Coconut oil is produced by
crushing copra, the dried
kernel, which contains about 60-
65% of the oil. The oil has the natural
sweet taste of coconut and contains
92% of saturated fatty acids(in the
form of triglycerides), most of them
(about 70%) are lower chain
saturated fatty acids known as
medium chain fatty acids (MCFAs).
MCFAs are not common to different
vegetable oils with lauric acid at 45-
56%. Various fractions of coconut oil
have medium chain triglycerides and
are excellent solvent for flavours,
essences, emulsifiers etc. These fatty
acids are used in the preparation of
emulsifiers, as drugs and also in
cosmetics. Its metabolism is different
from that of the normal vegetable oils
containing long chain fatty acids.
Hence, it cannot be generalized as an
oil similar in properties to that of a
92% long chain saturated fatty acids
containing oil/fat. More studies are
required to prove the good effects of
coconut oil, medium chain
triglycerides (MCT) and the fatty
acids on humans especially on the ill
effects on cardiovascular and other
diseases. The review covers the
production of coconut oil, its chemistry, MCT and its applications
taking a holistic approach on the good
and bad effects of coconut oil reported
in the literature.

/pdf/coconut-oil-chemistry-production-and-its-applications-a-51dvuyamo9.pdf

Coconut Oil: Chemistry,Production and Its Applications -A Review

Erucic acid is the trivial name of the fatty acid cis-13-docosenoic acid and occurs at high concentrations mainly in the seeds of species of the Brassicaceae (e.g. rape seed or mustard seed). The European Commission requested EFSA to deliver a scientific opinion on the risks for animal and human health related to the presence of erucic acid in feed and food. For most humans, the main contributor to dietary exposure to erucic acid was the food group ‘Fine bakery wares’. In ‘Infants’, ‘Food for infants and small children’ was the main contributor to exposure. The heart is the principal target organ for toxic effects after exposure. Myocardial lipidosis was identified as the critical effect for chronic exposure to erucic acid. This effect is reversible and transient during prolonged exposure. A tolerable daily intake (TDI) of 7 mg/kg body weight (bw) per day for erucic acid was established, based on a no observed adverse effect level of 0.7 g/kg bw per day for lipidosis in young rats and newborn piglets. Mean chronic exposure of the different groups of the population did not exceed the TDI. The 95th percentile dietary exposure level was highest in infants and other children, ranging from 1.3 to 7.4 mg/kg bw per day; the higher level being at the level of the TDI. This may indicate a risk for young individuals with high erucic acid exposure. In pigs, levels of erucic acid are unlikely to represent a health concern. However, for poultry, the small margin between the lowest observed adverse effect level (LOAEL) and the estimated exposure may indicate a health risk where maximum inclusion rates are applied. Due to the absence of adequate data, the risk for ruminants, horses, fish and rabbits could not be assessed.

https://efsa.onlinelibrary.wiley.com/doi/pdf/10.2903/j.efsa.2016.4593

Erucic acid in feed and food

Brassicaceae germplasm diversity for agronomic and seed quality traits under drought stress

Male Sprague-Dawley rats were fed diets for 1 or 16 weeks, containing 20% by weight vegetable oils differing widely in their oleic, linoleic and linolenic acid content. No significant changes were observed in the level of the cardiac lipid classes. The fatty acid composition of the 2 major phospholipids, phosphatidylcholine and phosphatidylethanolamine, showed a remarkable similarity between diets in the concentration of total saturated, C22 polyunsaturated and arachidonic acids. Monounsaturated acids were incorporated depending on their dietary concentration, but the increases were moderate. Dietary linolenic acid rapidly substituted C22 polyunsaturated fatty acids of the linoleic acid family (n-6) with those from the linolenic acid family (n-3). The results suggest that dietary linolenic acid of less than 15% does not inhibit the conversion of linoleic to arachidonic acid but the subsequent conversion of arachidonic acid to the C22 polyunsaturates was greatly reduced. Significant amounts of dietary monounsaturated fatty acids were incorporated into cardiac cardiolipin accompanied by increases in polyunsaturated fatty acids, apparently to maintain an average of 2 double bonds/molecule. The cardiac sphingomyelins also accumulated monounsaturated fatty acids depending on the dietary concentration. It is quite evident from the results of this study that the incorporation of oleic acid and the substitution of linolenic for linoleic acid-derived C22 polyunsaturated fatty acids into cardiac phospholipids was related to the dietary concentration of these fatty acids and was not peculiar to any specific oil. Even though it is impossible to estimate the effect of such changes in cardiac phospholipids on membrane structure and function, results are discussed which suggest that the resultant membrane in the Spragu-Dawley male rat is more fragile, leading to greater cellular breakdown and focal necrosis.

