Coconut oil

Coconut Oil (Cocos nucifera L.): A Comprehensive Reference

1. Identity, Botanical Classification, and Natural Source

Botanical name: Cocos nucifera L., family Arecaceae (the palm family). The common name "coconut oil" refers to the fixed oil expressed or extracted from the dried or fresh kernel (endosperm) of the fruit of this monocotyledonous palm tree.

Coconut oil, with its rich history and versatile applications, has been a vital component of tropical life for thousands of years. This natural product is extracted from the kernel or meat of mature coconuts harvested from the coconut palm, and has been revered not only for its nutritional value but also for its medicinal and cosmetic properties.

Approximately 84% of the fatty acids contained in coconut oil are saturated fatty acids (SFAs), and approximately 47% of the SFA are lauric acid with 12 carbon atoms. Coconut oil is 82% saturated fat, 2% PUFAs, and 6% MUFAs.

1.1 Common Forms and Preparations

Several distinct commercial and culinary preparations of coconut oil exist, which differ substantially in processing, chemical profile, and intended use:

• Virgin coconut oil (VCO): VCO is produced from fresh coconut milk obtained from the kernels of fresh and ripe coconuts by mechanical or natural means, with or without the use of heat, without undergoing chemical refining, bleaching, or deodorizing, which does not cause a change in oil properties.
• Refined, bleached, and deodorized (RBD) oil: RBD oil is made from dried coconut kernels or flesh produced by smoke drying, sun drying, or combining the two methods.
• Extra virgin coconut oil (EVCO): An additional designation used in some markets for unrefined oil processed at low temperatures from fresh coconut; it is often used interchangeably with VCO but has no universally regulated definition.
• MCT oil derived from coconut: A further-processed fraction. MCT oil derived from coconuts surpasses traditional coconut oil in efficiency and speed of energy conversion due to its higher concentration of readily metabolizable MCTs.

In traditional extraction methods, coconut meat was grated and manually pressed to obtain the oil — a labor-intensive process yielding a highly valuable product. The oil was used in various traditional practices, from cooking and lighting to skin care and hair treatment, embedding itself deeply in the cultural fabric of these societies.

2. Traditional and Historical Use

2.1 Geographic Origins and Timeline

Historical records trace coconut oil usage back over 4,000 years in Southeast Asia, India, and the Pacific Islands. These tropical regions saw the coconut not just as food, but as a source of healing, protection, and sustenance.

It was primarily in Southeast Asia and the Pacific Islands where coconut and coconut oil cultivation and use became extensive, serving as a dietary staple and an essential for cooking and medicinal practices.

2.2 Ayurvedic and South Asian Traditions

Coconut oil, or narikela taila as it is traditionally known, is celebrated in Ayurvedic texts dating as far back as 1500 BC. These ancient scriptures, including the Charaka Samhita and Sushruta Samhita, often advocate for the use of coconut oil for its "cooling" properties. In the Ayurvedic context, coconut oil is known to balance the "Pitta" dosha, responsible for metabolic processes involving digestion, absorption and body temperature.

Origins of such practices can be traced back to Ayurveda, the traditional Hindu system of medicine originating thousands of years ago in India. In Ayurvedic teachings, coconut oil is considered a vital element balancing the body's natural energies, known as "doshas," and promoting holistic health and wellbeing.

In India, Ayurvedic medicine used coconut oil for treating inflammation, skin diseases, digestive disorders, and hair care.

2.3 Pacific Island, Filipino, and Sri Lankan Traditions

In Pacific cultures like Polynesia and Micronesia, coconut oil protected skin from sun and saltwater, and even preserved wooden tools and instruments.

Island nations like the Philippines, Samoa, Fiji, and Sri Lanka also heavily incorporate coconut oil into their medicinal practices. It is revered for its supposed antimicrobial, anti-inflammatory, and general healing attributes. Topical application of the oil is common in wound healing and skin care, while internal use is believed to aid digestion, improve heart health, and boost the immune system.

Coconut oil is an integral part of Sri Lankan and many South Asian diets.

2.4 Western Pharmacopoeial and 18th–19th Century Use

Even in Western countries, during the 18th century, pharmacists regularly incorporated coconut oil into a multitude of medicinal preparations, recognizing its therapeutic potencies.

3. Key Constituents and Active Compounds

3.1 Fatty Acid Profile

Coconut oil contains predominantly saturated fatty acids — caprylic acid, capric acid, lauric acid, myristic acid, palmitic acid, and stearic acid — and less than 10% unsaturated fatty acids (oleic acid and linoleic acid).

