Could Coconut Oil be nature’s answer to Tamiflu?
The current Swine Flu pandemic is like nothing ever experienced before. The illness is milder but this strain is more infectious than previous ones. The government has made a tremendous effort to make the Tamiflu antiviral available and the media has played its part in galvanising the population into hysteria and a sense of panic. So how good is Tamiflu which offers about a 20% reduction in severity and duration of infection. Are there any side effects to cause concern and is there an alternative? The answer to both of these questions is yes.
The public perception is that all saturated fats are bad for you - and many of them are. However, recent research (not widely publicised in the press) shows some saturated fats are essential and give a huge boost to the immune system. One such example is Coconut oil which, although it contains high levels of saturated fat, these are part of a group known as MCTs (medium chain triglycerides). Coconut Oil is not something new and has been known to have health promoting properties and no side effects for about nearly 4000 years. Rural communities in places like Indonesia and Thailand, with no sanitation or fresh water supply rely on up to 60% of their daily energy requirements from coconuts. Yet, despite meagre diets young children play in murkey canals and infested river waters remaining apparently happy, healthy and free of infection.
The same cannot be said about the Tamiflu experience in Japan. A “New Scientist” Health report dated 18 November 2005 states that 12 children taking Tamiflu had died and 32 others were reported to suffer neuropsychiatric events such as hallucination, convulsions and brain inflammation. By 2007 of 54 identifiable deaths reported, 18 were of children dying of self-destructive behaviour; mostly aged between 10 and 19 years. As a result Tokyo’s Ministry of Health issued a warning not to give Tamiflu to patients aged between 10 and 19 because of irrational behaviour (Times on line 21st March 2007). One 14 year old after taking two tablets straddled the balcony of an eleventh floor apartment and, despite his mother’s warning cries fell to his death. Another 17 year old walked to his death in front of a truck, in a blizzard, wearing only pyjamas. According to the driver he was smiling at the moment of impact. During the same three year period 36 adult deaths were considered due to specific organ failures. These are worrying figures since Japan has to date, prescribed more than 60% of the world’s supply of Tamiflu. Europe and the US have decided this difference may be due to neuropsychiatric events associated with some cases of influenza in general and not to Tamiflu - evidence of this link however is thin. With Tamiflu not yet widely prescribed in the UK it is still too early to say what effects may be uncovered.
The truth on Tamiflu will only become clear as Swine Flu spreads. Looking at an alternative however there is now good scientific evidence that most of the fats in Coconut oil have strong complementary antimicrobial properties which will help you to fight off infection. In 1994, a US patent was granted for development of the most active antiviral ingredient, “monolaurin” which can now be obtained as a concentrate. Published data from the same research group describe these concentration dependent benefits as cumulative indicating regular consumption could provide a substantial level of protection. The first clinical trial in the Philippines in 2000 showed Coconut oil to be more effective in reducing HIV virus load in AIDs patients than monolaurin capsules. The antiviral in Coconut oil is only effective against viruses with a fatty coat which includes Swine Flu virus. This may, therefore, be a safer alternative, particularly for children and young adults given the current time frame for a massive increase in spread in Swine Flu later this year. Of course the benefits do not stop at Swine Flu as the antimicrobial protection works against a wide variety of infections.
Coconut Oil is not the only substance to contain the good MCT fats – other common sources include mother’s milk. butter and cream.
Ultimately we must all make up our own minds on how to protect ourselves from the almost inevitable bout of Swine Flu in the coming winter. By introducing some good fat into your diet you may be able to fight off the infection that much better.
Tuesday, 4 August 2009
Saturday, 1 August 2009
Health Benefits of Coconut Oil
Will Coconut Oil Protect You Against Swine Flu’?
