Coconuts are grown on coconut palms and coconut oil is made from the nut (fruit) of the coconut.
Coconut oil contains 91% saturated fatty acids, of which a quarter are saturated long chain fatty acids, with more than 12 carbons, while all the rest are saturated fatty acids of medium chain length, i.e. 4 – 12 carbons. 7% of coconut oil are MUFA’s, while only 2% of the oil are PUFA’s. Thus coconut oil is high in a saturated fat, called medium chain triglycerides (MCT’s).
When coconut oil is claimed to be “virgin”, it generally means it has not been bleached, deodorized or refined. Sometimes the claim is also made that it is “cold pressed”, which in general terms implies that the mechanical pressing of the oil out of the nut, was done without the use of any outside heat source. The high pressure needed for such pressing does generate heat naturally, but the temperature is controlled so that it does not exceed 49 C or 120 F.
When applied to skin, coconut oil has a moisturizing effect – thus it is frequently found in creams, soaps and body washes. The use of coconut oil is a popular choice for sweet and biscuit manufacturers, because it gives a pleasant sensation in the mouth – the way a biscuit melts in the mouth is very important! For the same reason, coconut oil is often one of the “hidden” fats in processed food. Coconut oil is very stable, and as a more saturated oil, there is no problem of oxidation by air and light, producing off-flavors.
Digestion of MCT’s
Triglycerides are the major fat in the human diet because they are the major storage fat in plants and animals, contributing to our diet. Triglycerides consist of a glycerol backbone to which 3 free fatty acids are attached, and in the lumen of the intestine, this molecule is digested through hydrolysis by pancreatic lipase, to free fatty acids and monoacylglycerol. However, the route depends to some extent on the chain length of the fatty acids. Lingual lipase (produced by cells at the back of the tongue) and gastric lipases (produced in the stomach) preferentially digest short and medium chain fatty acids (less than 12 carbons in chain length) from dietary triglycerides. Therefore they are most active in babies and younger children, who generally drink lots of cow’s milk, rich in triglycerides with short and medium chain fatty acids.
Absorption of MCT’s
The fatty acids and monoacylglyerols produced by digestion in the intestines are packaged into tiny droplets, emulsified by bile salts, called micelles. Other dietary lipids such as cholesterol and fat soluble vitamins, are also found in these micelles. These micelles are then absorbed by the microvilli on the surface of the intestinal epithelial cells; repackaged as chylomicrons in the intestinal cells (similar to micelles) and from there they move into the small lymphatic vessels (lacteals) inside the microvilli. Triglycerides are transported in lipoprotein particles (chylomicrons is one example) as they are insoluble in water.
Short and medium chain fatty acids (4-12 carbons in length) do not require bile salts for their absorption. They are absorbed directly into the intestinal epithelial cells and as they do not need packaging into chylomicrons, they enter the portal blood (rather than the lymph), travelling to the liver carried by serum albumin in the blood. As fatty acids are hydrophobic, those with more than 4 carbons in chain length are usually transported attached to proteins – therefore in the blood stream attached mostly to albumin, being the most abundant protein in plasma.
Metabolism of medium chain fatty acids
Once inside body cells, fatty acids must be activated, before they can be oxidized for energy. Fatty acids of medium chain length (4-12 carbons) cross the mitochondrial membrane with ease and are then activated inside the mitochondrial matrix, before being oxidized to provide the cell with energy. (MCAD coupled to beta oxidation).
Ketone bodies are formed in the liver only, whenever the fatty acid levels in the blood are elevated, such as during fasting, starvation or as a result of a high fat, low carbohydrate diet.
A major factor stimulating ketone body production (4 carbons in length) is increased availability of fatty acids. An increased mobilization of fatty acids from adipose tissue (fat tissue), with consequential increase in free fatty acid levels in the liver, may be sufficient to stimulate ketone body formation (ketosis) in the liver. Increased release of free fatty acids from adipose tissue occurs during fasting and starvation, when the glucagon/insulin ratio increases. A diet that provides over 85% of its energy in the form of fat, can also result in ketosis.
Drug resistant epileptics are often treated with such ketogenic diets, high in medium chain triglycerides. Coconut oil would be an excellent source. The medium chain triglycerides are not stored as fat, but are immediately transported into the mitochondria, where they are oxidized to supply energy, as discussed above. The only problem with the diet is its unpalatability.
Ketone bodies are freely soluble in plasma and when their levels in the bloodstream are high, they are a valuable source of energy for various tissues, but especially the brain. As glucose is limited in such times (e.g. fasting), the brain resorts to using primarily ketones for energy. Evidence suggests that ketone bodies reduce epileptic seizures by changing the metabolism of glutamate and aspartate, two amino acid neurotransmitters in the brain.
Nola Dippenaar
April 2016