Coconut Oil Market Metabolism

Coconut

Coconut oil: an overview

COCONUT OIL: MARKET AND CONSUMPTION

Coconut products are now part of people's diets worldwide, although only some Asian populations, such as Sri Lankans, Minangkabau, and Filipinos, have coconut as part of their daily diet. As expected, the Asian continent holds the largest area of coconut tree plantations, where coconut palm cultivation is intended for commercial fruit copra (dried coconut meat) exploitation for oil production and dehydrated dried coconut (18). The Philippines, Indonesia, and India are the three most important coconut oil producers worldwide (19).

In the past few years, international coconut oil consumption and production, especially that of virgin unrefined coconut oil, has increased significantly (6). It is estimated that 640,000 tons of coconut oil were consumed in the Philippines, 449,000 tons in India, and 468,000 tons in the United States in 2016 (20). The same is observed in Europe, where the United Kingdom stands out as one of the main importers of coconut oil, having been responsible for around 7% of Sri Lanka's coconut exports in 2015 (21). There are no records regarding Brazilian consumption of coconut oil until 2020, when an online survey of graduate students and laymen in southern Brazil found that 59.1% of the responders consumed coconut oil (22). However, its use for food preparation or as a dietary supplement was uncommon until the mid-2010s. As it is rich in SFA, a type of fat well known as being related to increased plasma levels of low-density lipoprotein (LDL-C) and increased cardiovascular risk, the consumption of coconut oil was not recommended by scientific societies (10).

Human studies testing the effects of coconut oil on cardiometabolic health date back to the 1990s (23,24), but it was only after the publication and possibly dissemination of the results of other studies (25,26) at

scientific meetings and on social networks that coconut oil sparked people's interest as a new option for consumption and for healthy diet prescriptions.

These short-term studies showed a slight improvement in lipid and anthropometric profiles with coconut oil intake in healthy adult populations (25,26).

However, their results were based on surrogate markers of cardiometabolic health, and no

studies to date have actually evaluated the potential benefit of coconut oil consumption in preventing diabetes and hard cardiovascular outcomes.

Furthermore, it is also possible that these studies set off an interest in the food industry to market coconut oil as a healthy food by broadcasting its benefits on websites, blogs, health professionals’ social media profiles, and in clinical practice, spreading the news that coconut oil is healthy to cook with or to add to salads and other meals .

Coconut oil was an unusual component of westernized dietary patterns until the mid-2010s.

In spite of being rich in saturated fatty acids, there has been a surge in beliefs that coconut oil is healthy and possibly superior to other oils in improving cardiometabolic outcomes (1),

without support from strong scientific evidence (2-5).

This phenomenon has been accompanied by a rise in consumption rates in the last decade (6)

and might be explained by the spread of misinformation in internet-based and traditional media (7,8).

This review aims to summarize the current knowledge on coconut oil's general characteristics, its effects on cardiometabolic and anthropometric markers, and the possible role of misinformation spread as the catalyst for the observed change in dietary patterns in the West.

COCONUT OIL: CHARACTERISTICS AND METABOLISM

Approximately 91% of coconut oil fatty acids (FAs)

are saturated (SFAs), of which 46.2% are lauric acid (C12:0), 18.5% myristic acid (C14:0), 9.5% palmitic acid (C16:0), 7.5% caprylic acid (C8:0), and 6% capric acid (C10:0). The remaining FAs are monounsaturated (MUFAs) (7%) and polyunsaturated (PUFAs) (2%). Coconut oil is low in linoleic acid (18:2) and contains no linolenic acid (18:3) [both essential fatty acids] (Figure 1) (9).

Figure 1. Coconut oil fatty acid composition. C4:0 = butyric; C6:0 = caproic acid; C8:0 = caprylic acid; C10:0 = capric acid; C12:0 = lauric acid; C14:0 = myristic acid; C16:0 = palmitic acid; C18:0 = stearic acid; C18:1: = oleic acid; C18:2 = linoleic acid.

Dietary fats are composed of a mixture of fatty acids (SFAs, MUFAs, and PUFAs), and their composition varies according to their source: animal or vegetable. Fats with a higher proportion of MUFAs and PUFAs are generally

liquid at room temperature and are referred to as “oils,” whereas fats with a higher proportion of SFAs, especially long-chain FAs, are usually solid at room temperature and are called “fats” (10,11). Hence, “coconut oil,” as it is popularly known, is not the most correct term, since it is solid at room temperature precisely due

to its high amount of SFAs and is, therefore, considered a solid fat for nutritional purposes (11).

Lauric acid, the main FA contained in coconut oil, can be classified as both a medium-chain fatty acid (MCFA) and a long-chain fatty acid (LCFA); thus, it is a FA

with intermediate properties (12). MCFAs, mainly composed of caprylic (C8:0) and capric (C10:0) acids,

are absorbed in the small intestine bound to albumin and reach the liver via the portal system without increasing triglyceridemia (13). Conversely, 70% to 75% of lauric acid is absorbed within

chylomicrons (similarly to LCFA absorption) (6), and its presence in chylomicrons is dose-dependent (14). Overall, MCFAs (C8:0 and C10:0) have a low molecular weight (512 on average), unlike LCFAs, which have a higher molecular weight (the molecular weight of coconut oil is 638).

FAs with lower molecular weights facilitate

pancreatic lipase action, being hydrolyzed more

efficiently in the small intestine compared to

FAs with longer chains (15).

LCFAs are esterified in enterocytes,

where they form triglycerides (TGs) that are

transported to the bloodstream via the

lymphatic system by chylomicrons.

Lipoprotein lipase hydrolyzes chylomicron TGs, releasing FAs to peripheral tissues, which can either be used as an

energy source or be re-esterified into new

TGs for storage (10). LCFAs require the

transporter carnitine palmitoyl transferase in the

outer mitochondrial membrane to be internalized

into the organelle and oxidized to acetyl-CoA to serve as an energy source (16,17). By contrast, MCFAs are absorbed directly into the bloodstream and are not significantly

incorporated in chylomicrons and

very-low-density lipoproteins (VLDL).

Hence, they are considered a quick source of energy, because, as they pass through the enterocytes, MCFAs reach the portal circulation and are transported to the liver bound to albumin,

where they are oxidized. It has been speculated that,

due to their rapid metabolism

, MCFAs could stimulate thermogenesis,

decreasing their deposition in adipose tissue, which would increase satiety without increasing serum total cholesterol (TC) levels (10). However, there are no experimental

studies that prove these theories, and

even if there were, these findings

could not be extrapolated to coconut oil

due to its high concentration of lauric acid, which is not absorbed, transported, and metabolized in this manner

Ref Arch Endocrinol Metab. 2023 Jun 19;67(6):e000641. doi: 10.20945/2359-3997000000641