Coconut Oil

Coconut oil is a highly saturated oil derived from coconuts, made of up of medium chain fatty acids. It is a popular cosmetic.

This page features 98 unique references to scientific papers.


Confused about what actually Works?
MUST GET: Supplement Stack Guides - Saving You Money & Time

   

Coconut oil is an oil product derived from Cocos nucifera, commonly known as the coconut.

Coconut oil is used frequently in cosmetics as a topically-applied moisturizer. The effects of coconut oil on skin and hair after ingestion have not been studied.

The majority of coconut oil (65%) is made up of medium chain triglycerides (MCT), which are triglycerides and fatty acids with a carbon length chain of 6 – 12. Studies suggest replacing calories with MCTs without exceeding daily caloric requirements can result in a small, but significant, increase in the rate of fat loss over time. This effect appears to be slightly more powerful in overweight people.

Coconut oil may also temporarily increase metabolic rate and the speed at which fats are broken down to release fatty acids, a process known as lipolysis. This effect occurs when coconut oil is first added to the diet and disappears after two weeks. Coconut oil also creates more ketone bodies than longer chain fatty acids when it is broken down. One study has provided evidence that this mechanism is what causes coconut oil to provide obese people with a muscle preserving effect during caloric restriction. This effect has not been replicated in lean people.

Adding coconut oil to a diet is unlikely to cause noticeable fat loss effects, but it can replace other dietary fatty acids in order to fine-tune a diet plan.

Follow this Page for updates

Confused about Supplements?
Get the Stack Guides

Also Known As

Cocos nucifera, Coconut, Medium Chain Triglycerides (partially synonymous but commonly touted as such)


Things to Note

  • Although single-use heating of coconut oil appears to be free of harm (use as a home cooking oil) multiple heating (deep frying) may be associated with production of polyaromatic hydrocarbons, a carcinogenic compound, which is common to all tested fatty acids

Is a Form of


Goes Well With

  • Vitamin E (enhanced topical absorption when using medium chain triglycerides as base)

Caution Notice

Examine.com Medical Disclaimer

Coconut oil is most effective when about 5- 10g of medium chain triglycerides are included in the diet. This is approximately 7.7 – 15g of coconut oil.

Coconut oil can be used in cooking, as long as cooking is done below the smoke point of the oil (350°F/175°C).

Replacing other dietary fatty acids with coconut oil may negate any potential fat loss effects if the caloric content of coconut oil is greater than the previously consumed fatty acids.


The Human Effect Matrix looks at human studies (excluding animal/petri-dish studies) to tell you what effect Coconut Oil has in your body, and how strong these effects are.
GradeLevel of Evidence
ARobust research conducted with repeated double blind clinical trials
BMultiple studies where at least two are double-blind and placebo controlled
CSingle double blind study or multiple cohort studies
DUncontrolled or observational studies only
Level of Evidence
EffectChange
Magnitude of Effect Size
Scientific ConsensusComments
CMetabolic Rate

Minor

Appears to be a short lived and of small magnitude increase in metabolic rate.

CProcessing Speed

Minor

Study was unable to properly assess coconut oil as it was used as an active control; some benefit appears apparent relative to fish oil.

CWorking Memory

Insufficient evidence to support an increase in working memory

CSkin dryness

Notable

Appears to be comparable to mineral oil, which is usually the active control in these studies.

CSkin moisture

Notable

Appears to be comparable to mineral oil, the active control

DBlood Glucose

Insufficient evidence to support alterations in blood glucose.

DInsulin Sensitivity

Minor

May improve insulin sensitivity in diabetics, requires more evidence though as the one study was confounded with fat loss.

DTriglycerides

Insufficient evidence to support changes in serum triglycerides.

