Essential Fatty Acids (EFAs) are critical to good nutrition. Our bodies cannot make them; they must be supplied through the diet. Humans must consume EFAs in far greater quantities than vitamins. A diet low in EFAs increases the risk of hormone abnormalities, cardiovascular disease, and decreased brain and immune functions. Essential Fats, EFAs, PUFAs		cular disease, or nutritional deficiencies) cannot make enough EFA derivatives, and must eat them. Generally, vegetables have parent EFAs but no daughter EFAs. EFA derivatives are found in animal fat (mostly w6) and fish fat (mostly w3). Most w3 in the body is in the form of w3 derivatives; most w6 is linoleic acid, the parent EFA. Relative excesses or deficiencies of one fatty acid alter the effects of the others, leading to cell damage. All excess calories, even those from carbohydrates or protein, are converted by the body to SFAs & MUFAs. If you eat foods low in EFs, most of		The altered structure, which resembles straight SFAs, is known as a trans fatty acid (TFA). TFAs have no known desirable function, increase the risk of heart disease, and may interfere with normal EF activity. Cell walls cannot be constructed properly with TFAs. Eating hydrogenated oils causes TFAs to accumulate in the blood and tissues. Although cholesterol has been blamed for heart disease, high cholesterol levels can actually be a symptom of EFA deficiency. Since the body is trying to make cell membranes out of "stiff" SFAs, MUFAs, and TFAs, it needs cholesterol to soften them and make them more flexible. If one eats more EFs, cholesterol levels often decrease as membranes become more fluid. A few MUFAs are converted to nonessential w7 + w9 PUFAs. With EFA deficiency, levels of w7 + w9 PUFAs increase. Blood levels of these fatty acids are used as markers of EF status. See diagram+fig 2.
Fats are a mixture of fatty acids: + Saturated fatty acids (SFAs), such as beef fat, form solid foods at room temperature because they are straight molecules and can pack tightly together. + Monounsaturated fatty acids (MUFAs), such as olive oil, have one "kink" or bend. They form liquid foods at room temperature, but pack together as solids when refrigerated. + Polyunsaturated fatty acids (PUFAs), like flax seed oil, have 2 or more kinks. They remain liquid even when refrigerated, because the molecules cannot pack together. Two PUFAs (w3 and w6) are EFAs. Others (w7 and w9) are not EFAs. The human body can make MUFAs & SFAs, but not w3 or w6.
			"Essential Fats" (EFs) = EFA precursors + EFA derivatives = linolenic (w3) + linoleic (w6) + + (w3 derivatives) + (w6 derivatives). PUFAs = PUFA w3 + PUFA w6 + some w9, mostly with EFA deficiency.
			the fat in your body will be solid, your arteries will become hard, and you will develop hypertension. Eating foods high in EFs maintains soft arteries and prevents clots. EFs are used for energy, to make cell membranes, and to modulate the balance of eicosanoids (hormones which regulate many body functions). Eicosanoid balance is critical to life (for clot formation, immune defenses, inflammation, etc.). Nutrients (vitamins and minerals) protect EFs from oxidation. Hydrogenation is a process that changes oil into a more stable solid which is less likely to turn rancid.
