2016/02/16 by S. Lockyer, Sara Stanner · 1 citation
Chemistry · Engineering · Nursing · #Coconut Research and Applications #Advanced Chemical Sensor Technologies #Fatty Acid Research and Health
paper · pdf · doi:10.1111/nbu.12188
openalex publication_date 2016/02/16 · openalex created_date 2025/10/10 · openalex updated_date 2026/07/29
The increasing popularity of edible coconut products, such as coconut oil and coconut water, is difficult to miss. Coconut oil, in particular, has been endorsed by celebrities and chefs for use in cooking and baking, with fashion models reportedly eating it in an attempt to speed up their metabolic rate (The Telegraph 2015a). According to leading market research providers Mintel, coconut oil in food and beverages accounted for 26% of food and drink new product launches in 2012, and one in ten 16–24 year-olds currently buys coconut oil (Mintel 2015). Whole Foods reportedly sold six tonnes of coconut oil across the UK in the month of February 2015 (The Telegraph 2015a). Recipe books, advertisements and some journal articles are claiming that coconut oil is a cure-all product that has weight reduction, cholesterol-lowering, wound healing and immune system, energy and memory-boosting effects and can be used to treat Crohn's disease, irritable bowel syndrome, thyroid conditions, diabetes, as well as Alzheimer's and Parkinson's diseases (DebMandal & Mandal 2011; Positivemed.com 2015). Such claims have led to a significant amount of press coverage (The Independent 2014, 2015b, The Daily Mail 2015b; The Telegraph 2015a), comment from the scientific community (Cunningham 2011; DeDea 2012; Inayat et al. 2013; Varteresian & Lavretsky 2014) and the inclusion of coconut oil within food products as a perceived health-boosting ingredient, with companies using it as a unique selling point. Additionally, a recent story suggested that coconut oil produces fewer aldehydes than unsaturated oils when heated and is therefore better for health (The Telegraph 2015b), a claim that was based on unpublished data. As a beauty product, coconut oil has been advocated as being useful for frizzy hair, stretch marks, as a moisturiser and make-up remover. Swilling around the mouth has even been encouraged to prevent tooth decay (The Independent 2015b). Whilst topical use of coconut oil and indeed the consumption of coconut water [containing around 20 calories per 100 g and providing small quantities of micronutrients (USDA 2015)] are unlikely to be of concern for public health, high consumption of saturated fatty acid-laden coconut oil may well be. In America, for example, big-brand food manufacturers have started selling fat spreads made with coconut oil (Foodnavigator.com 2015). Considering the widespread use of fat spreads as an everyday product, is this a good idea? Coconut oil is a colourless to brown-yellow edible oil derived from mature coconuts. Standard coconut oil is normally produced by firstly drying the kernel (to produce something known as copra) and secondly refining, bleaching and deodorising the extracted oil. So-called virgin coconut oil is instead made via a 'wet process', either being extracted from coconut milk or from fresh kernel which is not subjected to drying or chemical refining (Babu et al. 2014). Coconut oil comprises 99.9% fatty acids; of these, 91.9% are saturated fatty acids (SFA), 6.4% are monounsaturated fatty acid acids (MUFA) and 1.5% are polyunsaturated fatty acids (PUFA), and coconut oil contains no dietary cholesterol (PHE 2015). The individual fatty acid composition of coconut oil can be seen in Figure 1. The principal fatty acids are lauric (C12:0), myristic (C14:0) and palmitic (C16:0) acids. Virgin coconut oil has been found to contain up to seven times higher concentrations of polyphenols than standard coconut oil, with total polyphenol contents of up to 80 mg gallic acid equivalents/100 g oil reported in virgin coconut oil (a figure comparable to extra virgin olive oil), although concentrations differ depending on coconut variety (Nevin & Rajamohan 2004a; Seneviratne & Sudarshana Dissanayake 2008; Marina et al. 2009). The lower levels in standard coconut oil are likely to be due to minor components being destroyed during the manufacturing process and also because polyphenols are polar compounds and therefore have a higher affinity for liquid coconut milk and fresh copra as opposed to dried copra (Seneviratne & Sudarshana Dissanayake 2008). Despite the difference in concentrations, the mixture of phenolics present (including ferulic, p-coumaric, caffeic, gallic and syringic acids and catechin) (Seneviratne & Sudarshana Dissanayake 2008; Seneviratne et al. 2009) is thought to be largely the same in standard and virgin coconut oils (Seneviratne & Sudarshana Dissanayake 2008). Phenolic composition has been characterised only in a small number of publications and further verification is needed, particularly in terms of quantities. Of the compounds identified so far, all are found in a variety of other plant foods. For example, ferulic acid is present in much higher quantities in wholegrain bread flour (72 