Skip to main content

Why is coconut oil healthy?

What do coconut oil, butter, and other kinds of fat from animals have in common? They are all saturated fats.

Yet coconut oil is supposedly good for us with health benefits such as weight loss, increasing good cholesterol levels, and decreasing risk of cardiovascular diseases. On the other hand, the American Heart Association recommends us to limit saturated fat consumption. So ... what explains the benefits of coconut oil?

The difference between coconut oil and fat from animals is in the length of the fatty acids. Coconut oil is a medium-chain fatty acid (MCFA) while fat from animals are long-chain fatty acids (LCFA). MCFAs have a carbon backbone of 7-12 carbons, while LCFAs have more than 12 carbons.

The body digests these fats differently. LCFAs are digested through the lymphatic system. LCFAs are packaged into chylomicrons which circulate through the body before reaching the liver. LCFAs are released from the chylomicron by lipoprotein lipase. All cells secrete this enzyme into their nearby extracellular space in order to intake fatty acids. But, the enzyme is secreted at different levels depending on the level of the hormone insulin. When insulin is high, fat cells secrete more lipoprotein lipase, thus releasing the LCFAs which can then get stored into the fat cells. At the same time, other cells (like muscle cells) secrete less lipoprotein lipase so that they take in and metabolize more glucose. Thus, if the LCFAs are stored in chylomicrons, the secretion of lipoprotein lipase is necessary for all cells in the body to uptake LCFAs. Once the LCFAs are released from its chylomicron package and stored into the fat cells, they are released from the fat cells into the bloodstream as free fatty acids, not packaged into chylomicrons.

MCFAs are digested through the hepatic portal system. The MCFAs are small enough to get absorbed straight into the bloodstream where it travels directly to the liver. These MCFAs are not packaged into chylomicrons, which means they are accessible to all cells in the body. They are not controlled by insulin levels, which means even when glucose levels are high, MCFA metabolism is not hindered. Rather, they are absorbed by whatever cell needs energy, which means only a limited amount of MCFAs are stored in fat cells.

The difference between how MCFAs and LCFAs are digested by the body can explain most of the health benefits of consuming coconut oil:
  • Weight loss is promoted because less fat is stored. In addition, when you burn more fat, ketones (a product of fat metabolism) is increased in the body which reduces our hunger and appetite.
  • Reduces inflammation and increases immune function because the MCFA in coconut oil is called lauric acid which inhibits certain bad bacteria in the gut and in the body. Moreover, during digestion, lauric acid is converted into monolaurin which has antibacterial, antiviral, and antifungal properties. Fewer harmful pathogens result in less inflammation. A study by Newell-Fugate et al. also suggests that the change in the gut microbiome caused by lauric acid and monolaurin might further reduce inflammation.
  • Brain function is enhanced because ketones can cross the blood-brain barrier and provide energy for the brain. Particularly in Alzheimer's patients, the brain might lack glucose even when glucose levels in the body are high. Moreover, parts of the brain in Alzheimer's patients have a reduced ability to metabolize glucose, making ketones especially important for their brain to function.
While consuming coconut oil does seem to improve your health, it is important to note that coconut oil is only 50% MCFAs. The rest of the fatty acids are LCFAs (coconut oil is 90% saturated fat). The almost equivalent percentage of LCFAs in coconut oil could result in decreased or even reversal of the health benefits of consuming MCFAs.

Some studies have shown an increase in good cholesterol (HDL) and a reduction in bad cholesterol (LDL). However, a molecular explanation for this is still unknown: on the one hand, MCFAs could increase HDL and lower LDL, but at the same time, LCFAs increase LDL. Since coconut oil is only 50% MCFAs, the increase and decrease of LDL caused by LCFAs and MCFAs seem to conflict with each other. Furthermore, there has been conflicting data about whether lauric acid actually increases or decreases HDL and LDL levels.

Further questions about this topic:
  • How does MCFAs and LCFAs influence cholesterol?
  • How are HDL and LDL formed in the liver?
  • How does lauric acid and monolaurin affect microbes?
  • Polyunsaturated and monounsaturated fats are all LCFAs. Why are they good for us?
  • Are short-chain fatty acids also good for us?

Sources:

Gunnars, Kris. “Top 10 Evidence-Based Health Benefits of Coconut Oil.” Healthline, Healthline Media, 11 Jan. 2018, www.healthline.com/nutrition/top-10-evidence-based-health-benefits-of-coconut-oil.

Newell-Fugate A., et al. Effects of coconut oil on glycemia, inflammation, and urogenital microbial parameters in female Ossabaw mini-pigs. PLoS One. 2017; 12(7).

Bruner, Sandra. “Lipoprotein Lipase.” Lipoprotein Lipase, www.physiologymodels.info/lipoproteins/LPL.htm.

Barba, Christine. “Which Is a Better 'Fuel for the Brain': Ketones or Sugar?” Being Patient, 29 Oct. 2018, www.beingpatient.com/ketones-for-alzheimers/.

Schönfeld P. and Wojtczak L. Short- and medium-chain fatty acids in energy metabolism: the cellular perspective. J Lipid Research. 2016; 57(6): 943–954.