Health & Nutritional Benefits, coconut board of india

l 9 Indian Coconut Journal

Health and nutritional benefitsfrom coconut oil and its

advantages over competing oilsMary G. Enig, Ph.D., F.A. C.N.

Director, Nutritional Sciences Division, Enig Associates Inc., Maryland, USA

Introduction

Two important areas will becovered in this paper. In the first

part, a review of the major healthchallenge facing coconut oil todayhas been included. This challenge isbased on a supposed negative roleplayed by saturated fat in heartdisease. It is proposed to dispel anyacceptance of this notion with theinformation that will be presentedhere.

In the second part some newdirections where important positivehealth benefits are seen for coconutoil are suggested. These benefitsstem from coconut oilís use as a foodwith major antimicrobial and anti-cancer benefits. The rationale for thiseffect and some of the literature willbe reviewed here. The health andnutritional benefits derived fromcoconut oil are unique andcompelling. They are under-appreciated today by both theproducer and the consumer. Betterrecognised are the functionaladvantages coconut oil has, overcompeting oils, in many foodproducts. Historically, coconuts andtheir extracted oil have served manas important foods for thousands ofyears. The use of coconut oil as ashortening was advertised in theUnited States in popular cookbooks

The lauric acid in coconut oilis used by the body to make

the same disease-fighting fattyacid derivative monolaurinthat babies make from the

lauric acid they get from theirmothersí milk. The

monoglyceride monolaurin isthe substance that keeps

infants from getting viral orbacterial or protozoal

infections.

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at the end of the 19th century. Notethat both the health-promotingattributes of coconut oil and thosefunctional properties useful to thehouse maker were recognized 100years ago. These same attributes, inaddition to some newly discoveredones, should be of great interest toboth the producing countries as wellas the consuming countries.

Origins of the Diet/ Heart Hypothesis

The literature of epidemiologicalstudies usually attribute an in-creased risk of coronary heartdisease (CHD) to elevated levels ofserum cholesterol, which in turn arethought to be derived from a dietaryintake of saturated fats andcholesterol. But, saturated fats maybe considered a major culprit forCHD only if the links between serumcholesterol and CHD, and betweensaturated fat and serum cholesterolare each firmly established. Decadesof large scale tests and conclusionsthere from have purported toestablish the first link. In fact, thisrelationship has reached the level ofdogma. Through the years metabolicward and animal studies haveclaimed that dietary saturated fatsincrease serum cholesterol levels,thereby supposedly establishing thesecond link. But the scientific basisfor these relationships has now been

10 lSeptember 2010

challenged as resulting from largescale misinterpretation andmisrepresentation of the data. (Enig1991, Mann 1991, Smith 1994,Rvnskov 1995). Ancel Keys islargely responsible for starting theanti-saturated fat agenda in theUnited States. From 1953 to 1957Keys made a series of statementsregarding the atherogenicity of fats.These pronouncements were: ìAllfats raise serum cholesterol; Nearlyhalf of total fat comes from vegetablefats and oils; No difference betweenanimal and vegetable fats in effecton CHD (1953); Type of fat makesno difference; Need to reducemargarine and shortening (1956); Allfats are comparable; Saturated fatsraise and polyunsaturated fats lowerserum cholesterol; Hydrogenatedvegetable fats are the problem;Animal fats are the problem (1957-1969).î

As can be seen, his findings wereinconsistent. What about the role ofedible oil industry in promoting thediet/ heart hypothesis? It is importantto realise that at this time (1960s) theedible oil industry in the UnitedStates seized the opportunity topromote its polyunsaturates. Theindustry did this by developing ahealth issue focusing on Keyís anti-saturated fat bias.

With the help of the edible oilindustry lobbying in the UnitedStates, federal government dietarygoals and guidelines were adoptedincorporating this mistaken idea thatconsumption of saturated fat wascausing heart disease. This anti-saturated fat issue became theagenda of government and privateagencies in the US and to an extentin other parts of the world. This is

the agenda that has had such adevastating effect on the coconutindustry for the past decade.Throughout the 1960s, the 1970s andthe 1980s the anti-saturated fatrhetoric increased in intensity. Aneditorial by Harwardís WalterWillett, M.D. in the AmericanJournal of Public Health (1990)acknowledged that even though ìthefocus of dietary recommendations isusually a reduction of saturated fatintake, no relation between saturatedfat intake and risk of CHD wasobserved in the most informativeprospective study to date.î Anothereditorial, this time by FraminghamísWilliam P. Castelli in the Archihivesof Internal Medicine (1992),declared for the record thatî...inFramingham, Mass, the moresaturated fat one ate, the morecholesterol one ate, the more caloriesone ate, the lower the personís serumcholesterol... the opposite of what theequations provided by Hegsted et al(1965) and Keys et al (1957) wouldpredict. ìCastelli further admittedthatî...In Framingham, for example,we found that the people who ate themost cholesterol, ate the mostsaturated fat, ate the mostcalories,weighted the least, and werethe most physically active.î