mg/100 g vs. 0.3 mg/100 g reported in virgin coconut oil), catechin is present in much higher quantities in cocoa (108 mg/100 g vs. 0.3 mg/100 g reported in virgin coconut oil) and p-coumaric acid is higher in dried dates (5.8 mg/100 g vs. 0.2 mg/100 g reported in virgin coconut oil) (Neveu et al. 2010). Various biological effects of coconut oil, such as blood pressure and cholesterol lowering, reduction in low-density lipoprotein cholesterol (LDL-C) oxidation and potential as an Alzheimer's treatment, as have been reported in animal and in vitro studies, have been attributed to the phenolic content (Nevin & Rajamohan 2004a; Nurul-Iman et al. 2013; Fernando et al. 2015). Coconut oil also contains small amounts of vitamin E (0.66 mg/100g) and vitamin K (1 μg/100 g) (PHE 2015). Historically, coconut oil has been described as 'one of the most potent agents for elevating serum cholesterol level' (The Inter-Society Commission for Heart Disease Resources 1970). This is due to its very high saturated fatty acids content (up to around 92 g/100 g), which exceeds other edible fats (see Fig. 2), including butter that contains around 52 g/100 g (PHE 2015). The plasma lipid raising potential of saturated fatty acids and the positive association between plasma cholesterol and heart disease risk have long been established in the literature (Keys et al. 1965; Castelli et al. 1992; Hu et al. 2001). This is the rationale behind current UK dietary guidelines (and similar guidelines around the world) for cardiovascular disease (CVD) prevention, which recommend that saturated fatty acid intake should be limited to no more than 11% of food energy, which, in the context of average energy needs, equates to a maximum of 30 g per day for men, 20 g for women and less for children (DH 1991). The link between saturated fat and heart disease has been recently questioned and debated at length in the press (The Daily Mail 2015a; The Independent 2015a), due to the publication of some journal articles concluding that there is no association between the two (Siri-Tarino et al. 2010; Malhotra 2013; Chowdhury et al. 2014). This topic is currently being examined by a BNF Task Force report on cardiovascular disease (due for publication in 2017) and the UK Scientific Advisory Committee on Nutrition. The view that the consumption of saturated fatty acids is not detrimental for health, largely based on observational evidence, has been used to support the use of coconut oil. It is important to note that claims relating to potential health benefits of coconut oil are often based solely on animal or in vitro studies (Nevin & Rajamohan 2004a, 2008; Hayatullina et al. 2012; Nurul-Iman et al. 2013; Wang et al. 2015), or human studies feeding one component of coconut oil rather than the whole food (Inayat et al. 2013). Overall, human studies on coconut oil itself are limited and largely non-UK based. A handful of observational studies have examined the prevalence of CVD risk markers in populations for whom coconut represents an important part of the diet. A study of 1839 Filipino women using 24-hour dietary recall reported that coconut oil consumption was not associated with raised levels of triacylglycerides (TAG), LDL-C or with ratio of total cholesterol to high-density lipoprotein cholesterol (TC/HDL-C) (Feranil et al. 2011). In pre-menopausal women, the highest tertile of coconut oil intake was associated with higher total cholesterol levels compared to the lowest tertile, and moderate and high intakes were associated with significantly higher HDL-C levels. However, these relationships were not identified in post-menopausal women and the paper did not detail how low, moderate and high intakes were classified in terms of amounts of oil. In a comprehensive study of two island populations of Polynesians (436 Pukapukans and 939 Tokelauans), for which coconuts are a staple food, carried out in the years 1964–1971 (Prior et al. 1981), all foods consumed by a subsection of randomly selected families (13 families in Pukapuka and 18 families in Tokelau) over a 7-day period were weighed and recorded by researchers and dishes were analysed chemically to determine fatty acid composition. Pigs and chickens on the islands also had high intakes of coconuts, which added to the saturated fatty acid content of animal foods in the diets. Twenty-four-hour recall was also used to obtain dietary data, though only in a subsample of individuals aged 25–54 years [n = 165 Pukapukans (74% of the age group) and n = 77 in Tokelauans (46% of the age group)]. In the Tokelauan diet, coconuts supplied 63% of energy and the diet contained 54% energy from fat and 48% energy from saturated fatty acids. In the Pukapukan diet, coconuts contributed 34% of energy and the diet contained 37% energy from fat and 28% energy from saturated fatty acids. The groups with the highest mean cholesterol concentrations among the Pukapukans were males aged 35–44 years (4.71 mmol/l) and females aged 55–64 years (5.03 mmol/l), and among Tokelauans were males aged 45–54 years (5.7 mmol/l) and females aged 55–64 years (6.4 mmol/l). For