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Americans (and probably Europeans) in modern society (with refrigerators and indoor heat) need a minimum amount of omega 3 (w3) and omega-6 (w6) fatty acids (which I named "essential fats"). I invented technology to accurately measure fatty acids in human tissue. Since the early 1980s I analyzed over 2,000 blood samples from patients, subjects from the Framingham Heart Study and many more. Roughly (see references), about 75% have low levels of w3s, about 25-50% have low levels of w6s. Sometimes people have so much fat in their blood (usually due to overweight) that it creates a relative deficiency of essential fats. There is HUGE variability in FAP (Fatty Acid Profiles). Good analysis is very difficult, takes over 2 hours per sample and sophisticated computers to calculate the quantity of each fatty acid (due to superimposition of peaks in chromatography, integration errors, etc.).
Based on my biochemical tests, most Americans eat too many processed fats high in isomers (Trans are just one type of isomers). The storage and use of oils rich in PUFAs may convert some of the EFAs (Essential Fatty Acids) to an undesirable isomer. These isomers are VERY difficult to measure (and rarely done); in particular, isomers of very long chain PUFA (such as EPA, DHA) are almost impossible to measure with commonly used technology (almost no data are reported on them, but some fish oils could be high in isomers).
My recommendations are that most people need to eat diets with more w3s and w6s, with a higher ratio of w3/w6 (the ideal ratio is unknown, and depends on geography, genes, body composition). Eating merely more w6s, as a population strategy to prevent heart disease, is unlikely to be useful. Part of the problem is that the oils used may not have the essential fats in the optimal biological configuration (e.g., they are on the wrong part of a triglyceride molecule, they are isomers, etc.). The best population strategy is EAT LESS; lose weight (do not smoke, etc.). However, I suggest people use conventional soybean oil as a raw oil instead of olive or safflower. Soybean oil has w3s and w6s and, in my experience using it, even with its high w6/w3 ratio, it raises EPA, DHA levels in the blood (notice that other oils may raise it more, but measurements rarely distinguish between biologically active w3s and other w3s). The better solution is to eat more natural foods rich in membranes that are rich in essential fats (vegetables, eggs, etc.).
Good dietary recommendations are fairly consistent (and reported in BMJ): eat foods close to their natural state (avoid highly processed fat, carbohydrates), more vegetables and fruit. CUT calories. With these recommendations, Americans and Europeans would save 100s of Billions in health care (at least $500B/year in the US because healthy diets are the best treatment x cardiovascular disease, diabetes Type 2, etc.).
It is substantially undisputed that linoleic and linolenic acid are essential nutrients (there is a dispute about their derivatives, so it is not certain that humans can eat only a vegetarian diet, EFA derivatives are usually found in foods from animals, plants rarely elongate the EFAs to their derivatives). Being essential, there must be an optimal intake between zero and infinite. Due to huge human variability, I cannot make a general recommendation about eating more or less w6s.
For most overweight people, like apparently the subjects in this study, by far the decisive factor in heart disease is weight. Other factors include temperature, smoking, fatty acid body composition and other factors not considered in the study. Without those factors, the implicit model that predicts deaths is likely to have low predictability (validity).
The statistical analysis and underlying mathematical models linking the dependant to the independent variables are confusing. The specific equations are not shown. Measures of validity (accuracy or predictability of the model, such as R squares) and reliability (e.g., reproducibility of results after splitting the data into 3 subsets) are not shown. But I suspect critical variables such as FAPs are missing. Incorporating weight in the analysis model is very tricky (unless the authors can prove that their model has high predictability).
There are no data on the storage means for the oil from production to consumption. Safflower oil can deteriorate at room temperatures, likely increasing the production of isomers. There are no adequate data explaining how the subjects used the safflower oil. Given common practice, it is unlikely that they took it via a spoon, directly from the container to the mouth (the preferred method). It seems likely that the oil was cooked. Thus, the linoleic acid may have changed to undesirable isomers (not just Trans).
Because the experimental group did not gain weight from the extra oil, they replaced some foods. Given the very small # of deaths, some subjects who died may have eaten far fewer w3s or modified molecules of linoleic acid/
The control group apparently ate more eggs. Eggs are high in omega-3s. This could mean that the experimental group ate fewer omega3s.
Given the very small mortality and small sample size, the difference in mortality between the experimental and control group was about 12 people. There was likely huge variability in body weight, smoking, eating and most relevant factors; it seems likely that a unique combination of undesirable factors could account for the 12 extra deaths. Perhaps they were in colder parts of the country. Perhaps they went out more often in the cold. We know that cold is associated with higher cardiovascular mortality. Could it be that some subjects in the experimental group were under colder conditions? (knowing the season, temperature, time and activity at the time of the cardiovascular event would have helped answer these questions). Or perhaps they had unique anatomic conditions or genes.