The individual fatty acids present are:

• Lauric acid (C12:0): The dominant fatty acid. The major MCFA of oils from coconut are lauric acid (47.0–50.0%).
• Myristic acid (C14:0), palmitic acid (C16:0), stearic acid (C18:0): Present in lower proportions. The fatty acid composition also includes caprylic acid (C8:0), capric acid (C10:0), caproic acid (C6:0), oleic acid (C18:1), and linoleic acid (C18:2).

The most saturated fatty acid content in Virgin Coconut Oil (VCO) is approximately 90.9% of total fatty acids.

3.2 Classification Controversy: Medium-Chain vs. Long-Chain

Lauric acid makes up approximately half of the fatty acids in coconut oil; likewise, medium-chain triglycerides which contain lauric acid account for approximately half of all triacylglycerides in coconut oil. Based on biochemical and nutritional evidence, lauric acid (C12) has distinctive properties that are not shared with longer-chain saturated fatty acids: myristic acid (C14), palmitic acid (C16), and stearic acid (C18). Because medium-chain saturated fatty acids C6 to C12 show sufficiently different metabolic and physiological properties from long-chain saturated fatty acids C14 to C18, the term "saturated fatty acid" does not convey nutritionally accurate information.

Lauric acid's carbon chain length is intermediate between medium and long-chain fatty acids (LCFAs). Lauric acid (C12:0), which has distinctive metabolic characteristics including rapid energy conversion that are not found in long chain fatty acids (LCFA, C14–C18), is still ambiguously classified since some studies define MCFA as C6–C10 only.

3.3 Monolaurin: Key Bioactive Metabolite

The lauric acid present in coconut kernel and the extracted oil is proven to have antimicrobial effects. The human body metabolizes lauric acid, converting it to monolaurin, a monoglyceride. Monolaurin is found to be an active antimicrobial agent.

In humans, the oral ingestion of VCO stimulates the conversion of lauric acid, the most abundant MCFA (45 to 52%), to monolaurin, a key component of breast milk that boosts the baby immune system and has the potential to damage bacteria's lipid membranes.

3.4 Polyphenols and Minor Constituents

Virgin coconut oil also contains phenolic compounds. A robust body of evidence shows that lauric acid and other phenolic compounds are responsible for the VCO protection against toxicities and pharmacological efficacies. These minor constituents are largely absent or reduced in heavily processed or refined coconut oil.

4. Mechanisms of Action

4.1 Metabolic Handling of Medium-Chain Fatty Acids

MCFAs are absorbed and rapidly converted to energy as they are easily transported across the mitochondrial membrane without any carrier molecule and hence are rapidly metabolized in the liver. MCFAs are generally absorbed through portal veins, whereas long chain fatty acids (LCFAs) enter the lymphatic system.

After intestinal absorption, MCFAs enter the portal vein mainly in a non-esterified form and can be used as a rapid energy source in muscles, the liver, and heart tissues.

4.2 Ketogenesis and Brain Fuel

Coconut oil is rich in medium-chain triglycerides (MCTs), which are metabolized into ketone bodies (KBs) that can serve as an alternative energy source for the brain, especially in cases of Alzheimer's disease (AD) where glucose metabolism is impaired. While MCTs in CO may not directly cross the blood-brain barrier, their metabolic byproducts, such as acetoacetate and β-hydroxybutyrate (β-HB), can support cognitive function by providing energy through alternative pathways.

4.3 Thermogenesis and Brown Adipose Tissue Activation

Coconut oil showed a better effect than isolated MCFA in activating brown adipose tissue (BAT) to increase thermogenesis and energy metabolism to combat obesity, which may be attributed to the cooperation of MCFA and other substances in CO. This finding, however, is derived from animal studies and has not been confirmed in large human trials.

4.4 Antimicrobial Mechanisms

The antimicrobial, antifungal, and antiviral properties can be attributed to the destruction of the cell membrane in bacteria, fungi, and viruses due to both hydrogen and hydrophobic interaction between antibacterial lipid compounds with functional groups present in the membrane.

Another widely accepted theory on microbial inactivation — applicable to viruses — is that coconut oil prevents the maturation of pathogens and precludes pathogen binding to the host cell. Lauric acid treatment can increase the production of triacylglycerols in the host cell, which in turn penetrates the plasma membrane and alters its membrane fluidity. This alteration in membrane lipid composition severely affects the reproduction of those viruses which are dependent on the host plasma membrane for the development of their envelopes. Lauric acid is converted to monolaurin inside the human body, which is responsible for disrupting the phospholipid layers in the membranes of enveloped viruses.