DTotal Cholesterol

Minor

A decrease in total cholesterol (both the LDL and HDL portions) has been noted with coconut oil to a minor degree relative to longer chain fatty acids

DWeight

Minor

Appears somewhat effective in reducing weight of obese persons to a greater degree than an isocaloric amount of longer chain fatty acids

DLDL-C

Minor

Not an overly significant reduction of LDL-C, but it does appear to be present relative to longer chain fatty acids

DHDL-C

Minor

Decrease in HDL-C is minor and likely not practically relevant.

DApolipoprotein B

No significant alterations in Apolipoprotein B levels

DInsulin

No significant influence detected on fasting insulin levels following coconut oil consumption

DApolipoprotein A

No significant changes in apo-A levels with dietary inclusion of coconut oil

DThermic Effect of Food

Insufficient evidence to support alterations in the thermic effect of food compared to other oils

DKetone Bodies

Minor

Has been implicated in increasing serum ketones more than other fatty acids.

DFat Mass

Minor

May decrease fat mass to a greater degree than an isocaloric amount of long chain fatty acids.

DSkeletal Muscle Atrophy

Minor

Was able to attenuate the rate of skeletal muscle loss during a hypocaloric diet in obese persons; unknown if this applies to lean persons and may be related to ketone production.

DFat Oxidation

Minor

Appears to increase the percentage of calories derived from lipids in obese persons; no comparator.

DInfant Growth

Disagree? Join the Coconut Oil Discussion

Table of Contents:


Edit1. Sources and Composition

1.1. Sources

Coconut oil is a term used to refer to the oil derived from coconuts (Cocos nucifera of the family Arecaceae[1]) 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;[2] usage in noncosmetic products for the functional properties of coconut oil extends to soaps, edible fats, chocolate, candies, candles, and night lights.[2]

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%[1]); with the fatty acids being extracted via refinement followed by bleaching and deodorizing to produce RBD coconut oil with no aroma nor taste;[2] 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)[1] 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.[1]

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

1.2. Composition

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%[1]
  • Capric acid at 7%[1]
  • Lauric acid (49%[3]) a 12 carbon saturated fatty acid (SFA) with the designation 12:0
  • Myristic acid (17.5-18%[1][3]) a SFA with 14 carbons (14:0)
  • Palmitic acid (8-9%[1][3]) a 16 carbon SFA (16:0)
  • Stearic acid (2-3%[1][3]) an 18 carbon SFA (18:0)
  • Oleic acid (5-6%[1][3]) as an omega-9 monounsaturated fatty acid with the designation 18:1
  • Linoleic acid (1.8-2%[1][3]) and omega-6 with the designation 18:2

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.[5][2] Of these fatty acids, approximately 65% are designated as medium-chain triglycerides.[1]

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[2] Triglycerides from coconut oil can be altered with mixing of the oil with other oils, a process known as interesterification.[6][7]

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)


Edit2. Neurology

2.1. Appetite

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.[8]

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)

2.2. Pain

In an acetic-acid, formalin, and hot plate pain tests coconut oil (either fermented or regular) exert dose-dependent pain-reducing effects.[9]

2.3. Amyotrophic lateral sclerosis and Processing Speed

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[10] relative to fish oil in otherwise healthy adults.[11]

In a position statement from ALSUntangled (expert panel)[12] 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[13] and impairment of complex I is common to some neurodegenerative diseases such as ALS;[14][15] the authors noted that simply being a provision of calories could also be a possible mechanism as lipid metabolism is linked to ALS pathology.[16] ALSUntangled[12] 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.[17][18]

There is currently insufficient evidence to support the role of Coconut Oil in treatment or prevention of ALS


Edit3. Cardiovascular Health

3.1. Triglycerides and Lipoproteins

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.[19] 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)[20][21] and coconut oil has been associated with increased HDL-C in survey research, with with no association to lower LDL-C.[22] When coconut oil is associated with increased LDL-C, it may be due to the myristic and caprylic acid content.[23]

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.[3] 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.[24] Lauric acid rich foods have also noted reduced total cholesterol relative to transfats,[25] and increases cholesterol more in general relative to both oleic and palmitic (due to both LDL-C and HDL-C)[26] as well as beef tallow or safflower oils.[27]

