l 15 Indian Coconut Journal

A simpler approach tounderstand coronary heart

disease, fat facts and itscorrelation with consumption of

coconut oilDr Dipak Kr. Ghosh1 and Dr Arpita Ghosh2

C. Manojkumar and K. Samsudeen1Sr.Lecturer, AICRP on Palms, Dept of Spices and Plantation Crops

Bidhan Chandra Krishi Viswavidyalaya, Kalyani-741235, Nadia, WB.2MBBS, Medical Officer WBHS, Ex- Kolkata Medical College

Abstract

The WHO has drawn attentionthat Coronary Heart Disease

(CHD) is one our modern epidemics.CHD syn. Ischemic (lack of oxygen)Heart Disease has been defined asimpairment of heart function due toinadequate blood flow to the heartcompared to its need caused byobstructive changes in the coronarycirculation to the heart(atherosclerosis). The risk factors forCHD are (i) non modifiable : age,sex, genetic factor, personality etcand (ii) modifiable : cigarettesmoking, high blood pressure,elevated serum cholesterol, diabetes,obesity stress etc. Smoking has beenidentified as a major CHD riskfactor. Hypertension acceleratesthe atherosclerotic process.Serum cholesterol concentration isan important risk factor for CHD atlevels 220 mg/dl or more. The riskof CHD is 2-3 times higher indiabetics and high alcohol intake.Being rich in saturated fatty acid(SFA) coconut oil is bracketed with

animal fats having cholesterogenicproperties creating a fear complexabout consumption of coconut oilresulting in elevated cholesterol. Butthe actual fact is that dominated fattyacid present in coconut oil are mediumchain fatty acids, which are easilydigestable and do not circulate in theblood stream and not deposite in thebody like long chain fatty acids.Studies conducted by different workershave revealed beneficial /neutralresults of coconut oil on animal orhuman health. The incidence of CHDcould be better linked withconsumption of cholesterol rich animaloriginated food, the sedentary habitsassociated with a tension riddenmechanical society.

Coronary heart disease

Coronary heart disease(sym:ischemic heart disease) has beendefined as impairment of heartfunction due to inadequate bloodflow to the heart compared to itsneeds, caused by obstructivechanges in the coronary circulation

HEALTH

The incidence of CHD couldbe better linked with

consumption of cholesterolrich animal originated food,

the sedentary habitsassociated with a tension

ridden mechanical society.

16 lOctober 2008

to the heart. It is the cause of 25 -30 per cent of death in mostindustrialized countries. The WHOhas drawn attention to the fact thatCHD is one of our modern epidemic.Depending on the rate ofdevelopment of the ischemia and itsultimate severity CHD may manifestitself in many presentation: a)Angina pectoris,(AP) (b) myocardialinfarction, (MI) (c) irregularities ofthe heart, (d) cardiac failure, (e)sudden death.

Coronary artery disease (CAD)is a complex degenerative diseasethat causes reduced or absent bloodflow in one or more of the arteriesthat encircle the heart. The principalcause of coronary artery disease iscoronary artery atherosclerosiswhich is a disease of the arteriescharacterized by endothelialdysfunction, vascular inflammationand the build up of lipids,cholesterol, calcium and cellulardebris within the intima of the vesselwall. CAD refers to the presence ofatherosclerotic changes with thewalls of the coronary arteries, whichcauses impairment or obstruction ofnormal blood flow with resultantmyocardial ischemia. Ischemiarefers to lack of oxygen due toinadequate perfusion, which resultsfrom an imbalance between oxygensupply and demand. Ischemic heartdisease (IHD) is the most common,serious, chronic, life-threateningdisease of the US.

