Coconut oil boom
- Coconut oil is surging in popularity as a “health food,” after being demonized since the 1950s because of its high saturated fat content.
- Coconut oil has a variety of uses: as a cooking oil, shortening, nutritional supplement, personal care ingredient, antimicrobial agent, and biofuel.
- Many of the properties of coconut oil can be traced to medium-chain fatty acids (MCFAs) such as lauric acid (C12:0), which are metabolized differently from long-chain fatty acids (LCFAs).
Coconut is the oil du jour, attracting endorsements from athletes and celebrities for its alleged health-promoting effects. The oil, once considered exotic outside of the tropics, is showing up in supermarkets and health food stores everywhere, often advertised as a “functional food.” Yet not long ago, coconut oil was reviled by health experts, lumped in the same unhealthful category as lard and tallow because of its high content of saturated fat. As saturated fat has embarked on the long road to exoneration, many people are starting to appreciate the unique physical and chemical characteristics of coconut oil, not only as a cooking oil, but also as a cosmetic ingredient, an antimicrobial agent, a biofuel, and even a possible medicine for ailments ranging from obesity to Alzheimer’s disease. But does the scientific evidence of coconut oil’s benefits justify the hype?
Boom and bust
Although new to many consumers in the West, coconut oil has been used as a food ingredient and folk medicine for millennia in the tropical regions where coconut trees grow, such as India, the Philippines, Sri Lanka, Malaysia, Polynesia, and Indonesia (Fig. 1). The oil attracted the attention of European traders in the late 19th century, a time of increased demand for edible oils and oils for soapmaking in Europe and the United States. As a result, Europeans established coconut plantations in the Caribbean, Southeast Asia, and the South Pacific from the 1890s to the 1920s, and coconut oil was widely used as a cooking oil in Europe and the United States until about 1940. Then, World War II cut off the supply of coconut oil to the West. “There was quite a desperate shortage of edible oil in the U.S., and the soy industry got a huge boost from that,” says Mike Foale, a coconut consultant in Queensland, Australia, and retired agronomist at Australia’s Commonwealth Scientific and Industrial Research Organization (CSIRO). “The price of coconut oil was so high, and the soy oil industry expanded very rapidly indeed during that period.”
When the war ended, coconut-producing countries were eager to resume coconut oil exports. However, by this time the saturated fat scare had taken hold. Based mainly on incomplete epidemiological data, in the 1950s prominent US nutrition researcher Ancel Keys formulated a hypothesis that dietary saturated fat raises cholesterol levels in the blood, which in turn clogs arteries and causes heart disease. Because coconut oil is about 93% saturated fat, it was viewed as less healthful than edible oils composed of primarily unsaturated fats, such as soybean oil.
Apparently bolstering Keys’ hypothesis, several studies showed that rodents fed coconut oil as the sole dietary fat had higher cholesterol levels and were much less healthy than animals fed corn or soybean oil (e.g., Williams, M. A., et al., J. Nutr., 1972). However, according to Foale, these studies were flawed because coconut oil lacks the essential omega-3 fatty acids. Therefore, the animals fed coconut oil were suffering from a dietary deficiency, rather than from negative effects of the oil per se. “In the real world, coconut users of the tropics generally eat fish, which are rich in omega-3 fatty acids,” says Foale. “So the combination has always been a healthy one, and heart disease isn’t an issue among traditional coconut users.” Moreover, in these studies the researchers typically used hydrogenated coconut oil, which could contain trans fats. Trans fats are now recognized to have adverse effects on serum cholesterol levels and human health.
Despite firmly entrenched biases against saturated fat within the medical community, mounting evidence has begun to exonerate saturated fat as a contributing factor to heart disease. Coconut oil has likely benefited from this recent development. Like other saturated fats, coconut oil raises the total serum cholesterol level, which concerns some health experts. However, more than any other type of fat, saturated fats raise the level of high-density lipoprotein (HDL) cholesterol, the so-called “good” cholesterol that has been correlated with a reduced risk of heart disease (Cassiday, L, Inform, 2015). Although saturated fat also raises the serum level of low-density lipoprotein (LDL), or “bad,” cholesterol, the type of LDL particles increased are of the large, buoyant type, which are less strongly associated with cardiovascular disease than small, dense LDL particles.