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.[28]

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

In diabetics, 18g of medium chain triglycerides (relative to 18g long chain triglycerides) for 90 days is assocaited with a reduction of total cholesterol (12%), LDL-C (17%), and a reduction in HDL-C (16%) with no influence on triglycerides.[29]


Edit4. Interactions with Glucose Metabolism

4.1. Interventions

A 90 day trial using 18g of medium chain triglycerides, relative to 18g long chain triglycerides, in type II diabetics noted that alongside a small weight reducing effect that there was a 17% improvement in insulin resistance as assessed by HOMA-IR while control experiencing a worsening (7.3%); the difference was significant, although differences existed at baseline and there was no apparent influence on fasting glucose.[29]


Edit5. Fat Mass and Obesity

5.1. Mechanisms

Medium chain triglycerides (65% of coconut oil by weight), relative to long chain fatty acids, appear to have a greater propensity for oxidation which is shown in animal studies on substrate utilization[30][31][32] and has been demonstrated in humans.[33][34][35] Consumption of medium chain triglycerides in humans has once been noted to enhance oxidation of long chain fatty acids in addition to medium chain fatty acids[36] which is thought to have important implications for obesity as it has been observed obese persons have less long chain fatty acid oxidation relative to lean counterparts, but no impairments in medium chain oxidation are noted.[37]

This may be related to the enzyme carnitine palmitoyltransferase (CPT), the rate limiting step in fatty acid oxidation, not being required for fatty acids of medium or short chain length.[38]

The class of medium chain triglycerides (65% of coconut oil) appears to be more readily oxidized via lipolysis ('fat burning') relative to longer chain fatty acids, which may be important in obesity as impaired long chain fatty acid oxidation has been noted in obese persons

In animal studies in which the animals are overfed, there appears to be less weight gain associated with medium chain fatty acid ingestion relative to long chain fatty acid ingestion although a degree of weight gain is still present.[39][40][41][42]

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;[43] 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.[44]

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

5.2. Ketogenesis

Ingestion of medium chain triglycerides in obese persons (BMI above 30 and and 9.9g MCTs) paired with a hypocaloric diet (578.4kcal) has been associated with a higher blood ketone body (beta hydroxy-butyrate) level and reduced nitrogen excretion which have been thought to exert protein sparing effects; this study noted that for weight loss obtained over 2 weeks, that a greater percentage (56%) was from fat mass relative to long chain triglycerides (22%) or low fat control (25%).[45]

5.3. Interventions

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[36] 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.[46]

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).[3] 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).[47]

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.[48] This may be related to the aforementioned impairment in long chain fatty acid oxidation noted in obese persons[37] that may be alleviated with medium chain triglycerides.[36]

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%)[47] 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.[29]

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)


Edit6. Exercise and Performance

6.1. Bioenergetics

It has been reported that medium chain triglycerides in general, when replacing long chain fatty acids in the diet, do not appear to confer additional performance enhancing benefits[49] or at least the benefits are highly controversial[50] despite theoretically being a more readily catabolized source of fatty acids for energy production during exercise.[51]

For studies assessing glycogen, there does not appear to be a significant interaction for for normal distance aerobic exercise[52][53] or ultradistances[54] with or without additional carbohydrates.[55]

There is not a large amount of convincing evidence that calories from medium chain triglycerides and coconut oil are somehow better for performance than carbohydrates or long chain fatty acids, although the calories themselves may confer an ergogenic property


Edit7. Inflammation and Immunology

7.1. Mechanisms

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).[9]

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.[56] 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,[3] as weight circumference is related to low-grade chronic inflammation.[57][58]

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.[59]

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


Edit8. Interactions with Organ Systems

8.1. Oral Cavity

Decoction obtained from coconut tree roots appear to have traditional usage as mouthwash or gargle,[1] which may be related to the low toxicity in general and potential anti-infective properties secondary to lauric acid.[60] Coconut (husk fiber) has demonstrated anti-bacterial properties against various strains of oral bacteria[61] 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[1][61] 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.[62]