Essential Fats (EFs), a term coined by Dr. Siguel, consist of two families, omega-3s (w3s) and omega-6s (w6s). The letter "omega", abbreviated "w", refers to the "kinks" or "bends" in EF chemical structure. Each family is divided into parents (precursors) and daughters (derivatives). Using information gained by distinguishing precursors from their metabolic derivatives, nutritionists can determine fatty acid needs. Siguel distinguished these groups because there is interconversion among the derivatives, and the key limiting delta-6-desaturase enzyme separates them from their precursors. The two EFAs (the "parents") are linolenic and linoleic acid. From the EFAs, most humans can make all the EFA derivatives they need. However, some people (diabetics, alcoholics, the elderly, infants not breast fed, and people with severe fat malabsorption, AIDS, cardiovas
				Case History: Genetically induced heart disease aggravated by low fat diet Paul W, 66 yo male with advanced, genetically accelerated heart disease, previous heart attack, CABG, and advancing atherosclerosis, was placed on a strict reversal program consisting of a very low fat diet (little meat or fish), cholesterol lowering drugs, one aspirin, beta carotene, + 800mg vit E every day. After 3 months, triglycerides (TG) increased from 107 to 152, HDL decreased from 56 to 35, and TC/HDLC ratio increased from 2.9 to 4.1. Patient felt much worse than he had before starting the very low fat diet. He lacked energy, was tired most of the day, was sleepy after

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	lunch, and could no longer work as he used to. Fatty acid profile EFA-SR™ found low levels of w3 and w6 fatty acids. Paul was placed on 2-3 tablespoons/day of oils rich in w3 and w6, told to avoid processed carbohydrates (bread, pasta, cereals) as well as SFAs and MUFAs (i.e., olive oil). He was allowed to eat chicken, lean beef, fish, eggs, and foods he liked in the context of a low-calorie diet. Within 12 months, Paul's TGs declined to 53, HDL increased to 50, and TC/HDLC decreased to 2.5. His "energy" level improved considerably. Paul now works many more hours, exercises more frequently and for longer periods of time, and feels much better. A heart scan revealed regression of stenosis. Before a patient starts on a very low fat diet, he/she should be evaluated for EF abnormalities. EFs should be provided to correct deficiencies or imbalances to achieve ideal levels. Eating the right EFs aids in the prevention & treatment of: 0 Cardiovascular disease; stroke; atherosclerosis; poor blood circulation; abnormal cholesterol; high triglycerides; hypertension (EFs reduce the risk of heart disease, while TFAs & SFAs increase it); 0 Complications of diabetes; kidney disease; arthritis; 0 Inflammatory bowel disease; celiac disease; cystic fibrosis; 0 Neurological and psychological abnormalities such as Alzheimer's disease; depression; reduced brain function associated with aging; impaired vision; 0 Abnormalities in children fed diets low in EFAs or breast milk from mothers with insufficient levels of EFs); pregnancy complications; preeclampsia; prematurity; 0 Malnutrition; wasting states; seborrheic dermatitis; dry skin;	coagulation disorders; AIDS and immune deficiencies; reduced cell survival; impaired wound healing. Fatty Acid Abnormalities EF abnormalities may be caused by genetic disorders or by deficiencies/excesses of dietary fatty acids. Many genetic abnormalities which are associated with severe imbalances of EFAs can cause premature heart disease or abnormal lipid levels. People rarely develop severe EFA deficiency (EFAD) with signs such as scaling of the skin or hair loss, but most are deficient enough to develop chronic diseases. Severe EFAD is found in newborns and premature infants without enough EFAs, in small children fed diets low in EFAs, and in very thin patients who do not eat enough or have severe intestinal disease which interferes with fat absorption. Diagnoses of EF abnormalities Using the blood test EFA Status Report (EFA-SR™), a health provider can determine how to plan a diet to correct an imbalance or insufficiency of EFs. This test reveals which fatty acids are needed or should be avoided. When EF levels are low, w7, w9, and 16:1w7 increase. The ratio 20:3w9/20:4w6 = Trienoic/ Tetraenoic (T/T) also increases. Some nutritional deficiencies inhibit one's ability to make EFA derivatives. Here 20:3w9 does not increase, and T/T may go down. Current dietary intake of EFs is often insufficient. More than 25% of adults (+ many children and infants) have w6 EFA deficiencies and more than 50% have low w3 levels. People who have a greater deficiency of w3s than w6s should eat proportionately more w3s than w6s. EF abnormalities develop because people: Eat too much fat in their diets: SFAs, MUFAs, TFAs, or Medium Chain Triglycerides (MCT). The