Because of the opposing effects of HDL and LDL cholesterol, the total serum cholesterol level has proven to be a poor predictor of cardiovascular risk. Instead, the ratio of total cholesterol to HDL cholesterol (total:HDL) is a more reliable estimate, with lower levels correlating with reduced risk. Whereas unsaturated fats lower total:HDL cholesterol, and trans fats raise the ratio, saturated fats typically have no effect, suggesting a neutral influence on heart disease risk.
A different saturated fat
Although saturated fats are often considered a single nutritional entity, studies have shown that molecular chain length greatly influences a fatty acid’s metabolic and physiologic properties. Coconut oil is unique in its fatty acid composition, containing more than 65% medium-chain fatty acids (MCFAs)—commonly defined as fatty acids with chains of 6 to 12 carbon atoms (C6–C12) (Fig. 2). In contrast, saturated fats in animal fats and most other vegetable oils are mainly long-chain fatty acids (LCFAs), which contain 14 to 18 carbon atoms (C14–C18). Triacylglycerides (TAGs) composed of MCFAs are more water-soluble and readily digestible than TAGs containing LCFAs.
FIG. 2. Examples of medium-chain fatty acids (MCFA) and medium-chain triglycerides (MCT)
Among vegetable oils, coconut oil, palm oil, and palm kernel oil have the highest levels of saturated fat (coconut, 93%; palm, 50%; palm kernel, 82%), making them semi-solid at room temperature. All three oils are derived from palm trees, but from different species or parts of the fruit: Coconut oil is extracted from the meat, or kernel, of the coconut fruit of the palm Cocos nucifera, whereas palm and palm kernel oil are derived from the pulp and kernel, respectively, of the fruit of the oil palm Elaeis guineensis.Palm oil contains mostly LCFAs, such as palmitic acid (C16) at 44%, whereas coconut and palm kernel oils contain predominantly MCFAs, such as lauric acid (C12) at about 48% and 46%, respectively (Dubois, V., et al., http://doi.org/10.1002/ejlt.200700040, 2007) (Fig. 3).
FIG. 3. Fatty acid composition of coconut oil. Adapted from data in Dayrit, F. M. (2015) “The properties of lauric acid and their significance in coconut oil.” J. Am. Oil Chem. Soc. 92: 1–15.
Coconut and palm kernel oils have similar fatty acid profiles, but they have different triacylglyceride (TAG) compositions (Dayrit, F. M., http://doi.org/10.1007/s11746-014-2562-7, 2015). In one study, researchers found that the predominant TAGs in coconut oil are trilaurin (3C12), 1-capro,2,3-dilauryl glyceride (C10-C12-C12), and 1-capro,2-lauryl,3-myristyl glyceride (C10-C12-C14). In contrast, palm kernel oil contains mostly trilaurin (3C12), 1-myristyl,2-stearyl,3-lauryl glyceride (C14-C18-C12), and 1,3-oleyl,2-lauryl glyceride (C18:1-C12-C18:1). Unlike coconut oil, palm kernel oil is not commonly consumed in the diet because of the presence of residual extraction solvents, says Foale.
The two main types of coconut oil—copra and virgin—have similar fatty acid profiles, but virgin coconut oil has a higher content of bioactive components such as tocotrienols and tocopherols (forms of vitamin E), sterols (precursors to fat-soluble vitamins and steroid hormones), and polyphenols (antioxidants). The two types of coconut oil differ in their extraction processes (Table 1). Copra is produced by crushing dried coconut kernels to extract the oil, which is then typically refined, bleached, and deodorized (RBD). This coconut oil was the type commonly used in the United States and Europe for frying and shortening in the early twentieth century. In contrast, virgin coconut oil (VCO) is made by pressing shredded wet coconut kernel to squeeze out the oil and coconut milk, which form an emulsion that is then separated by various techniques. Unlike RBD copra oil, VCO is not refined, and thus not subjected to the high temperatures of free fatty acid distillation and deodorization, which can volatilize or otherwise destroy heat-labile components.
