Coconut oil is a term used to refer to the oil derived from coconuts (Cocos nucifera of the family Arecaceae) that is commonly used as cooking oil, for its fatty acid content and related health properties, or in cosmetics for the functional properties and/or aroma of coconut; usage in noncosmetic products for the functional properties of coconut oil extends to soaps, edible fats, chocolate, candies, candles, and night lights.
Coconut oil is derived from the copra of the coconut (the dried meat of the coconut) which is 60-70% fatty acids, 4-10% water, and has a protein and carbohydrate content (protein of less than 10% and non-sugar carbohydrate less than 20%); with the fatty acids being extracted via refinement followed by bleaching and deodorizing to produce RBD coconut oil with no aroma nor taste; skipping these processes and merely using bulk fatty acids results in virgin coconut oil (this form being commonly used in food preparation). For cosmetic purposes, RBD coconut oil may subsequently be hydrogenated for the physicochemical properties such as an increased melting point.
Coconut oil has a history of usage in Indian medicine and may qualify as Ayurveda, with the tree bearing coconuts (coconut palm) refered to as Kalpavriksha (giving-all tree) and medicinal usage of coconut oil being for the purposes of treating hair loss, burns and heart problems while other traditional usage extends to treating intestinal worms and having antiblenorrhagic, antibronchitis, febrifugal, and antigingivitic properties.
Coconut oil is the fatty acid component from coconuts, which has historically been used for cosmetic and anti-microbial properties in addition to merely being a food product
Coconut oil fatty acids are:
Note: Fatty acid designations follow a schematic of the number of carbons in the side chain followed by the number of double bonds; a 14:2 designation is a 14 carbon chain with two double bonds. Any fatty acid with an x:0 designation without double bonds is a saturated fatty acid, and anything with a carbon chain between 6 and 12 is designation a medium chain triglyceride (MCT)
Caprylic acid at 8%
Capric acid at 7%
Lauric acid (49%) a 12 carbon saturated fatty acid (SFA) with the designation 12:0
With components in coconut oils but not fatty acids being:
Of the above fatty acids, 90% appear to be designated as saturated fats with monounsaturated comprising 7% (mostly oleic) and the rest coming from linoleic acid and and trace alpha-linolenic acid. Of these fatty acids, approximately 65% are designated as medium-chain triglycerides (MCTs). However, lauric acid has a higher propensity to be absorbed via the lymphatic system than other MCTs and be treated as a long-chain saturated fatty acid. Coconut oil does not result in the same blood ketone response observed with other medium-chain triglycerides.
The triglycerides (three fatty acids bound to a glycerol backbone; standard storage form for fatty acids) tend to mostly be trimyristin, trilaurin, tripalmitin, and tristearin Triglycerides from coconut oil can be altered with mixing of the oil with other oils, a process known as interesterification.
The fatty acid component of coconut oil appears to be up to 90% saturated fats mostly from medium chain fatty acids (65% of total fatty acids or so being those with medium length chains)
A study assessing fatty acid length in relationship to hunger in otherwise healthy lean men has failed to note any differences between short chain fatty acid (dairy fat), medium chain fatty acids (coconut oil), and long chain fatty acids (beef tallow) when calories are held constant at a test meal.
Currently not enough evidence to support an appetite suppressing effect relative to other fat sources (fatty acids do have some satiating properties inherently, coconut oil may not be more suppressive than others)
In an acetic-acid, formalin, and hot plate pain tests coconut oil (either fermented or regular) exert dose-dependent pain-reducing effects.
A study using coconut as a placebo to test the effects of fish oil noted that 1,200mg of coconut oil daily for 4 weeks was involved with improvements in the Trail Making Test relative to fish oil in otherwise healthy adults.
In a position statement from ALSUntangled (expert panel) noted that it is possible coconut oil could impair mitochondrial complex I, as this is observed in vitro following incubation with ketone bodies produced from medium chain triglycerides and impairment of complex I is common to some neurodegenerative diseases such as ALS; the authors noted that simply being a provision of calories could also be a possible mechanism as lipid metabolism is linked to ALS pathology. ALSUntangled failed to find any direct evidence between coconut oil and ALS pathology in existence (2012 study), and found some weak rodent evidence that suggests a protective effect of high fat or ketogenic diets on ALS pathology.
There is currently insufficient evidence to support the role of Coconut Oil in treatment or prevention of ALS
A recent meta-analysis (of prospective epidemiological studies) investigating the role of saturated fatty acids per se failed to find evidence to support any link between saturated fatty acids and serum cholsterol. This may be due to heterogeneity between SFAs, as lauric acid (up to half of coconut oil by caloric weight) as well as myristic acid are said to increase HDL and lower LDL (short reviews and position statements) and coconut oil has been associated with increased HDL-C in survey research, with with no association to lower LDL-C. When coconut oil is associated with increased LDL-C, it may be due to the myristic and caprylic acid content.
