Fw: [Mr_Tracys_Corner] The Health Benefits Of Coconuts & Coconut Oil. Part 2 of 2

[Guest guest]

- Walt

Tracys

Thursday, October 14, 2004 9:42 AM

[Mr_Tracys_Corner] The Health Benefits Of Coconuts & Coconut Oil. Part 2 of 2

SEARCH:HOME | CURRENT ISSUE | BACK ISSUES | ARTICLES | SUBSCRIBE | PRODUCTS |ADVERTISING | WHO, WHAT, WHERE | LINKS | COMMENTS | SURVEYThe Health Benefits of Coconuts & Coconut OilPart 2 of 2Scientific research proves that the saturated fatty acids and derivativecompounds found in coconuts and coconut oil have significant benefits for ahealthy immune system and metabolism.(Go to Part 1)--Extracted from Nexus Magazine, Volume 9, Number 3 (April-May 2002)PO Box 30, Mapleton Qld 4560 Australia. editorTelephone: +61 (0)7 5442 9280; Fax: +61 (0)7 5442 9381From our web page at: www.nexusmagazine.comby Mary G. Enig, PhD, FACN© 1999, 2001DirectorNutritional Sciences DivisionEnig Associates, Inc.12501 Prosperity Drive, Suite 340 Silver Spring, MD 20904-1689, USATelephone: +1 (301) 680 8600Fax: +1 (301) 680 8100Email: marye--(The following is the text of a talk and paper, "Coconuts: In Support ofGood Health in the 21st Century", presented by Dr Mary Enig at the AsianPacific Coconut Community (APCC) meeting held in Pohnpei in the FederatedStates of Micronesia in 1999. Note that it does make several references toanimal experiments, and that NEXUS does not condone animalexperimentation. --Editor)VI. THE LATEST ON THE TRANS FATTY ACIDSBoth the United States and Canada will soon require labelling of the transfatty acids, which will put coconut oil in a more competitive position thanit has been in the past decade. (In 2001, Canada published examples of thelabels it plans to use, while the US is still to finalise its labels.)A fear of the vegetable oil manufacturers has always been that they wouldhave to label trans fatty acids. The producers of trans fatty acids haverelied on the anti-saturated fat crusade to protect their markets. However,the latest research on saturated fatty acids and trans fatty acids shows thesaturated fatty acids coming out ahead in the health race.It has taken a decade, from 1988 to 1998, to see changes in perception.During this period, the trans fatty acids have taken a deserved drubbing.Research reports from Europe have been emerging since the seminal report byMensink and Katan in 1990 that the trans fatty acids raised the low-densitylipoprotein (LDL) cholesterol and lowered the high-density lipoprotein (HDL)cholesterol in serum. This has been confirmed by studies in the US (Judd etal., 1994; Khosla and Hayes, 1996; Clevidence, 1997).In 1990, the Lipids Research Group at the University of Maryland published apaper (Enig et al., 1990) correcting some of the erroneous data sponsored bythe food industry in the 1985 review of the trans fatty acids by the LifeSciences Research Office of the Federation of American Societies forExperimental Biology (LSRO-FASEB) (Senti, 1985).In 1993, a group of researchers at Harvard University, led by ProfessorWalter Willett, reported a positive relationship between the dietary intakeof the trans fatty acids and coronary heart disease in a greater than 80,000cohort of nurses who had been followed by the School of Public Health atHarvard University for more than a decade.Pietinen and colleagues (1997) evaluated the findings from the large cohortof Finnish men who were followed in a cancer prevention study. Aftercontrolling for the appropriate variables including several coronary riskfactors, the authors observed a significant positive association between theintake of trans fatty acids and the risk of death from coronary disease.There was no association between the intake of saturated fatty acids ordietary cholesterol and the risk of coronary death. This is another exampleof the differences between the effects of the trans fatty acids and thesaturated fatty acids, and a further challenge to the dietary cholesterolhypothesis.The issue of the trans fatty acids as a causative factor in cancer remainsunderexplored, but recent reports have found a connection. Bakker andcolleagues (1997) studied the data for the association between breast cancerincidence and linoleic acid status across European countries, since animaland ecological studies had suggested a relationship. They found that themean fatty acid composition of adipose did not show an association withomega-6 linoleic acid and breast, colon or prostate cancer. However, cancersof the breast and colon were positively associated with the trans fattyacids. Kohlmeier and colleagues (1997) also reported that data from theEURAMIC study showed adipose tissue concentration of trans fatty acidshaving a positive association with postmenopausal breast cancer in Europeanwomen.In 1995, a British documentary on the trans fatty acids was aired on a majortelevision station in the UK. This documentary included an exposé of thebattle between the edible oil industry and some of the major researchers ofthe trans fatty acids. Just this year [1999], this same documentary wasaired on television in France, where it had been requested by a majortelevision station. Several of the early researchers into the transproblems, including Professor Fred Kummerow and Dr George Mann, havecontinued their research and/or writing (Kummerow, 1999, 2000; Mann, 1994,2000). The popular media have continued to press the issue of the amounts oftrans in foods, for which there are still no comprehensive governmentdatabases.A recently published paper from a US Department of Agriculture researcherstates: "Because trans fatty acids have no known health benefits and strongpresumptive evidence suggests that they contribute markedly to the risk ofdeveloping CHD, the results published to date suggest that it would beprudent to lower the intake of trans fatty acids in the US diet" (Nelson,1998).Professor Meir Stampfer from Harvard University refers to trans fats as "oneof the major nutritional issues of the nation", contending that "they have alarge impact" and that "we should completely eliminate hydrogenated fatsfrom the diet" (Gottesman, 1998).Lowering the trans fatty acids in foods in the US can only be done byreturning to the use of the natural, unhydrogenated and more saturated fatsand oils.Predictions can be made regarding the future of trans fatty acids. Ourability to predict has been pretty good; for example, when Enig Associatesstarted producing the