5. Scientific Evidence by Area of Use

5.1 Cardiovascular Health and Blood Lipids

This is the most extensively studied and most clinically contested area for coconut oil use.

Systematic reviews and meta-analyses:

A systematic review published in Circulation (2020) examined the effect of coconut oil consumption on blood lipids and other cardiovascular risk factors compared with other cooking oils using data from clinical trials. Researchers searched PubMed, SCOPUS, Cochrane Registry, and Web of Science through June 2019, and selected trials comparing the effects of coconut oil consumption with other fats lasting at least 2 weeks. In this comprehensive systematic review, coconut oil consumption resulted in higher LDL-cholesterol than non-tropical vegetable oils.

Compared with nontropical vegetable oils, coconut oil significantly increased total cholesterol, LDL cholesterol, and HDL cholesterol but not triglycerides, body measurements, glycemia, or C-reactive protein.

A second systematic review and meta-analysis, published in Lipids in Health and Disease (2022), reached partially different conclusions. The amount of coconut oil consumed in reviewed studies varied from 12 to 30 ml/day to 6 to 54.4 g/day. Coconut oil intake did not significantly decrease body weight, waist circumference, % body fat, LDL-C, or triglyceride levels. However, coconut oil intake was associated with a small increase in HDL-C (MD 3.28 mg/dL, 95% CI 0.66 to 5.90 mg/dL). Overall risk of bias was high, and certainty of evidence was very-low. Study limitations include the heterogeneity of intervention methods, in addition to small samples and short follow-ups, which undermine the effects of dietary intervention in metabolic parameters. Coconut oil intake revealed no clinically relevant improvement in lipid profile and body composition compared to other oils/fats.

Key individual RCTs:

The Khaw et al. (2018) RCT compared changes in blood lipid profile, weight, fat distribution and metabolic markers after four weeks' consumption of 50 g daily of one of three different dietary fats — extra virgin coconut oil, butter, or extra virgin olive oil — in healthy men and women in the general population. This largest RCT to date in generally healthy participants showed that LDL-cholesterol was increased for butter compared to coconut oil, with no differences in the change in LDL-cholesterol for coconut oil compared to olive oil; coconut oil resulted in higher HDL-cholesterol levels compared to butter and olive oil.

In another RCT (Nikooei et al. 2021), consumption of 30 g/day of virgin coconut oil improved HDL-cholesterol and triacylglycerols, but worsened LDL-cholesterol and total cholesterol. This trial included 48 participants with metabolic syndrome aged 20–50 years. Compared to a control group, consumption of 30 g/day of virgin coconut oil did not result in differences in anthropometric outcomes and blood pressure. However, virgin coconut oil improved HDL-C (0.19 mmol/L, 95% CI: 0.12 to 0.26) and triacylglycerols (−0.61 mmol/L, 95% CI: −0.91 to −0.30).

A separate RCT comparing coconut oil and corn oil reported that changes from baseline for the two conditions were: LDL cholesterol (−2.7% for corn oil compared with +4.6% for coconut oil), non-HDL cholesterol (−3.0% compared with +5.8%), and total cholesterol (−0.5% compared with +7.1%). When incorporated into the habitual diet, consumption of foods providing approximately 54 g of corn oil/day produced a more favorable plasma lipid profile than did coconut oil in adults with elevated cholesterol.

AHA position: The American Heart Association (AHA) has emphasized the role of saturated fats in its recommendations over the years. Saturated fats such as coconut oil and other oils that are tropically derived should be replaced with unsaturated fatty acids, according to a scientific guideline statement issued by the AHA in 2017. Coconut oil was found to elevate dangerous LDL cholesterol levels in seven studies reviewed by the AHA. Since then, the AHA recommended that coconut oil should therefore be avoided, and all saturated fat should be limited.

Despite some claims in the literature, the AHA Advisory determined that coconut oil is not expected to have cardiovascular benefit given the causal role of LDL in CVD. Although coconut oil also increases HDL-cholesterol levels, the value of this parameter as a risk predictor is currently being questioned, as clinical trials of HDL modulators have failed to provide evidence of CVD benefits.

Evidence strength: Mixed to unfavorable for cardiovascular outcomes. Multiple meta-analyses and the AHA 2017 advisory point to LDL-raising effects relative to unsaturated oils. HDL increases are observed but their clinical significance is unclear. Overall certainty of evidence is rated low to very-low in meta-analyses due to small sample sizes, short durations, and heterogeneous study designs.

