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The fatty acid profile EFA-SRÔ

 

Contents

 Rationale for measuring plasma Fatty Acid Profiles using the profile EFA-SRÔ.

 We need to treat EFA abnormalities for the same reasons that we treat abnormalities of other essential nutrients (B12, folate, iron, Mg, K, etc.)

 The diagnosis of abnormal EFA profiles leads to nutritional treatment that is likely to reduce those abnormalities.

 Plasma EFA profiles can identify individuals at risk for premature cardiovascular death.

 Distinguishing features of the fatty acid profile EFA-SRÔ.

 References

Rationale for measuring plasma Fatty Acid Profiles using the profile EFA-SRÔ

The purpose of the fatty acid profile EFA-SRä is to diagnose deficiencies of EFAs and EFA derivatives, abnormalities of fatty acid metabolism, imbalances of w3s vs. w6s, and excesses of harmful fatty acids such as trans fatty acids.

The fatty acid profile is medically necessary because these abnormalities cannot be diagnosed on clinical examination or by any other tests.

In contrast to many purely diagnostic tests such as ultrasound, PET scans, cholesterol, HDL, Lp(a), isoenzymes, apoproteins, genetic testing, the EFA profile determines the nature of the disorder, provides clues to its cause, and suggests the means to correct the abnormalities found. EFAs are vital nutrients the body must have for proper functioning. These nutrients come only from diet, the body is not capable of  making them from other substances. Diagnosing the type and extent of EF abnormalities gives immediate clues for proper  treatment. For example, while Apoproteins, blood pressure, and blood flow describe body status, “you cannot eat more or less of blood flow or apoproteins or blood pressure to change them” However, a person can eat more essential fats to correct a deficiency of essential fats.

There are more than 30 different types of fatty acids. Different diseases are associated with different types of fatty acid abnormalities.  They can only be corrected after having been diagnosed by a proper fatty acid profile. Numerous  studies have shown that EFA deficiencies or abnormalities, unless treated promptly and effectively, lead to abnormal cell function, abnormal cell histology, premature cell death (in organs like the heart, kidney, and brain), dermatitis, hair loss, cardiovascular disease, and neurological damage. For example, low blood levels of EFAs may damage the heart, because the body cannot make EFAs  needed for the optimal functioning of cell membranes.

We need to treat EFA abnormalities for the same reasons that we treat abnormalities of other essential nutrients (B12, folate, iron, Mg, K, etc)

EFAs are of special importance in nutrition because humans cannot synthesize them. Thus, they must be obtained from the diet in a manner similar to vitamins, but in far greater quantities. It is impossible to predict EFA status from clinical or nutritional intake data alone. EFA status depends on many factors, including EFA intake during a lifetime, intake of other nutrients (carbohydrates, protein, other fat), EFA utilization by the individual, cooking methods, and the extent of processing of the foods consumed (i.e., hydrogenation or isomer formation).

The amounts of EFAs used or needed by the body are determined by numerous factors including disease conditions, infection, burns, oxidation (caused by smoking or other factors), environmental temperature, accidents, and other lifetime variables that we cannot measure. Therefore, the only way to properly diagnose EFA abnormalities is by body tissue measures of fatty acids (i.e., plasma, red cell or adipose tissue fatty acid profiles).

The US Surgeon General's Report on Nutrition and Health identified the type of fat that people eat as being one of the most significant factors in health and disease. In recent years, studies have shown that EFA abnormalities are associated with a far wider range of clinical disorders than previously known. EFA abnormalities have been documented in patients at risk for nutritional deficiencies as well as in patients suffering from coronary heart disease (CHD), diabetes mellitus, hypertension, inflammatory bowel disease (IBD), dermatitis, brain dysfunction, and behavioral disorders. In addition, patients on unusual diets (such as parenteral alimentation or elemental diets), and patients who follow a low-fat diet, low in EFAs, for a prolonged period, are also at risk for developing EFA deficiency.

Using samples from the Framingham Heart Study, Dr. Siguel found that more than 25% of adults had biochemical evidence of w3 or w6 deficiency. At least 5% had deficiency so severe that it would reduce life expectancy and impair body function unless promptly treated.

The need to diagnose and treat EFA deficiencies was established more than 10 years ago and is now standard medical practice. Tens of thousands of patients have been treated with EFAs for EFA abnormalities. Many case studies have been published and presented at scientific meetings, such as the American Society for Parenteral and Enteral Nutrition and the International Society for the Study of Fatty Acids and Lipids. With the advent of parenteral alimentation and intravenous lipid infusions, it has become possible to treat EFA deficiencies even in individuals who suffer from fat malabsorption. As a result, the established protocols for total parenteral nutrition (TPN) require the use of intravenous lipid solutions rich in EFAs to prevent or treat EFA deficiencies.