Scientific Assessment of Evidence (2009)
The health promoting activity of coconut oil was recognized in Ayurvedic medicine almost 4000 years ago. It was valued for its ability to nourish the body, increase body strength and to protect the skin from bacterial, protozoal and viral infections and promote luxurious hair growth. The first scientific evidence of antimicrobial activity to appear was a report by Chester1 in 1940 that showed oleic acid in soaps could inactivate epidemic influenza virus. The first major break through came from Karbara’s group (Karbara, 1978, 1985, and 1990, 2,3,4) and Sands (1978,5). After non-productive screening of some 300 synthetic lipids for antimicrobial activity Karbara decided to investigate the natural lipids in tropical oils and mother’s milk and showed that only they possessed real healing powers, described as miraculous, and their research identified the most active species was monolaurin, which possesses a broad range of antimicrobial activity without any evidence of toxicity or side effects,1
The main antimicrobial fatty acids in coconut oil are myristic, caprylic, capric and lauric acids which can provide the body with biologically active monoglycerides. Lauric acid is the most abundant (> 50%) and most potent as an antiviral agent. A similar array of these saturates is found in mother’s milk. Butter provides about 12% as lauric acid which is found in all dairy products. Furthermore, all four acids provide protection against a wide range of pathogenic bacteria, fungi and protozoa and are a vital protective component in mother’s milk during the first six months while newborns develop independent immune responses. A mother whose diet is short of saturates will produce underweight offspring more prone to a variety of infections.
Coconut oil has a saturated fat content in excess of 92%. The caprylic, capric and lauric acids total more than 60% and belong to a sub group of saturates known as medium chain fatty acids (MCT’s) which are now known to be easily solubilised and absorbed through intestine mucosa and transported directly to the liver. They do not to enter the cholesterol transport system. Instead they provide a rapid and immediate source of energy, cell membrane repair and new cell growth to epithelial cells throughout the body. Very little is deposited as fat in adipose cells
In 1987 Thormar,6 demonstrated that short chain and long chain saturated fatty acids possessed little or no antiviral effects whereas medium chain saturated and certain long chain unsaturated fats were highly active against enveloped viruses. Viral inactivation varied by as much as 20-fold after enzyme conversion of these fatty acids into monoglycerides; formed during storage of human milk at 4C. The most active substance, monolaurin; a monoglyceride of lauric acid was shown to be released in our bodies, primarily by salivary lipases. Patents were granted in the US in 1989 (Bistrian)7, 1989 (Hierholzer and Kabara)8 and in 1989 and 1994 to Isaac’s group. The last relates more specifically to development of substances which kill enveloped viruses, (Isaacs 1994)9. The viruses listed include influenza, measles and herpes group viruses which include the AIDs virus.
Viruses use our own DNA or RNA to reproduce and, in the case of enveloped viruses, our own fats to form their outer coat. Monolaurin interferes with this process without preventing viral RNA or protein synthesis; a process accompanied by a nine fold increase in cellular synthesis of triacylglycerols. These are thought to bind to cell membrane preventing virus maturation and release (Hornung 1994)10. Lauric acid effects are dose dependent, cumulative and total concentrations critical (Isaacs and Thormar 1990) suggesting regular availability is needed from the diet.
The results from a small trial in 2001,11 suggests that coconut oil is, if anything, more effective in reducing viral loads in HIV patients than monolaurin capsules. Further studies are in progress. Evidence of its immunity boosting effects is reviewed by Enig and Fallon 12,13. This is particularly evident in native communities who derive up to 60% of their energy from coconuts, are exposed to high levels of parasite and bacterial agents because of poor sanitation and untreated water,12 yet still have healthy, smiling children swimming the murky waters of Bangkok’s canals.