5.2 Skin Health and Dermatology

VCO displays several biological activities including anticancer, antimicrobial, analgesic, antipyretic, and anti-inflammatory properties in vivo. Traditionally, coconut oil is used to moisturize and treat skin infections. The emollient effect of coconut oil has been successfully demonstrated in atopic dermatitis patients, thereby showing that coconut oil is a potent natural emollient to be used in treatment of xerosis.

Used as a moisturizer to treat mild-to-moderate dry skin, coconut oil has demonstrated comparable efficacy and safety to mineral oil. In a review of clinical studies conducted by Poljšak and Kocevar Glavac in 2022, coconut oil was among three oils used in patients with atopic dermatitis and outperformed mineral oil.

In 2014, Evangelista and colleagues conducted a randomized, double-blind clinical trial to compare the effects of topical virgin coconut oil and mineral oil on SCORAD values, transepidermal water loss (TEWL), and skin capacitance in 117 pediatric patients with mild-to-moderate atopic dermatitis over 8 weeks. The coconut oil group performed better along every metric, with both oils diminishing the signs of atopic dermatitis. The investigators concluded that topical virgin coconut oil was superior to mineral oil for pediatric patients with mild-to-moderate atopic dermatitis in terms of clinical and instrumental evaluations.

In a double-blind controlled trial comparing virgin coconut oil (VCO) and virgin olive oil (VOO) in adult atopic dermatitis patients randomized to apply each oil twice daily over 4 weeks: 26 subjects received each oil. Of those on VCO, 20 were positive for Staphylococcus aureus (SA) colonies at baseline versus 12 on VOO. Post-intervention, only 1 (5%) VCO subject remained positive versus 6 (50%) of those on VOO. Relative risk for VCO was 0.10, significantly superior to that for VOO (p = 0.0028; 95% CI, 0.01–0.73); the number needed to treat was 2.2.

The following year, Nangia and colleagues determined that coconut oil application decreased TEWL without elevating skin colonization in very low birthweight neonates. In 2018, Strunk and colleagues conducted an open-label, randomized controlled trial to assess the viability, safety, and effectiveness of topical coconut oil to treat the skin of 72 very preterm infants (less than 30 weeks' gestation). No adverse effects emerged from the study, which found that topically applied coconut oil was a feasible treatment. The Neonatal Skin Condition Score in the coconut oil group was maintained throughout the study, whereas it decreased in the control group.

Evidence strength: Moderate and favorable for topical use as a moisturizer and for reducing S. aureus colonization in atopic dermatitis; well-supported by multiple RCTs. The evidence base for neonatal skin care is smaller but promising.

5.3 Oral Health (Oil Pulling)

Coconut oil is used in the practice of "oil pulling" — a traditional Ayurvedic technique involving swishing oil in the mouth — for improving dental and oral hygiene.

Results from included randomized controlled trials demonstrated evidence that coconut oil pulling has a significant effect on plaque index score when compared to the control group. The evidence for coconut oil pulling having a reduction in salivary bacterial colony count was variable; both studies detected a reduction, however there was no reported statistical difference in one. With regards to salivary Streptococcus mutans count, the evidence suggests that coconut oil pulling has no change when compared to a control after two weeks of the intervention.

In comparison to baseline values, both the gingival and the plaque indices substantially reduced during the period of assessment. There was a steady decline in both the plaque index and the gingival index values from day 7. The average gingival index score on day 30 was down to 0.401 and the plaque index score was 0.385. Statistical analysis using the paired t-test showed that the decrease was statistically significant.

In a separate trial, there was a statistically significant decrease in S. mutans count from both the coconut oil and chlorhexidine groups from baseline to 30 days. The study also showed that in comparison of coconut oil and chlorhexidine there is no statistically significant change regarding the antibacterial efficacy. Coconut oil is as effective as chlorhexidine in the reduction of S. mutans.

All systematic reviews conclude that the evidence on oral health effects of oil pulling is limited due to the absence of high-quality studies.

Evidence strength: Preliminary and limited. Some RCTs show benefits for plaque index and gingivitis, and one small trial found coconut oil pulling equivalent to chlorhexidine for S. mutans reduction, but effect sizes and study quality are variable. No large, high-quality RCTs confirm these effects definitively.

5.4 Cognitive Function and Alzheimer's Disease

Alzheimer's disease (AD) is the most common form of dementia and affects approximately 50 million individuals worldwide. Interest in coconut oil as a potential dietary intervention has surged owing to its substantial medium-chain triglyceride (MCT) content.