TABLE 1. Coconut Oil Production
Credit: Oi-Ming Lai
“Most of the health benefits of coconut oil, whether VCO or RBD coconut oil, have been attributed to the high content of lauric acid,” says Fabian M. Dayrit, professor of chemistry at Ateneo de Manila University, in Quezon City, Philippines. “Additional health benefits of VCO have been attributed to the presence of polyphenols.”
About 60% of coconut TAGs contain the MCFAs lauric (C12) or capric (C10) acid at the sn-1 or sn-3 positions (Fig. 4). This placement is important because lipases in the body hydrolyze TAGs more rapidly if MCFAs occupy the sn-1and sn-3 positions, rather than LCFAs. Upon ingestion, TAGs undergo stepwise hydrolysis. First, lipases in the gastrointestinal tract cleave off a fatty acid at the sn-1 or sn-3 position of the TAG to yield a diacylglyceride and a free fatty acid. Then, lipases hydrolyze a second fatty acid (sn-1or sn-3) to produce 2-monoacylglyceride and another free fatty acid. In the third hydrolysis step, the fatty acid at the sn-2 position is hydrolyzed to yield glycerol and the remaining free fatty acid. Alternatively, 2-monoacylglyceride can undergo isomerization to 1-monoacylglyceride, which can then be hydrolyzed to glycerol and a free fatty acid.
FIG. 4. Lauric acid in the triacylglyceride (TAG) structure of coconut oil
After lipases liberate fatty acids from TAGs, enterocytes of the small intestine absorb the free fatty acids. From there, LCFAs and MCFAs have very different metabolic fates. LCFAs are predominantly re-esterified into TAGs, and then combined with phospholipids, proteins, and cholesterol to form complexes called chylomicrons. Chylomicrons enter the lymphatic system, where they circulate in the bloodstream and enter tissues, contributing to fat accumulation. In contrast, MCFAs are more water-soluble than LCFAs due to their shorter chain length, so they do not require packaging into chylomicrons. Instead, most MCFAs are conducted to the hepatic portal vein, which directly links the gastrointestinal tract to the liver. In experiments using rat intestine, the proportion of saturated fatty acids entering the portal vein was inversely correlated with carbon number: C12 (72%), C14 (58%), C16 (41%), and C18 (28%) (Dayrit, F. M., Philipp. J. Sci., 2014). As a result, most ingested MCFAs are transported directly to the liver, where they are converted to energy and other metabolites rather than being stored as fat. Indeed, among fatty acids, lauric acid contributes the least to fat accumulation.
Upon arrival at the liver, MCFAs enter the mitochondria. Unlike LCFAs, MCFAs can freely diffuse across the mitochondrial membrane without requiring carnitine-assisted transport. MCFAs are then rapidly metabolized by one of two pathways (Fig. 5). The major pathway, β-oxidation, yields acetyl CoA. Acetyl CoA either enters the citric acid cycle to produce energy, or is further metabolized to ketone bodies. Ketone bodies are three water-soluble molecules (acetoacetate, β-hydroxybutyrate, and acetone) that are transported from the liver to other tissues, such as the brain, muscle, and heart. There, enzymes can convert the ketone bodies to acetyl CoA for use as an energy source. The second pathway, ω-oxidation, accounts for only 10–20% of total liver fatty acid oxidation under normal conditions. This pathway produces 11- and 12-hydroxyl fatty acids, which can be further oxidized to dicarboxylic acids. The ω-oxidation pathway may help remove excess fatty acids from the mitochondrial respiratory chain (Dayrit, F. M., Philipp. J. Sci., 2014).