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

8.2. Liver

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.[63] 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.[64]

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).[65] This decrease in LPL has been noted with coconut water (although the reduction in HMG-CoA was absent)[66] 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[67][66] and in fat-fed rats 40mL/kg bodyweight is comparable to 0.1mg/kg lovastatin for cholesterol reduction.[67]

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


Edit9. Interactions with Aesthetics

9.1. Hair

Coconut oil appears to be a traditionally applied hair remedy in India alongside amla oil and mustard oil.[68]

It is known to penetrate hair follicles when directly applied[69][70][71] 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[72] 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.[73]

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[74] which may be related to an oil coating of the hair.[71]

In usage of coconut oil as a shampoo, it does not appear to have any ocular irritant properties[75] (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)

9.2. Skin

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)[76] 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.[77] This lack of effect has been noted in animal studies,[75] 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.[77]

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.[78] 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;[79] 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.[79]

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.[80]

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.[81] Staphylococcus aureus in atopic dermatitis has also been reduced with coconut oil applied topically,[79]

Coconut oil, as a component of hand wash, can exert anti-microbial properties which is thought to be related to the monolaurate content


Edit10. Sexuality and Pregnancy

10.1. Benefits to Child

It is thought that coconut oil can promote neonatal growth in part due to topical absorption of fatty acids, and in part due to tactile kinesthetic stimulation.[82][83]

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.[83] Neurobehavioural outcomes were unaffected by either coconut oil or mineral oil.[83]

Massages of coconut oil to the newborn appear to have preliminary evidence to suggest improved weight gain


Edit11. Nutrient Nutrient Interactions

11.1. CLA

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[84][85] and also in mice fed fat-free diets,[85][86] one other study has noted that pairing CLA with coconut oil trended to outperform coconut oil alone but this was insignificant;[86] in isolated fat cells measuring biomarkers of lipolysis, they appear to be synergistic.[86]

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

11.2. Vitamin E

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;[87] 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.[87] This has been noted with another branded formulation of coconut oil MCTs (Henkel)[88] 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


Edit12. Safety and Toxicology

12.1. Cosmetic usage

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[2]

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.[89] This report was expanded upon by expert panel[2] 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[90][91][92][93] reaffirmed the safety of cosmetic usage of coconut oil.[2]

12.2. Genotoxicity

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.[94] This is not necessarily unique to coconut oil, as it has been noted with repeatedly heated sunflower oil[95] and adverse effects (artherosclerotic) have been noted with repeatedly heated soy oil[96] and palm oil.[97][98]

