Wednesday, 29 July 2009

Lipids in Health and Disease

Do Fats Really Matter?
The Importance of Lipid Balance in Health and Disease

At the turn of the 20th century improved sanitation and housing reduced levels of mortality from infectious diseases. Death rates from heart disease in the USA were 10% or less and far lower than from tuberculosis and pneumonia. By 1950 the incidence of coronary heart disease (CHD) had rose to 30% and by 1960 mortality from myocardial infarction (MI), virtually non-existent in 1910, increased from 3,000 recorded in 1930 to around 500,000. Over a similar time scale butter consumption declined by more than 50%, margerine consumption rose 4-fold and the use of vegetable oils for cooking and shortenings in biscuits and other baked goods increased 400% as the food industry switched from coconut and palm oils to those derived from a variety of seeds such as cotton and corn using processes which introduced trans fats into diets (Enig 1990 1, 1995,2). Within four decade’s, under the influence of agricultural groups, the health of nations was changed and government agencies introduced dietary guidelines to limit consumption of saturated fats; now considered unhealthy.

A modernised form of the lipid hypothesis, first described in 1856 3, suggesting that saturated fats and cholesterol are the cause of heart disease was proposed by Duff,4; apparently endorsing the work of Kritchevsky (1954, 5) and supported by Keys,6. Previously, atherogenesis was recognised as a normal part of the aging process and current levels of CHD did not exist. However, in 1964 Garrett, 7 noted that cholesterol levels did not relate to the distribution and severity of atherosclerosis in 1700 surgically treated patients. Nor did the cumulative frequency values of serum levels cited in their report, differ remarkably from those reported by others; including Key’s. Controversy continued into the 1990’s when a report by Lakland, 8 showed that high levels of dietary fat do not increase cholesterol levels and several population surveys were unable to provide information to support these claims, 9,10. Furthermore, in 1969 Shorland, 11 showed that fatty acid (FA) distribution in the adipose tissue of Polynesians reflected dietary intakes and that serum cholesterol levels remained low, despite a high saturated fat intake; mostly from coconut oil. Prior, 12 confirmed these findings in 1981 while Pitskhelauri, 13 noted in 1982 that the long-lived inhabitants of Georgia, Russia, who eat the most fat, live the longest. Yet the Seven Countries Study, 14, published 1995, concluded that saturated and trans fats and dietary cholesterol were important determinants in developing CHD. This data, however, based on analysis of food data on dietary intakes of 12,763 middle aged men from seven different countries between 1958 and 1964, had been ‘re-constructed’ to reflect the fatty acid content in their diets because detailed information about these FAs was not available from the original data pool. This was during a period when trans fats in average diets were at their highest levels; up to 37g/day in the USA.

Saturated fats, like the unsaturates, are not a single family but consist of subgroups defined according to the number of carbons in the fatty acid chain. Short chain triglycerides contain 2- 6 carbons (SCT’s), medium chain 8 -12 (MCT’s) and long chain 14 – 24 (LCT’s). Each subgroup differs in metabolic, biological and pharmacological functions depending on the binding locations of one (mono-), two (di-) or three (tri-) glycerides each of which can be derived from fatty acids of different lengths binding to the same molecule of glycerol. Unsaturated fatty acids are defined according to the number of hydrogen bonds introduced into the chain. Monounsaturated fats (MUFA’s – omega 9) contain one unsaturated hydrogen molecule, the rest are defined as polyunsaturated (PUFA’s) with the position of the extra hydrogens’ denoted according their position in the chain (omega-3; fish oils and omega-6; vegetable oils). Saturated fats are very stable, unlike unsaturates, which can be dehydrogenated to form trans fats. Structurally, these are mirror images of the unsaturated fatty acids from which they were derived (the ‘cis’ form). These can be incorporated into cell membranes making them less rigid, more prone to lipid oxidation and reduction and nutrient transfer less efficient.