Coconut oil has been observed to reduce the secretion of amyloid-β (Aβ) peptides, which are implicated in AD pathology, possibly by downregulating the transport protein ARF1.

A small number of clinical trials and animal studies using a formulation of MCT have reported significant improvement of cognition in AD patients. At the same time, studies in which the diet has been supplemented with saturated fat, particularly hydrogenated coconut oil, have reported deleterious effects on hippocampal morphology and behaviour, and increased plasma LDL levels.

Evidence suggests that despite coconut being a saturated fat, it may not pose the usual negative effects on lipid profiles; however, the influence on neuronal function and survival, as well as cardiovascular effects, remains unknown. While the nutritional components of coconut are well accepted, inconsistencies in the data suggest that further research needs to be undertaken before broadly advocating the use of coconut oil in addition to existing fat consumption or in substitution.

Simply adding coconut oil to the diet would not provide brain cells with an alternative energy source in the manner of a strict ketogenic diet. The NHS and World Health Organization advise against consuming a large amount of coconut oil as it contains high levels of saturated fat, which can lead to high cholesterol levels.

There is no credible scientific evidence to back up claims of coconut oil treating Alzheimer's disease. Since rigorous, extensive research studies on the effectiveness of coconut oil in treating Alzheimer's disease are lacking, we do not know if it works or not. Due to the absence of large-scale studies, we cannot say whether coconut oil genuinely helps people with Alzheimer's.

Evidence strength: Very weak and preliminary for Alzheimer's disease specifically. The MCT-ketone body hypothesis has theoretical support and modest backing from small MCT-specific (not whole coconut oil) trials. No large RCTs using coconut oil itself in AD patients have been conducted.

5.5 Antimicrobial Activity

Lauric acid and monolaurin can be used as antibacterial, antifungal, and antiviral compounds with broad-spectrum inhibition. Lauric acid and monolaurin have a strong ability to destroy gram-positive bacteria, especially S. aureus, fungi such as C. albicans, and viruses including vesicular stomatitis virus (VSV), herpes simplex virus (HSV), and visna virus (VV).

Coconut oil has been shown to have significant antimicrobial activity against Escherichia vulneris, Enterobacter spp., Helicobacter pylori, Staphylococcus aureus, Candida spp., including C. albicans, C. glabrata, C. tropicalis, C. parapsilosis, C. stellatoidea and C. krusei. Studies also show that coconut oil is effective against S. mutans and C. albicans in an in vitro oral biofilm model.

Modern scientific research into monolaurin is extremely limited and mostly takes place in a petri dish. The results, however, are promising.

Evidence strength: Largely in vitro (cell culture) and animal studies. Clinical translation to humans remains limited. The topical antibacterial evidence (notably against S. aureus in atopic dermatitis) is better-supported than claims about systemic antimicrobial effects following oral ingestion.

5.6 Body Weight and Metabolic Outcomes

Medium-chain fatty acids contained in virgin coconut oil could enhance the growth of Bifidobacterium and Lactobacillus, improving metabolic and cognitive functions. Medium-chain triglycerides (MCTs) promote energy expenditure, weight loss, and lipid catabolism by improving gut microbial equilibrium and gut barrier function.

While long-chain fatty acids impair insulin sensitivity and lipid metabolism, MCFAs seem to protect against obesity and associated metabolic derangements. However, this is largely derived from animal and mechanistic studies rather than large human RCTs with whole coconut oil.

In meta-analysis, coconut oil intake did not significantly decrease body weight (MD −0.24 kg, 95% CI −0.83 kg to 0.34 kg), waist circumference (MD −0.64 cm, 95% CI −1.69 cm to 0.41 cm), or % body fat (−0.10%, 95% CI −0.56% to 0.36%).

Evidence strength: Weak to null for body weight reduction from whole coconut oil consumption in humans. Mechanistic and animal study evidence for thermogenic effects exists, but is not confirmed in well-powered human trials.

5.7 Anti-inflammatory Properties

Beyond its usage in cooking, coconut oil has attracted attention due to its hypocholesterolemic, anticancer, antihepatosteatotic, antidiabetic, antioxidant, anti-inflammatory, antimicrobial and skin moisturizing properties.

The medium-chain triglyceride derivatives of MCFAs are bioactive forms with versatile pharmacological properties that can help in boosting the immune system, treating various pathologies such as cardiovascular, gastrointestinal, and inflammatory disorders. They have the capability to fight off numerous bacterial, fungal, and viral infections.

