Coconut oil – good or bad?

The coconut palm tree, fruit and oil (Cocus nucifera) have a long history of use in Malaysia, India, the South Pacific and the Philippines for many religious, dietary and medicinal purposes.[1,2] The multifaceted application of coconut by traditional paradigms has also been observed in recent years with a resurgence in the popularity of coconut oil, particularly for dietary and medicinal purposes.[1,3,4] The role of saturated fatty acids (SFA) in health and disease is a hotly debated topic in nutritional medicine and, as a concentrated source of SFA, coconut oil has been part of this debate.[5,6] This article reviews the current evidence regarding the beneficial, harmful or neutral impact of coconut oil on health outcomes.

Classification and composition

Coconut oil is classified as copra or virgin according to the type of extraction and processing it undergoes, which naturally influences the structural and functional properties of the end material.[4,7]

Copra oil is formed by crushing dried coconut kernels, followed by refinement, distillation, bleaching and deodarisation, producing an oil with a higher degree of saturation more stable for single-use frying than virgin coconut oil (VCO). Alternatively, VCO, considered to be the purest form of coconut oil, is produced by pressing wet coconut kernels to extract an oil/milk emulsion, with the oil subsequently separated via physical extraction, fermentation or enzymatic processes. Consequently, VCO has a lower smoke point and higher concentration of phenolic acids [caffeic, syringic, p-coumaric, vanillic and ferulic acids], flavonoids (flavanones and dihydroflavonols) and vitamins (A and E).[4,7]

VCO is classified as a SFA because it is comprised of approximately 90% saturated fats and 10% unsaturated fats. Around 50-70% of the SFAs are medium-chain (MCFA: C6-C12) and short-chain (SCFA) (C2-C4) fatty acids, predominantly lauric and myristic acids, with smaller amounts of stearic, capric, caprylic, stearic and palmitic acids; while the unsaturated fatty acid portion is comprised of oleic, linoleic and linolenic acids.[1,3,4,6,8,9]

Absorption and metabolism

As with any ingested substance, the structure of fatty acids influences the digestive processes and metabolic pathways used by the body for their utilisation or storage.

SCFA are absorbed directly through the intestinal mucosal layer, while MCFA are hydrolysed and absorbed in both the stomach and small intestine. This rapid absorption can be partly attributed to the highly water-soluble nature of SCFAs and MCFAs. Following absorption, both SFCA and MCFA travel to the liver via the portal circulation. Here they are preferentially converted to acetoacetate and beta-hydroxybutyrate that are subsequently used as a rapid energy source by the brain, organs and muscles.[4,5,9]

Conversely, following hydrolysation and absorption via the rate-limiting active carnitine transport system, long-chain fatty acids (LCFA) attach to proteins to form lipoproteins that circulate in the bloodstream. They can be stored (in adipocytes and arterial walls) or used for energy or structural purposes.[4,5]

The utilisation of SCFA and MCFA from coconut oil as an energy source, as opposed to storage in adipose or other body tissues as occurs with LCFA, is a key factor to consider in the context of the potential health impact of coconut oil.[10,11]

Mechanisms of action

As well as being an energy source, VCO and the MCFA and SCFA that are naturally present have demonstrated a range of physiological actions in mechanistic studies. (Refer to Table 1.) The endogenous metabolism, utilisation and mechanisms of MCFA and SCFA underlie the impact of coconut oil on health and disease outcomes that have been investigated to-date.