Coconut oil and the diet/hearthypothesis

For the past several decadesanimal and human studies feedingcoconut oil have purportedly showedincreased indices for cardiovascularrisk. Blackburn et a1 (1988) havereviewed the published literature ofìcoconut oilís effect on serumcholesterol and atherogenesisî andhave concluded that whenì...[coconut oil is] fed

physiologically with other fats oradequately supplemented withlinoleic acid, coconut oil is a neutralfat in terms of atherogenicity.î Thequestion then is, how did coconut oilget such a negative reputation? Theanswer quite simply is, initially, thesignificance of those changes thatoccurred during animal feedingstudies were misunderstood. Thewrong interpretation was thenrepeated until ultimately themisinformation and disinformationtook on a life of its own. Theproblems for coconut oil started fourdecades ago when re-searchers fedanimals hydrogenated coconut oilthat was purposefully altered tomake it completely devoid of anyessential fatty acids. Thehydrogenated coconut oil wasselected instead of hydrogenatedcottonseed, corn or soybean oilbecause it was a soft enough fat forblending into diets due to thepresence of the lower meltingmedium chain saturated fatty acids.The same functionality could not beobtained from the cottonseed, cornor soybean oils if they were madetotally saturated, since all their fattyacids were long chain and highmelting and could not be easilyblended nor were they as readilydigestible. The animals fed thehydrogenated coconut oil (as theonly fat source) naturally becameessential fatty acid deficient; theirserum cholesterol levels increased.Diets that cause an essential fattyacid deficiency always produce anincrease in serum cholesterol levelsas well as an increase in theatherosclerotic indices. The sameeffect has also been seen when otheressential fatty acid deficient, highlyhydrogenated oils such as

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l 11 Indian Coconut Journal

cottonseed, soybean or corn oilshave been fed; so it is clearly afunction of the hydrogenatedproduct, either because the oil isessential fatty acid (EFA) deficientor because of trans fatty acids (TFA).

What about the studies whereanimals were fed with unprocessedcoconut oil?

Hostmark et al (1980) comparedthe effects of diets containing 10 percent coconut fat and 10 per centsunflower oil on lipoproteindistribution in male Wistar rats.Coconut oil feeding producedsignificantly lower levels (p = <0.05)of pre-beta lipoproteins (VLDL) andsignificantly higher (p = <0.01)alpha-lipoproteins (HDL) relative tosunflower oil feeding. Awad (1981)compared the effects of dietscontaining 14 per cent coconut oil,14 per cent safflower oil or a 5 percent ìcontrolî (mostly soybean) oilon accumulation of cholesterol intissues in male Wistar rats. Thesynthetic diets had 2 per cent addedcorn oil with a total fat of 16 per cent.Total tissue cholesterol accumulationfor animals on the safflower diet wassix times greater than for animals fedthe coconut oil, and twice that of theanimals fed the control oil.

A conclusion that can be drawnfrom some of this animal research isthat feeding hydrogenated coconutoil devoid of essential fatty acids(EFA) in a diet otherwise devoid ofEFA leads to EFA deficiency andpotentiates the formation ofatherosclerosis markers. It is of notethat animals fed regular coconut oilhave less cholesterol deposited intheir livers and other parts of theirbodies. What about the studies wherecoconut oil is part of the normal diet

of human beings? Kaunitz andDayrit (1992) have reviewed someof the epidemiological andexperimental data regardingcoconut-eating groups and noted thatthe ìavailable population studiesshow that dietary coconut oil doesnot lead to high serum cholesterolnor to high coronary heart diseasemortality or morbidity.î They notedthat in 1989 Mendis et al reportedundesirable lipid changes whenyoung adult Sri Lankan males werechanged from their normal diets bythe substitution of corn oil for theircustomary coconut oil [Table 1].Although the total serum cholesteroldecreased 18.7 per cent from 179.6to 146.0 mg/dl and the LDLcholesterol decreased 23.8 per centfrom 131.6 to 100.3 mg/dl, the HDLcholesterol decreased 41.4 per centfrom 43.4 to 25.4 mg/dl (putting theHDL values below the accept-ablelower limit) and the LDL/ HDL ratioincreased 30 per cent from 3.0 to 3.9.These later two changes would beconsidered quite undesirable.