The diagnosis of abnormal EFA profiles leads to nutritional treatment that is likely to reduce those abnormalities.

Fatty acid analysis is cost effective because it identifies both the problem and the solution. Optimal nutritional treatment is less expensive and often more effective than lifetime treatment with drugs. Addictive behaviors such as smoking, and entrenched cultural preferences such as physical inactivity, are difficult to change. In contrast, modifications to the balance of EFAs can be achieved by supplementing the diet with oil, oil capsules, or EFA-rich foods.

Using foods rich in EFAs to prevent and treat cardiovascular disease, high blood pressure, abnormal cholesterol levels, and other health problems could save billions of health care dollars and improve our overall quality of life.

The purpose of treatment is to bring the EFA profile of a patient closer to the profile of a healthy population.

EFAs are essential nutrients; therefore, eating more EFAs or their derivatives will increase the levels of these nutrients in the body. Individuals who cannot absorb fat well (such as patients with Crohn’s disease or Cystic Fibrosis) can receive these fats intravenously. The fatty acid profile helps determine whether individuals with fat malabsorption require infusions of intravenous lipids, and how often these lipids should be infused.

Shifting the EFA fatty acid profile of a person deficient in EFAs or with EFA imbalances closer to the EFA profile of a healthy person can lower the risk of cardiovascular disease and future organ failure. There are several other "incidental" benefits that can often be achieved by correcting EFA abnormalities. These include improvement in brain function and in skin texture. Dietary intervention studies have provided evidence that eating PUFA and fish oils reduces the risk of cardiovascular disease. It is also well established that increased dietary PUFA reduces the TC/HDLC ratio. A reduction in TC/HDLC leads to regression of CHD and reduces the risk of angiographic progression.

Plasma EFA profiles can identify individuals at risk for premature cardiovascular death.

Not only are abnormal plasma EFA profiles associated with biochemical risk of CHD, they are also directly associated with premature death from heart disease. It is well known that fatty acid abnormalities are found in patients with various types of atherosclerosis and in those with myocardial infarction. Patients who suffered sudden cardiac death were also found to have lower levels of polyunsaturated fatty acids (PUFAs) in their blood phospholipids.

Recently, researchers have shown that fatty acid patterns can predict myocardial infarction, and low dietary intake of linoleic acid predisposes one to myocardial infarction. In fact, linoleic acid in serum total lipids is the single most effective predictor of cardiovascular death in postinfarction middle-aged men. Thus, correction of abnormally low levels of EFAs has major clinical implications for heart disease and other disorders.

It would be unethical and a malpractice to withhold EFAs in a patient deficient in EFAs. Similarly, it could be unethical and a malpractice not to inform a patient that he/she needs to be tested for a likely fatty acid abnormality.

If we suspect that a patient has a deficiency of an essential nutrient (such as potassium or B12), we do a blood test to diagnose the deficiency. If we find that a patient has a deficiency, we give supplements of the specific nutrient. A doctor can easily prescribe the RDA of many nutrients without likely harm because the body either does not absorb or excretes the excessive (surplus) nutrients.

However, the same approach cannot be followed with EFAs. Patients with EFA abnormalities or deficiencies need to take supplements for many months, and often years. These supplements, equivalent to several tablespoons of oil per day, are difficult to take and must contain the proper balance of w3s and w6s. While it is possible to take a month’s requirement of some vitamins (such as vitamin B12) in one day, it is impossible to eat a gallon of oil in a day. For these reasons, correcting EFA abnormalities can take months to years and must be carefully monitored.

The purpose of treatment is to bring the EFA profile of a patient closer to the profile of a healthy population.

Distinguishing features of the fatty acid profile EFA-SRÔ.

1. The Fatty Acid Profile EFA-SRÔ provides percentages, ratios, and concentrations for fatty acids. The use of percentages and concentrations as reported in the Fatty Acid Profile EFA-SRÔ has been deemed unique and useful to receive the US Patent No. 5075101, "Method And Apparatus for Diagnosis of Fatty Acid or Lipid Abnormalities." These numbers are critical to the proper diagnosis of abnormalities caused by a Relative vs. an Absolute deficiency of EFAs. Relative deficiencies are in part caused by excessive amounts of saturated and monounsaturated fatty acids (SFAs and MUFAs). Such deficiencies often respond to weight loss in combination with moderate amounts of PUFA supplements to correct fatty acid imbalances. Absolute deficiencies require large quantities of EFAs to bring adipose tissue stores up to healthy levels. In some cases intravenous lipids are needed. For guidelines about the diagnosis of these abnormalities in patients with elevated plasma lipids, see Siguel and Lerman, "Fatty Acid Patterns in Patients With Angiographically Documented Coronary Artery Disease. Metabolism 1994; 43:982-993." For the diagnosis of these abnormalities in patients with low plasma lipids caused by fat malabsorption, such as Inflammatory Bowel Disease and Cystic Fibrosis, see Siguel and Lerman, "Fatty Acid Patterns in Patients with chronic intestinal disease". Metabolism 1996.