marketing newsletter Market Insights, written by EricEnig, we predicted that trans fatty acids would eventually be swept out ofthe market. It appears that this prediction may be close to coming true.Also in the early 1990s, Market Insights predicted that the Center forScience in the Public Interest (CSPI) would change its mind about the transfatty acids, which it had spent years defending. CSPI did change its mind,and in fact went on the attack regarding the trans, but CSPI never admittedthat it had originally been promoting trans or that the high levels of transfatty acids found in the fried foods in fast food and other restaurants andin many other foods are directly due to CSPI lobbying. While its change waswelcome, CSPI's revisionist version of its own history of support ofpartially hydrogenated oils and trans fatty acids would have fittedperfectly into George Orwell's Nineteen Eighty-Four.VII. COMPARISON OF SATURATED FATS WITH THE TRANS FATSThe statement that trans fatty acids are like saturated fatty acids is notcorrect for biological systems. A listing of the biological effects ofsaturated fatty acids in the diet versus the biological effects of transfatty acids in the diet is in actuality a listing of the good (saturated)versus the bad (trans).When one compares the saturated fatty acids and the trans fatty acids, wesee that:1) saturated fatty acids raise HDL cholesterol, the so-called "goodcholesterol", whereas the trans fatty acids lower HDL cholesterol (Mensinkand Katan, 1990; Judd et al., 1994);2) saturated fatty acids lower the blood levels of the atherogeniclipoprotein (a), whereas trans fatty acids raise the blood levels oflipoprotein (a) (Khosla and Hayes, 1996; Hornstra et al., 1991; Clevidenceet al., 1997);3) saturated fatty acids conserve the elongated omega-3 fatty acids(Gerster, 1998), whereas trans fatty acids cause the tissues to lose theseomega-3 fatty acids (Sugano and Ikeda, 1996);4) saturated fatty acids do not inhibit insulin binding, whereas trans fattyacids do inhibit insulin binding;5) saturated fatty acids are the normal fatty acids made by the body andthey do not interfere with enzyme functions such as the delta-6-desaturase,whereas trans fatty acids are not made by the body and they interfere withmany enzyme functions such as delta-6-desaturase; and6) some saturated fatty acids are used by the body to fight viruses,bacteria and protozoa and they support the immune system, whereas transfatty acids interfere with the function of the immune system.VIII. WHAT ABOUT THE UNSATURATED FATS?The arteries of the heart are also compromised by the unsaturated fattyacids. When the fatty acid composition of the plaques (atheromas) in thearteries has been analysed, the level of saturated fatty acids in thecholesterol esters is only 26% compared to that in the unsaturated fattyacids, which is 74%. When the unsaturated fatty acids in the cholesterolesters in these plaques are analysed, it is shown that 38% arepolyunsaturated and 36% are mono-unsaturated. Clearly, the problem is notwith the saturated fatty acids.As an aside, you need to understand that the major role of cholesterol inheart disease and cancer is as the body's repair substance and thatcholesterol is a major support molecule for the immune system, an importantantioxidant and a necessary component of neurotransmitter receptors. Ourbrains do not work very well without adequate cholesterol. It should beapparent to scientists that the current approach to cholesterol has beenwrong.The pathway to cholesterol synthesis starts with a molecule of acetyl CoA[coenzyme A] that comes from the metabolism of excess protein-formingketogenic amino acids and from the metabolism of excess carbohydrates aswell as from the oxidation of excess fatty acids. Grundy in 1978 reportedthat the degree of saturation of the fat in the diet did not affect the rateof synthesis of cholesterol. However, research reported by Jones in 1997showed that the polyunsaturated fatty acids in the diet increase the rate ofcholesterol synthesis relative to other fatty acids. Furthermore, researchreported in 1993 (Hodgsons et al.) showed that dietary intake of the omega-6polyunsaturated fatty acid, linoleic acid, was positively related tocoronary artery disease.Thus, those statements made by the consumer activists in the United States,to the effect that the saturated fatty acids increase cholesterol synthesis,are without any foundation.What happens when there is an increase or a decrease of cholesterol in theserum is more like a shift from one compartment to another as the body triesto rectify the potential damage from the excess polyunsaturated fatty acids.Research by Dr Hans Kaunitz (1978) clearly showed the potential problemswith excess polyunsaturated fatty acids.IX. RESEARCH SHOWING BENEFICIAL EFFECTS OF EATING THE MORE SATURATED FATSOne major concern expressed by the nutrition community is related to whetheror not people are getting enough elongated omega-3 fatty acids in theirdiets. The elongated omega-3 fatty acids of concern are eicosapentaenoicacid (EPA) and docosahexaenoic acid (DHA). Some research has shown that thebasic omega-3 fatty acid, linolenic acid, is not readily converted to theelongated forms in humans or animals, especially when there is ingestion ofthe trans fatty acids and the consequent inhibition of thedelta-6-desaturase enzyme. One recent study (Gerster, 1998), which usedradioisotope-labelled linolenic acid to measure this conversion in adulthumans, showed that if the background fat in the diet was high in saturatedfat, the conversion was approximately 6% for EPA and 3.8% for DHA; whereas,if the background fat in the diet was high in omega-6 polyunsaturated fattyacids (PUFA), the conversion was reduced 40-50%.Nanji and colleagues (1995) reported that a diet enriched with saturated butnot unsaturated fatty acids reversed the alcoholic liver injury in theiranimals which was caused by dietary linoleic acid. These researchersconcluded that this effect may be explained by the down-regulation of lipidperoxidation. This is another example of the need for adequate saturated fatin the diet.Cha and Sachan (1994) studied the effects of saturated fatty acid andunsaturated fatty acid diets on ethanol pharmacokinetics. The hepatic enzymealcohol dehydrogenase and plasma carnitines were also evaluated. Theresearchers concluded that dietary saturated fatty acids protect the