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excessive fat makes it difficult for the blood to carry enough EFs to the body organs. Eat too many processed "low fat" foods (EFs are removed to extend shelf life). Eat too many calories from sugar-like substances: grains, cereals, pasta, low fat dairy products, fruit juices, pastries. [These diets can cause people to consume extra calories, because their bodies don't find the nutrients they need and continue to signal "hunger." Extra calories cause weight gain stored as SFA.] Eat fat substitutes or substances that interfere with fat absorption to lose weight. Have gastrointestinal disease with fat malabsorption; anorexia nervosa, or bulimia. Eat primarily infant formulas, adult liquid foods or food supplements without enough EFs. How much EFs do we need? Dr. Siguel suggests consuming about 1/3 gram EFs per kg of ideal body weight [20-30 grams per day for the average man that weighs 150 lbs; and 15-25 grams for the average woman that weighs 120 lbs]. The proportion of w3:w6 should be between 1:1 and 1:10. Because EFs accumulate in the body, one may eat more some days and less other days. There is huge variability in individual needs. The need for EFs increases with increased cell turnover (i.e. burns, pregnancy, gastrointestinal disease, inflammation, growth). Growing children and pregnant women need proportionately more EFs, particularly w3s, than average adults.	To reduce your chances of becoming deficient in EFs, you should eat more natural foods in their unprocessed state. These foods are high in cell membranes, which contain plenty of EFs and the appropriate antioxidants. Green vegetables, many seeds and oils such as soybean oil, flax, and wheat germ are often high in EFs. Fish, poultry & egg yolks contain mixtures of EFs. Lean meats and eggs from animals fed EF-rich feeds, such as EggsPlus from Pilgrim's Pride, are high in w3s and w6s. EFs can be added to spreads, desserts, baked products, salad dressings + many other foods. EF deficient patients need supplements of EF oils or EF-rich foods. Select one that has been properly processed, evaluated and shown to have a mixture of unaltered EFs. In general, the diet that works best for prevention or treatment of CAD may also work to prevent other diseases, including cancer. A low-fat diet can be healthy, but only when eating foods that are intrinsically low in fat and high in EFs. The treatment diet is designed to correct deficiencies identified by the fatty acid profile EFA-SR™, using foods and oil supplements. Eating more EFs using oil or oil extracts should be accompanied by increased amounts of antioxidants like Vits. E, C, Se & Beta Carotene. Website www.efafood.com This website contains links to manufacturers of foods rich in EFs and health-related sites, comments on nutritional articles, guidelines to diagnose and treat fatty acid abnormalities, and disease information for health professionals, news media and consumers.	Resources Natl Ctr Nutr & FA Res, Inc. Non-profit R&D + education on EFs. Tax deductible donations welcomed. PO Box 10187 dept C, Gaithersburg MD 20898
Major Fatty Acids & Their Pathways Essential Fats (EFAs + EFA Derivatives) Linolenic acid (18:3w3) ^delta 6 desaturase> 18:4w3 ^elongase> 20:4w3 ^delta 5 desaturase> 20:5w3 (EPA) ^elongase> 22:5w3 (DPA) ^delta 4 desaturase> 22:6w3 (DHA). ^Other pathways> 24:6w3*. Linoleic acid (18:2w6) ^delta 6 desaturase> 18:3w6 (GLA) ^elongase> 20:3w6 (DGLA) ^delta 5 desaturase> 20:4w6 (AA) ^elongase> 22:4w6 (adrenic) ^delta 4 desaturase> 22:5w6. ^Other pathways> 20:2w6* and 24:5w6*. Non-essential Unsaturated Fatty Acids (Not EFs) Made from dietary saturated fat, proteins, & carbohydrates 18:0 (stearic) ^delta 9 desaturase> Oleic acid (18:1w9 ***) ^delta 6 desaturase> 18:2w9** ^elongase> 20:2w9** ^delta 5 desaturase> 20:3w9* (Mead, ***) ^elongase> 22:3w9** ^delta 4 desaturase> 22:4w9**. ^Other pathways> 20:1w9 and 24:1w9. 16:0 (palmitic) ^delta 9 desaturase> 16:1w7*** Palmitoleic ^delta 6 desaturase> 16:2w7** ^elongase> 18:2w7** ^delta 5 desaturase> 18:3w7** ^elongase> 20:3w7**. ^Other pathways> 18:1w7. * = rare (pathways less active); ** = very rare. *** = increased with EF deficiency Indicators of EFAD: 20:3w9, 16:1w7. Fatty acids found in fish oils: EPA, DPA, DHA Pathways share enzymes. Enzyme preference explains relative amounts: w3 >w6 >w9 >w7 Compare concentrations vs. %, fig 4; FA1 vs. FA2, Fig 2, 3, 5