Evidence strength: Primarily in vitro and animal data. Consumption of coconut oil is still underrated due to a lack of supportive scientific evidence. Even though studies done in Asian countries claim a favorable impact on cardiac health and serum lipid profile, the limitations in the number of studies conducted among Western countries impede the endorsement of the real value of coconut oil.

6. Body Systems and Health Areas Associated with Coconut Oil

• Cardiovascular system: Effects on LDL-C, HDL-C, and triglycerides (contested, studied extensively in RCTs and meta-analyses)
• Integumentary system (skin): Moisturization, atopic dermatitis, wound healing, neonatal skin care (moderate clinical evidence)
• Oral cavity: Plaque reduction, gingivitis, S. mutans count (preliminary clinical evidence via oil pulling)
• Neurological system: Potential ketogenic substrate in Alzheimer's disease and dementia (very preliminary; no large RCTs)
• Immune/antimicrobial: Antibacterial, antifungal, antiviral activity via lauric acid and monolaurin (primarily in vitro)
• Metabolic/endocrine: Energy expenditure, body composition, gut microbiota modulation (animal and mechanistic data; weak human evidence)
• Gastrointestinal tract: Potential gut microbiome modulation; traditional use for digestive disorders

7. Dosage Forms and Dosages Reported in Studies

The following dosages are reported directly from clinical studies and meta-analyses; they are not recommendations:

• Oral (internal) intake: Studies have used 12 to 30 ml of coconut oil per day (in 5 studies), or 6 to 54.4 g/day (in 5 studies), or a portion of total caloric energy intake of 15 to 21% (in 6 studies).
• Khaw et al. RCT (2018): 50 g of extra virgin coconut oil per day, consumed for four weeks.
• Nikooei et al. RCT (2021): 30 g/day virgin coconut oil in 48 participants with metabolic syndrome aged 20–50 years.
• Oil pulling (oral hygiene): Participants were asked to routinely perform oil swishing with coconut oil every day in the morning after brushing for 2–3 minutes. Participants were instructed to continue oil swishing for 30 days.
• Topical (dermatology): Patients applied VCO or VOO twice daily at two noninfected skin sites in the atopic dermatitis double-blind controlled trial.

8. Safety Considerations and Notable Interactions

8.1 Saturated Fat and Cardiovascular Risk

The AHA report notes that 82% of the fat present in coconut oil is saturated, whereas butter has only 63% saturated fat, beef fat 50%, and pork lard 39%.

A recent systematic review showed that lauric, myristic, and palmitic fatty acids — the major components of coconut oil — are responsible for the highest increase in low-density lipoprotein cholesterol (LDL-C) levels, which is a major risk factor for CVD.

Despite potential benefits in some areas, the high saturated fat content of coconut oil poses cardiovascular risks, leading to caution in its dietary use.

8.2 Distinction Between Refined and Virgin Forms

Data suggested that unrefined, virgin coconut oil did not seem to raise LDL cholesterol as much as refined coconut oil. Glycerol-derived process contaminants glycidyl esters and monochloropropandiol (MCPD) increased with processing. Addition of glycidyl or MCPD to virgin coconut oil had similar effects to processing on cholesterol metabolism in vitro, while addition of phenolic antioxidants to fully refined CO reduced those effects. The authors conclude that harsh processing creates contaminants that raise cholesterol levels in vitro, consistent with a role as a contributing atherosclerotic factor.

8.3 Regulatory and Institutional Positions

The NHS and World Health Organization advise against consuming a large amount of coconut oil as it contains high levels of saturated fat which can lead to high cholesterol levels.

The Food and Drug Administration (FDA) has not approved coconut oil as a treatment for any condition.

8.4 Topical Safety

In a 2018 open-label RCT assessing the viability, safety, and effectiveness of topical coconut oil to treat the skin of 72 very preterm infants (less than 30 weeks' gestation), no adverse effects emerged from the study, which found that topically applied coconut oil was a feasible treatment. Topical coconut oil is generally considered well-tolerated, though individuals with tree nut sensitivities should be aware of potential cross-reactivity, a consideration not yet extensively studied in large trials.

8.5 Limitations of the Overall Evidence Base

Studies that analyzed how coconut oil intake affects weight, lipid and glycemic levels are mostly based on small, short-term observational studies and clinical trials. Although its anti-obesity and hypoglycemic effects are backed by emerging scientific literature, many questions remain unanswered. Long-term clinical trials are warranted.

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