liverfrom alcohol injury by retarding ethanol metabolism, and that carnitine maybe involved.Hargrove and colleagues (1999) noted the work of Nanji et al. and postulatedthat they would find that diets rich in linoleic acid would also cause acuteliver injury after acetaminophen injection. In the first experiment, twolevels of fat (15g/100g protein and 20g/100g protein), using corn oil orbeef tallow, were fed. Liver enzymes indicating damage were significantlyelevated in all the animals except for those animals fed the higher level ofbeef tallow. These researchers concluded that "diets with high [linoleicacid] may promote acetaminophen-induced liver injury compared to diets withmore saturated and mono-unsaturated fatty acids".X. RESEARCH SHOWING GENERAL BENEFICIAL EFFECTS FROM CONSUMING COCONUT OILResearch that compares the feeding of coconut oil with other oils to answera variety of biological questions is increasingly finding beneficial resultsfrom the coconut oil.Obesity is a major health problem in the United States and the subject ofmuch research. Several lines of research dealing with metabolic effects ofhigh-fat diets have been followed. One study used coconut oil to enrich ahigh-fat diet and the results reported were that the "coconut oil-enricheddiet is effective in...[producing]...a decrease in white fat stores"(Portillo et al., 1998).Cleary et al. (1999) fed genetically obese animals high-fat diets of eithersafflower oil or coconut oil. Animals fed safflower oil had higher hepaticlipogenic enzyme activities than did animals fed coconut oil. When thenumber of fat cells was measured, the safflower oil fed also had more fatcells than the coconut oil fed.Many of the feeding studies produce results at variance with the popularconception. High-fat diets have been used to study the effects of differenttypes of fatty acids on membrane phospholipid fatty acid profiles. When sucha study was performed on mice, the phospholipid profiles were similar fordiets high in linoleic acid from high-linoleate sunflower oil relative todiets high in saturated fatty acids from coconut oil. However, those animalsfed diets high in oleic acid (from the high-oleate sunflower oil) or high inelongated omega-3 fatty acids (from menhaden fish oil) were not onlydifferent from the other two diets, but they also resulted in enlargedspleens in the animals (Huang and Frische, 1992).Oliart-Ros and colleagues (1998) at the Instituto Tecnológico de Veracruz,Mexico, reported on effects of different dietary fats on sucrose-inducedcardiovascular syndrome in rats. The most significant reduction inparameters of the syndrome was obtained by the n-3 PUFA-rich diet. Theseresearchers reported that the diet thought to be PUFA-deficient presented atissue lipid pattern similar to the n-3 PUFA-rich diet (fish oil), whichsurprised and puzzled them. When the researchers were questioned, it turnedout that the diet was not really PUFA-deficient, but rather just a normalcoconut oil (nonhydrogenated) which conserved the elongated omega-3 andnormalised the omega-6 to omega-3 balance.A recent study measured the effect of high-fat diets, fed for more thanthree months to neonatal pigs, on the HMG-CoA reductase enzyme's functionand gave some surprises. There were two feeding protocols: one with theadded cholesterol and one without added cholesterol, but both with coconutoil. The hepatic reductase activity, which was the same in all groups at thebeginning of the feeding on the third day and similar on the 42nd day, wasincreased with and without added cholesterol on the 13th day and thendecreased on the 25th day. The data were said to suggest that dietarycholesterol suppressed hepatic reductase activity in the young pigsregardless of their genetic background, that the stage of development was adominant factor in its regulation, and that both dietary and endogenouslysynthesised cholesterol were used primarily for tissue building in veryyoung pigs (McWhinney et al., 1996). The feeding of coconut oil did not inany way compromise the normal development of these animals.When compared with feeding coconut oil, feeding two different soybean oilsto young females caused a significant decrease in HDL cholesterol. Bothsoybean oils, one of which was extracted from a new mutant soybean thoughtto be more oxidatively stable, were not protective of the HDL levels (Lu etal., 1997).Trautwein et al. (1997) studied cholesterol-fed hamsters on different oilsupplements for plasma, hepatic and biliary lipids. The dietary oilsincluded butter, palm stearin, coconut oil, rapeseed oil, olive oil andsunflowerseed oil. Plasma cholesterol concentrations were higher (9.2millimoles/litre) for olive oil than for coconut oil (8.5 mmol/L), hepaticcholesterol was highest in the olive oil group, and none of the diet groupsdiffered for biliary lipids. Even in this cholesterol-sensitive animalmodel, coconut oil performed better than olive oil.Smit and colleagues (1994) had also studied the effect of feeding coconutoil compared with feeding corn oil and olive oil in rats, and measured theeffect on biliary cholesterol. Bile flow was not different between the threediets, but the hepatic plasma membranes showed more cholesterol and lessphospholipid from corn and olive oil feeding relative to coconut oilfeeding.Several studies (Kramer et al., 1998) have pointed out problems with canolaoil feeding in newborn piglets, which results in a reduction in the numberof platelets and alteration in their size. There is concern for similareffects in human infants. These undesirable effects can be reversed whencoconut oil or other saturated fat is added to the feeding regimen (Krameret al., 1998).Research has shown that coconut oil is needed for good absorption of fat andcalcium from infant formulas. The soy oil (47%) and palm olein (53%) formulagave 90.6% absorption of fat and 39% absorption of calcium, whereas the soyoil (60%) and coconut oil (40%) gave 95.2% absorption of fat and 48.4%absorption of calcium (Nelson et al., 1996). Both fat and calcium are neededby the infant for proper growth. These results clearly show the folly ofremoving or lowering the coconut oil content in infant formulas.XI. RESEARCH SHOWING A ROLE FOR COCONUT IN ENHANCING IMMUNITY AND MODULATINGMETABOLIC FUNCTIONSCoconut oil appears to help the immune system response in a beneficialmanner. Feeding coconut oil in the diet completely abolished the expectedimmune