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Oil, the Nectar of Good Health
||Dr. D.M. Vasudevan, Principal (Retd.), Amrita Institute of Medical Sciences, Kochi|
There are strong evidences to state that the risk of coronary artery disease (CAD) is related with elevated levels of serum cholesterol, which in turn is correlated with an increased intake of saturated fats. A fear complex has been created among the general public that consumption of coconut oil results in elevated cholesterol levels. This myth is primarily due to the high content of saturated fats in coconut oil. It is known that saturated fatty acids will generally increase, while unsaturated fatty acids will tend to lower the cholesterol levels in blood.
Commonly occurring unsaturated fatty acids are linoleic acid (in ground nut oil) and linolenic acid (sun flower oil). Thus people started to take these vegetable oils with reduced usage of coconut oil. Within the last 50 years, per capita consumption of coconut oil in Kerala has been reduced to one-third. But during the same period in the same population, the incidence of myocardial infarction has increased to three folds. This fact alone is enough to disprove the anti-propaganda against coconut oil.
It may be stressed that all saturated fats are not harmful. Now we know that saturated fatty acids in coconut oil are of the medium chain variety. Nearly 55 % of the fatty acids in coconut oil are lauric acid (12 carbon atoms) and 20% myristic acid (14 carbon atoms), both medium chain fatty acids. On the other hand, the fats that cause heart disease are saturated long chain fatty acids with 16 or 18 carbon atoms in their structure.
Differences between coconut oil and other oils
Coconut oil is chemically different from all other oils containing saturated fatty acids. Medium chain fatty acids (in coconut oil) have certain definite advantages over other long chain fatty acids.
(a) The digestion of coconut oil is faster and undergoes complete digestion in upper intestine; this process does not require the help of pancreatic juice lipase. (b) They are absorbed as fatty acids, and are directly entering into the portal blood.
(c) Thus fatty acids from coconut oil are entering the liver directly to undergo rapid oxidation to release energy.
(d) So, fatty acids of coconut oil are not deposited in tissues.
On the other hand, other oils containing long chain fatty acids have definite disadvantages.
(a) They need pancreatic lipase for their digestion.
(b) They are absorbed as triglycerides and are first incorporated into large insoluble particles called chylomicrons by the intestinal cells.
(c) These are then absorbed to the lymph vessels and then to circulatory system, thereby going round all parts of the body before going to the liver for final oxidation.
(d) This transportation in blood needs the help of lipoproteins. Fats in lipoproteins are deposited into various organs, including heart vessels. Thus the long chain fatty acids also cause increase in the blood fat content. <>In short, coconut oil is the most easily digestible and absorbed class of fats and does not circulate in the blood stream and is not deposited.
Coronary artery disease (CAD) is a complex degenerative disease that causes reduced or absent blood flow in one or more of the arteries that encircle the heart. Atherosclerosis is the principal cause of CAD and is the single largest killer of both men and women, all over the world. The most deadly presentation of CAD is acute myocardial infarction (AMI).
The earliest pathologic lesion of atherosclerosis is the fatty streak, which may progress to lipid accumulation and the migration and proliferation of smooth muscle cells. Thus a fibrous plaque is formed. Activated platelets and macrophages will further contribute to vascular inflammation and later, thrombosis at these sites. Then a fibrous cap is formed that overlies a core of lipid-laden foam cells. Growth of the fibrous plaque results in vascular remodeling, progressive luminal narrowing, blood-flow abnormalities, and compromised oxygen supply to the heart muscle.
A number of large epidemiological studies have identified that an increase in serum cholesterol level is associated with increased risk of death from heart disease. For every 10% lowering of cholesterol, CAD mortality was reduced by 13%. In healthy persons, cholesterol level varies from 150 to 200 mg/dl. If other risk factors are present, cholesterol level should be kept preferably below 180 mg/dl. Values around 220 mg/dl will have moderate risk and values above 240 mg/dl need treatment.