Although any artery may beaffected by atherosclerosis, themajor targets are aorta, coronary andcerebral arteries. Atherothromboticdisease of the cerebral vessels is the

major cause of brain infarcts, the socalled strokes. Fatty streaks developas circulating monocytes migrateinto intima, take up oxidized LDLfrom plasma become foam cell.When it dies, smooth muscle cellthen migrate into and proliferatewithin the plaque. It encroaches intothe lumen of the vessel. Plaquerupture may lead to rapid occlusionof vessel and cause most acutesyndrome. The pattern of CHD inIndia has been reported to be asfollows : (a) The peak period isattained between 51 -60 yrs, (b)males are affected more thanfemales, (c) hypertension anddiabetes account for about 40% ofall cases, (d) heavy smoking isresponsible in a good number ofcases (Park 2000). The aeteology ofCHD is multifactorial. The greaterthe number of risk factors present, itis more likely to develop CHD. Theprincipal risk factors are as below:

Smoking has been identified asa major CHD risk factor with severalmechanisms – carbon monoxideinduced atherogenesis, nicotinestimulation raising both bloodpressure and myocardial oxygendemand. Hypertension acceleratesthe atherosclerotic process. In theFramingham study, men aged 45-62with BP 160/95 mm Hg had morethan 5 fold greater risk of IHD. Thereis a triangular relationship between

Risk factors for CHD

Non - modifiable Modifiable

Age Cigarette smoking

Sex High blood pressure, Dietory factors

Family history Elevated serum cholesterol

Genetic factor Diabetes, haemostatic variables

Personality Obesity, sedentary habits, stress etc.

habitual diet, blood cholesterol –lipoprotein levels and CHD.

Serum cholesterol concentr-ation is an important risk factor forCHD at levels 220 mg/dl or more(Keys A,1980). When we look at thevarious type of lipoprotein it is thelevel of low density lipoprotein(LDL) cholesterol is most directlyassociated with CHD ( Gordon etal 1977). Very low densitylipoprotein (VLDL) has also beenshown to be associated withpremature atherosclerosis. Highdensity lipoprotein (HDL)cholesterol is protective againstCHD (Gordon et al 1977). HDLshould be more than 30 mg/dl.Cholesterol/HDL ratio less than 3.5has been recommended as a clinicalgoal for CHD prevention (Superkoet al 1985). Regular physicalexercise increase HDLconcentration and decrease the body

weight and blood pressure, reducedblood clotting, promote colateralvessel which are beneficial tocardiovascular health. The risk ofCHD is 2-3 times higher indiabetics. High alcohol intake isanother risk factor for CHDhypertension and all cardiovasculardisease.

Genetic factors are determinantsof an individuals TC and LDL levelsdetermines the CHD risk. Type A

HEALTH

l 17 Indian Coconut Journal

behaviour associated withcompetitive restlessness, hestilityand impatience are more prone toCHD than the calmer type Bindividuals.

Haemostatic factors – High levelsof fibrinogen and factor VII areassociated with increased risk of MI(coronary thrombosis). Obesity,physical inactivity etc are also riskfactors. Other dietary factors – Lowlevel of of vit. C, vit. E and otherantioxidants may enhance theproduction of oxidized LDL whichfavours CHD. By dietary modificationand controlling the risk factors whereapplicable reduced the risk of CHD.

Some facts about fats

What people eat is not caloriesbut food and consideration offlavour and variations of appetite canmake nonsense of the dietician’stheories. Good nutrition means“maintaining a nutritional status thatenables us to grow well and enjoygood health. The food according tochemical composition is divided intoprotein, fat, carbohydrates, vitamins& minerals. In the Indian dietarythey contribute to the total energyintake as follows.

Protein - 7 – 15%

Fats - 10 – 30%

Carbohydrate - 65 – 80%

In developed countries fatsprovide 30-40% of total energyintake. The WHO expert committeeon prevention of CHD hasrecommended only 20-30% of totaldietary energy to be provided by fat.

Fats are classified as

a) Simple lipids eg – triglycerides

b) Compound lipids eg –phospholipids

c) Derived lipis eg – cholesterol

Fats yield fatty acids and glycerolon hydrolysis. Fatty acids aredevided into saturated fatty acid (eg– lauric, palmitic, stearic acids etc)and unsaturated fatty acids which arefurther divided into monounsaturated (eg – oleic acid) andpoly unsaturated fatty acid (eglinoleic acid).