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Case History: Coronary Artery Disease (CAD) with hyperlipidemia + high trans fatty acids 48 y.o female, 15% overweight, with elevated cholesterol (TC), angina, mildly elevated markers of low EF status (indicating EF insufficiency), slightly reduced levels of EFs in blood (indicating EFA insufficiency), increased trans (TFAs), low levels of both w3s and w6s, reduced w3/w6, no family history of premature death. Recommendations. Reduce weight; avoid processed food (e.g. doughnuts, pastries); avoid beef and hydrogenated oils which contain TFAs. Because plasma concentrations of all fats are elevated (a consequence of hyperlipidemia), weight loss and a slight increase in PUFA intake will reduce plasma concentrations of SFAs and MUFAs. Only a slight increase in PUFA intake is needed, because the patient has a small deficit of EFs, some of which is often corrected with weight loss. If the deficit was high, or the patient were not losing weight, she would need to take more EFs. Treatment. 5 ml (about 1 tsp) of soybean oil, one tsp of flax seed oil (or 1 tbsp of flax seeds), and 100 I.U. Vit. E per day. This plan aims to decrease the TC/HDLC ratio, lower TC and TG, reduce platelet aggregation, cause increased blood fluidity, and reduce the risk of cardiovascular disease. A diet very low in TFAs is needed, to give the body time to burn its excessive TFAs. [If the patient did not have such high TFAs in his blood, we would not enforce a diet severely restricted in TFAs.] After the TFAs return to more reasonable levels, the patient can continue to eat foods with some TFAs, such as beef or baked foods made with hydrogenated oils. (We restrict beef rather than fish, poultry, turkey, or pork, because beef is usually higher in TFAs than other animal products. However, there are huge variations from one brand to another. Animals fed foods high in TFAs would themselves contain large amounts of TFAs.) Results. After three months, the patient returns for repeat blood testing. Depending on the test results of the fatty acid profile EFA-SR™, blood pressure, lipids (TC, HDL, TG) and weight, the patient is told to eat more or less calories, exercise more (if current program is not enough), and change the mixture of EFs to improve the ratio of ratio w3/w6 in the blood. For example, if TGs, HDL, and platelet coagulation are low, while blood pressure and w3s remain high, and the skin is dry, the patient may need more w6s. If TGs are still high, the patient may need more w3s.
References Siguel EN. Cancerostatic effect of vegetable diets. Nutr and Cancer, 4:285-289, 1983. Schaefer EJ, Rees DG, Siguel EN. Nutrition, Lipoproteins, and Atherosclerosis. Clinical Nutrition, 5:99-111, 1986. Siguel EN, Blumberg JB, Caesar J. Monitoring the Optimal Infusion of Intravenous Lipids: Detection of EFAD. Arch Path Lab Med. 110: 792-797, 1986. Siguel E, Maclure, M. Relative enzyme activity of unsaturated fatty acid metabolic pathways in humans, Metabolism, 36: 664-669, 1987. Siguel EN,Chee KM,Gong J,Schaefer EJ Criteria for EFA Deficiency in Plasma as assessed by Capillary Column GLC. Clin Chem, 1987;33:1869-1873. Warren SE, Siguel EN, et al.. Effects of cod liver oil on plasma lipids, eicosanoids, platelet aggregation, and exercise in stable angina pectoris. J. Applied Cardiology, 3(4):227-236, 1988. Siguel EN, Schaefer EJ. Aging & Nutritional Requirements of EFAs. In: Beare J, ed. Dietary Fats, AOCS, 1989. Chee KM, Gong JX, Rees DMG, Meydani M., Ausman L, Johnson J, Siguel EN, Schaefer EJ Fatty Acid Content of Marine Oil Capsules. Lipids 25, 1990:523-527. London SJ Sacks FM, Caesar J, Stampfer MJ, Siguel, EN, Willett, WC. FA Composition of Subcutaneous Adipose Tissue & Diet Among Postmenopausal US Women. Am.J.Clin.Nutr, 1991; 54:340-5. Siguel EN, Lerman, RH. TFA patterns in patients with angiographically doc. CAD. Am J Card 1993; 71:916-920. Siguel E, Lerman, R. FA Patterns in Patients With Angiographically docum. CAD. Metabolism 1994; 43:982-993.