factor responses to endotoxin that were seen with corn oil feeding.This inhibitory effect on interleukin-1 production was interpreted by theauthors of the study as being largely due to a reduced prostaglandin andleukotriene production (Wan and Grimble, 1987). However, the damping may bedue to the fact that effects from high omega-6 oils tend to be normalised bycoconut oil feeding.Another report from this group (Bibby and Grimble, 1990) compared theeffects of corn oil and coconut oil diets on tumour necrosis factor-alphaand endotoxin induction of the inflammatory prostaglandin E2 (PGE2)production. The animals fed coconut oil did not produce an increase in PGE2,and the researchers again interpreted this as a modulatory effect thatbrought about a reduction of phospholipid arachidonic acid content.Another study from the same research group (Tappia and Grimble, 1994) showedthat omega-6 oil enhanced inflammatory stimuli, but that coconut oil, alongwith fish oil and olive oil, suppressed the production of interleukin-1.Several recent studies are showing additional helpful effects of consumingcoconut oil on a regular basis, thus supplying the body with the lauric acidderivative, monolaurin. Monolaurin and the ether analogue of monolaurin havebeen shown to have the potential for damping adverse reactions to toxicforms of glutamic acid (Dave et al., 1997). Lauric acid and capric acid havebeen reported to have very potent effects on insulin secretion (Garfinkel etal., 1992). Using a model system of murine splenocytes, Witcher et al.(1996) showed that monolaurin induced proliferation of T-cells and inhibitedthe toxic shock syndrome toxin-1 mitogenic effects on T-cells.Monserrat and colleagues (1995) showed that a diet rich in coconut oil couldprotect animals against the renal necrosis and renal failure produced by adiet deficient in choline (a methyl donor group). The animals had less or nomortality and increased survival time as well as decreased incidence orseverity of the renal lesions when 20% coconut oil was added to thedeficient diet. A mixture of hydrogenated vegetable oil and corn oil did notshow the same benefits.The immune system is complex and has many feedback mechanisms to protect it,but the wrong fat and oils can compromise these important mechanisms. Thedata from the several studies show the helpful effects of coconut fat.Additionally, there are anecdotal reports that consumption of coconut isbeneficial for individuals with the chronic fatigue and immune dysfunctionsyndrome known as CFIDS.XII. US PATENTS FOR MEDICAL USES OF LAURIC OILS, MEDIUM-CHAIN FATTY ACIDSAND THEIR DERIVATIVES SUCH AS MONOLAURINA number of patents have been granted in the United States for medical usesof lauric oils, lauric acid and monolaurin. Although one earlier patent wasgranted to Professor Kabara more than three decades ago, the rest of thesepatents have been granted within the past decade.In 1989 a patent was issued to the New England Deaconess Hospital (Bistrianet al., 1989) for the invention titled "Kernel Oils and Disease Treatment".This treatment requires lauric acid as the primary fatty acid source, withlauric oils constituting up to 80% of the fat in the diet "using naturallyoccurring kernel oils".In 1991 and 1995, two patents were issued to the group of researchers whosework has been reviewed above.The first invention (Isaacs et al., 1991) was directed to antiviral andantibacterial activity of both fatty acids and monoglycerides, primarilyagainst enveloped viruses. The claims are for "a method of killing envelopedviruses in a host human...wherein the enveloped viruses are AIDSviruses...[or]...herpes viruses...[and the]...compounds selected from thegroup consisting of fatty acids having from 6 to 14 carbon atoms andmonoglycerides of said fatty acids...[and]...wherein the fatty acids aresaturated fatty acids".The second patent (Isaacs et al., 1995) was a further extension of theearlier one. This patent also includes discussion of the inactivation ofenveloped viruses, and it specifically cites monoglycerides of caproic,caprylic, capric, lauric and myristic acids. These fatty acids make up morethan 80% of coconut oil. Also included in this patent is a listing ofsusceptible viruses and some bacteria and protozoa.Although these latter patents may provide the owners of the patents with theability to extract royalties from commercial manufacturers of monoglyceridesand fatty acids, they cannot require royalties from the humangastrointestinal tract when it is the "factory" that is doing themanufacturing of the monoglycerides and fatty acids.Clearly, though, these patents serve to illustrate to us that thehealth-giving properties of monolaurin and lauric acid are well recognisedby some individuals in the research arena, and they lend credence to ourappropriate choice of lauric oils for promoting health and as an adjuncttreatment of viral diseases.XIII. HOW CAN WE GET SUFFICIENT COCONUT FAT INTO THE FOOD SUPPLY?I would like to review for you my perception of the status regarding thecoconut and coconut products markets in the United States and Canada at theend of the 20th century and the beginning of the 21st century.Coconut products are trying to regain their former place in several smallmarkets. The extraction of oil from fresh coconut has been reported in thepast decade and my impression is that this is being considered as adesirable source of minimally processed oil with desirable characteristicsfor the natural foods market.There have been some niche markets for coconut products developing duringthe past half-decade. These are represented primarily by the natural foodsand health foods producers. Some examples are the new coconut buttersproduced in the US and Canada by Omega Nutrition and Carotec, Inc. And thisis no longer as small a market as it has been in past years. Desiccatedcoconut products, coconut milk and even coconut oil are appearing on theshelves of many of these markets. After years of packaging coconut oil forskin use only, one of the large suppliers of oils to the natural foods andhealth foods stores has introduced coconut oil for food use, and it hasappeared within the last few months on shelves in the Washington, DC,metropolitan area, along with other oils. I believe I indirectly hadsomething to do with this turn of events.XIV. CONCLUSIONS AND RECOMMENDATIONSThere is much to be gained from pursuing the functional