FIG. 5. Metabolism of lauric acid (an MCFA) in the liver
The unique metabolism of MCFAs may help explain some of coconut oil’s physiological effects. Despite warnings against saturated fats in general, epidemiological studies have demonstrated no correlation between coconut oil consumption and coronary heart disease (Dayrit, F. M., http://doi.org/10.1007/s11746-014-2562-7, 2015). Indeed, traditional coconut-consuming populations, such as the Polynesians, typically show a favorable lipid profile, low levels of atherosclerosis, and a low incidence of heart disease. As early as 1960, a human feeding study of C6–C12 saturated fatty acids showed only a transient rise in serum cholesterol with consumption of the MCFAs (Hashim, S. A., et al., Lancet). A 2003 meta-analysis of 60 controlled trials concluded that ingestion of lauric acid—the predominant fatty acid in coconut oil—increased total cholesterol, but much of this increase was due to HDL cholesterol, resulting in a decreased total:HDL ratio (Mensink, R. P., et al., Am. J. Clin. Nutr., 2003).
In an animal study comparing VCO and RBD copra oil, rats fed VCO showed reduced levels of total cholesterol, triglycerides, and LDL cholesterol, and increased levels of HDL cholesterol, compared with rats fed RBD copra oil (Nevin, K., and Rajamohan, T., Clin. Biochem., 2004). The researchers attributed the difference to the presence of polyphenols in VCO. When the researchers isolated the polyphenols from VCO, they found that the antioxidants prevented in vitro LDL oxidation. Oxidized LDL cholesterol increases inflammation in arteries and promotes atherosclerosis.
Because of their rapid metabolism in the liver, MCFAs do not contribute to fat accumulation or obesity nearly as much as other dietary fatty acids. In one study, 40 Brazilian women with abdominal obesity were given 1 ounce soybean oil or 1 ounce coconut oil per day, along with a hypocaloric diet. After 12 weeks, both groups of women had lost an average of about 1 kg of body mass. However, the average waist circumference in the soybean oil group increased by 0.6 cm, whereas the average waist circumference in the coconut oil group decreased by 1.4 cm (Assunção, M. L., http://doi.org/10.1007/s11745-009-3306-6, 2009). Similarly, a pilot study of 20 obese but otherwise healthy Malay volunteers showed that supplementing their normal diet with 1 ounce VCO per day decreased waist circumference by an average of 2.86 cm after only one month (Liau, K. M., http://doi.org/10.5402/2011/949686, 2011). Although these reductions are modest, they represent a statistically significant response to a relatively minor dietary modification.
Coconut oil may help people lose weight simply by increasing their satiety so that they do not overeat. Also, coconut oil may stimulate fat loss by increasing thermogenesis—a process that generates body heat directly from fat instead of producing ATP—in brown adipose tissue (Dayrit, F. M., Philipp. J. Sci., 2014). In animal studies, a coconut-oil-rich diet increased thermogenesis by activating a mitochondrial protein called uncoupling protein 1 (UCP1). Found only in brown adipose tissue, UCP1 dissipates the proton-motive force in the mitochondria that normally drives ATP synthesis, and the energy is instead released in the form of heat. Thermogenesis has been linked to weight loss.
Foale notes that many health-conscious people are now incorporating coconut oil into their diets, whether as a cooking oil or as an addition to their morning cereal, smoothies, or desserts. “People who are a bit skeptical about the advice that ‘this is a saturated fat and it’s bad for you’ are prepared to try it,” says Foale. “And then they discover that they feel better with it: Their general well-being is improved, and they feel more energetic.” Many athletes find that coconut oil sustains their energy during exhaustive competitions, Foale says, possibly due to the ketone bodies formed from MCFAs. Ketone bodies can serve as an alternative energy source in muscles during strenuous exercise, when glucose reserves may be lagging.