Table 1: Physiological actions of fatty acids from coconut oil

Action	Mechanism
Antioxidant	Increases antioxidant status via catalase, SOD, glutathione, peroxidase and glutathione enzyme activity and tissue levels[1,4,9] Reduces lipid peroxidation[4]
Cardioprotective	Increased serum HDL-C, decreased LDL-C, TC, TG VLDL-C[4,10,12] Reduces gene expression of apolipoprotein B-48 lipid transporter à downregulation of high-TG chylomicrons[5] Decreases hepatic TG synthesis, VLDL-C secretion and postprandial plasma TG levels[5] Increases lipoprotein lipase activity à increased clearance of high-TG lipoproteins[5] Hypotensive[1,10] Antithrombotic via inhibition of platelet and coagulation factor activation[9]
Lipid metabolism	Increases lipolysis and decreases lipogenesis-activating transcription factors, lipogenic enzymes and fatty-acid uptake-associated enzymes[3,13] Shifts cells from global lipid anabolism to lipid catabolism[13] Increases thermogenesis[13] Decreases visceral and subcutaneous fat deposition, body weight gain and body fat mass[13]
Hepatoprotective	Reduces hepatic triacylglycerols Decreases lipid peroxidation Increases hepatic glutathione enzyme activity[1,4,14]
Glucose metabolism	Amelioration of blood glucose levels by regulating blood sugar and increasing insulin activity and binding affinity[1,9]
Antimicrobial Antifungal Antiviral Antiparasitic	Inhibition of gram-negative and gram-positive microbes [Staphylococcus aureus, Helicobacter pylori, Campylobacter jejuni, Listeria monocytogenes, Clostridium perfringens, Vibrio cholera, Escherichia coli and Proteobacteria, Prevotella, Bacteroidetes phyla][9,12,15] Inhibition of Candida species[9] Inhibition of Giardia lamblia[9]
Immune modulation	Interact with immune cells [macrophages, monocytes, granulocytes, neutrophils and B and T cells] via G-protein-coupled receptor (GPR84)[15]

SOD (superoxide dismutase); LDL-C (low-density lipoprotein cholesterol); TG (triglycerides); TC (total cholesterol); HDL-C (high-density lipoprotein cholesterol); VLDL-C (very low density lipoprotein cholesterol)

Health and disease outcomes associated with coconut oil

In recent years, there has been a significant focus on the potential health and disease-promoting outcomes associated with the regular dietary intake of coconut oil in heterogeneous populations. Currently the evidence does not allow for a definitive consensus to be made due to study outcomes variably demonstrating beneficial, harmful and neutral effects of coconut oil consumption for a range of disease states.

Cardiovascular disease (CVD)

The primary concern highlighted for the potential harmful impact of coconut oil on cardiovascular health is attributed to its classification as a SFA. However, the ‘saturated fat is bad’ messaging has been called into question due to evidence demonstrating no correlation between SFA intake and health outcomes (total mortality, CVD mortality, fatal- and non-fatal myocardial infarctions, coronary heart disease events and mortality), partly attributed to the positive effect of SFA on HDL-C compensating for its observed negative effect on LDL-C.[6,9]

Clinical trials investigating the effect of VCO specifically on CVD incidence demonstrated a reduction in heart disease associated with improved blood lipid profiles,[9] while a separate study showed a neutral effect on lipid profiles, antioxidant mechanisms and endothelial function following two years of dietary intake. Most of the evidence demonstrating a beneficial effect of VCO on CVD incidence is based on animal trials, with further human evidence required to confirm efficacy.[12]

More studies have been conducted on the impact of VCO on lipid profiles in both healthy and diseased populations. The evidence involving healthy subject groups is mixed, demonstrating that VCO both increased and decreased HDL-C and TGs, and increased or had neutral or non-significant effects on total, LDL-C, VLDL-C and intermediate-density lipoprotein levels.[4,5,8,12,17]

These variable results have also been observed in studies involving subjects with existing heart disease (CAD, hypercholesterolaemia), with VCO associated with both elevated and reduced LDL-C levels, and positive and neutral effects on HDL-C and total cholesterol concentrations.[10,16,17]

Glycaemic control

Mechanistic data demonstrates that VCO regulates blood sugar levels by enhancing insulin activity and binding affinity.[1,9] However, while there is not a significant amount of research, it does suggest that VCO may have a beneficial or neutral effect on glycaemic control.

One clinical trial showed that VCO ingested with a carbohydrate-rich meal by healthy subjects reduced the peak of the postprandial glucose response at 30 and 45-minutes.[18] In two other trials, VCO consumed over a two-year period, by subjects with stable CAD and for 4-weeks by healthy subjects, resulted in minimal effects on glycosylated haemoglobin, insulin and fasting blood glucose levels, respectively.[8,16] Conversely, acute ingestion of VCO by relatives of diabetes mellitus type 2 subjects was associated with a non-significant insulin response.[19] These results warrant further investigation, particularly to ascertain the effect of VCO on subjects with glycaemic-control-associated issues.

Body composition

While animal evidence has shown that VCO stimulates thermogenic and lipid catabolic pathways and reduces body weight and fat mass[3,13], the proposed role and general use of VCO for improving body composition parameters is not robustly supported by human clinical evidence due to inconsistent study results.