properties ofcoconut for improving the health of humanity.On the occasion of the 30th anniversary of the Asian Pacific CoconutCommunity, at this 36th meeting of APCC, I wanted to bring you a messagethat I hope will encourage you to continue your endeavours on behalf of allparts of the coconut industry. Coconut products for inedible and especiallyedible uses are of the greatest importance for the health of the entireworld.Some of what I have been telling you, most of you already know. But insaying these things for the record, it is my intention to tell those who didnot know all the details until they heard or read this paper about thepositive properties of coconut.Coconut oil is a most important oil because it is a lauric oil. The lauricfats possess unique characteristics for both food industry uses and also forthe uses of the soaps and cosmetics industries. Because of the uniqueproperties of coconut oil, the fats and oils industry has spent untoldmillions to formulate replacements from those seed oils so widely grown inthe world outside the tropics. While it has been impossible to trulyduplicate coconut oil for some of its applications, many food manufacturershave been willing to settle for lesser quality in their products. Consumershave also been willing to settle for a lesser quality, in part because theyhave been fed so much misinformation about fats and oils.Desiccated coconut, on the other hand, has been impossible to duplicate, andthe markets for desiccated coconut have continued. The powdered form ofdesiccated coconut now being sold in Europe and Asia has yet to find amarket in the United States, but I predict that it will become anindispensable product in the natural foods industry. Creamed coconut, whichis desiccated coconut very finely ground, could be used as a nut butter.APCC needs to promote the edible uses of coconut, and it needs to promotethe re-education of the consumer, the clinician and the scientist. Theresearcher H. Thormar (Thormar et al., 1999) concluded his abstract with thestatement that monocaprin "is a natural compound found in certain foodstuffssuch as milk and is therefore unlikely to cause harmful side effects in theconcentrations used". It is not monocaprin that is found in milk, but capricacid. It is likely safe at most any level found in food. However, the levelin milk fat is at most 2%, whereas the level in coconut fat is 7%.One last reference for the record. Sircar and Kansra (1998) have reviewedthe increasing trend of atherosclerotic disease and type-2 diabetes mellitusin the Indians from both the subcontinent of India and abroad. They notethat over the time when there has been an alarming increase in theprevalence of these diseases, there has been a replacement of traditionalcooking fats with refined vegetable oils that are promoted asheart-friendly, but which are being found to be detrimental to health. Theseastute researchers suggest that it is time to return to the traditionalcooking fats like ghee, coconut oil and mustard oil.There are a number of areas of encouragement. The nutrition community in theUnited States is slowly starting to recognise the difference betweenmedium-chain saturated fatty acids and other saturated fatty acids. Wepredict now that the qualities of coconut, both for health and foodfunction, will ultimately win out.--About the Author:Dr Mary G. Enig holds an MS and PhD in Nutritional Sciences from theUniversity of Maryland in the USA. She is a consulting nutritionist andbiochemist of international renown and an expert in fats/oils analysis andmetabolism, food chemistry and composition and nutrition and dietetics.Dr Enig is Director of the Nutritional Sciences Division of Enig Associates,Inc., President of the Maryland Nutritionists Association and a Fellow ofthe American College of Nutrition. She is also Vice President of the WestonA. Price Foundation and Science Editor of the Foundation's publication. DrEnig has many years of experience as a lecturer and has taughtgraduate-level courses for the Nutritional Sciences Program at theUniversity of Maryland, where she was a Faculty Research Associate in theLipids Research Group, Department of Chemistry and Biochemistry, Universityof Maryland. She also maintains a limited clinical practice for patientsneeding nutritional assessment and consultation.Dr Enig has extensive experience consulting and lecturing on nutrition toindividuals, medical and allied health groups, the food processing industryand state and federal governments in the US. She also lectures and acts as aconsultant to the international health and food processing communities.Since 1995 she has been invited to make presentations at scientific meetingsin Europe, India, Japan, Vietnam, Indonesia, the Philippines and Micronesia.Dr Enig is the author of numerous journal publications, mainly on fats andoils research and nutrient/drug interactions. She also wrote the book KnowYour Fats (Bethesda Press, Silver Spring, MD, May 2000). She is a popularmedia spokesperson and was an early critic speaking out about the use oftrans fatty acids and advocating their inclusion in nutritional labelling.One of Dr Enig's recent research topics dealt with the development of anutritional protocol for proposed clinical trials of a non-drug treatmentfor HIV/AIDS patients. Her articles, "The Oiling of America" and "Tragedyand Hype: The Third International Soy Symposium", written with nutritionist/researcher Sally Fallon, were published in NEXUS 6/01 6/02 and 7/03respectively.References: a.. Aveywardena MY and Charnock JS. Dietary lipid modification ofmyocardial eicosanoids following ischemia and reperfusion in the rat. Lipids1995;30:1151-1156. b.. Awad AB. Effect of dietary lipids on composition and glucoseutilization by rat adipose tissue. Journal of Nutrition 1981;111:34-39. c.. Bakker N, Van't Veer P, Zock PL. Adipose fatty acids and cancers ofhte breast, prostate and colon: an ecological study. EURAMIC Study Group.International Journal of Cancer 1997;72:587-591. d.. Bergsson G, Arnfinnsson J, Karlsson SM, Steingrimsson O, Thormar H. Invitro inactivation of Chlamydia trachomatis by fatty acids andmonoglycerides. Antimicrobial Agents and Chemotherapy 1998;42:2290-2294. e.. Bibby DC, Grimble RF. Tumour necrosis factor-alpha and endotoxininduce less prostaglandin E2 production from hypothalami of rats fed coconutoil than from hypothalami of rats fed maize oil. Clinical Science (Colch)1990;79:657-62. f.. Bierenbaum JL, Green DP, Florin A, Fleishman AI, Caldwell AB.Modified-fat dietary management of the young male with coronary disease: afive-year report. Journal of the American Medical Association1967;202:1119-1123. g.. Blackburn GL, Kater G, Mascioli EA, Kowalchuk M, Babayan VK, BistrianBR. A reevaluation of coconut oil's effect on serum cholesterol andatherogenesis. The Journal of the Philippine Medical Association1989;65:144-152. h.. Boddie, RL and Nickerson, SC. Evaluation of postmilking teatgermicides containing Lauricidin, saturated fatty acids, and lactic acid.Journal of Dairy Science 1992;75:1725-1730. i.. Castelli WP. Editorial: Concerning the possibility of a nut. Archivesof Internal Medicine 1992;152:1371-2. j.. Cha YS, Sachan DS. Opposite effects of dietary saturated andunsaturated fatty acids on ethanol-pharmacokinetics, triglycerides andcarnitines. Journal of the American College of Nutrition 1994;13:338-343. k.. Chen A, Li W, Yang Y. [Detection of human cytomegalovirus DNA invascular plaques of atherosclerosis by in situ hybridization] (translationfrom Chinese). Chung Hua I Hsueh Tsa Chih 1995;10:592-593, 638. l.. Cleary MP, Phillips FC, Morton RA. Genotype and diet effects in leanand obese Zucker rats fed either safflower or coconut oil diets. Proceedingsof the Society for Experimental Biology and Medicine 1999;220:153-161. m.. Clevidence BA, Judd JT, Schaefer EJ, Jenner JL, Lichtenstein AH,Muesing RA, Wittes J, Sunkin ME. Plasma lipoprotein (a) levels in men andwomen consuming diets enriched in saturated, cis-, or trans-mono-unsaturatedfatty acids. Arterioscler Thromb Vasc Biol 1997;17:1657-1661. n.. Cohen LA, Thompson DO, Maeura Y, Choi K, Blank M, Rose DP. Dietary fatand mammary cancer. I. Promoting effects of different dietary fats onN-nitrosomethylurea-induced rat mammary tumorigenesis. Journal of theNational Cancer Institute 1986;77:33. o.. Cohen LA, Thompson DO, Choi K, Blank M, Rose DP. Dietary fat andmammary cancer. II. Modulation of serum and tumour lipid composition andtumour prostaglandins by different dietary fats: Association with tumourincidence patterns. Journal of the National Cancer Institute 1986;77:43. p.. Crouch AA, Seow WK, Whitman LM, Thong YH. Effect of human milk andinfant milk formulae on adherence of Giardia intestinalis. Transactions ofthe Royal Society of Tropical Medicine and Hygiene 1991;85:617-619. q.. Dave JR, Koenig ML, Tortella FC, Pieringer RA, Doctor BP, Ved HS.Dodecylglycerol provides partial protection against glutamate toxicity inneuronal cultures derived from different regions of embryonic rat brain.Molecular Chemistry and Neuropathology 1997;30:1-13. r.. Dodge JA and Sagher FA. Antiviral and antibacterial lipids in humanmilk and infant formula. Archives of Disease in Childhood 1991;66:272-273. s.. Ellis RW. Infection and coronary heart disease. Journal of MedicalMicrobiology 1997;46:535-539. t.. Enig MG. Diet, serum cholesterol and coronary heart disease, in MannGV (ed): Coronary Heart Disease: The Dietary Sense and Nonsense. JanusPublishing, London, 1993, pp 36-60. u.. Enig, MG. Lauric oils as antimicrobial agents: theory of effect,scientific rationale, and dietary applications as adjunct nutritionalsupport for HIV-infected individuals. In Nutrients and Foods in AIDS (RRWatson, ed), CRC Press, Boca Raton, 1998, pp 81-97. v.. Enig MG, Atal S, Sampugna J and Keeney M. Isomeric Trans Fatty Acidsin the US Diet. Journal of the American College of Nutrition 1990;9:471-486. w.. Epstein SE, Speir E, Zhou YF, Guetta E, Leon M, Finkel T. The role ofinfection in restenosis and atherosclerosis: focus on cytomegalovirus.Lancet 1996;348 Supplement 1:S13-17. x.. Eraly MG. IV. Coconut oil and heart attack. Coconut and Coconut Oil inHuman Nutrition, Proceedings. Symposium on Coconut and Coconut Oil in HumanNutrition, 27 March 1994. Coconut Development Board, Kochi, India, 1995, pp63-64. y.. Felton CV, Crook D, Davies MJ, Oliver MF. Dietary polyunsaturatedfatty acids and composition of human aortic plaques. Lancet1994;344:1195-1196. z.. Fletcher RD, Albers AC, Albertson JN, Kabara JJ. Effects ofmonoglycerides on Mycoplasma pneumoniae growth. In The PharmacologicalEffect of Lipids II (JJ Kabara, ed), American Oil Chemists' Society,Champaign, IL, 1985, pp 59-63. aa.. Florentino RF, Aquinaldo AR. Diet and cardiovascular disease in thePhilippines. The Philippine Journal of Coconut Studies 1987;12:56-70. ab.. Garfinkel M, Lee S, Opara EC, Akkwari OE. Insulinotropic potency oflauric acid: a metabolic rational for medium chain fatty acids (MCF) in TPNformulation. Journal of Surgical Research 1992;52:328-333. ac.. Gerster H. Can adults adequately convert alpha-linolenic acid(18:3n-3) to eicosapentaenoic acid (20:5n-3) and docosahexaenoic acid(22:6n-3)? International Journal of Vitamin and Nutrition Research1998;68:159-173. ad.. Gottesman S. Making Sense of Shortenings. Baking Buyer August 1998,pp 45-49. ae.. Grundy SM. Cholesterol metabolism in man, Western Journal of Medicine128:13;1978. af.. Halden VW, Lieb H. Influence of biologically improved coconut oilproducts on the blood cholesterol levels of human volunteers. Nutr Dieta1961;3:75-88. ag.. Hargrove JL, Hwang J, Wickwire K, Liu J. Diets with corn oil orsoybean oil increase acute acetaminophen hepatotoxicity compared to dietswith beef tallow. The FASEB Journal 1999;13:A222, Abstract 204.1. ah.. Hashim SA, Clancy RE, Hegsted DM, Stare FJ. Effect of mixed fatformula feeding on serum cholesterol level in man. American Journal ofClinical Nutrition 1959;7:30-34. ai.. Hegsted DM, McGandy RB, Myer ML, Stare FJ. Quantitative effects ofdietary fat on serum cholesterol in man. American Journal of ClinicalNutrition 1965;17:281-295. aj.. Hernell O, Ward H, Blackberg L, Pereira ME. Killing of Giardialamblia by human milk lipases: an effect mediated by lipolysis of milklipids. Journal of Infectious Diseases 1986;153:715-720. ak.. Hierholzer, J.C. and Kabara, J.J. In vitro effects of monolaurincompounds on enveloped RNA and DNA viruses. Journal of Food Safety1982;4:1-12. al.. Hodgson JM, Wahlqvist ML, Boxall JA, and Balazs ND. Can linoleic acidcontribute to coronary artery disease? American Journal of ClinicalNutrition 1993;58:228-234. am.. Holland KT, Taylor D, Farrell AM. The effect of glycerol monolaurateon growth of, and production of toxic shock syndrome toxin-1 and lipase byStaphylococcus aureus. Journal of