Although experimental evidence is lacking, some researchers have theorized that the ketone bodies generated from MCFAs in coconut oil could help treat neurological disorders such as Alzheimer’s disease. Scientists have already established that a ketogenic diet—a high-fat, low-carbohydrate, adequate-protein eating plan—can drastically reduce the rate of seizures in epileptic children who are resistant to drug therapies (Watkins, C., Inform, 2016). The lack of carbohydrates in the ketogenic diet forces the liver to convert fat into ketone bodies, which can cross the blood-brain barrier and be used as a source of energy by the brain. However, the mechanism by which ketone bodies can help prevent epileptic seizures in some patients is still unknown.
In Alzheimer’s disease, certain parts of the brain have an impaired ability to use glucose, partially due to disruption of insulin signaling. Thus, ketone bodies may help alleviate symptoms of Alzheimer’s by providing an alternative energy source for the brain. Researchers have also proposed that polyphenols and plant hormones called cytokinins in VCO may prevent aggregation of amyloid-β, the peptide that forms plaques in the brains of people with Alzheimer’s disease. Antioxidants such as polyphenols also scavenge free radicals that cause oxidative stress, a condition that has been linked to Alzheimer’s disease.
Some small clinical trials and animal studies using formulations of medium-chain triacylglycerides have reported cognitive improvements in Alzheimer’s disease (Fernando, W. M., et al., http://doi.org/10.1017/S0007114515001452, 2015). In an in vitro study, neurons treated with amyloid-β showed higher survival rates if they were co-treated with coconut oil. However, no large randomized clinical trials have been conducted on coconut oil and Alzheimer’s disease, so much research is needed before coconut oil can be recommended as an effective treatment for this neurological disorder.
Lauric acid and its derivative monolaurin have antimicrobial activity against gram-positive bacteria and some fungi and viruses. Lauric acid is the most active antimicrobial among saturated fatty acids, and monolaurin is more active than lauric acid (Dayrit, F. M., http://doi.org/10.1007/s11746-014-2562-7, 2015). In fact, many commercial products contain lauric acid or monolaurin as antimicrobial agents. Synthetic monolaurin is used as an antimicrobial compound in a number of food and non-food applications.
The antimicrobial properties of lauric acid can be traced to three main mechanisms: destruction of the cell membrane of gram-positive bacteria and lipid-coated viruses, interference with microbial processes such as transcription and signal transduction, and stabilization of human cell membranes. Thus far, bacteria have not been able to evolve resistance to lauric acid or monolaurin, possibly due to their multiple antimicrobial mechanisms (Dayrit, F. M., http://doi.org/10.1007/s11746-014-2562-7, 2015).
Like its predominant fatty acid, coconut oil likewise has antimicrobial properties, says A. G. Gopala Krishna, retired chief scientist at the Central Food Technological Research Institute (CSIR) in Mysore, India. “Coconut oil kills bacteria that cause diseases such as pneumonia, sore throats, dental cavities, urinary tract infections, meningitis, gonorrhea, and food poisoning,” he says. “It also kills the causes of fungal infections such as candida, ringworm, athlete’s foot, thrush, jock itch, and diaper rash. It kills viruses having a lipid coating, such as herpes, HIV, hepatitis C, influenza, and mononucleosis.”
In the early twentieth century, a prominent American dentist named Weston A. Price traveled to the South Pacific and observed that Polynesians had excellent dental health. “He attributed that to, among other things, the regular use of coconut oil in their diets and the antibiotic effects of some of the fatty acids,” says Foale. The traditional Indian practice of “oil pulling,” or swishing coconut oil around in the mouth, is increasing in popularity. Although evidence of its efficacy is mostly anecdotal at this point, coconut oil pulling has been reported to reduce or prevent bad breath, gingivitis, and tooth decay.
Coconut oil is a common ingredient in personal care products such as soaps, lotions, and cosmetics. Also, lauric acid and its derivatives (e.g., lauryl sulfate) are used as detergents and surfactants in cleansers. Rubbing VCO directly on the skin can boost the skin’s moisture and lipid content, similar to mineral oil (Agero, A. L., and Verallo-Rowell, V. M., Dermatitis, 2004). Coconut oil may confer antiseptic properties to lotions or moisturizers that could benefit people with certain skin conditions.