	Siguel E. The role of EFAs in Health and Disease. Comprehensive Ther, Nutrition Issue. 1994; 20(9):500-510. Siguel E, Lerman RH. The role of EFAs: Dangers in the USDA dietary recommendations ("pyramid") and in low fat diets. Am. J Clin. Nut, 1994; 60:973-9; The role of EFAs: Reply to the USDA. Am J Clin. Nutr, 1995; 63:973-9. Siguel E, Lerman, RH. Fatty Acid Patterns in Patients With chronic intestinal disease. Metabolism. 1996; 45(1):12-23. (Jan) Siguel, E. A new relationship between PUFAs and TC/HDL Cholesterol. Lipids, 1996; 31, S51-S56. Siguel E. Dietary Sources of Long-Chain n-3 PUFAs. JAMA, 1996; 275:836. Siguel E, Lerman R. The effects of Low-Fat Diet on Lipid Levels. JAMA, 1996; 275:759. Siguel E, Lerman R, MacBeath, B. Low-Fat Diets for CHD: Perhaps, But Which One?. JAMA, 1996:275: 1402-1403. Siguel, E. Issues and problems in the design of foods rich in EFAs. Lipid Technology, 8(4):81-86, 1996. Siguel, E. Dietary Fat: How low can or should you go? Abstr Am. Oil. Chem Society annual meeting 1997. Articles featuring Siguel's research Brody J. Study suggests 2 FAs may help keep hearts healthy. NY Times, 9/24/94. New Twist: Very Low-Fat Diet May Imperil Heart. Chicago Trib, 8/24/94. Is too little fat bad for your health? Self Magazine, 9/94, p.48 Brandon, Richard, PhD. Is Low-Fat Eating Aging You? Longevity, 9/94. 10% of Population May Have EFA Shortage. The Nutrition Post, Fall 1994. Nash, JM. Is a Low-Fat Diet Risky? Time magazine,9/15/94, p.62. Vaughan, D. Fat-Free Diets can hurt your Heart. Your Health 11/94.	Key concepts *TC/HDLC decreases with increased PUFA intake; it increases with increased SFA or TFA intake. *The effects of various fats on TC/HDLC, one of the best risk markers for heart disease, follow this order: PUFA > MUFA > SFA > TFA. *Pathway activity: w3 >w6 >w9 >w7. *Weight gain (as saturated fat) = Calories In - Calories Burned. *Low fat diets, if low in PUFAs, may increase the risk of cardiovascular disease and reduce brain function.
		The fatty acid profile EFA-SR™ uses methods to diagnose fatty acid abnormalities which are covered by the US Patent No 5075101, "Method and Apparatus for Diagnosis of Fatty Acids or Lipid Abnormalities". The graphs and diagrams in this brochure are licensed from the patent holder. Use without prior written approval is not allowed.
			Warning/disclaimer: This simplified brochure is not intended to provide diagnosis or treatment advice. No representations, either express or implied, are made or given regarding the medical consequences of opinions herein presented. Each person is different, thus, these general guidelines may not apply to you.
			For information + references, read "Essential Fatty Acids in Health & Disease" by Edward Siguel MD PhD. To order, write Edward Siguel, PO Box 10187, Gaithersburg MD 20898-0187. Include $28.95 + $5.95 S&H priority mail, and a self-addressed mailing label). Purchases are non-refundable.
			Copyright 1997 by Edward Siguel. All rights reserved.