Blood levels of LDL cholesterol (bad cholesterol) should be kept under 130 mg/dl. Levels between 130 and 159 mg/dl are borderline; while above 160 mg/dl carry definite risk. HDL cholesterol (good cholesterol) levels above 60 mg/dl protect against heart disease. A level below 40 mg/dl increases the risk of CAD. For every 1 mg/dl drop in HDL, the risk of heart disease rises 3%. If the ratio of total cholesterol / HDL is more than 3.5, it is dangerous. Similarly, LDL : HDL ratio more than 2.5 is also detrimental.
Hypertension is an important risk factor for the development of atherosclerosis, atherosclerotic cardiovascular disease and stroke. Diabetes mellitus is commonly associated with hyperlipidemia, hypertension, abnormalities of coagulation, platelet adhesion, atherosclerosis and myocardial infarction. Good control of diabetes may also reduce the risk of complications of CAD. Smoking has been identified as a major and modifiable risk factor for atherosclerosis and is associated with an increased relative risk of dying from vascular disease.
Convincing evidences are
available to show that lowering serum cholesterol reduces the risk of
subsequent coronary heart disease and overall mortality. The
primary treatments of hypercholesterolemia are diet and exercise.
This includes restriction of calorie intake; reduction in intake of
saturated fats and avoidance of cholesterol-containing food stuff.
Limiting the amount of fat to no more than 25 to 30% of daily calories
is recommended. The type of fat consumed is important. It is better to
take saturated (coconut oil), mono unsaturated (Gingelly oil) and poly
unsaturated (sunflower oil) in 1:1:1 ratio. A diet containing
mono-unsaturated or omega-3 fats will reduce the incidence of
atherosclerosis. Eating fruits and vegetables daily will also decrease
the risk of coronary artery disease.
Coconut oil does not produce atherosclerosis
There are dozens of animal and human studies in world literature to disprove allegations about coconut oil enhancing the risk of a CAD. There is not even one paper in the whole literature directly showing that coconut oil increases cardiac diseases. In fact, coconut oil is neutral with respect to atherogenicity (plaque formation).
Blackburn et al (1989) have reviewed the published literature and concluded that coconut oil will neither increase nor decrease the cholesterol level, and is a neutral fat in terms of atherogenicity. Kurup and Rajmohan (1995) conducted a study on 64 volunteers and found no statistically significant alteration in the serum total cholesterol, HDL cholesterol, LDL cholesterol, and triglycerides from the baseline values. Kaunitz and Dayrit (1992) have noted that the available population studies show that dietary coconut oil does not lead to high serum cholesterol or to high coronary heart disease mortality or morbidity. Sundaram et al (1994) fed coconut oil containing diets to healthy males. Their findings indicate that a favorable alteration in serum lipoprotein balance was achieved when coconut oil was included in the diet. Coconut is the chief source of energy for populations of Polynesian islands. But vascular disease is uncommon in these populations and there is no evidence of the high saturated fat intake having a harmful effect in these populations (Prior et al, 1981). When coconut oil was fed as 7% of energy to patients recovering from heart attacks, the patients had greater improvement compared to untreated controls, and no difference compared to patients treated with corn or safflower oils (Bierenbaum et al 1967). When compared with feeding coconut oil, feeding of soybean oils caused a significant decrease in HDL cholesterol (good cholesterol) (Lu et al 1997).
Hostmark et al (1980) compared the effects of diets containing 10% coconut fat and 10% sunflower oil on lipoprotein distribution in rats. Coconut oil feeding produced significantly lower levels of LDL (bad cholesterol) and significantly higher HDL (good cholesterol) relative to sunflower oil feeding. Awad (1981) compared the effects of diets containing coconut oil versus safflower oil on accumulation of cholesterol in tissues in rats. The total tissue cholesterol accumulation for animals on the safflower diet was six times greater than for animals fed the coconut oil. In mice studies, the phospholipids profiles were similar for diets on sunflower oil as well as on diets with coconut oil (Huang and Frische 1992). In studies with neonatal pigs, the feeding of coconut oil did not in any altered the blood composition of animals (McWhinney et al 1996). Trautwein et al (1997) studied cholesterol-fed hamsters on different oil supplements. Plasma cholesterol concentrations were higher for olive oil than for coconut oil (8.5 mmol/l). Even in this cholesterol-sensitive animal model, coconut oil performed better than olive oil. In summary, studies that supposedly showed a hypercholesterolemic effect of coconut oil feeding, in fact, usually have only shown that coconut oil was not as effective at lowering the serum cholesterol as was the more unsaturated fat being compared.