Anti-microbial Chemotherapy 1994;33:41-55. an.. Hornstra G, van Houwelingen AC, Kester AD, and Sundram K. A palmoil-enriched diet lowers serum lipoprotein(a) in normocholesterolemicvolunteers. Atherosclerosis 1991;90:91-93. ao.. Hornung B, Amtmann E, Sauer G. Lauric acid inhibits the maturation ofvesicular stomatitis virus. Journal of General Virology 1994;75:353-361. ap.. Hostmark AT, Spydevold O, Eilertsen E. Plasma lipid concentration andliver output of lipoproteins in rats fed coconut fat or sunflower oil.Artery 1980;7:367-383. aq.. Huang SC, Frische KL. Alteration in mouse splenic phospholipid fattyacid composition and lymphoid cell populations by dietary fat. Lipids1992;27:25-32. ar.. Isaacs CE, Thormar H. Membrane-disruptive effect of human milk:inactivation of enveloped viruses. Journal of Infectious Diseases1986;154:966-971. as.. Isaacs CE, Thormar H. Human milk lipids inactivated envelopedviruses. in Breastfeeding, Nutrition, Infection and Infant Growth inDeveloped and Emerging Countries (Atkinson SA, Hanson LA, Chandra RK, eds)Arts Biomedical Publishers and Distributors, St John's, NF, Canada, 1990. at.. Isaacs CE, Thormar H. The role of milk-derived antimicrobial lipidsas antiviral and antibacterial agents. In Immunology of Milk and the Neonate(Mestecky J, et al., eds), Plenum Press, New York, 1991. au.. Isaacs CE, Schneidman K. Enveloped Viruses in Human and Bovine Milkare Inactivated by Added Fatty Acids (FAs) and Monoglycerides (MGs). FASEBJournal 1991;5, Abstract 5325, p A1288. av.. Isaacs CE, Kashyap S, Heird WC, Thormar H. Antiviral andantibacterial lipids in human milk and infant formula feeds. Archives ofDisease in Childhood 1990;65:861-864. aw.. Isaacs CE, Litov RE, Marie P, Thormar H. Addition of lipases toinfant formulas produces antiviral and antibacterial activity. Journal ofNutritional Biochemistry 1992;3:304-308. ax.. Isaacs CE, Kim KS, Thormar H. Inactivation of enveloped viruses inhuman bodily fluids by purified lipids. Annals of the New York Academy ofSciences 1994;724:457-464. ay.. Jones PJH. Regulation of cholesterol biosynthesis by diet in humans.American Journal of Clinical Nutrition 1997;66:438-446. az.. Judd JT, Clevidence BA, Muesing RA, Wittes J, Sunkin ME, and PodczasyJJ. Dietary Trans Fatty Acids: Effects on Plasma Lipids and Lipoproteins ofHealthy Men and Women. American Journal of Clinical Nutrition1994;59:861-868. ba.. Kabara JJ. Fatty acids and derivatives as antimicrobial agents: Areview. In The Pharmacological Effect of Lipids (JJ Kabara, ed), AmericanOil Chemists' Society, Champaign IL, 1978. bb.. Kabara JJ. Inhibition of Staphylococcus aureus. In ThePharmacological Effect of Lipids II (JJ Kabara, ed), American Oil Chemists'Society, Champaign IL, 1985, pp.71-75. bc.. Kaunitz H. Toxic effects of polyunsaturated vegetable oils. InSymposium on the Pharmacological Effect of Lipids (JJ Kabara, ed), AmericanOil Chemists' Society, Champaign, IL, 1978, pp 203-210. bd.. Kaunitz H, Dayrit CS. Coconut oil consumption and coronary heartdisease. Philippine Journal of Internal Medicine 1992;30:165-171. be.. Keys A, Anderson JT, Grande F. Prediction of serum-cholesterolresponses of man to changes in the diet. Lancet 959;1957. bf.. Khosla P and Hayes KC. Dietary trans-mono-unsaturated fatty acidsnegatively impact plasma lipids in humans: critical review of the evidence.Journal of the American College of Nutrition 1996;15:325-339. bg.. Kohlmeier L, Simonsen N, van't Veer P, Strain JJ, Martin-Moreno JM,Margolin B, Huttunen JK, Fernandez-Crehuet Navajas J, Martin BC, Thamm M,Kardinaal AF, Kok FJ. Adipose tissue trans fatty acids and breast cancer inthe European Community Multicenter Study on Antioxidants, MyocardialInfarction, and Breast Cancer. Cancer Epidemiology and Biomarkers Prev1997;6:705-10. bh.. Kramer JK, Sauer FD, Farnworth ER, Stevenson D, Rock GA.Hematological and lipid changes in newborn piglets fed milk-replacer dietscontaining erucic acid. Lipids 1998;33:1-10. bi.. Kurup PA, Rajmohan T. II. Consumption of coconut oil and coconutkernel and the incidence of atherosclerosis. Coconut and Coconut Oil inHuman Nutrition, Proceedings. Symposium on Coconut and Coconut Oil in HumanNutrition, 27 March 1994. Coconut Development Board, Kochi, India, 1995, pp35-59. bj.. Lim-Sylianco CY. Anticarcinogenic effect of coconut oil. ThePhilippine Journal of Coconut Studies 1987;12:89-102. bk.. Lu Z, Hendrich S, Shen N, White PJ, Cook LR. Low linolenate andcommercial soybean oils diminish serum HDL cholesterol in young free-livingadult females. Journal of the American College of Nutrition 1997;16:562-569. bl.. Macallan DC, Noble C, Baldwin C, Foskett M, McManus T, Griffin GE.Prospective analysis of patterns of weight change in stage IV hulmanimmunodeficiency virus infection. American Journal of Clinical Nutrition1993;58:417-24. bm.. Mann GV. A short history of the diet/heart hypothesis. In Mann GV(ed), Coronary Heart Disease: The Dietary Sense and Nonsense. JanusPublishing, London, 1993, pp 1-17. bn.. McWhinney VJ, Pond WG, Mersmann HJ. Ontogeny and dietary modulationof 3-hydroxy-3-methylglutaryl-CoA reductase activities in neonatal pigs.Journal of Animal Science 1996;74:2203-10. bo.. Melnick JL, Adam E, DeBakey ME. Cytomegalovirus and atherosclerosis.Archivum Immunologiae et Therapiae Experimentalis (Wroclaw) 1996;44:297-302. bp.. Mendis S, Kumarasunderam R. The effect of daily consumption ofcoconut fat and soyabean fat on plasma lipids and lipoproteins of youngnormolipidaemic men. British Journal of Nutrition 1990;63:547-52. bq.. Mendis S, Wissler RW, Bridenstine RT, Podbielski FJ. The effects ofreplacing coconut oil with corn oil on human serum lipid profiles andplatelet derived factors active in atherogenesis. Nutrition ReportsInternational 40:4, Oct 1989. br.. Mensink RP and Katan MB. Effect of Dietary Trans Fatty Acids onHigh-Density and Low-Density Lipoprotein Cholesterol Levels in HealthySubjects. The New England Journal of Medicine 1990;323:439-445. bs.. Monserrat AJ, Romero M, Lago N, Aristi C. Protective effect ofcoconut oil on renal necrosis occurring in rats fed a methyl-deficient diet.Renal Failure 1995;17:525-537. bt.. Nanji AA, Sadrzadeh SM, Yang EK, Fogt F, Maydani M, Dannenberg AJ.Dietary saturated fatty acids: a novel treatment for alcoholic liverdisease. Gastroenterology 1995;109:547-554. bu.. Nelson GJ. Dietary fat, trans fatty acids, and risk of coronary heartdisease. Nutrition