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

References

  1. DebMandal M, Mandal S. Coconut (Cocos nucifera L.: Arecaceae): in health promotion and disease prevention. Asian Pac J Trop Med. (2011)
  2. Burnett CL, et al. Final report on the safety assessment of Cocos nucifera (coconut) oil and related ingredients. Int J Toxicol. (2011)
  3. Assunção ML, et al. Effects of dietary coconut oil on the biochemical and anthropometric profiles of women presenting abdominal obesity. Lipids. (2009)
  4. Loki AL, Rajamohan T. Hepatoprotective and antioxidant effect of tender coconut water on carbon tetrachloride induced liver injury in rats. Indian J Biochem Biophys. (2003)
  5. Misra A, Singhal N, Khurana L. Obesity, the metabolic syndrome, and type 2 diabetes in developing countries: role of dietary fats and oils. J Am Coll Nutr. (2010)
  6. Soares FA, et al. Chemical interesterification of blends of palm stearin, coconut oil, and canola oil: physicochemical properties. J Agric Food Chem. (2012)
  7. Reena MB, Lokesh BR. Hypolipidemic effect of oils with balanced amounts of fatty acids obtained by blending and interesterification of coconut oil with rice bran oil or sesame oil. J Agric Food Chem. (2007)
  8. Poppitt SD, et al. Fatty acid chain length, postprandial satiety and food intake in lean men. Physiol Behav. (2010)
  9. Zakaria ZA, et al. In vivo antinociceptive and anti-inflammatory activities of dried and fermented processed virgin coconut oil. Med Princ Pract. (2011)
  10. Trail Making Test (TMT)
  11. Karr JE, Grindstaff TR, Alexander JE. Omega-3 polyunsaturated fatty acids and cognition in a college-aged population. Exp Clin Psychopharmacol. (2012)
  12. ALSUntangled Group. ALSUntangled 15: coconut Oil. Amyotroph Lateral Scler. (2012)
  13. Tieu K, et al. D-beta-hydroxybutyrate rescues mitochondrial respiration and mitigates features of Parkinson disease. J Clin Invest. (2003)
  14. Swerdlow RH, et al. Mitochondria in sporadic amyotrophic lateral sclerosis. Exp Neurol. (1998)
  15. Martin LJ. Mitochondrial pathobiology in ALS. J Bioenerg Biomembr. (2011)
  16. Dorst J, et al. Patients with elevated triglyceride and cholesterol serum levels have a prolonged survival in amyotrophic lateral sclerosis. J Neurol. (2011)
  17. Dupuis L, et al. Evidence for defective energy homeostasis in amyotrophic lateral sclerosis: benefit of a high-energy diet in a transgenic mouse model. Proc Natl Acad Sci U S A. (2004)
  18. Zhao Z, et al. A ketogenic diet as a potential novel therapeutic intervention in amyotrophic lateral sclerosis. BMC Neurosci. (2006)
  19. Siri-Tarino PW, et al. Meta-analysis of prospective cohort studies evaluating the association of saturated fat with cardiovascular disease. Am J Clin Nutr. (2010)
  20. Kris-Etherton PM, et al. Position of the American Dietetic Association and Dietitians of Canada: dietary fatty acids. J Am Diet Assoc. (2007)
  21. Cunningham E. Is there science to support claims for coconut oil. J Am Diet Assoc. (2011)
  22. Feranil AB, et al. Coconut oil is associated with a beneficial lipid profile in pre-menopausal women in the Philippines. Asia Pac J Clin Nutr. (2011)
  23. Tsai YH, et al. Mechanisms mediating lipoprotein responses to diets with medium-chain triglyceride and lauric acid. Lipids. (1999)
  24. Müller H, et al. The serum LDL/HDL cholesterol ratio is influenced more favorably by exchanging saturated with unsaturated fat than by reducing saturated fat in the diet of women. J Nutr. (2003)
  25. de Roos N, Schouten E, Katan M. Consumption of a solid fat rich in lauric acid results in a more favorable serum lipid profile in healthy men and women than consumption of a solid fat rich in trans-fatty acids. J Nutr. (2001)
  26. Temme EH, Mensink RP, Hornstra G. Comparison of the effects of diets enriched in lauric, palmitic, or oleic acids on serum lipids and lipoproteins in healthy women and men. Am J Clin Nutr. (1996)