In assessing studies measuring LDL cholesterol (LDL-C) and HDL-C, adding 30mL (270kcal) of coconut oil in addition to a standardized hypocaloric diet (and compared to a control of soy bean oil) noted an 8.2% increase in HDL relative to control and improvements in the LDL:HDL ratio, but the soybean oil control experienced increases in total cholsterol and LDL relative to baseline in these overweight women. In high fat (38%) diets differing only by their fatty acid composition, coconut oil was associated with an increase in HDL-C by 17.3%, increased LDL (2.5%) and decreased vLDL (14%) relative to the control group of a monounsaturated and polyunsaturated fatty acid mixture. Lauric acid rich foods have also noted reduced total cholesterol relative to transfats, and increases cholesterol more in general relative to both oleic and palmitic (due to both LDL-C and HDL-C) as well as beef tallow or safflower oils.
In contrast, one study (20% of total calories from the test oil, additional 10% from the diet) noted that soy oil reduced cholesterol to a greater degree than coconut oil (the latter increasing LDL-C) with no influence on HDL-C in either group; the addition of psyllium reduced cholesterol independent of fatty acid composition.
Coconut oil is said to improve the LDL:HDL ratio and beneficially influence cardiovascular health, and the limited evidence in existence right now supports this idea somewhat. HDL-C appears to be increased following coconut oil inclusion in the diet as does LDL-C, with the increase in HDL-C being more than LDL-C for some studies. As is the nature of dietary studies and not being able to be compared against placebo (instead being compared against another fatty acid) the evidence is not as reliable as some other interventions for cholesterol
One study in humans comparing coconut oil (40% of calories being fat, from which 80% of that is coconut oil) against long chain fatty acid control (beef tallow at the same amount) noted that after fourteen days there was an increase in metabolic rate assocaited with coconut oil by 4.3% which was detected 7 days after ingestion, but not 14; this has been noted elsewhere in otherwise healthy young women where the increase in metabolic rate detected on day 7 failed to be present subsequently on day 14.
Is associated with an increased metabolic rate, but these effects are short lived (not being present at 2 weeks) and are unlikely to contribute to long term fat loss
This section notes studies on coconut oil per se (65% medium chain triglycerides, or MCTs) and supplemental MCTs themselves. In areas where long chain triglycerides are used as an active control, the acronym LCT is used
The increase in long chain fatty acid oxidation in obese persons has also been seen alongside an increase in fat oxidation in overweight persons (BMI 25-33) that may be independent of weight loss over 6 weeks (40% of diet as fat, 75% thereof being test oil) when medium chain triglycerides are compared to the control of olive oil.
In women with abdominal obesity given either 30mL of coconut oil or 30mL of the control oil (soybean, both at 270kcal) for 12 weeks paired with a hypocaloric carbohydrate-rich diet and a walking regimen noted that while both groups experienced a similar reduction in weight and BMI only the coconut oil group reduced waist circumference (1.4cm). A reduction in waist circumference has been noted elsewhere with 1.7g daily in persons with an average BMI of 24.6-24.7 for 12 weeks to exceed control oil, although this study noted weight loss in both groups (MCT usage being associated with more weight loss and waist circumference loss).
10g of MCTs, relative to 10g long chain fatty acids (both paired with a 2,200kcal intake and 60g fatty acids), MCTs were associated with more fat loss after 12 weeks (3.86+/-0.3kg) than LCTs (2.75+/-0.2kg) only in persons with a BMI greater than 23, whereas there was no significant difference with persons with a lower BMI. This may be related to the aforementioned impairment in long chain fatty acid oxidation noted in obese persons that may be alleviated with medium chain triglycerides.
One study using a test bread (14g fatty acids of which 1.7g were MCTs) daily for 12 weeks noted that the body weight reduction in the MCT group was greater (6.1+/-0.5%) than the LCT group (4.5+/-0.5%) and a study in type II diabetics which noted improvements in HbA1c with consumption of 18g MCTs also noted a 2.6% weight loss over 90 days (132 to 128.6lbs average) where the control of LCTs was inactive.
There appears to be a fat reducing effect of coconut oil and MCTs that exceeds other oils used, which is more readily apparent in obese persons than lean persons. The magnitude of this effect is not astounding (with some studies not noting a weight reducing effect)
One study using in vivo inflammation tests in rats noted that while coconut oil ingestion exerted anti-inflammatory effects in an acute inflammation model (carrageenan-induced paw edema) it failed to have any significant effect chronically (cotton-pellet-induced granuloma test).