Saturated fatty acids contain nodouble bond, unsaturated fatty acidscontains one or more double bonds.

important EFA which serves as abasis for production of other EFA.

Coconut oil and coronary heartdisease

Coconut oil constitutes the mostimportant source of dietary fat inmany countries. But, of late, theconsumption of coconut oil has beenlinked with the incidence ofCoronary Heart Disease andsustained campaign against its useis going on. Being rich in saturatedfatty acid, coconut oil is oftenbracketed with animal fats such aslard, butter and egg products ashaving cholesterogenic properties.

Fatty acid content of different fats(%)

Fats Saturated F.A. Mono unsaturated F.A. Poly unsaturated F.A.

Coconut oil 92 6 2

Palm oil 46 44 10

Cotton seed oil 25 25 50

Ground nut oil 19 50 31

Safflower oil 10 15 75

Sunflower oil 8 27 65

Corn oil 8 27 65

Soya bean oil 14 24 62

Butter 60 37 3

margarine 25 25 50

Fatty acid composition of coconut oil (% )wt. of total fatty acids

Medium chain saturated % Monounsaturated %

Capric acid (C:10) 6 Oleic acid (C18:1:9) 6

Lauric acid (C:12) 47 Poly unsaturated

Myristic acid (C:14) 18 Linoleic acid(Omega 6C18:2) 2

Palmitic acid (C:16) 9 Omega 3 fattyacid Nil

Stearic acid (C:18) 3

(Rajan 2006)

Mono unsaturated fatty acidcontains one double bond. Polyunsaturated fatty acid (PUFA)contains two or more double bond.Essential fatty acids (EFA) are thosethat can not be synthesized byhumans. They can be derived fromfood. Linoleic acid is the most

Chemically all the saturated fattyacids are not alike in their dietaryproperties. The difference isbasically in the length of the carbonchain or the number of carbonspresent in the fatty acid. Thedominant fatty acid present incoconut oil are medium chain fatty

HEALTH

18 lOctober 2008

acids (MCFA). These MCFA areabsorbed directly through the portalvein into the liver and do not requirethe carnitine transport for their entryinto the cells and subsequentmetabolism. They are immediatelymade available to the body unlikelong chain fatty acid which requireemulsification in the intestine forabosorbtion and they reach thesystemic circulation via the lymphaticsystem. Because of their distributionto all parts of the body before reachingto the liver, they are more prone tobe deposited in the different tissues.In simple word coconut fats are easilydigestable and not cerenlate in theblood stream and not stored. Mediumchain fatty acds (MCFAs) are notdeposited in the adipose tissue butare readily oxidized in the body toprovide quick energy favourable foruse in sports nutrition and in slimingdiet products (Kaunitz 2001). MCFAsare beneficial for people sufferingfrom fat mal absorbtion and used ininfant formulations. The lauric acidin coconut oil is used by the body asdisease fighting derivativemonolaurin that babies make from thelauric acid they get from their mothersmilk (Mary Enig).

Coconut oil & palm oil are calledlauric oils which make them uniquefrom other vegetable oils. Onhydrolysis coconut oil yields 85%fatty acids and 15% glycerol. Thelimitation in the use of coconut oil isthat it contains very low amount ofessential fatty acids (EFA). Some fishoil, soya bean oil sunflower oil,peanut oil etc. are rich source ofessential fatty acids. These deficiencycan be meet up through the use ofvariety of food particularly fish.

In the developed countries theunsaturated vegetable oils aregenerally consumed afterhydrogenation. On hydrogenerationpart of the unsaturated fats getsconverted into saturated long chainfatty acid (LCFA) trans fatty acids thatcause elevation in cholesterol (Enig1990). Contrary to this coconut oilboth in its natural state andhydrogenated form will have majorityof its fatty acids as medium chain fattyacids which on consumption will notelevate cholesterol levels. Coconut oilis also a preferred oil in the house holdculinary preparations because it couldbe reheated in subsequent uses. Butother vegetable oils are not amenableto such uses as they produce toxin tohealth in the process of heatingcooling and reheating.