  27. Reiser R, et al. Plasma lipid and lipoprotein response of humans to beef fat, coconut oil and safflower oil. Am J Clin Nutr. (1985)
  28. Ganji V, Kies CV. Psyllium husk fiber supplementation to the diets rich in soybean or coconut oil: hypocholesterolemic effect in healthy humans. Int J Food Sci Nutr. (1996)
  29. Han JR, et al. Effects of dietary medium-chain triglyceride on weight loss and insulin sensitivity in a group of moderately overweight free-living type 2 diabetic Chinese subjects. Metabolism. (2007)
  30. Souza PF, Williamson DH. Effects of feeding medium-chain triacylglycerols on maternal lipid metabolism and pup growth in lactating rats. Br J Nutr. (1993)
  31. Lieber CS, et al. Difference in hepatic metabolism of long- and medium-chain fatty acids: the role of fatty acid chain length in the production of the alcoholic fatty liver. J Clin Invest. (1967)
  32. Johnson RC, et al. Medium-chain-triglyceride lipid emulsion: metabolism and tissue distribution. Am J Clin Nutr. (1990)
  33. Watkins JB, et al. Diagnosis and differentiation of fat malabsorption in children using 13C-labeled lipids: trioctanoin, triolein, and palmitic acid breath tests. Gastroenterology. (1982)
  34. Metges CC, Wolfram G. Medium- and long-chain triglycerides labeled with 13C: a comparison of oxidation after oral or parenteral administration in humans. J Nutr. (1991)
  35. Schoeller DA, et al. 13C abundances of nutrients and the effect of variations in 13C isotopic abundances of test meals formulated for 13CO2 breath tests. Am J Clin Nutr. (1980)
  36. Papamandjaris AA, et al. Endogenous fat oxidation during medium chain versus long chain triglyceride feeding in healthy women. Int J Obes Relat Metab Disord. (2000)
  37. Binnert C, et al. Influence of human obesity on the metabolic fate of dietary long- and medium-chain triacylglycerols. Am J Clin Nutr. (1998)
  38. Carnitine Palmitoyltransferase 1A Deficiency
  39. Geliebter A, et al. Overfeeding with medium-chain triglyceride diet results in diminished deposition of fat. Am J Clin Nutr. (1983)
  40. Dulloo AG, et al. Differential effects of high-fat diets varying in fatty acid composition on the efficiency of lean and fat tissue deposition during weight recovery after low food intake. Metabolism. (1995)
  41. Crozier G, et al. Metabolic effects induced by long-term feeding of medium-chain triglycerides in the rat. Metabolism. (1987)
  42. Lavau MM, Hashim SA. Effect of medium chain triglyceride on lipogenesis and body fat in the rat. J Nutr. (1978)
  43. White MD, Papamandjaris AA, Jones PJ. Enhanced postprandial energy expenditure with medium-chain fatty acid feeding is attenuated after 14 d in premenopausal women. Am J Clin Nutr. (1999)
  44. Papamandjaris AA, White MD, Jones PJ. Components of total energy expenditure in healthy young women are not affected after 14 days of feeding with medium-versus long-chain triglycerides. Obes Res. (1999)
  45. Krotkiewski M. Value of VLCD supplementation with medium chain triglycerides. Int J Obes Relat Metab Disord. (2001)
  46. Roynette CE, et al. Structured medium and long chain triglycerides show short-term increases in fat oxidation, but no changes in adiposity in men. Nutr Metab Cardiovasc Dis. (2008)
  47. Kasai M, et al. Effect of dietary medium- and long-chain triacylglycerols (MLCT) on accumulation of body fat in healthy humans. Asia Pac J Clin Nutr. (2003)
  48. Tsuji H, et al. Dietary medium-chain triacylglycerols suppress accumulation of body fat in a double-blind, controlled trial in healthy men and women. J Nutr. (2001)
  49. Clegg ME. Medium-chain triglycerides are advantageous in promoting weight loss although not beneficial to exercise performance. Int J Food Sci Nutr. (2010)
  50. Does medium chain triglyceride play an ergogenic role in endurance exercise performance?