A rat study assessing IL-6 release from adipocytes (basal or epinephrine stimulated) comparing coconut oil against both sunflower oil and olive oil noted that ingestion of coconut oil and olive oil were not associated with an epinephrine-induced increase in IL-6 (although coconut oil was consistenly higher than olive oil) while sunflower oil was low initially and increased IL-6 secretion in response to epinephrine. These localized anti-inflammatory effects may be related to the one human study noting a reduction in waist circumference independent of overall weight changes with coconut oil, as weight circumference is related to low-grade chronic inflammation.
A human study assessing serum IL-8 after a test meal noted that while fish oil and linseed had differential effects, that cakes enriched with coconut oil had no significant effect.
Ingestion of coconut oil, relative to other dietary fatty acids, may be associated with anti-inflammatory effects although they do not appear to be of remarkable magnitude
Decoction obtained from coconut tree roots appear to have traditional usage as mouthwash or gargle, which may be related to the low toxicity in general and potential anti-infective properties secondary to lauric acid. Coconut (husk fiber) has demonstrated anti-bacterial properties against various strains of oral bacteria which may be related to the glycolipid sucrose monolaurate, which has been noted to reduce oxidative of Streptococcus mutans at 0.05% and reduced dental plaque in vitro and has shown these properties in a human study (although to a lesser degree of efficacy) using coconut soap on dentures, where there were protective effects against denture stomatitis.
The husk fiber of coconut appears to have anti-bacterial effects in the oral cavity; the oil component may (demonstrated elsewhere) although usage in the oral cavity is not common which may be related to the fiber being chewed and oil ingested
In response to paracetamol-induced liver injury, 10mL/kg of coconut oil was able to outright reverse the increase in liver weight induced by paracetemol (the reference drug, Silymarin from milk thistle at 100mg/kg, was also effective) while 1-5mL/kg were wholly ineffective; similar changes were noted in serum liver enzymes and histopathological analysis of the liver. This may be independent of anti-oxidant induction, as dietary ingestion of 15% coconut oil in rats for 8 weeks has failed to show such an antioxidative effect.
Relative to other oils (copra, olive, and sunflower), coconut oil appears to downregulate hepatic lipogenesis in rats after 45 days of 8% dietary inclusion which coincided with reduced activity of HMG-CoA and more activity of lipoprotein lipase (LPL). This decrease in LPL has been noted with coconut water (although the reduction in HMG-CoA was absent) whereas the water portion appears to be associated with increased HMG-CoA reductase activity but increased bile acid efflux, resulting in a net hypocholesterolemic effect and in fat-fed rats 40mL/kg bodyweight is comparable to 0.1mg/kg lovastatin for cholesterol reduction.
The oil may have protective effects at higher doses (preliminary evidence) while in rats some benefitical effects on lipid synthesis and degradation (less synthesis, more degradation) are noted with chronic ingestion of both coconut oil and water
Coconut oil appears to be a traditionally applied hair remedy in India alongside amla oil and mustard oil.
It is known to penetrate hair follicles when directly applied and appears to be more protective of physical damage (from combing techniques in vitro) relative to both mineral oil and sunflower oil as assessed by protein losses and when applied directly to hairs; these protective effects were noted on normal and bleached by not boiled hair follicles and was more protective when applied prior to the stressor rather than after and have been confirmed in humans as assessed by the hair breakage index (HBI) where coconut oil for 16 weeks was associated with less physical hair damage.
Studies that are conducted on isolated hair follicles or strands note increased moisture resorption with coconut oil relative to mineral oil secondary to reducing moisture loss which may be related to an oil coating of the hair.
In usage of coconut oil as a shampoo, it does not appear to have any ocular irritant properties (in case shampoo reaches the eye).
Coconut oil appears to have direct protective and moisture preserving effects on hair when applied, and may have a role in shampoos (if the physical properties, stickiness and solidifying at room temperature, are considered)
A topical irritation assessment noted that, of 480 persons with active skin diseases, only 5 persons (0.9%) appeared to have a response to coconut oil (15µL of a 5% potassium cocoate solution applied via patch) and in 12 persons known to have an allergic response to cocamidopropyl betaine a 100% solution of coconut oil failed to exert an allergic reaction. This lack of effect has been noted in animal studies, and elsewhere in humans where both isolated lauric acid and coconut oil were not associated with significant allerginity in persons confirmed to be allergic to coamidopropyl betaine.