References:
1. Chester C, Francis, T. J Exp Med 1940:71, 661-668
2. Karbara, JJ. “Fatty Acids and Derivatives as Antimicrobial Agents – A review in The Pharmacological Effects of Lipids” (Karbara JJ, ed). American Oil Chemists’ Society, Champaign IL, 1978
3. Pharmacological Effects of Lipids Volumes 1,2, and 3 edited by JJ Karbara, AOCS Press, Champaign Illinois, 1978, 1985, 1990, respectively
4. Karbara JJ. Inhibition of staphylococcus aureus in ‘The Pharmacological Effects of Lipids II (JJ Karbara, ed) American Oil Chemists’ Society Champaign IL, 1985, pp. 71-75
5. Sands JA, Auperin DD, Landin PD, Reinhardt A, Cadden SP. Antiviral effects of fatty acids and derivatives: lipid-containing bacteriophages as a model system in ‘The Pharmacological Effects of Lipids (JJ Karbara, ed) American Oil Chemists’ Society Champaign IL, 1978, pp 75-95
6. Thormar H, Isaacs CE, Brown HR, PessollanoT. Inactivation of enveloped viruses and killing of cells by fatty acids and monoglycerides. Antimicrobial Agents and Chemotherapy 1987; 31: 27-31
7. Bistrian BR, Babayan VK, Blackburn GL. Kernel oils and disease treatment. US Patent No: 4,810,726, 1989
8. Hierholzer JC, Karbara JJ. In vitro effects of monolaurin compounds on enveloped RNA and DNA viruses. J Food Safety 1982; 4: 1-12 US Patent No: 4841023 1989
9. Isaacs CE, Kim KS, Thormar H. Inactivation of enveloped viruses in human bodyily fluids by purified lipids. Annals of the New York Academy of Sciences 1994; 724: 457-464
10. Hornung B, Amtmann E, Sauer G. Lauric acid inhibits the maturation of vesicular stomatitis virus. Journal of General Virology 1994; 75: 353-361
11. Dayrit, CS, Presentation to 37th Cocotech Meeting, India, March 5th 2001, see: http://www.lauric.org/
12. Enig MG. Address to the APPC. Coconut: In support of good health in the 21st century. 2000 www.cocniutresearchcentre.org/article10147.htm
13. Fallon, S. Enig. MG, “Thailand – Land of the Coconut”, Price-Pottinger Nutrition Foundation Health Journal, 1999, 22: No 4.
Scientific Assessment of Evidence (2009)
The health promoting activity of coconut oil was recognized in Ayurvedic medicine almost 4000 years ago. It was valued for its ability to nourish the body, increase body strength and to protect the skin from bacterial, protozoal and viral infections and promote luxurious hair growth. The first scientific evidence of antimicrobial activity to appear was a report by Chester1 in 1940 that showed oleic acid in soaps could inactivate epidemic influenza virus. The first major break through came from Karbara’s group (Karbara, 1978, 1985, and 1990, 2,3,4) and Sands (1978,5). After non-productive screening of some 300 synthetic lipids for antimicrobial activity Karbara decided to investigate the natural lipids in tropical oils and mother’s milk and showed that only they possessed real healing powers, described as miraculous, and their research identified the most active species was monolaurin, which possesses a broad range of antimicrobial activity without any evidence of toxicity or side effects,1
The main antimicrobial fatty acids in coconut oil are myristic, caprylic, capric and lauric acids which can provide the body with biologically active monoglycerides. Lauric acid is the most abundant (> 50%) and most potent as an antiviral agent. A similar array of these saturates is found in mother’s milk. Butter provides about 12% as lauric acid which is found in all dairy products. Furthermore, all four acids provide protection against a wide range of pathogenic bacteria, fungi and protozoa and are a vital protective component in mother’s milk during the first six months while newborns develop independent immune responses. A mother whose diet is short of saturates will produce underweight offspring more prone to a variety of infections.
Coconut oil has a saturated fat content in excess of 92%. The caprylic, capric and lauric acids total more than 60% and belong to a sub group of saturates known as medium chain fatty acids (MCT’s) which are now known to be easily solubilised and absorbed through intestine mucosa and transported directly to the liver. They do not to enter the cholesterol transport system. Instead they provide a rapid and immediate source of energy, cell membrane repair and new cell growth to epithelial cells throughout the body. Very little is deposited as fat in adipose cells
In 1987 Thormar,6 demonstrated that short chain and long chain saturated fatty acids possessed little or no antiviral effects whereas medium chain saturated and certain long chain unsaturated fats were highly active against enveloped viruses. Viral inactivation varied by as much as 20-fold after enzyme conversion of these fatty acids into monoglycerides; formed during storage of human milk at 4C. The most active substance, monolaurin; a monoglyceride of lauric acid was shown to be released in our bodies, primarily by salivary lipases. Patents were granted in the US in 1989 (Bistrian)7, 1989 (Hierholzer and Kabara)8 and in 1989 and 1994 to Isaac’s group. The last relates more specifically to development of substances which kill enveloped viruses, (Isaacs 1994)9. The viruses listed include influenza, measles and herpes group viruses which include the AIDs virus.