As it is already mentioned anexcess of cholesterol in the blood andof blood fats in general are caused notonly by the fat component of a normaldiet but by other factors as well. Theyare related to heredity, disease ofthyroid gland, pancreas, liver, kidneyetc. obesity, sedentary habits,prolonged mental stress and intake ofcholesterol rich food eg – dairyproduct, eggs, red meat etc. Thevegetable oil including coconut oil donot contain cholesterol as in animalfood.

An excessive intake of cholesterolrich food will lead to a gradualincrease in the serum cholesterol leveland cause blood lipid abnormalities.

High serum cholesterol is one of themajor risk factor of coronary heartdisease. But the consumption ofcoconut oil has not been proved tohave any relationship either with theincidence of the disease (CHD) orwith hypercholesterolaeia orhyperlipidaemia. Coconut kernelcontains 7-8% dietary fiber whichbeneficially influences serumcholesterol(Sindhu & Rajmohan2006).

Studies conducted in manycountries by different workers on theeffects of dietary Fatty acid onhuman health have revealedbeneficial results from the use ofcoconut oil. In most of the studiescoconut oil has proved to be neutral.Many animal experiment showsbeneficial or harmless effects ofcoconut oil consumption. Coconutoil feeding produced significantlyhigher alpha lipoproteins (HDL)relative to sunflower oil feeding inrats (Host mark et al 1980). Totaltissue cholesterol accumulation foranimals on the safflower diet was 6times greater than on coconut oil dietand twice that of soybean oil diet(Award 1981).CHD is unknownamong Polynesian population whosestaple diet is coconut. In anepidemiological and experimentalobservation Kamitz and Dayzil(1992) reviewed that dietary coconutoil does not lead to high serumcholesterol or high CHD. Prior etal 1981 had shown that when a

HEALTH

The reported figures are

Vegetable oil cholesterol Animal fats cholesterol

Palm oil 18 ppm egg 5000 ppm

Soybean oil 28 ppm butter 3150 ppm

Corn oil 50 ppm cheese 1100 ppm

Coconut oil 0 – 14 ppm Lardmilk 3500 ppm150 ppm

l 19 Indian Coconut Journal

population lowered their intake ofcoconut oil their total cholesteroland LDL increased and HDL(goodcholesterol) decreased. Ng et al 1991reported that by supplying 75% fatfrom coconut oil total cholesterolincreased 1.1% bnt, HDL cholesterolincreased 21.4% resulting LDL/HDL ratio decreased by 3.6%.

From the experiments it can beobserved that effect of coconut oil onserum cholesterol is that there maybe a rise in total cholesterol, LDL andHDL who have lower serumcholesterol, but there is lowering oftotal cholesterol and LDL (badcholesterol) in hypercholestrolemics.Clinical studies done at the NewEngland Deaconess Hospital, aHavard Medical School affiliate,showed that coconut oil is neutral inits effects on blood lipids and willnot cause an increase in cholesterolor cause cardio vascular disease.Coconut oil even increased the HDL(good cholesterol) reducing the riskfor CHD.

Saturated fats may be consideredas a major culprit for CHD becausethere is some association betweenserum cholesterol and CHD andbetween saturated fat and serumcholesterol. However, a fearcomplex has been created among thegeneral public that consumption ofcoconut oil result in elevatedcholesterol level. This myth wasprimarily due to equating coconut oilwith saturated fat without knowingeverything about saturated fat. Thesaturated fat in coconut oil is of shortchain and medium chain fatty acid.All saturated fats are not harmful.The real problematic fat is thehydrogenated vegetable fats or

animal fats.Black burn et al (1988)concluded that when coconut oil isfed with other fats or supplementedwith linoleic acid, coconut oil is aneutral fat in terms ofatherogenecity. Kurup andRajmohan (1994) also found nostatistically significant alteration inthe serum total cholesterol, HDL,LDL, HDL/total cholesterol ratioand LDL/HDL ratio of triglyceridesfrom the baseline values.