Reviews 1998;56:250-252. bv.. Nelson SE, Rogers RR, Frantz JA, Ziegler EE. Palm olein in infantformula: absorption of fat and minerals by normal infants. American Journalof Clinical Nutrition 1996;64:291-296. bw.. New York Times, Medical Science, Tuesday, January 29, 1991. Commonvirus seen as having early role in arteries' clogging (byline SandraBlakeslee). bx.. Ng TKW, Hassan K, Lim JB, Lye MS, Ishak R. Nonhypercholesterolemiceffects of a palm-oil diet in Malaysian volunteers. American Journal ofClinical Nutrition 1991;53:1015S-1020S. by.. Oh DH and Marshall DL. Antimicrobial activity of ethanol, glycerolmonolaurate or lactic acid against Listeria monocytogenes. InternationalJournal of Food and Microbiology 1993;20:239-246. bz.. Oliart-Ros RM, Torres-Marquez ME, Badillo A, Guerrero OA. Effects ofdietary polyunsaturated fatty acids on sucrose-induced cardiovascularsyndrome in rats. 89th AOCS Annual Meeting Abstracts, H & N 5: General Healthand Nutrition II, p 76, Chicago, IL, May 10-13, 1998. ca.. Petschow BW, Batema RP, Ford LL. Susceptibility of Helicobacterpylori to bactericidal properties of medium-chain monoglycerides and freefatty acids. Antimicrobial Agents and Chemotherapy 1996;40:302-306. cb.. Pietinen P, Ascherio A, Korhonen P, Hartman AM, Willett WC, AlbanesD, Virtamo J. Intake of fatty acids and risk of coronary heart disease in acohort of Finnish men. The Alpha-Tocopherol, Beta-Carotene Cancer PreventionStudy. American Journal of Epidemiology 1997;145:876-887. cc.. Portillo MP, Serra F, Simon E, del Barrio AS, Palou A. Energyrestriction with high-fat diet enriched with coconut oil gives higher UCP1and lower white fat in rats. International Journal of Obesity and RelatedMetabolic Disorders 1998;22:974-9. cd.. Prior IA, Davidson F, Salmond CE, Czochanska Z. Cholesterol,coconuts, and diet on Polynesian atolls: a natural experiment: the Pukapukaand Tokelau Island studies. American Journal of Clinical Nutrition1981;34:1552-1561. ce.. Projan SJ, Brown-Skrobot S, Schlievert PM, Vandenesch F, Novick RP.Glycerol monolaurate inhibits the production of beta-lactamase, toxic shocktoxin-1, and other staphylococcal exoproteins by interfering with signaltransduction. Journal of Bacteriology 1994;176:4204-4209. cf.. Ravnskov U. Quotation bias in reviews of the diet-heart idea. Journalof Clinical Epidemiology 1995;48:713-719. cg.. Raza-Ahmad A, Klassen GA, Murphy DA, Sullivan JA, Kinley CE,Landymore RW, Wood JR. Evidence of type-2 herpes simplex infection in humancoronary arteries at the time of coronary artery bypass surgery. CanadianJournal of Cardiology 1995;11:1025-1029. ch.. Reddy BS, Maeura Y. Tumour promotion of dietary fat inazoxymethane-induced colon carcinogenesis in female F 344 rats. Journal ofthe National Cancer Institute 1984;72:745-750. ci.. Reiner DS, Wang CS, Gillin FD. Human milk kills Giardia lamblia bygenerating toxic lipolytic products. Journal of Infectious Diseases1986;154:825-832. cj.. Saikku P. Chlamydia pneumoniae and atherosclerosis - an update.Scandinavian Journal of Infectious Diseases Supplement 1997;104:53-56. ck.. Sircar S, Kansra U. Choice of cooking oils - myths and realities.Journal of the Indian Medical Association 1998;96:304-307. cl.. Sands JA, Auperin DD, Landin PD, Reinhardt A, Cadden SP. Antiviraleffects of fatty acids and derivatives: lipid-containing bacteriophages as amodel system. In The Pharmacological Effect of Lipids (JJ Kabara, ed),American Oil Chemists' Society, Champaign, IL, 1978, pp 75-95. cm.. Smit MJ, Wolters H, Temmerman AM, Kuipers F, Beynen AC, Vonk RJ.Effects of dietary corn and olive oil versus coconut fat on biliarycholesterol secretion in rats. International Journal of Vitamin andNutrition Research 1994;64:75-80. cn.. Smith RL. The Cholesterol Conspiracy. Warren H Green Inc., St Louis,Missouri, 1991. co.. Sugano M, Ikeda I. Metabolic interactions between essential andtrans-fatty acids. Current Opinions in Lipidology 1996;7:38-42. cp.. Sundram K, Hayes KC, Siru OH. Dietary palmitic acid results in lowerserum cholesterol than does a lauric-myristic acid combination innormolipemic humans. American Journal of Clinical Nutrition 1994;59:841-846. cq.. Tappia PS, Grimble RF. Complex modulation of cytokine induction byendotoxin and tumour necrosis factor from peritoneal macrophages of rats bydiets containing fats of different saturated, mono-unsaturated andpolyunsaturated fatty acid composition. Clinical Science (Colch)1994;87:173-178. cr.. Tholstrup T, Marckmann P, Jespersen J, Sandstrom B. Fat high instearic acid favorably affects blood lipids and factor VII coagulantactivity in comparison with fats high in palmitic acid or high in myristicand lauric acids. American Journal of Clinical Nutrition 1994;59:371-377. cs.. Thormar H, Isaacs EC, Brown HR, Barshatzky MR, Pessolano T.Inactivation of enveloped viruses and killing of cells by fatty acids andmonoglycerides. Antimicrobial Agents and Chemotherapy 1987;31:27-31. ct.. Trautwein EA, Kunath-Rau A, Dietrich J, Drusch S, Erberdobler HF.Effect of dietary fats rich in lauric, myristic, palmitic, oleic or linoleicacid on plasma, hepatic and biliary lipids in cholesterol-fed hampsters.British Journal of Nutrition 1997;77:605-620. cu.. Visseren FL, Bouter KP, Pon MJ, Hoekstra JB, Erkelens DV, DieperslootRJ. Patients with diabetes mellitus and atherosclerosis; a role forcytomegaloviorus? Diabetes Research and Clinical Practice (Limerick)1997;36:49-55. cv.. Wan JM, Grimble RF. Effect of dietary linoleate content on themetabolic response of rats to Escherichia coli endotoxin. Clinical Science(Colch) 1987;72:383-385. cw.. Wang LL and Johnson EA. Inhibition of Listeria monocytogenes by fattyacids and monoglycerides. Applied and Environmental Microbiology 1992;58:624-629. cx.. Willett W. Editorial: Challenges for public health nutrition in the1990s. American Journal of Public Health 1990;80:1295-1298. cy.. Witcher KJ, Novick RP, Schlievert PM. Modulation of immune cellproliferation by glycerol monolaurate. Clinical and Diagnostic LaboratoryImmunology 1996;3:10-13. cz.. Zhou YF, Buetta E, Yu ZX, Finkel T, Epstein SE. Human cytomegalovirusincreases modified low-density lipoprotein uptake and scavenger receptormRNA expression in vascular smooth muscle cells. Journal of ClinicalInvestigation 1996;98:2129-2138.The homepage and the place to sign up for Tracy's Corner is: Mr_Tracys_CornerFor complaints or assistance contact xootsuit26