comparison, in the UK, the average diet comprises 34.6% energy from fat and 12.6% energy from saturated fatty acids (PHE 2014) and total cholesterol levels are estimated to be 5.5 mmol/l in women and 5.4 mmol/l in men (WHO 2009). The fact that total cholesterol was higher in the Tokelau population than in Pukapukans could indicate a deleterious effect of higher coconut consumption on cholesterol; however, as dietary data were not obtained for all participants, blood samples were not taken in the same year as dietary measurements and the study was observational in design, it is difficult to draw firm conclusions from these data. It was observed that among Tokelauan individuals who migrated to New Zealand, LDL-C levels increased, despite the percentage of energy from fat decreasing from 57% to 43%. This finding is often used in support of coconut oil consumption due to the low incidence of vascular disease in the indigenous populations. However, this scenario is, of course, completely uncontrolled and does not account for other dietary and lifestyle factors which may have impacted on the lipid profile of these migrants. A case–control study carried out in South India found no differences in coconut oil intake between coronary heart disease patients and healthy matched controls (Kumar 1997). Average daily intakes of coconut oil were 13.6 ml among patients and 12.5 ml among controls, around 2–3 teaspoons. However, subjects had a mean age of 57 years and were asked to recall their dietary habits from age 15 years onwards, a methodology of questionable validity. Similarly, a study of diabetic cases and controls in South India found no significant differences in lipid profile or antioxidant enzymes between individuals who used coconut oil in cooking, contributing 13–20% of their total energy intake, and those consuming similar amounts of sunflower oil (Sabitha & Vasudevan 2010). In a study of 71 endarterectomy samples (atherosclerotic plaques removed from artery linings), it was reported that despite coconut oil consumers having significantly higher plasma myristic acid concentrations than sunflower oil consumers, this was not reflected in plaque fatty acid composition (Palazhy et al. 2012). However, interestingly, the author reported that the atheromas mostly comprised saturated fatty acids, in stark contrast to earlier studies which had reported that unsaturated fatty acids were the principle component (Lausada et al. 2007). Neither plasma nor plaque lauric acid concentrations were significantly higher in the coconut oil group; however, capric acid was identified in some plaques, providing evidence of the deposition of medium-chain fatty acids (MCFAs) in tissues (see 'Medium-chain triglycerides' section below). Plaque kinetics are complex and fatty acid composition is not restricted to dietary sources. The authors speculated that medium-chain triglycerides (MCTs) may be converted to longer-chain SFAs before plaque incorporation. As dietary fatty acid intake has been associated with atherosclerotic plaque stability (Calder 2012), the effect of coconut oil within this context is certainly of relevance but it is important to note that the study was uncontrolled and the duration and amount of oil consumed varied between subjects. Although many papers cite observational data as principal evidence for the effects of coconut oil, as always with this type of study a cause and effect relationship cannot be established. In addition, the methods of dietary analysis used in all but one of the aforementioned observational studies (Prior et al. 1981) relied on recall and self-report which can lead to misreporting and therefore biased data (Castro-Quezada et al. 2015). Robust randomised controlled trial (RCT) evidence is likely to provide more insight. The majority of the RCTs in this area have focused on lipid-modifying effects of coconut oil, usually in comparison with other dietary fatty acids. The duration of the dietary interventions has ranged from 7 days to 12 months, with many studying the effects after 4 weeks of coconut oil consumption. A summary of the evidence can be seen in Tables 1 and 2. n = 10 (five men and five women) Normolipidaemic ↑TC ↑LDL-C ↑TAG ↑TC ↑IDL-C + LDL-C ↑HDL-C ↑TAG ↓TC ↓LDL-C ↑TC ↑LDL-C ↑HDL-C in women only n = 41 (24 men and 17 women) Normolipidaemic ↑TC ↑LDL-C ↑HDL-C ↑TC ↑LDL-C (P = 0.08) ↑HDL-C ↓TAG ↑TC ↑LDL-C ↑HDL-C Butterfat: ↑TC by 60–65% at 38% energy All meals provided under controlled conditions. Butterfat was the most potent cholesterol-raising agent. Coconut oil was the second most potent Coconut oil: ↑TC by 41% at 22%E ↑TC by 56% at 38%E ↑HDL-C ↓TAG Diet 3 resulted in the most favourable lipid profile Free-living ↑TC ↑LDL-C ↑HDL-C n = 20 (13 women and 7 men) Obese (using Malaysian criteria, BMI ≥ 25 kg/m2) n = 114 (92 in the coconut oil group and 22 in the control group) Coronary artery disease patients n = 16 men Healthy ↓TC ↓LDL-C ↓HDL-C ↑TAG n = 83 (22 women and 61 men) Healthy ↓TC ↓LDL-C ↓HDL-C ↓TAG ↓TC ↓LDL-C ↓HDL-C ↓TC ↓LDL-C Phase 2: 9.3%E reduced to 4.7%E ↓TC ↓LDL-C ↑HDL-C ↓TC:HDL ratio ↓TC ↓LDL-C ↑HDL-C ↑TAG ↓TC:HDL