Whenever we deal with a very small frequency of outcome events we must consider the high probability that specific events outside those analyzed by researchers contributed to variations in outcome data.
My research indicates as follows. The most significant nutrition risk factor for CVD is overweight (eating too many calories). After that, deficiencies and imbalances of the w3 and w6s essential fats; we need to eat diets with higher w3/w6 ratio because most Americans have too high a ratio of w6/w3 in their blood. Furthermore, most Americans need to eat more w3s in absolute terms, and some need to eat more w6s. Merely shifting calories from saturated fats to w6s is unlikely to be beneficial because it increases the body ratio of w6/w3, and, depending on how the diet is implemented, may lower intake of w3s. Lowering Trans and isomers comes next.
Siguel E, Maclure, M. Relative Activity of Unsaturated Fatty Acid Metabolic Pathways in Humans. Metabolism, 1987; 36: 664-69.
Siguel E, Chee, KM, Gong J, Schaefer, EJ. Criteria for Essential Fatty Acid Deficiency in Plasma as Assessed by Capillary Column Gas-Liquid Chromatography. Clin.Chem, 1987; 33:1869-73.
Chee KM, Gong JX, Rees DMG, Meydani M., Ausman L, Johnson J, Siguel E, Schaefer EJ. Fatty Acid Content of Marine Oil Capsules. Lipids 1990; 25:523-27.
Siguel, E. Method and Apparatus for Diagnosis of Fatty Acid or Lipid Abnormalities. U.S. Patent No. 5075101, Issue date 12/24/91.
Siguel E, Lerman, RH. Trans Fatty Acid Patterns in Patients with Angiographically Documented Coronary Artery Disease. Am. J. Cardiology, 1993; 71:916-20.
Siguel E, Lerman, RH. Altered Fatty Acid Metabolism in Patients With Angiographically Documented Coronary Artery Disease. Metabolism 1994; 43:982-93.
Siguel E. Essential Fatty Acids in Health and Disease. 1994, P.O. Box 10187, Dept F, Gaithersburg, MD 20898 (book).
Siguel E, Lerman RH. The Role of Essential Fatty Acids: Dangers in the USDA Dietary Recommendations ("Pyramid") and in Low Fat Diets. Am. J. Clin. Nutrition, 1994; 60:973-79 (let).
Siguel E. Does Linoleic Acid Contribute to Coronary Artery Disease? Am. J. Clin. Nutrition, 1995; 61:397-98 (let).
Siguel E, Lerman, RH. The Role of Essential Fatty Acids: Reply to the USDA. Am. J. Clin. Nutrition, 1995; 63:973-79 (let).
Siguel, E. A New Relationship between Total/HDL Cholesterol and Polyunsaturated Fatty Acids. Lipids, 1996; 31:S51-6.
Siguel E, Lerman RH. The Effects of Low-Fat Diet on Lipid Levels. JAMA, 1996; 275:759-60.
Siguel E, Lerman RH, MacBeath, B. Very Low-Fat Diets for Coronary Heart Disease: Perhaps, but Which One? JAMA, 1996; 275: 1402-03. Erratum in: JAMA 1996; 276(12):954 (let).
Siguel, E. Issues and Problems in the Design of Foods Rich in Essential Fatty Acids. Lipid Technology, 1996; 8(4):81-86 (July).
Siguel, E. Identification and Quantification of Fatty Acids. J.Parent.Ent.Nutr. 1998; 22(6):401-02.
Siguel, E. Deficiencies and Abnormalities of Essential Fats in Gastrointestinal and Coronary Artery Disease. Journal of Clinical Ligand Assay 2000; 23:104–11.
Siguel, E. Clinical Impact of Methodological Issues in the Diagnosis of Deficiencies and Abnormalities of Essential Fats. Journal of Clinical Ligand Assay 2000; 23:112–21.
Siguel, E. n-3 Fatty Acids and the Risk of Sudden Death. N.Engl.J.Med. 2002; 347(7):531-33 (let).
Siguel, E. Some Thoughts to Ponder Before Condemning Trans Fatty Acids. Viewpoint. Inform, (Am. Oil Chem Society), 2002; 13:339 (April).
Competing interests: Author has a patent to measure fatty acids. Author has a book about fatty acids and writes articles about fatty acids
essentialfats.com, PO Box 10187, Gaithersburg, MD 20898, USA
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