The observation and otherevidences suggest that coconut oilis more beneficial to human body asa dietary fat than the natural orhydrogenated form of unsaturatedvegetable oil. The incidence ofcoronary heart disease could bebetter linked with the consumptionof cholesterol rich food of animalorigin and the sedentary habitsassociated with a tension riddenmechanical society.

References

Award AB. (1981). effect of dietary lipids oncomposition and glucose utilization by ratadipose tissue. J Nutriticn 111: 34 -39.

Black burn GL, Kater G, Mascioli EA,Kowlchuk M, Babayan VK and Bistri anBR, (1989). A reevaluation of coconut oil’seffect on serum cholesterol andatherogenesis. The J. of the PhillipineMed. Assoc. 65 : 144 – 152.

Davidson’s Principales and Practices ofMedicine 17th ed. ELBS – ChurchillLivingstone.

Enig MG (1990) Fats and oils : Understandingthe functions and properties of partiallyhydrogenated fats and oils and theirrelationship to unhydrogenated fats andoils. PJCS X V: 1 pp 27-31.

Gordon T et al (1977) Am. J. Med, 62: 707.

Harisson’s Principales of Internal Medicines15 th ed. Mc Grow – Hill.

Hostmark A T, Spydevold O and Eilertseen E.(1980). Plasma lipid concentration and

HEALTH

liver output of lipoprotein in rats fedcoconut fat or sunflower oil. Artery 7: 367-383.

Kaunitz H (2001) The ABC of MCT’S,Coconut Today. Special Issue. UCAP.

Kauntiz H and Dayrit CS (1992). Coconut oilconsumption and coronary heart disease,Philipp. J of internal Med. 30 : 165 – 171.

Keys A (1980) seven countries, a multivariateanalysis of death and CHD, HavardUniversity Press, Cambridge MA.

Kumar V, Cotran R.S. Robbuis S L (1992)Basic Pathology, Prism Books Pvt Ltd 5th

ed.

Kurup PA and Rajmohan T. (1994).Consumption of coconut oil and kerneland the incidence of atherosclerosis.Proceedings symp. Coconut and coconutoil in human nutrition 27th March Kochi.India, PP 35 -59.

Murray RK, Ganner KD, Mayes AP, RodwellWV (1994) Harper’s Biochemistry 21 eds.

Ng T K W, Hanan K, Lim J B Lye M S andIshak R (1991). Non hypercholesterolemiceffects of a palm oil diet in MalaysiamVolunteers. Am. J. Clin. Nutrition 53:101.

Park K (2000) Pork’s Text book of Preventiveand Social Medicine 16ed. Banarsidas B.Publication (India) Appeleton & Lange.

Prior I A, Davidson F, Satmond C E andEzochans Kaz, (1981.) Cholesterol,coconuts and diet on polynesion atolls :anatural experiment: the Pukpuka andTokelan Island stdues. Am. J. Clin.Nutrition 34: 1552 – 1561.

Rajan R(2006). Coconut oil – The healthiestoil on earth. Indian coconut Journal 37:2

Sindhu J A and Rajmohan T (2006) coconutfiber – a natural hypolipidemic andhypoglycemic agent. Indian Coconut J.37(3): 21-23.

Superko H R et al (1985) Am J Med, 78:826.

Sundaram K, Hayes K C and Siru OH (1994).Dietary palmistic acid results in lowercholesterol than does a lauric – mystricacid combination in normolipemichumans. Am. J. Clim. Nutrition 59: 841 –846.

Thampam PK(1993). Hand book on coconutpalm 3rd ed. Oxford & IBH Publishingco.Pvt Ltd.