ratio Most of the RCT evidence available demonstrates that coconut oil raises total cholesterol, LDL-C and HDL-C and removing coconut oil from the diet reduces total cholesterol and LDL-C with varying effects on HDL-C depending on the study. This is perhaps unsurprising considering the known cholesterol-raising effects of coconut oil's principal saturated fatty acids lauric, myristic and palmitic acids (Flock & Kris-Etherton 2013). The TC/HDL-C ratio has been advocated as a marker of CVD risk (Mensink et al. 2003), with a lower ratio being more favourable, but all of the RCTs not report this as an on its fatty acid coconut oil is to TC/HDL-C ratio when fats in an average diet (Mensink et al. 2003), although to a than and oil (Mensink et al. However, the of HDL-C as a risk account its in to cholesterol has recently been that coconut oil raises HDL-C may not indicate a the may be more complex et al. 2015). Despite a number of around the individual study in human RCTs coconut oil and plasma are which can the study in terms of and the it difficult to the between studies of a with no or an period may also be to the of the Whilst lipid profile is a very significant marker of health et al. there is a of studies the effect of coconut oil on such as blood vascular and study reported a reduction in after the consumption of coconut oil vs. oil, which to a in blood et al. two studies reported no significant difference in blood pressure effects between coconut oil and oil after 7 days & or coconut oil and no after 3 et al. 2015). two studies the of a period of with g coconut oil per day the same of oil in patients reported no significant differences et al. and significantly raised blood pressure et al. in the coconut oil however, the composition of the coconut oil had been in cases to contain 63% and capric acids, that these cannot be to whole coconut oil. RCT = coconut oil and virgin olive oil at of energy for weeks reported no significant differences in the markers and and but significant in plasma and after the consumption of and coconut oil compared to virgin olive oil et al. 2015). It is to determine the of coconut oil on from a due to the of the and its in is, however, some evidence that saturated fatty acids are et al. 2013; et al. 2015). As the link between saturated fatty acids, plasma and CVD risk has recently been and is indeed all saturated fatty acids are in terms of with for example, thought to have but a of evidence has that the principal fatty acids within coconut oil, lauric, myristic and palmitic acids, total cholesterol and LDL-C (Mensink et al. 2008; et al. 2010). food to have an For example, the consumption of products to be either or CVD et al. despite lauric, myristic and palmitic acids up around of the fatty acids present and foods being one of the of saturated fatty acids in the UK diet (PHE 2014). The for this is to be but evidence this may be due to the high et al. 2009) or effects on et al. The has to provide for intakes of fatty acids to their biological effects 2010). This the that intakes of lauric, myristic and palmitic acids should be limited to less than of energy due to their In terms of and from the UK (DH and and (WHO 2008; to intake of all saturated fatty acids may be for the public to This is particularly as all foods provide a mixture of fatty acids, reduced intake of foods high in saturated fatty acids in than to the intake of individual saturated fatty acids. fatty acids are not an part of the human diet. A recent including 15 RCTs with a total of found that saturated fatty acid intake led to a reduction in the risk of CVD et al. 2015). this and indicate that saturated fatty acids with small amounts of unsaturated fatty acids produces more favourable plasma lipid than with & 2010). of observational studies concluding that there is no relationship between saturated fatty acid intake and CVD risk did not between studies to which had been used to saturated fatty acids in the diet. these of studies all a biased of coconut oil claim that some of the saturated fatty acids present in coconut oil, those of medium-chain health benefits (Babu et al. 2014). are triglycerides of saturated fatty acids with a length of acid and acid et al. to their and have been used the for such as total and et al. In addition, the from animal studies and some human studies have suggested that the consumption of weight in reduced daily food intake and energy compared to other of fatty acids at a of of up to of energy, though in these studies are often small & acid and acid are also to as However, there is as to should be classified in this of these fatty acids are in the coconut oil could be described as around However, it unlikely that lauric acid is in the a of fatty acids, because of its potent cholesterol-raising potential (Mensink et al. used and those used in the majority of human studies potential biological such as increasing energy of and capric acids & 2010; et al. 2012). Considering that lauric acid represents around 48% of the fatty acid content present in coconut oil and and capric acids only around studies feeding oils of only