Short and medium chain fatty acids are absorbed directly through gut epithelium and transported via the portal vein to the liver to provide an immediate source of energy for new cell membranes and repair around the body. Only LCT’s are involved in the cholesterol transport system and able to contribute to heart disease or influence cholesterol metabolism and levels. Studies showing the harmful effects of so-called ‘tropical oils’ were generally carried out in the absence of essential fatty acids (EFA). During the past 10 years analysis of lipid oxidation pathways have shown that the ratio of n-3 to n-6 PUFA’s is crucial in determining the way we store and release energy from fat tissues and burn off excess fat. In a diet rich in MCTs available n-3 PUFA modulates the release of LCT’s deposited in adipose tissue making significant weight loss, 15,16 possible by natural means.

The body produces its own cholesterol through a highly regulated process (Jones, 199717). Increased meal frequency patterns reduce levels of synthesis and consumption of foods rich in polyunsaturated fats, while reducing serum cholesterol levels and increasing the rate cholesterol synthesis compared with other fats. Dietary sources of cholesterol found in powdered milk, eggs, and in meats and fats heated to high temperatures during cooking are, however, associated with oxidised lipids found in atherogenesis, 18 and a higher proportion of deposited unsaturates to saturates (Felton, 19, 1994). The role of dietary fat in assessing coronary risk in the Strong Heart Study and its comparison with results from 17 other major studies spanning 30years by Xu et al in 2006, 20 demonstrate the difficulties in establishing relational significances. Future progress to unravel such levels of contradiction within the published literature seems now more dependent upon studies which analyse the balance of dietary fat sub groups able to modify fat metabolism, as discussed earlier.

There is also interesting and mounting evidence of the benefits of sterols and stanols. These are a plant’s equivalent of cholesterol and interfere with intestinal cholesterol absorbance and lower total and LDL cholesterol. Serum levels are found to be inversely related to the overall rate of cholesterol synthesis (Miettinen and Gylling 1999, 21). Useful amounts are found in nuts, seeds, grains and unprocessed vegetable oils. High levels found in wheat germ seem to be particularly effective (Ostund 2003, 22). Sterols also possess anti-oxidation, anti-inflammatory and anti-atherosclerotic activities which combine to provide significant protection against CHD and a variety of cancers. However, vegetable oil quality varies. In a report by Pederson, 23 rapeseed oil is now shown to be more beneficial in this regard than olive oil.

One clear way forward would be to re-assess food labelling laws and nutritional dietary guidelines. In 2003 Canada introduced labelling of trans fats. The subsequent study by Freisen, 24 on human milk over two years showed that consumption of trans fats dropped from 4 to 2.2g/day. The USA introduced this change in 2004. Yet again the UK has failed to recognise the true facts behind fats and there is now an urgent need to introduce a comprehensive strategy to eliminate trans fats from our diets through education, food labelling and new legislation which, time will show, would likely prevent tens of thousands from CHD and the continued increase in levels of obesity and diabetes; with real savings in health and support costs.

Medium chain fatty acids provide many health benefits including reduced onset of atherogenesis and aging25 and it is time to recognise the real value of tropical oils. In the words of Kabara26, “our body, similar to our car, may be in need of an oil change if we want it to function properly and to reach our optimum health”.


References:

1. Enig, MG, et al, “Isomeric Trans Fatty Acids in the U.S Diet”, J Am College of Nutrition, 1990, 9:471- 86
2. Enig, MG, Trans Fatty Acids in the Food Supply: A Comprehensive Report Covering 60 Years of Research, 2nd Edition, Enig Associates, Inc, Silver Spring, MD, 1995 pp 4-8
3. Virchow, R ‘Phlogose und Thrombose im Gefassystem. In: Gesammelte Abhandlungen zur wissenschaftlichen Medizin. Frankfurt 1856
4. Duff, GL, McMillan, GC. “Pathology of Atherosclerosis”. American Journal of Medicine, 1951, 11: 92 - 108
5. Kritchevsky, D et al, “Effect of Cholesterol Vehicle in Experimental Atherosclerosis”, Am J Physiology, 1954, 178: 30-32
6. Keys, A, “Atherosclerosis: a problem in newer public health” Journal of the Mount Sinai Hospital, New York. 20: (2): 118-39. PMID 13085148
7. Garrett, HE, et al. “Serum Cholesterol Values in Patients Treated Surgically for Atherosclerosis”. JAMA. 1964, 189: 655-59
8. Lakland, DT, Wheeler, FC, “The Need for Accurate Nutrition Survey Methodology: The South Carolina Experience1,2 “. Journal of Nutrition, 1990, 120: 1437 – 39
9. Kang-Jey Ho, et al, “Archeology Pathology”, 1972, 91: 387
10. Mann GV et al, American Journal of Epidemiology, 1972, 95: 26 – 37
11. Shorland, FB, et al, “Studies on the Fatty Acid Composition of Adipose Tissue and Blood Lipids in Polynesians1,2 “, American Journal of Clinical Nutrition, 1969, 22: 594 – 605
12. Prior, IA, et al, “Cholesterol, coconuts and Diet on Polynesian Atolls: a natural experiment: the Pukapuka and Tokelau Island Studies” , American Journal of Clinical Nutrition1981, 34: 1552 -1561
13. Pitskhelauri, GZ, “The longest living of Georgia”, 1982, Human Sciences Press, New York, NY
14. Kromhout, D et al., “Dietary Saturated and Trans Fatty Acids and Cholesterol and 25-year Mortality from Coronary Heart Disease: The Seven Countries Study”, Preventive Medicine , 1995, 24: 308 -315
15. Beermann, C et al., “Short Term Effects of Dietary Medium-Chain Fatty Acids and n-3 Long Chain Polyunsaturated Fatty Acids on the Fat Metabolism of Healthy Volunteers”, 2003, 2: http://www.lipidworld.com/content/2/1/10
16. St-Onge, MP, Jones, PJH, “Greater Rise in Fat Oxidation with Medium-Chain Triglyceride Consumption Relative to Long-Chain Triglyceride is Associated with Lower Initial Body Weight and Greater Loss of Subcutaneous Adipose Tissue”, International Journal of Obesity, 2003, 27: 1565 -1571
17. Jones, PJH, “ Regulation of Cholesterol Biosynthesis by Diet in Humans1,2 “, American Journal of Nutrition, 1997, 66: 438 – 446
18. Addis, Paul, Food and Nutrition News, 1990, 62; 7 – 10
19. Felton, CV, “Dietary Polyunsaturated Fatty Acids and Composition of Human Aortic Plaques”, The Lancet, 1994, 344: 1195 – 1196
20. Xu, J et al., “Dietary Fat Intake and Risk of Coronary Heart Disease: The Strong Heart Study1-4., American Journal of Nutrition, 2006, 84: 894 -902
21. Mietttinen, TA, Gylling, H, “Regulation of Cholesterol Metabolism by Dietary Plant Sterols”, Current Opinions in Lipidology, 1999,10: 9 – 14
22. Ostund, RE, Racette, SB, Stensen, WF, “ Inhibition of Cholesterol Absoption by Phytosterol-replete Wheat Germ Compared with Phytosterol-Depleted Wheat Germ “, American Journal of Nutrition, 2003, 77: 1385 -1389
23. Pederson, A et al., “An Olive Oil-Rich Diet Results in Higher Concentrations of LDL Cholesterol and a Higher Number of LDL Subfraction Particles than Rapeseed Oil and Sunflower Oil Diets”, Journal of Lipid Research, 2000, 41:1901 – 1911
24. Freisen, R, Innis, SM, “Trans Fatty Acids in Human Milk in Canada Declined with the Introduction of Trans Fat Food Labelling” Journal of Nutrition, 2006, 136: 2558 -2561
25. Dean, W, English, J “Medium Chain Triglycerides (MCT’s): Beneficial Effects on Energy, Atherosclerosis and Aging” http://www.nutritionreview.org/library/mcts.phpKabara, JJ, “Health Oils from the Tree of Life (Nutritional and Health Aspects of Coconut Oil)”, http://www.apccsec.org/document/Kabara.pdf

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