Some of the studies wherecoconut oil was the major dietary fatsource reported thirty and more yearsago should have cleared coconut oilof any implication in thedevelopment of coronary heartdisease (CHD). For example, whenFrantz and Carey (1961) fed anadditional 810 kcal/day fatsupplement for a whole month tomales with high normal serumcholesterol levels, there was nosignificant difference from theoriginal levels even though the fatsupplement was hydrogenatedcoconut oil. Halden and Lieb (1961)also showed similar results in agroup of hypercholesterolemicswhen coconut oil was included intheir diets. Original serumcholesterol levels were reported as170 to 370 mg/dl. Straight coconutoil produced a range from 170 to 270mg/dl. Coconut oil combined with 5per cent sunflower oil and 5 per centolive oil produced a range of 140 to240 mg/dl. Earlier, Hashim andcolleagues (1959) [Table 2] hadshown quite clearly that feeding a fatsupplement to hypercholesterolemics,where half of the supplement (21 percent of energy) was coconut oil (andthe other half was safflower oil),resulted in significant reduction intotal serum cholesterol. Thereductions averaged -29 per cent andranged from -6.8 to -41.2 per cent.And even earlier, Ahrens andcolleagues (1957) had shown thatadding coconut oil to the diet ofhypercholesterolemics lowers serumcholesterol from 450 mg/ dl to 367mg/dl. This is hardly a cholesterol-raising effect.

Bierenbaum et al (1967)followed 100 young men withdocumented myocardial infarction

Table 1. Substituting corn oil for coconut oil

Total cholesterol ! 18.7 %LDL cholesterol ! 23.8%HDL cholesterol ! 41.4%LDL/HDL ratio " 30%

Adapted from Mendis et al (1989)

Previously, Prior et al (1981) hadshown that islanders with high in-take of coconut oil showed noevidence of the high saturated fatintake having a harmful effect inthese populations. ìWhen thesegroups migrated to New Zealandhowever, and lowered their intake ofcoconut oil, their total cholesteroland LDL cholesterol increased, andtheir HDL cholesterol decreased.

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12 lSeptember 2010

for 5 years on diets with fat restrictedto 28 per cent of energy. There wasno significant difference between thetwo different fat mixtures (50/ 50corn and safflower oils or 50/50coconut oil and peanut oils), whichwere fed as half of the total fatallowance; both diets reduced serumcholesterol. This study clearlyshowed that 7 per cent of energy ascoconut oil was as beneficial to the50 men who consumed it as for the50 men who consumed 7 per cent ofenergy as other oils such as corn oilor safflower. Both groups faredbetter than the untreated controls.More recently, Sundram et al (1994)[Table 3] fed whole food diets tohealthy normocholesterolemicmales, where approximately 30 percent of energy was fat. Lauric acid(C 12:0) and myristic acid (C14:0)from coconut oil suppliedapproximately 5 per cent of energy.

Relative to the baselinemeasurements of the subjects priorto the experimental diet, this lauricand myristic acid rich diet showedan increase in total serum cholesterolfrom 166.7 to 170.0 mg/ dl (+1.9%),

a decrease in low density lipoproteincholesterol (LDLC) from 105.2 to104.4 mg/dl (-0.1%), an increase inhigh density lipoprotein cholesterol(HDL-C) from 42.9 to 45.6 mg/dl(+6.3%). There was a 2.4% decreasein the LDL-C/HDL-C ratio from2.45 to 2.39. These findings indicatethat a favourable alteration in serumlipoprotein balance was achievedwhen coconut oil was included in awhole food diet at 5 per cent ofenergy. Tholstrup et al (1994) reportsimilar results with whole foods dietshigh in lauric and myristic acids frompalm kernel oil. The HDLcholesterol levels increasedsignificantly from baseline values(37.5 to 46.0 mg/dl, P<0.01) and theLDL-C/HDL-C ratios decreasedfrom 3.08 to 2.69. The increase intotal cholesterol was from 154.7(baseline) to 170.9 mg/dl on theexperimental diet. Ng et al (1991)