Viruses use our own DNA or RNA to reproduce and, in the case of enveloped viruses, our own fats to form their outer coat. Monolaurin interferes with this process without preventing viral RNA or protein synthesis; a process accompanied by a nine fold increase in cellular synthesis of triacylglycerols. These are thought to bind to cell membrane preventing virus maturation and release (Hornung 1994)10. Lauric acid effects are dose dependent, cumulative and total concentrations critical (Isaacs and Thormar 1990) suggesting regular availability is needed from the diet.
The results from a small trial in 2001,11 suggests that coconut oil is, if anything, more effective in reducing viral loads in HIV patients than monolaurin capsules. Further studies are in progress. Evidence of its immunity boosting effects is reviewed by Enig and Fallon 12,13. This is particularly evident in native communities who derive up to 60% of their energy from coconuts, are exposed to high levels of parasite and bacterial agents because of poor sanitation and untreated water,12 yet still have healthy, smiling children swimming the murky waters of Bangkok’s canals.
References:
1. Chester C, Francis, T. J Exp Med 1940:71, 661-668
2. Karbara, JJ. “Fatty Acids and Derivatives as Antimicrobial Agents – A review in The Pharmacological Effects of Lipids” (Karbara JJ, ed). American Oil Chemists’ Society, Champaign IL, 1978
3. Pharmacological Effects of Lipids Volumes 1,2, and 3 edited by JJ Karbara, AOCS Press, Champaign Illinois, 1978, 1985, 1990, respectively
4. Karbara JJ. Inhibition of staphylococcus aureus in ‘The Pharmacological Effects of Lipids II (JJ Karbara, ed) American Oil Chemists’ Society Champaign IL, 1985, pp. 71-75
5. Sands JA, Auperin DD, Landin PD, Reinhardt A, Cadden SP. Antiviral effects of fatty acids and derivatives: lipid-containing bacteriophages as a model system in ‘The Pharmacological Effects of Lipids (JJ Karbara, ed) American Oil Chemists’ Society Champaign IL, 1978, pp 75-95
6. Thormar H, Isaacs CE, Brown HR, PessollanoT. Inactivation of enveloped viruses and killing of cells by fatty acids and monoglycerides. Antimicrobial Agents and Chemotherapy 1987; 31: 27-31
7. Bistrian BR, Babayan VK, Blackburn GL. Kernel oils and disease treatment. US Patent No: 4,810,726, 1989
8. Hierholzer JC, Karbara JJ. In vitro effects of monolaurin compounds on enveloped RNA and DNA viruses. J Food Safety 1982; 4: 1-12 US Patent No: 4841023 1989
9. Isaacs CE, Kim KS, Thormar H. Inactivation of enveloped viruses in human bodyily fluids by purified lipids. Annals of the New York Academy of Sciences 1994; 724: 457-464
10. Hornung B, Amtmann E, Sauer G. Lauric acid inhibits the maturation of vesicular stomatitis virus. Journal of General Virology 1994; 75: 353-361
11. Dayrit, CS, Presentation to 37th Cocotech Meeting, India, March 5th 2001, see: http://www.lauric.org/
12. Enig MG. Address to the APPC. Coconut: In support of good health in the 21st century. 2000 www.cocniutresearchcentre.org/article10147.htm
13. Fallon, S. Enig. MG, “Thailand – Land of the Coconut”, Price-Pottinger Nutrition Foundation Health Journal, 1999, 22: No 4.
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
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:
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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
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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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