There appears to be low allergenicity and immune reactivity of coconut oil and its components when topically applied to the skin, suggesting it can be useful for those with sensitive or reactive skin
In persons with xerosis (dry and itchy skin) which is normally treated with moisturizers, coconut oil applied topically was as effective as the active control of mineral oil in reducing symptoms of skin dryness. This moisturizing effects has been noted in adults with atopic dermatitis to a potency greater than that of olive oil (control group for blinding purposes) with reductions in the objective-SCORAD severity index (46.8% reduction from baseline) after 5mL oil application to infected areas twice daily; for those adults that were positive for Staphylococcus aureus infection (readily colonizes atopic dermatitis) only 1 out of 20 remained positive after coconut oil application for 4 weeks.
Coconut oil appears to have moisturizing properties on skin and may also have these effects in atopic dermatitis, where it may also have additive anti-bacterial effects
One study in rats using coconut oil topical application of a wound (first dose 24 hours after the wound, applied to 10 days once a day) noted that coconut oil was assocaited with improved healing rates relative to control.
Glycerol monolaurate (one lauric acid fatty acid bound to glycerol), sometimes referred to as Lauricidin, is as effetive as a 70% isopropyl alcohol mixture (when lauricidin itself is at 1.5%) in eradicating the bacteria Serratia marcescens when applied to the hands. Staphylococcus aureus_ in atopic dermatitis has also been reduced with coconut oil applied topically,
Coconut oil, as a component of hand wash, can exert anti-microbial properties which is thought to be related to the monolaurate content
In neonates given an oil massage with either coconut oil or mineral oil (with another control group) four times daily starting on the second day of life (massage given by trained professional) and continued until a month of life (continued up until this point by mother), the coconut oil group appeared to be associated with increased infant weight and length gain relative to the controls. Neurobehavioural outcomes were unaffected by either coconut oil or mineral oil.
Massages of coconut oil to the newborn appear to have preliminary evidence to suggest improved weight gain
Conjugated Linoleic Acid (CLA) is a fatty acid touted to reduce fat mass, but seems highly unreliable at doing so.
CLA-induced fat loss in mice is augmented when paired with coconut oil relative to being paired with soybean oil and also in mice fed fat-free diets, one other study has noted that pairing CLA with coconut oil trended to outperform coconut oil alone but this was insignificant; in isolated fat cells measuring biomarkers of lipolysis, they appear to be synergistic.
Appears to be synergistic in regards to anti-obesity effects with CLA, but due to the lack of human evidence for the combination and the known species differences with CLA these results should be taken with caution
A study using topical vitamin E (succinate) noted that, with using a coconut oil product (Myritol 318; the medium chain triglycerides of coconut oil) as a base, that absorption was enhanced by approximately 50% relative to other oils tested; 61.2% of vitamin E reached solubility with Myritol 318, which was higher than walnut (43.4%), olive (42.6%), sesame (40.1%), soy (39.6%), sunflower (39.4%), safflower (36%), and canola (24%) and these trends followed for circulating levels of free tocopherol following topical administration in mice. This has been noted with another branded formulation of coconut oil MCTs (Henkel) suggesting that the MCTs per se influence absorption rather than branded products.
Medium chain triglycerides in coconut oil may enhance vitamin E topical absorption relative to other fatty acids, coconut oil has a naturally occurring Vitamin E content
Coconut oil appears to be a heavily used cosmetic ingredient, and as of 2007 the FDA reports it is contained within 626 products for a total of 142 total uses
A 1986 safety assessment noted that coconut oil was free from any reported skin irritation, sensitization, toxicity, and very minimal associations with products containing coconut oil and allergic breakouts; safety of coconut oil up to 50% concentration in cosmetics was seen as very safe. This report was expanded upon by expert panel reviewing coconut oil fatty acids and other conjugates thereof that may be found in cosmetics (Glycerol cocoate, Lanolin acid and alcohol, Butylene glycol, etc.) and in reviewing other safety data reaffirmed the safety of cosmetic usage of coconut oil.
Polyaromatic hydrocarbons (PAHs), a known carcinogen associated with highly smoked meats, appears to be present in concernable quantities following repeated but not single heating of coconut oil; ingestion of this repeatedly heated coconut oil to rats is associated with decreases in hepatic weight. This is not necessarily unique to coconut oil, as it has been noted with repeatedly heated sunflower oil and adverse effects (artherosclerotic) have been noted with repeatedly heated soy oil and palm oil.
Repeatedly heating oils (deep frying without changing the oil source, seen in commercial institutes) appears to be associated with adverse health effects, possible due to increased lipid peroxidation. Coconut oil may be more resistant to these effects (some antioxidant components, but mostly due to being saturated fatty acids) but does not appear to be free of the concern associated with repeated heating