2. For many years, textbooks of medicine have referred to the trienoic/tetraenoic or 20:3w 9/20:4w 6 (Mead/Arachidonic acid), or "T/T" ratio, as a test or marker for EFA deficiency. Using older, less sensitive technologies, researchers established that T/T values above 0.2 or 0.4 are indicators of EFA deficiency (this is still reported in many medical publications). Using modern technology, Dr. Siguel reported that levels of T/T above 0.02 are indicative of insufficient EFA levels. In recent years, other markers of EFA status have been developed.  The fatty acid profile EFA-SRÔ uses highly sophisticated technology to achieve narrow ranges for healthy reference levels; therefore, it is able to detect the biochemical changes that characterize the early onset of EFA deficiency. It is important to diagnose and treat an EFA abnormality before it becomes severe and causes cell damage.

3. Fatty acids are analyzed using High Resolution Capillary Column Gas Liquid Chromatography (GLC). The method quantifies plasma levels of the major fatty acids, including the EFAs, linoleic and linolenic acid. Similar methods can be used with red cells or adipose tissue. The fatty acid profile EFA-SRÔ measures fatty acids of chain length C14 up to C24, including the EFAs, arachidonic acid, eicosapentaenoic acid (EPA), docosahexaenoic acid (DHA), the eicosanoid precursors and key trans fatty acids. Several profiles are available to include major saturated and monounsaturated (w 7 and w 9) fatty acids, the EFAs (linoleic and linolenic), EFA derivatives, total w 6 and w 3, including 20:5w 3 (EPA), 22:5w 3 and 22:6w 3 (DHA). In addition, different types of trans fatty acids associated with hydrogenated oils or other processed fats can be measured. A physician usually orders a profile with 25-30 major cis fatty acids, or one with the cis and several trans fatty acids.

4. The methods used to prepare the fatty acid profile EFA-SRÔ have been called "state of the art" by the review committees of the National Institute of Health. A laboratory technician spends many hours analyzing each sample to obtain adequate peak identification. It takes more than 5 hours to prepare chemical extracts from each sample, more than 3 hours to have each sample analyzed by GLC (compared with minutes needed for the analysis of other substances), and additional time to review the chromatogram to insure that each peak is properly integrated (i.e., that the amount of each substance is properly calculated). Considerable time is spent on quality control. It is important to measure both cis and trans fatty acids (TFAs). TFAs, which have been shown to contribute to cardiovascular disease and abnormal lipids, are very difficult to distinguish from contaminants or isomers.

5. The Fatty Acid Profile EFA-SRÔ provides comparative values of a patient’s results in relation to healthy subjects as well as to other patients. The data presented identifies a relative vs. an absolute deficiency, a classification of fatty acid abnormalities described in Dr. Siguel’s patent and several peer-reviewed publications. This classification is critical to optimal diagnosis and treatment. The report includes charts and tables, designed using software developed by Dr. Siguel, which illustrates whether a patient is considered to have a relative or absolute deficiency. 6. Relative excesses or deficiencies of one fatty acid alter the metabolism of the others. The Fatty Acid Profile EFA-SRÔ provides guidelines for further diagnostic testing of defects in the metabolic conversion of EFA precursors to derivatives. This aspect of the test is in part described in US Patent No. 5075101 and is critical for the treatment of several disorders. The movie "Lorenzo’s oil" explained the use of special fatty acids to prevent the formation of long chain saturated fatty acids, which lead to neurological damage in some patients. In those patients, excessive levels of very long chain saturated fatty acids and low levels of EFAs are characteristic of the disease.