fed 75 per cent of the fat ration ascoconut oil (24 per cent of energy)to 83 adult normocholesterolemics(61 males and 22 females). Relativeto baseline values, the highest valueson the experimental diet for totalcholesterol was increased 17 per cent(169.6 to 198.4 mg/dl), HDLcholesterol was increased 21.4 percent (44.3 to 53.8 mg/dl), and theLDL-C/HDL-C ratio was decreased3.6 per cent (2.51 to 2.42). Whenunprocessed coconut oil is added toan otherwise normal diet, there isfrequently no change in the serumcholesterol although some studieshave shown a decrease in totalcholesterol. For example, whenGinsberg et al [Table 4j provided anì Average Americanî diet with 2-3times more myristic acid (C14:0),4.5 times more lauric acid (C12:0),and 1.2 times more palmitic andstearic acid (C16:0 and C18:0) thantheir ìMono [unsaturated]î diet andthe National Cholesterol EducationProgram ìStep 1î diet, there was noincrease in serum cholesterol, and infact, serum cholesterol levels for thisdiet group fell approximately 3 percent from 177.1 mg per cent to 171.8mg percent during the 22 week

Table 2. Effect of feeding 50 percent of fat ration ascoconut oil (21 % of energy ) to 10 adult male

hypercholesteromics

Serum cholesterol Serum cholesterol %Mg/dl Mg/dl change

Before added fat After coconut oil

364 214 -41.2358 272 -24.0353 281 -20.4336 240 -28.6315 198 -37.1416 274 -34.1348 245 -29.6331 265 -19.9489 361` -26.2310 289 -6.8Mean 362 256 -29.3

Adaptd from Hashim et al (1959)

Table 3. Coconut oil added at 5 % energy

Baseline Diet %change

Total cholesterol 166.7 mg% 170.0mg% +1.9%LDL cholesterol 105.2mg% 104.4mg% -0.1%HDL cholesterol 42.9mg% 45.6 mg% +6.3%LDL-C/HDL-C 2.45 2.39 -2.4%

Adapted from Sundaram et al (1994)

Table 4. Baseline values for serum cholesterol of subjects(36 males, 12/diet) prior to beginning one ot threediets identified as: Average American, American Heart Association(AHA) step 1 diet, and AHA step 1

diet with added monounsaturated (mono) fat

Diet (% of kcal from fat) Total cholesterol, mg/dl mM/L

Average American(38) 177.1+19.72 4.58AHA Step 1* 182.1+17.79 4.71Step1+Mono 191.4+11.20 4.95

%change from baseline for total cholesterol by 22 week

Diet % Mg/dl Total cholestreol, mg/dl final

Average American -3.0 -5.5 171.8AHA Step 1* -8.0 -14.6 167.5Step1+Mono -8.0 -15.3 176.1

*AHA Step = lower fat-the only real effect was between higher (38%) and lower (30%) as calories from fat.Adapted from Ginsberg et al (1990)

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l 13 Indian Coconut Journal

feeding trial. It appears from manyof the research reports that the effectcoconut oil has on serum cholesterolis the opposite in individuals withlow serum cholesterol values andthose with high serum values. Theremay be a rising of serum totalcholesterol, LDL cholesterol andespecially HDL cholesterol inindividuals with low serumcholesterol. On the other hand thereis lowering of total cholesterol andLDL cholesterol inhypercholesterolemics as notedabove.

Studies that supposedly showeda ìhypercholesterolemicî effect ofcoconut oil feeding, in fact, usuallyonly showed that coconut oil was notas effective at lowering the serumcholesterol as was the moreunsaturated fat being compared. Thisappears to be in part because coconutoil does not ìdriveî cholesterol intothe tissues as does the morepolyunsaturated fats. As noted inTable 5 analysis of the atheromashows that the fatty acids from thecholesterol esters are 74 per centunsaturated (41 per cent ispolyunsaturated) and only 24 percent are saturated. None of thesaturated fatty acids were re-portedto be lauric acid or myristic acid(Felton et al, 1994). There is anotheraspect to the coronary heart diseasepicture. This is related to theinitiation of the atheromas that arereported to be blocking arteries.Recent research is suggestive thatthere is a causative role for the herpesvirus and cytomegalovirus in theinitial formation of atheroscleroticplaques and the recloging of arteriesafter angioplasty (New York Times1991). What is so interesting is thatthe herpes virus and cytomegalovirus

are both inhibited by theantimicrobial lipid monolaurin; butmonolaurin is not formed in the bodyunless there is a source of lauric acidin the diet. Thus, ironically enough,one could consider therecommendations to avoid coconutand other lauric oils as contributingto the increased incidence ofcoronary heart disease. Perhaps moreimportant than any effect of coconutoil on serum cholesterol is theadditional effect of coconut oil on thedisease fighting capability of theanimal or person consuming thecoconut oil.