Fatty Acids (TFA)
excess, may be
Coconut oil has an advantage in these types of settings. Overweight person taking coconut oil, containing medium chain fatty acids, gradually over the months lose weight effortlessly (Geliebter 1980; Baba 1982; Bach and Babayan 1982). Replacing long chain fatty acids with medium chain fatty acids results in a decrease in body weight and a reduction in fat deposition (Bray 1980; Geliebter 1983; Hasihim and Tantibhedyangkul 1987). Coconut-oil-enriched diet was found to be effective in producing a decrease in fat stores (Portillo et al 1998). Cleary et al (1999) found that the safflower oil-fed animals had more fat cells than the coconut oil-fed.
Our idea is that when you
fat, you will gain weight. In this context, it may be a
paradoxical finding that overweight person taking coconut oil is losing
weight. The explanation is the following: Long chain fats will
almost always go into fat stores; this will eventually make the person
overweight and will cause dyslipidemia. However, as explained
previously, the medium chain fatty acids will be immediately utilised
for energy purposes, and will not be deposited in the body. Since
coconut oil will speed up metabolism and body will actually be burning
more calories in a day. This will help to reduce weight (Hill et
profile in persons
consuming coconut oil
This study was extended to analyse serum from 302 normal healthy persons, out of which 152 were consuming coconut oil and 150 were using sunflower oil for the past 2 years or more. There was no statistically significant difference in the cholesterol, HDL or LDL levels in coconut oil consuming population versus sunflower oil consuming population. Thus plasma fatty acid composition reflected no changes with dietary fat source. Lauric acid, the principal fatty acid of coconut oil was found in low concentrations among subjects of both groups. Higher intake of coconut oil did not cause any significant increase in the concentration of lauric acid in blood among coconut oil consumers.
oil consumers with disease
In various other studies throughout the world, chemical analysis of plaques did not show lauric acid or myristic acid (fats seen in coconut oil) (Felton et al 1994). Thus plaques from coronary artery are not due to intake of coconut oil. Moreover, fatty acid content of plaques from coconut oil group and sunflower group are the same. This clearly shows that coconut oil does not have an effect to produce plaque or heart disease.
Other beneficial effects of coconut oil
The major fat in mother’s milk is the same lauric acid that is seen in coconut oil. The lauric acid of coconut oil is used by the body to make the disease-fighting monolaurin in the skin. This monolaurin will inhibit viral, bacterial and protozoal infections. The medical community has largely overlooked this important benefit. Kabara (1978) and others have reported that medium chain fatty acids have inhibitory effects on various microorganisms such as bacteria, yeast, fungi, and enveloped viruses. The medium-chain saturated fatty acids disrupt the lipid membranes and kill the micro organisms (Isaacs et al 1992). Simple observations prove the stability of coconut oil and resistance to oxidative effects of the atmosphere. Coconut oil kept at room temperature for many months does not turn rancid as against other oils. It has been established that coconut oil reduces the need for Vitamin E.
The general advice given by physicians against the use of coconut oil needs re-evaluation. This mis-information arose, when long chain saturated fatty acids (LCSFA) were shown to increase cholesterol level. Since coconut oil also contains saturated fatty acids, people equated them with LCSFA. Now it is known that coconut oil contains medium chain fatty acids (MCFA). Metabolisms of LCFA and MCFA are drastically different. Coconut oil, within normal limits, neither decrease nor increase cholesterol levels. The advantages of coconut oil are that it does not affect serum cholesterol (neutral); it produces very little free radicals, as opposed to other oils (beneficial); it is rapidly absorbed, rapidly oxidized and is not deposited (beneficial) and it helps in resisting invading micro-organisms.
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