate (think about it: at this rate, every person who follows a low-fat diet may develop heart disease in about 4 years).
Although the subjects in the study were older and at risk of developing heart disease, Dr. Siguel believes that the high rate of heart disease associated with the study was probably a consequence of using low fat diets low in EFAs. In the experience of Dr. Siguel, low fat diets low in EFAs deplete the body of EFAs. The depletion of EFAs leads to cardiovascular disease. Depending on whether the depletion affects primarily the w3 or w6 fatty acids, the person may have heart disease, a stroke, or a heart attack (myocardial infarction).
The study also found that, in subjects who did not lose weight, HDL decreased and total TGs increased. This is consistent with the experience of other researchers and Dr. Siguel. Based on his conversations with many physicians regarding the clinical outcomes of patients on low fat diets, Dr. Siguel has determined that low fat diets utilizing processed low fat and non-fat foods deprived of essential fatty acids (EFAs) both decrease HDL levels and increase TGs. Some patients feel more tired and lack "energy."
Dr. Siguel has warned physicians that such low fat diets can increase Total/HDL cholesterol (TC/HDLC) ratios and deplete plasma and red cell (RBC) EFA levels. This often happens when the diets are used with patients that have low levels of PUFAs in their body, or in patients that have abnormalities of EFA metabolism. These diets can be deadly for many people. They may not kill right away, but they can lead to a weakening of the cardiovascular system and premature death from heart attack or stroke.
Other scientists have found similar results. For example, Siscovick et al reported that low levels of w3 PUFA in RBCs are associated with increased risk of sudden death, probably due to cardiac arrest.
Dr. Siguel asked Dr. Schaefer for a few hundred microliters of blood leftover from this study to evaluate the EFA status of the subjects. If and when such blood is provided, we will seek to have it analyzed, at no cost to the authors or the subjects, and will report the results. In this manner we can determine whether or not the subjects changed their EFA status.
The New York Times of September 20, 1995, presented interviews with Drs. Ornish and Gould regarding this article. In this study, Drs. Gould, Ornish et al reported that regression of coronary artery disease (CAD) can be obtained using very low fat diets.
The diet proposed by Dr. Ornish is vegetarian and very low in fat. Animal fat, including fish, is usually avoided. It is my understanding that, until 1995, Dr. Ornish recommended that oil supplements not be allowed with his diet. In this study, the authors found that over a period of 5 years the patients lost considerable weight. Using a technology known as the PET scan, the authors found that the patients had improvements in coronary blood flow.
Dr. Siguel wrote JAMA urging caution in treating patients with such diets. In the experience of Dr. Siguel, following low fat diets low in essential fatty acids (EFAs) without losing weight can lead to a substantial decline in HDL. This decrease in HDL causes an increase in total/HDL cholesterol (TC/HDLC).
The article presents the case of a 55 year old who had a family history of premature death due to heart disease and a personal history of heart disease. When this patient followed a low fat diet, he deteriorated. Dr. Siguel found biochemical evidence of EFA deficiency, using a highly sophisticated blood test that measures the different types of fatty acids in plasma and red cells. The patient was asked to eat more EFAs and he improved.
Dr. Siguel stated in his letter that "Very low fat diets deficient in EFAs are potentially dangerous for individuals of average weight (i.e., those who need not lose 10 or more pounds), and for patients with low HDL, high TGs and low levels of EFAs." "Before a patient starts on a very low fat diet he/she should be evaluated for EFA abnormalities. EFAs should be provided to correct deficiencies or imbalances."
Most commercial low-fat foods are composed of processed carbohydrates with practically no EFAs; some are high in TFAs. Commercials and government advertisements create the perceived "desirable" goal of eating no fat. "Today, the all-important index of healthfulness for many people is fat content." "As a result, health-conscious consumers have anointed all kinds of improbable products as nutritionally correct, such as pretzels, licorice, and candy." (Ono, see references below).
Mistaken nutritional recommendations emphasize artificially low fat foods deprived of EFAs. Rather than promoting good health, these recommendations are making more Americans deficient in EFAs and thus increasing the risk of heart disease. Given the low EFA content of most popular foods, it is practically impossible to obtain the 10 to 30 grams of PUFAs per day that Siguel's research indicates a person should eat.
Therefore, if a person were to eat a low-fat diet for many years, he/she would likely drastically reduce his/her intake of EFAs and would deplete his/her body stores of EFAs. Paradoxically, EFA insufficiency is more likely in some individuals who eat what they believe to be healthy diets than in those who eat animal products (chicken) and byproducts (eggs). We feed our pets (cats and dogs) a better balanced diet with plenty of EFAs (just read the labels and you will see that most pet foods contain plenty of EFAs).
Many Americans follow macrobiotic or vegetarian meals consisting mostly of breads, pasta, cereals and fruit (and practically zero EFAs). Even those who supplement their meals with seeds, vegetables, and soy products may not eat enough EFAs. This problem is particularly significant in people who are not losing weight. Individuals with large body stores of EFAs who lose weight may lose more non-EFAs than EFAs, thereby increasing their plasma ratio of PUFA/(SFA+MUFA) = PUFA/NoPUFA.
We routinely diagnose and treat abnormalities of PUFA metabolism as part of the treatment for dyslipidemia. Low fat diets often contain less than 5 grams of PUFA per day, well below Siguel's suggested levels of approximately 1/3 gram/kg of body weight. Dr. Siguel has shown that TC/HDLC is inversely proportional to plasma PUFA levels, and directly proportional to plasma SFA or MUFA levels. It is now possible to prescribe a diet high in PUFAs aimed at correcting specific PUFA deficiencies diagnosed by an appropriate blood test. In many patients, studies have shown that eating more PUFAs substantially lower TC/HDLC and TGs.
We recommend that people who eat low fat diets for many months without weight loss be tested for EFA abnormalities and be prescribed PUFA-rich foods to correct deficiencies or imbalances if present. |
Research has shown that low HDL and high TGs is one of the most common genetic abnormalities of lipid metabolism, a common cause of premature death, and a major factor in heart disease costs. Research by Dr. Siguel has found that the lipid values of these patients are particularly sensitive to PUFA deficiencies (unpublished data). While low-fat, low-PUFA diets are dangerous for many people, these diets may be deadly for patients with low HDL and high TGs. A patient with low HDL and high TGs may find that this type of diet further depletes his body of PUFAs, decreasing HDL and increasing TGs.
For these reasons, health providers and patients should be warned never to use low fat diets deficient in PUFA in patients with low HDL and high TGs, in patients with low PUFA levels, or as a long-term maintenance diet for the general population. |
Patients ought to be informed about the need for EFAs and how to obtain them from the diet.
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© 1998 Edward
Siguel. All rights reserved |
modified 1/15/00 |