of the adenocarcinomas in the colon,but in the small intestine animals fedcoconut oil did not develop anytumors while 7 per cent of animalsfed olive oil did.

Studies by Cohen et at (1986)showed that the non promotionaleffects of coconut oil were also seenin chemically induced breast cancer.In this model, the slight elevation ofserum cholesterol in the animals fedcoconut oil was protective as theanimals fed the morepolyunsaturated oil had reducedserum cholesterol and more tumors.The authors noted that ì...an overallinverse trend was observed betweentotal serum lipids and tumorincidence for the 4 [high fat]groups.î This is an area that needsto be pursued.

Coconut Oil Antimicrobialbenefits

I would now like to review someof the rationale for the use of coconutoil as a food that will serve as theraw material to provide potentiallyuseful levels of antimicrobial activityin the individual. The lauric acid incoconut oil is used by the body tomake the same disease-fighting fattyacid derivative monolaurin thatbabies make from the lauric acid theyget from their mothersí milk. Themonoglyceride monolaurin is thesubstance that keeps infants fromgetting viral or bacterial or protozoalinfections. Until just recently, thisimportant benefit has been largelyoverlooked. Recognition of theantimicrobial activity of themonoglyceride of lauric acid(monolaurin) has been reported since1966. The seminal work can becredited to Jon Kabara. This earlyresearch was directed at the virucidal

Table 5. Fatty acid composition of aoritic plaque,serum and adipose tissue

Weight % of fatty acidFatty acid Plaque Serum Adipose

class

All SFA 26.4 28.4 31.3All MUFA 32.6 26.5 55.1All ω PUFA 36.1 38.8 11.9All ω PUFA 5.0 6.3 1.3

Adapted from Table. CV Felton et al 1994SFA = saturated fatty acidsMUFA = monounsaturated fatty acidsPUFA = polyunsaturated fatty acids

Coconut Oil and Cancer

Lim-Sylianco (1987) hasreviewed 50 years of literatureshowing anticarcinogenic effectsfrom dietary coconut oil. Theseanimal studies show quite clearly thenonpromotional effect of feedingcoconut oil. In a study by Reddy etal (1984) straight coconut oil wasmore inhibitory than MCT oil toinduction of colon tumors byazoxymethane. Chemically inducedadenocarcinomas differed 10-foldbetween corn oil (32 per cent) andcoconut oil (3 per cent) in the colon.Both olive oil and coconut oildeveloped the low levels (3 per cent)

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effects because of possible problemsrelated to food preservation.

Some of the early work byHierholzer and Kabara (1982) thatshowed virucidal effects ofmonolaurin on enveloped RNA andDNA viruses was done inconjunction with the Center forDisease Control of the US PublicHealth Service with selectedprototypes or recognizedrepresentative strains of envelopedhuman viruses. The envelope ofthese viruses is a lipid membrane.Kabara (1978) and others havereported that certain fatty acids (e.g.,medium-chain saturates) and theirderivatives (e.g., mono-glycerides)can have adverse effects on variousmicro-organisms: those micro-organisms that are inactivatedinclude bacteria, yeast, fungi, andenveloped viruses. The medium-chain saturated fatty acids and theirderivatives act by disrupting the lipidmembranes of the organisms (Isaacsand Thormar 1991; Isaacs et al1992). In particular, envelopedviruses are inactivated in both humanand bovine milk by added fatty acids(FAs) and monoglycerides (MGs)(Isaacs et al 1991) as well as byendogenous FAs and MGs (Isaacs etal 1986,1990,1991,1992; Thormar etal 1987). All three monoesters oflauric acid are shown to be activeantimicrobials, i.e.O, -, Oí-, and 13-MG. Additionally, it is reported thatthe antimicrobial effects of the FAsand MGs are additive and totalconcentration is critical forinactivating viruses (Isaacs andThormar 1990).

