Quick Summary tl;dr
Coconut oil fatty acids are saturated fatty acids.
There are two (and potentially three) separate problems with the claim that coconut oil is ‘pure poison’ because it is virtually entirely saturated fat:
- • it assumes dietary saturated fat is poison;
- • it assumes coconut oil fatty acids (MCFAs) behave like more common longer-chain fatty acids (saturated or otherwise); and
- • most common sources of dietary saturated fats are pizza and doughnuts.
Evidence to date suggests coconut oil may have beneficial effects on cognition and saturated fats clearly aren’t ‘pure poison.’
Coconut oil has been unfairly vilified due to its saturated fat content, although this is fallacious on multiple accounts. The fats in coconut oil don’t really behave like saturated fats (SFAs), and even if they did, the evidence against saturated fats is mixed.
Coconut Oil Fatty Acids Are Unlike Other Fatty Acids
This has less to do with the fact that they’re mostly saturated and more to do with their markedly shorter chain length. Most dietary fats (LCFAs) are 16 to 18 carbons long whereas coconut oil fatty acids, collectively referred to as ‘medium-chain fatty acids’ (MCFAs), are 8 to 14.
Most nutrients are absorbed into the portal vein and then liver. LCFAs are different. The “why” is hotly debated — some people believe this is to spare LCFAs from tissues that don’t use them very much (eg, liver) for tissues that rely on them more (eg, heart) — but not the “how.” LCFAs are absorbed into the lymphatic system, bypassing liver, and entering the periphery directly.
Medium-chain fatty acids behave differently from other saturated fats. MCFAs, like those in coconut oil, are absorbed like most other nutrients — into the portal vein and then liver. They’re not efficiently stored as triacylglycerols or used for any other major purpose so instead of just floating around doing nothing or getting in the way, they’re partially oxidized into ketones. They’re not highly fully oxidized because liver is oxidizing other fuels and simply doesn’t need the energy.
Saturated Fat Per Se
As detailed above, MCFAs behave very differently from LCFAs (regardless of saturation status), and as such shouldn’t be directly compared to them or vilified because of their saturation.
That said, I remain skeptical on the vast claims against saturated fats per se. Most of the evidence is observational, meaning complicated statistical models are required in attempt to control for every possible confounding variable, which is nearly impossible, so in effect they basically just control for the obvious confounding variables and this is assumed to be ‘good enough.’ From a logical or scientific philosophy perspective, it’s not. Randomized controlled intervention trials are the sort we should be relying on for more accurate nutritional guidance.
Also, remember, coconut oil fatty acids (MCFAs) are saturated but much shorter than most dietary SFAs. Further, the most common source of dietary SFAs are junk foods like pizza and doughnuts… no wonder they get a bad rap!
However, when studied under more rigorous conditions, some studies show saturated fats aren’t so bad after all. Remember, these SFAs are not the same SFAs like those found in coconut oil, I’m just making the case against coconut oil being poison because of their saturated fatty acid content.
For example, one study showed replacing SFAs (eg, dairy) with monounsaturated fats (eg, canola oil) or polyunsaturated fats (eg, safflower or sunflower oil), HDL declined ( 1). In another study, increasing dietary SFAs were shown to modestly increase HDL ( 2). Lastly, a coconut oil-rich diet increased HDL in patients with coronary artery disease ( 3) (reminder, these were mainly MCFAs, not long-chain SFAs).
Coconut Oil and Cognition
It is thought that one reason cognition declines in dementia is due to reduced ability of brain to utilize glucose. As the brain is not dependent on insulin for glucose uptake, there is no clear fix on this aspect of fuel provisions.
However, brain will just as easily use ketones if they’re there ( 4). That is, glucose is considered to be the primary fuel of the brain because in most people, glucose is present in the bloodstream at much higher concentrations than ketones. Ramping up ketones either via a ketogenic diet or coconut oil or both, can compensate for the reduced glucose uptake and fill the energy void ( 5), although this may not be the only way ketones help. For example, one study showed a protective effect of ketones on neurons directly ( 6).
In one study on patients with Alzheimer’s disease, two-20 mL doses of coconut oil per day for 21 days significantly improved cognitive function ( 7). In another study of similar duration, a coconut oil-rich Mediterranean diet improved various measures of cognition ( 8). These are not isolated findings ( 9). A similar effect has been observed for isolated MCFAs ( 10) and ketones given directly ( 11). And elevated ketone levels have shown beneficial effects in a variety of animal models of Alzheimer’s disease ( 12).
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