Metabolic blocks can be diagnosed with this fatty acid profile. A metabolic block in the formation of EFA derivatives requires treatment with specific supplements to bypass the block. Metabolic blocks have been found in patients with various conditions, including diabetes mellitus, alcoholism and abnormal lipids. In addition to an absolute or relative deficiency of EFAs, most patients have an imbalance of w3 vs. w6 fatty acids, and an imbalance of EFA derivatives. The analysis of hundreds of patients and research subjects has revealed that imbalances of w3 vs. w6 fatty acids or fatty acid excesses require that one compare the levels of EFA derivatives for each level of the EFA precursors. See a physician’s guide to the diagnosis of EFA abnormalities by Siguel: "Essential and Trans Fatty Acid Metabolism in Health and Disease." Nutrition Issue. Contemporary Therapy, 1994; 20(9):500-510.

7. The Fatty Acid Profile EFA-SRÔ relies on an extensive database of test results from research subjects as well as patients with unusual metabolic problems. To our knowledge, nobody else has access to a similar database.

8. The Fatty Acid Profile EFA-SRÔ is based on reference values developed from subjects without known disease, as well as samples from a population group with "normal" lipid levels. The reference levels provide 5, 10, 25, 50, 75, 90 and 95 percentiles for cis and trans fatty acids. These values allow physicians to compare a patient with other subjects.

9. Research has identified the fatty acid profiles associated with abnormal TC/HDLC ratios, with high triglycerides, with low HDL, with diabetes mellitus, and with various other health conditions. Depending of the results of each profile, specific guidelines are provided to determine the mixture of fatty acids that are likely to lower TC/HDLC ratios towards values associated with a reduced risk of heart disease.

10. Individualized reports are prepared for each patient, leading to specific treatment recommendations by  a health provider.

References

Rivers JPW, Frankel TL. Essential fatty acid deficiency. Br Med Bull 37(1):59-64, 1981.
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; 60:973-9.
U.S. Department of Health and Human Services, PHS publication No. 88-50210, 1988.
Siguel, EN. Essential and Trans Fatty Acid Metabolism in Health and Disease. Comprehensive Therapy, 1994; 20(9):500-510.
Siguel E. Cost-Effectiveness of Modern Nutrition Care vs. Conventional Treatment for Hyperlipidemia and Cardiovascular Disease. International Conference on Health Policy Research, Health Outcomes Meeting, Am. Statistical Association, Mass. General Hospital, Boston, 1995.
Kingsbury KJ, Brett C, Stovold R, Chapman A, Anderson J, Morgan DM (1974). Abnormal fatty acid composition and human atherosclerosis. Postgraduate Med J 50,425-440.
Kingsbury KJ (1970). Polyunsaturated fatty acids and myocardial infarction. Lancet i,648-676.
Luostarinen R, Boberg M, Saldeen T (1993). Fatty acid composition in total phospholipids of human coronary arteries in sudden cardiac death. Atherosclerosis 99,187-193.
Miettinen TA, Naukkarinen V, Huttunen JK, Mattila S, Kumlin T (1982). Fatty-acid composition of serum lipids predicts myocardial infarction. Brit Med J 285,993-6.
Simpson HCR, Barker K, Carter RD, Cassels E, and Mann JI (1982). Low dietary intake of linoleic acid predisposes to myocardial infarction. Br. Med.J. 285,683.
Valek J, Hammer J, Kohout M, Grafnetter D, Vondra K, Topinka V (1985). Serum linoleic acid and cardiovascular death in postinfarction middle-aged men. Atherosclerosis 54,111-118.
Siguel E, Blumberg JB, Caesar J. Monitoring the Optimal Infusion of Intravenous Lipids: Detection of Essential Fatty Acid Deficiency. Archives of Pathology and Laboratory Medicine. 110: 792-797, 1986.
Harris WS. Fish oils and plasma lipid and lipoprotein metabolism in humans: a critical review. J Lipid Res; 1989: 30,785-807.
Horrobin DF, Manku MS. How do polyunsaturated fatty acids lower plasma cholesterol levels?. Lipids; 1983:18,558-562.
Warren SE, Siguel EN, Gervino E, Salzman EW, Smith M, Silverman KJ, Pasternak RC (1988). Effects of cod liver oil on plasma lipids, eicosanoids, platelet aggregation, and exercise in stable angina pectoris. J Applied Cardiology, 3(4),227-236.
Superko HR, Krauss RM (1994). Coronary Artery Disease Regression. Convincing evidence for the Benefit of Aggressive Lipoprotein Management. Circulation 90,1056-1069.
Paterson RW, Paat JJ, Steele GH, Hathaway SC, Wong JG (1994). Impact of Intensive Lipid Modulation on Angiographically Defined Coronary Disease: Clinical Implications. Southern Medical J 87,236-242.

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© 1998 Edward N. Siguel. All rights reserved
© 1999 Edward N. Siguel. All rights reserved
© 2000 Edward N. Siguel. All rights reserved

modified 1/15/00