the two are of relevance to the effects of coconut oil. A very small number of studies have reported the effects of coconut oil on in observational study of island populations consuming high amounts of coconuts much higher amounts of lauric and myristic acids, the two fatty acids present within coconut oil, in the than that of New who a more diet vs. and vs. (Prior et al. Of the two populations the who consumed higher amounts of coconut of energy derived from coconut vs. 34% in the Pukapukan were and had In an women aged years were to 30 ml or coconut oil per day instead of their cooking oil for 12 weeks et al. 2009). groups a reduction in However, the groups had also been to for per day and a healthy dietary and groups consumed less calories than at the coconut oil group had a reduced at the of the study (a reduction of the authors used 24-hour dietary recall at the and of the study period to the amounts of coconut oil consumed by subjects were not In a women and seven men aged with a mean BMI of consumed 30 ml virgin coconut oil per day for 4 weeks et al. 2011). A significant reduction in in subjects. A reduction of also in women but this was due to the in the data. this study had no control group and very small so firm conclusions cannot be In a recent study of patients with coronary artery disease, 92 individuals consumed ml coconut oil per day for 3 and 22 as controls et al. 2015). groups healthy dietary for a period and the The two groups consumed amounts of energy for the coconut oil the energy consumed as coconut oil was by reduction in the intake of significant differences of in and mmol/l in were observed in the coconut oil group compared with the However, this study has many including group methodology and the fact that subjects in the coconut oil group were to the oil or on its a further for coconut oil may lead to weight the that are by the rather than being are more than longer-chain and consumption up metabolic As the majority of studies that may weight due to the effects on energy cannot be to coconut oil due to the fact that coconut does not capric and acids, Additionally, a small study = that the effect of a coconut oil fatty on and and amount of food consumed at a did not differ to the effect of meals with fatty acids from or foods et al. 2010). there is no reported evidence of coconut oil increasing metabolic rate in there is good evidence at present to that the consumption of coconut oil to a reduction in The of coconut oil by coconut oil have been attributed to the saturated fatty acid lauric which is present in human & and known as and a of lauric acid which is to be produced in after the consumption of coconut oil 2014). and lauric acid reportedly have and but this has mostly been in vitro & 2012; & 2012; et al. et al. 2014) or in animal studies et al. 2010; et al. 2013). has as in the is used as an in food products and sold as a human evidence that may be at when used et al. Wang et al. 2014). However, how much is produced lauric acid and the benefits of this in no human studies have effects of coconut oil per in relating to coconut oil and the for Alzheimer's disease are largely based on animal studies and a small number of human studies which have reported that a product of acid one of the more minor fatty acids in coconut oil at around Fig. may in patients et al. et al. 2009). The of is thought to be to the of something which may the low metabolic rate of which is a of Alzheimer's studies have reported similar et al. 2015). However, to there are no human studies at the effects of coconut oil on in either healthy or those from coconut oil was not consumed as part of the UK diet, with no reported use by of the of the and Diet and (PHE 2014). However, the of to coconut oil from to and new products coconut oil in the market are likely to have consumption. Coconut oil on saturated fatty acids, of which are LDL-C and total cholesterol-raising lauric, myristic and palmitic acids. Such quantities are compared to all other food (see 1 and The Heart and UK of that due to its high saturated fatty acid coconut oil should be consumed only in small quantities and that of unsaturated fatty acids are a better for everyday use Heart The coconut oil within a of foods these on the only does using coconut oil in of other fats dietary guidelines which recommend intake of saturated fatty acids (DH at calories per fats are the most food consuming amounts of oil may positive energy and weight olive oil, for example, which is and by a of evidence its health benefits et al. 2011; & 2014) as well as a health claim et al. and oil, an fatty component of the dietary of 2012), there is evidence to support effects of coconut oil. The effect of coconut oil on CVD risk markers other than plasma is largely in although saturated fatty acids in have been to be deleterious et al. 2012; et al. 2015). to saturated fatty acids and heart disease, evidence that coconut oil raises plasma and a of human studies in health benefits of coconut oil, use of coconut oil should not be coconut oil high up the before eating the product on a The authors have no of to