Overall, evidence from various clinical trials has demonstrated that dietary VCO intake either improved or had insignificant effects on total fullness perception, satiety, abdominal obesity and fasting metabolic rates, but did reduce total daily food intake.[12,20] More research is required to confirm the impact of VCO intake on these parameters.

Other clinical effects

VCO may also be beneficial for other health and disease outcomes, having demonstrated clinically relevant effects on the: quality of life of breast cancer patients undergoing chemotherapy;[21] tissue plasminogen activator antigen concentrations (associated with blood clots);[22] bone histomorphometric parameters; plaque and gingivial indices; atopic dermatitis;[4] neurodegeneration and cognitive status in Alzheimer’s disease and anti-inflammatory effects.[12] Further research is warranted to determine the efficacy of VCO for these health outcomes.

Factors impacting on study results and future research

While these variable results make it challenging to make definitive conclusions regarding the beneficial, harmful or neutral effect of VCO on health outcomes, a number of factors need to be considered both in relation to these results and for future investigations due to their potential impact on the study outcomes.

These include the type of coconut oil being used [i.e. hydrogenated vs VCO, variability of processing methods and concentrations of phenolic acids], the structure, metabolism and physiological impact of the comparable oil or compound, what is being used as the control substance (i.e. is it ‘inert’ in regards to the primary study outcome?) and the general dietary intake (e.g. high sugar and processed-food diet vs healthy diet), ethnicity (Caucasian, Pacific Islander, Asian), genetics and lifestyle habits (e.g. smoking) of the study population.[4,8,19,22,23]

Taking these factors into account, further research is required to determine the long-term health impact of SFA intake, the efficacy of VCO for the disease states discussed earlier and the relevance of non-glyceride constituents of SFA on health outcomes.

References

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Panth N, Dias CB, Wynne K, et al. Medium-chain fatty acids lower postprandial lipemia: a randomised crossover trial. Clin Nutr 2019 Feb 16. [Abstract]
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Cardosa DA, Moreira AS, de Oliveira GM, et al. A coconut extra virgin oil-rich diet increases HDL cholesterol and decreases waist circumference and body mass in coronary artery disease patients. Nutr Hosp 2015;32[50:2144-2152. [Abstract]
da Silva DC, Tavares MG, do Nascimento CKB, et al. Can coconut oil and treadmill exercise during the critical period of brain development ameliorate stress-related effects on anxiety-like behaviour and episodic-like memory in young rats? Food Funct 2018;9(3):1492-1499. [Abstract]
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Narayanankutty A, Palliyil DM, Kuruvilla K, Raghavamenon AC. Virgin coconut oil reverses hepatic steatosis by restoring redox homeostasis and lipid metabolism in male Wistar rats. J Sci Food Agric 2018;98[5]:1757-1764. [Abstract]
Xiang MSW, Tan JK, Macia L. The Molecular Nutrition of Fats - Fatty acids, gut bacteria and immune cell function – Chaper 11. Elsevier: Sydney, 2019. [Source]
Vijayakumar M, Vasudevan DM, Sundaram KR, et al. A randomised study of coconut oil versus sunflower oil on cardiovascular risk factors in patients with stable coronary heart disease. Indian Heart J 2016;68 4]:498-506. [Abstract]
Feranil AB, Duazo PL, Kuzawa CW, Adair LS. Coconut oil is associated with a beneficial profile in pre-menopausal women in Philippines. Asia Pc J Clin Nutr 2011;20(2):190-195. [Abstract]
Tan SY, Wan-Yi Peh E, Marangoni AG, Henry CJ. Effects of liquid oil vs oleogel coingested with a carbohydrate-rich meal on human blood triglycerides, glucose, insulin and appetite. Food Funct 2017;8(1):241-249. [Abstract]
Pietraszek A, Hermansen K, Pedersen SB, et al. Effects of a meal rich in medium-chain saturated fat on postprandial lipemia in relatives of type 2 diabetics. Nutrition 2013;29[7-8]:1000-1006. [Abstract]
Assuncao ML, Ferreira HS, dos Santos AF, et al. Effects of dietary coconut oil on the biochemical and anthropometric profiles of women presenting abdominal obesity. Lipids 2009;44:593-601. [Abstract]
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Muller H, Lindman AS, Blomfieldt A, et al. A diet rich in coconut oil reduces diurnal postprandial variations in circulating tissue plasminogen activator antigen and fasting lipoprotein [a] compared with a diet rich in unsaturated fat in women. J Nutr 2003;133[11]:3422-3427. [Abstract]
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