The properties that determine theanti-infective action of lipids arerelated to their structure; e.g.,

monoglycerides, free fatty acids. Themonoglycerides are active,diglycerides and triglycerides areinactive. Of the saturated fatty acids,lauric acid has greater antiviralactivity than either caprylic acid (C-10) or myristic acid (C-14). Theaction attributed to monolaurin isthat of solubilizing the lipids andphospholipids in the envelope of thevirus causing the disintegration ofthe virus envelope. In effect, it isreported that the fatty acids andmonoglycerides produce theirkilling/inactivating effect by lysingthe (lipid bilayer) plasma membrane.However, there is evidence fromrecent studies that one antimicrobialeffect is related to its interferencewith signal transduction (Projan etal 1994). Some of the virusesinactivated by these lipids, inaddition to HIV, are the measlesvirus, herpes simplex virus-1 (HSV-1), vesicular stomatitis virus (VSV),visna virus, and cytomegalovirus(CMV).

Many of the pathogenicorganisms reported to be inactivatedby these antimicrobial lipids arethose known to be responsible foropportunistic infections in HIV-positive individuals. For example,concurrent infection withcytomegalovirus is recognized as aserious complication for HIV +individuals (Macallan et al 1993).Thus, it would appear to beimportant to investigate the practicalaspects and the potential benefit ofan adjunct nutritional supportregimen for HIV infectedindividuals, which will utilize thosedietary fats that are sources of knownantiviral, antimicrobial, andantiprotozoal monoglycerides andfatty acids such as monolaurin and

its precursor lauric acid. No one inthe mainstream nutrition communityseems to have recognized the addedpotential of antimicrobial lipids inthe treatment of HIV-infected orAIDS patients. These antimicrobialfatty acids and their derivatives areessentially non-toxic to man; theyare produced in vivo by humanswhen they ingest those commonlyavailable foods that contain adequatelevels of medium-chain fatty acidssuch as lauric acid. According to thepublished research, lauric acid is oneof best ìinactivatingî fatty acids, andits monoglyceride is even moreeffective than the fatty acid alone(Kabara 1978, Sands et al 1978,Fletcher et al 1985, Kabara 1985).Increasingly, over the past 40 years,the American diet has undergonemajor changes. Many of thesechanges involve changes of fats andoils. There has been an increasingsupply of the partially hydrogenatedtrans-containing vegetable oils anda decreasing amount of the lauricacid containing oils. As a result, therehas been an increased consumptionof trans fatty acids and linoleic acidand a decrease in the consumptionof lauric acid. This type of changein diet has an effect on the fatty acidsthe body has available for metabolicactivities. The lipid coated (envelop)vi-ruses are dependent on host lipidsfor their lipid constituents. Thisaccounts for the variability of fattyacids in the virus envelop and alsoexplains the variability ofglycoprotein expression.

Lauric Acid in Foods

In the United States today, thereis very little lauric acid in most ofthe foods. Until a year ago, some ofthe commercially sold popcorn, at

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least in movie theaters, had coconutoil as the oil. This means that forthose people lucky enough toconsume this type of popcorn thepossible lauric acid intake was 6grams or more in a three (3) cuporder. Some infant formulas (but notall) are still good sources of lauricacid for infants. Only one enteralformula contains lauric acid (e.g.,Impact); this is normally used inhospitals for tube feeding. The morewidely promoted enteral formulas(e.g., Ensure) are not made withlauric oils and in fact, many are madewith partially hydrogenated oils.

There are currently some candiessold in the US that are made withpalm kernel oil. These can supplysmall amounts of lauric acid (e.g.,Andes, KitKat). Cookies such asmacaroons, if made with desiccatedcoconut, are good sources of lauricacids, but they make up a smallportion of the cookie market. Mostcookies in the United States are nolonger made with coconut oilshortenings; however, there was atime when many US cookies (eg.Pepperidge Farm) were about 25 percent lauric acid.

Originally, one of the largestmanufacturers of cream soups usedcoconut oil in the formulation. Manypopular cracker manufacturers alsoused coconut oil as a spray coating.These products supplied a smallamount of lauric acid on a daily basisfor some people. It is not knownexactly how much food made withlauric oils is needed in order to havea protective level of lauric acid in thediet. Infants probably consumebetween 0.3 and 1g/kg of bodyweight if they are fed human milkor an infant formula that containscoconut oil.

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