Coconut oil also has applications in hair care. “Coconut oil has a high affinity for hair proteins and, because of lauric acid’s low molecular weight and straight linear chain, is able to penetrate inside the hair shaft,” says Oi-Ming Lai, professor of bioprocess technology at Universiti Putra Malaysia, in Serdang. “Coconut oil reduces protein loss for both undamaged and damaged hair when used as a pre-wash and post-wash grooming product.”
Coconut oil is perhaps best known for its use as a cooking oil, but it is also used extensively by the food industry in baked products, processed foods, and infant formulas. Because coconut oil is almost completely saturated fat, it is much less susceptible to heat-induced damage than unsaturated fats. The oil has a long shelf life, 2 years on average.
Many people find coconut oil to have attractive sensory attributes. “When coconut oil is solid, at room temperature, it’s pure white, and when it’s melted it looks just like water,” says Foale. “This lovely oil has a very gentle aroma and a subtle taste—a pleasant taste, but not a strong taste.” He says that coconut oil can replace butter or shortening in “all manner of recipes.”
Coconut oil can be used directly as a fuel, or can be converted into methyl esters that have similar combustion properties as diesel, says Dayrit. “Coco-biodiesel” offers many advantages over diesel, including reduced emissions of particulates, carbon monoxide, and nitric oxide; reduced toxicity; and improved safety due to a higher flash point. In addition to reducing air pollution, coco-biodiesel is environmentally friendly from the standpoint that is it renewable and biodegradable. “The use of coco-biodiesel is already being implemented in a number of countries,” says Dayrit. “In the Philippines, diesel fuel currently must contain at least 1% coco-biodiesel.”
For someone choosing to consume coconut oil for its suspected health benefits, VCO is a better choice than RBD copra oil because of the higher content of polyphenols and other bioactive compounds. But how can consumers be certain they are purchasing high-quality coconut oil? To ensure quality, Codex Alimentarius has established standards for VCO. Likewise, the Asian and Pacific Coconut Community (APCC), an intergovernmental agency of 18 coconut-producing countries that oversees global trade and other aspects of the coconut industry, has standards for VCO. “The guidelines are very simple,” says Foale. “The oil must be perfectly clear, there mustn’t be any cloudy material from suspended particles, no residual water, and it must not have been subjected to high temperatures [above 60 ºC] during preparation.”
According to Krishna, rancidity can be a problem for low-quality coconut oil. “If moisture is removed carefully before extraction of the oil, or not allowed to come in contact with the oil, a good-quality oil can be prepared,” he says. “Hydrolytic rancidity causes the oil to stink very badly and become unfit for human consumption or for use in cosmetic applications.” Krishna adds that a good-quality oil should have a bland or slightly coconut aroma, be light to slightly brown in color, and have very low levels of free fatty acids (below 1%).
Adulteration can also be a problem for VCO. Less-expensive oils such as palm kernel oil or RBD coconut oil can be added to VCO to cut costs. “Because of the increased demand for VCO in recent years, there is a need for methods to detect adulterated VCO,” says Lai. Proposed techniques include Fourier transform infrared spectroscopy (FTIR), NMR, differential scanning calorimetry (DSC), and an electronic nose (Marina, A. M., et al., http://doi.org/10.1016/j.tifs.2009.06.003, 2009).
Coconut oil has a long history of use in tropical regions, but people elsewhere are now just discovering the varied uses of the oil. “From a historical perspective, the current rise in popularity of coconut oil in the U.S. and Europe can be seen as a rediscovery, driven by the dissatisfaction with currently available vegetable oils in the West, which are dominated by soybean oil and trans fats,” says Dayrit. “Coconut oil, along with olive oil, have become popular as healthy alternative vegetable oils, which may have many beneficial properties in both food and non-food applications.” Dayrit adds that VCO also has a number of high-value co-products, such as coconut water, coco flour, charcoal, and coconut coir (a fiber used for doormats, brushes, etc.). “Very few plant products have as wide a range of uses as the coconut,” says Dayrit.