  51. Hawley JA, Brouns F, Jeukendrup A. Strategies to enhance fat utilisation during exercise. Sports Med. (1998)
  52. Horowitz JF, et al. Preexercise medium-chain triglyceride ingestion does not alter muscle glycogen use during exercise. J Appl Physiol. (2000)
  53. Misell LM, et al. Chronic medium-chain triacylglycerol consumption and endurance performance in trained runners. J Sports Med Phys Fitness. (2001)
  54. Goedecke JH, et al. The effects of medium-chain triacylglycerol and carbohydrate ingestion on ultra-endurance exercise performance. Int J Sport Nutr Exerc Metab. (2005)
  55. Angus DJ, et al. Effect of carbohydrate or carbohydrate plus medium-chain triglyceride ingestion on cycling time trial performance. J Appl Physiol. (2000)
  56. García-Escobar E, et al. Nutritional regulation of interleukin-6 release from adipocytes. Int J Obes (Lond). (2010)
  57. Steene-Johannessen J, et al. Waist circumference is related to low-grade inflammation in youth. Int J Pediatr Obes. (2010)
  58. Ackermann D, et al. Waist circumference is positively correlated with markers of inflammation and negatively with adiponectin in women with metabolic syndrome. Nutr Res. (2011)
  59. Myhrstad MC, et al. Effect of the fat composition of a single high-fat meal on inflammatory markers in healthy young women. Br J Nutr. (2011)
  60. Antimicrobial Effect of Coconut Flour on Oral Microflora: An in vitro Study
  61. Alviano WS, et al. In vitro antioxidant potential of medicinal plant extracts and their activities against oral bacteria based on Brazilian folk medicine. Arch Oral Biol. (2008)
  62. Barnabé W, et al. Efficacy of sodium hypochlorite and coconut soap used as disinfecting agents in the reduction of denture stomatitis, Streptococcus mutans and Candida albicans. J Oral Rehabil. (2004)
  63. Zakaria ZA, et al. Hepatoprotective activity of dried- and fermented-processed virgin coconut oil. Evid Based Complement Alternat Med. (2011)
  64. Dauqan E, et al. Effect of four different vegetable oils (red palm olein, palm olein, corn oil, coconut oil) on antioxidant enzymes activity of rat liver. Pak J Biol Sci. (2011)
  65. Arunima S, Rajamohan T. Virgin coconut oil improves hepatic lipid metabolism in rats--compared with copra oil, olive oil and sunflower oil. Indian J Exp Biol. (2012)
  66. Sandhya VG, Rajamohan T. Beneficial effects of coconut water feeding on lipid metabolism in cholesterol-fed rats. J Med Food. (2006)
  67. Sandhya VG, Rajamohan T. Comparative evaluation of the hypolipidemic effects of coconut water and lovastatin in rats fed fat-cholesterol enriched diet. Food Chem Toxicol. (2008)
  68. Garg AP, Müller J. Inhibition of growth of dermatophytes by Indian hair oils. Mycoses. (1992)
  69. Gode V, et al. Quantitative measurement of the penetration of coconut oil into human hair using radiolabeled coconut oil. J Cosmet Sci. (2012)
  70. Ruetsch SB, et al. Secondary ion mass spectrometric investigation of penetration of coconut and mineral oils into human hair fibers: relevance to hair damage. J Cosmet Sci. (2001)
  71. Keis K, et al. Investigation of penetration abilities of various oils into human hair fibers. J Cosmet Sci. (2005)
  72. Rele AS, Mohile RB. Effect of mineral oil, sunflower oil, and coconut oil on prevention of hair damage. J Cosmet Sci. (2003)
  73. Mhaskar S, et al. Hair breakage index: an alternative tool for damage assessment of human hair. J Cosmet Sci. (2011)
  74. Keis K, Huemmer CL, Kamath YK. Effect of oil films on moisture vapor absorption on human hair. J Cosmet Sci. (2007)
  75. Alviano DS, et al. Antinociceptive and free radical scavenging activities of Cocos nucifera L. (Palmae) husk fiber aqueous extract. J Ethnopharmacol. (2004)
  76. Santucci B, et al. Cutaneous response to irritants. Contact Dermatitis. (2003)
  77. Shaffer KK, et al. Allergenicity and cross-reactivity of coconut oil derivatives: A double-blind randomized controlled pilot study. Dermatitis. (2006)