Comparative studies on composition of cardiac phospholipids in rats fed different vegetable oils

It is widely recognized that dietary polyunsaturated fatty acids (PUFA’s) and cholesterol can profoundly influence the development of atherosclerotic plaques in coronary vessels, which may lead to myocardial infarction. The possibility that dietary fatty acids may also directly influence cardiac function has received less attention. We therefore reviewed the evidence of the effects of dietary fatty acids, in particular n-3 and n-6 PUFA’s, on myocardial phospholipid fatty acid composition and cardiovascular performance. Heart organelles appear to incorporate uncommon fatty acids like 22:1 and trans- 18:1. Diets enriched with 22:1 induce myocardial lipidosis. N-9, n-6 and n-3 families compete among membrane C20 and C22 acids. Several studies have dealt with the relation between diet-induced changes of cardiac membrane (sarcolemma, sarcoplasmic reticulum and mitochondria) phospholipids and membrane function. In view of the variety of diets used and of the membrane functions studied, the results do not permit equivocal interpretation. Several investigators have reported an altered stress response of the heart due to a change of PUFA’s in the diet. In rats fed with a low 18:2n-6/18:3n-3 ratio combined with relatively low amounts of saturated fatty acids, a high incidence of myocardial lesions has been observed. Pigs are less sensitive but more susceptible to the development of vitamin E deficiency, when the dietary PUFA content is high. Increased contractility and coronary flow rate have been reported for Langendorff-perfused hearts of rats fed 18:2n-6-rich diets. The effects on coronary flow rate are possibly related to alterations in eicosanoid synthesis, which may also contribute to the reduction by n-6 or n-3 PUFA’s in infarct size, magnitude of recovery of function and suppression of reperfusion arrhythmias following release of a coronary artery ligation. On the other hand, increased peroxidation of membrane lipids, due to their high content of n-3 PUFA, may be deleterious.

Dietary fatty acids and myocardial function

Male Wistar rats were fed semipurified diets containing 20% fat for 25 weeks. Ten different oils or oil blends were employed, including rapeseed oils, simulated rapeseed-type oils, and modified rapeseed-type oils. Safflower, soybean, and hydrogenated coconut oils served as control oils. Histopathological examination of the cardiac tissue was conducted at the end of the study and an incidence-severity rating assigned to the lesions induced by each fat. Oils containing high levels of erucic acid (26–30%) induced the most severe cardiac necrosis, irrespective of the source of erucic acid (rapeseed oil or nasturtium oil). Increasing the linoleic: linolenic acid ratio of the high erucic oils to that of soybean oil failed to reduce necrosis, but the absence of linolenic acid from a high erucic acid oil blend resulted in a markedly reduced lesion incidence-severity rating, comparable to those obtained for low erucic acid rapessed oil and soybean oil which were similar. Lowest lesion incidence was obtained with safflower oil and hydrogenated coconut oil. We have postulated that linolenic acid plays a role in the etiology of cardiac necrosis observed when rats are fed diets containing low erucic acid rapeseed oils.

B. L. Walker

Papers

Cardiopathogenicity of rapeseed oils and oil blends differing in erucic, linoleic, and linolenic acid content.