Although many consumers are raving about health benefits they have experienced from VCO, research into the oil is still in its infancy, and many nutritionists continue to caution against the oil because of its high saturated fat content. “I confess to some frustration that a food oil that has supported traditional healthy diets for millennia must now be proven to support good health because it was maligned and ousted from acceptance in the diet policies of the U.S. and Australia, in particular,” says Foale. “Once the coconut industry declined from the plantation production phase back to small-holder producers, there has been no adequate source of funding to comprehensively defend the reputation of coconut oil.” He adds that more research is needed to discover why consumers apparently thrive on the oil.
Laura Cassiday is an associate editor of Inform at AOCS. She can be contacted at firstname.lastname@example.org.
- Agero, A. L., and Verallo-Rowell, V. M. (2004) “A randomized double-blind controlled trial comparing extra virgin coconut oil with mineral oil as a moisturizer for mild to moderate xerosis.” Dermatitis 15: 109–116.
- Assunção, M. L., et al. (2009) “Effects of dietary coconut oil on the biochemical and anthropometric profiles of women presenting abdominal obesity.” Lipids 44: 593–601. http://doi.org/10.1007/s11745-009-3306-6.
- Cassiday, L. (2015) “Big fat controversy: changing opinions about saturated fat.” Inform 26: 343–349, 377 (June 2015).
- Dayrit, F. M. (2014) “Lauric acid is a medium-chain fatty acid, coconut oil is a medium-chain triglyceride.” Philipp. J. Sci. 143: 157–166.
- Dayrit, F. M. (2015) “The properties of lauric acid and their significance in coconut oil.” J. Am. Oil Chem. Soc. 92: 1–15. http://doi.org/10.1007/s11746-014-2562-7.
- Dubois, V., et al. (2007) “Fatty acid profiles of 80 vegetable oils with regard to their nutritional potential.” Eur. J. Lipid Sci. Technol. 109: 710–732. http://dx.doi.org/10.1002/ejlt.200700040.
- Fernando, W. M., et al. (2015) “The role of dietary coconut for the prevention and treatment of Alzheimer’s disease: potential mechanisms of action.” Br. J. Nutr. 114: 1–14. http://doi.org/10.1017/S0007114515001452.
- Hashim, S. A., et al. (1960) “Effect of a saturated medium-chain triglyceride on serum lipids in man.” Lancet 1: 1105–1108.
- Liau, K. M., et al. (2011) “An open-label pilot study to assess the efficacy and safety of virgin coconut oil in reducing visceral adiposity.” ISRN Pharmacol. 2011, 94686. http://doi.org/10.5402/2011/949686.
- Marina, A. M., Che Man, Y. B., and Amin, I. (2009) “Virgin coconut oil: emerging functional food oil.” Trends Food Sci. Technol. 20: 481–487. http://doi.org/10.1016/j.tifs.2009.06.003.
- Mensink, R. P., et al. (2003) “Effects of dietary fatty acids and carbohydrates on the ratio of serum total to HDL cholesterol and on serum lipids and apolipoproteins: a meta-analysis of 60 controlled trials.” Am. J. Clin. Nutr. 77: 1146–1155.
- Nevin, K. G., and Rajamohan, T. (2004) “Beneficial effects of virgin coconut oil on lipid parameters and in vitro LDL oxidation.” Clin. Biochem. 37: 830–835.
- Watkins, C. (2016) “Prescribing dietary fat: therapeutic uses of ketogenic diets.” Inform 27: 6–11 (February 2016).
- Williams, M. A., et al. (1972) “Hydrogenated coconut oil and tissue fatty acids in EFA-depleted and EFA-supplemented rats.” J. Nutr. 102: 847–855.