  78. Agero AL, Verallo-Rowell VM. A randomized double-blind controlled trial comparing extra virgin coconut oil with mineral oil as a moisturizer for mild to moderate xerosis. Dermatitis. (2004)
  79. Verallo-Rowell VM, Dillague KM, Syah-Tjundawan BS. Novel antibacterial and emollient effects of coconut and virgin olive oils in adult atopic dermatitis. Dermatitis. (2008)
  80. Nevin KG, Rajamohan T. Effect of topical application of virgin coconut oil on skin components and antioxidant status during dermal wound healing in young rats. Skin Pharmacol Physiol. (2010)
  81. Testing of Lauricidin Versus Isopropyl Alcohol for Antisepsis of Cutaneous Hand Microbes to Prevent Infection
  82. Darmstadt GL, et al. Impact of topical oils on the skin barrier: possible implications for neonatal health in developing countries. Acta Paediatr. (2002)
  83. Sankaranarayanan K, et al. Oil massage in neonates: an open randomized controlled study of coconut versus mineral oil. Indian Pediatr. (2005)
  84. Hargrave KM, et al. Influence of dietary conjugated linoleic Acid and fat source on body fat and apoptosis in mice. Obes Res. (2004)
  85. Hargrave KM, Azain MJ, Miner JL. Dietary coconut oil increases conjugated linoleic acid-induced body fat loss in mice independent of essential fatty acid deficiency. Biochim Biophys Acta. (2005)
  86. Ippagunta S, et al. Dietary conjugated linoleic acid induces lipolysis in adipose tissue of coconut oil-fed mice but not soy oil-fed mice. Lipids. (2011)
  87. Trevithick JR, Mitton KP. Uptake of vitamin E succinate by the skin, conversion to free vitamin E, and transport to internal organs. Biochem Mol Biol Int. (1999)
  88. Trevithick JR, Mitton KP. Topical application and uptake of vitamin E acetate by the skin and conversion to free vitamin E. Biochem Mol Biol Int. (1993)
  89. Final Report on the Safety Assessment of Coconut Oil, Coconut Acid, Hydrogenated Coconut Acid, and Hydrogenated Coconut Oil
  90. FINAL REPORT OF THE SAFETY ASSESSEMENT FOR ACETYLATED LANOLIN ALCOHOL AND RELATED COMPOUNDS
  91. [No authors listed. Annual review of cosmetic ingredient safety assessments-2004/2005. Int J Toxicol. (2006)
  92. Cosmetic Ingredient Review Expert Panel. Annual Review of Cosmetic Ingredient Safety Assessments--2002/2003. Int J Toxicol. (2005)
  93. Johnson W Jr; Cosmetic Ingredient Review Expert Panel. Final report on the safety assessment of PEG-25 propylene glycol stearate, PEG-75 propylene glycol stearate, PEG-120 propylene glycol stearate, PEG-10 propylene glycol, PEG-8 propylene glycol cocoate, and PEG-55 propylene glycol oleate. Int J Toxicol. (2001)
  94. Srivastava S, et al. Genotoxic and carcinogenic risks associated with the dietary consumption of repeatedly heated coconut oil. Br J Nutr. (2010)
  95. Srivastava S, et al. Genotoxic and Carcinogenic Risks Associated with the Consumption of Repeatedly Boiled Sunflower Oil. J Agric Food Chem. (2010)
  96. Adam SK, et al. Consumption of repeatedly heated soy oil increases the serum parameters related to atherosclerosis in ovariectomized rats. Tohoku J Exp Med. (2008)
  97. Adam SK, et al. Effects of repeatedly heated palm oil on serum lipid profile, lipid peroxidation and homocysteine levels in a post-menopausal rat model. Mcgill J Med. (2008)
  98. Leong XF, et al. Intake of repeatedly heated palm oil causes elevation in blood pressure with impaired vasorelaxation in rats. Tohoku J Exp Med. (2009)

(Common misspellings for Coconut Oil include cocont, cocnut, cacaonut, cocoanut)

(Common phrases used by users for this page include hair+oil+related+studies, difference between food coconut oil and cosmetic coconut oil, coconut science information, coconut lipolysis, coconut and olive oil for skin, Normal Acid value of 10g of coconut oil)

(Users who contributed to this page include , , dbarvinok, shrillthrill, ch1ll, KamalPatel)