The intermittent reminder of just how misled and unaware the public is of basic nutritional principles that can save their lives is an encouragement to continue writing about them. 

I spoke to an elderly woman whose husband’s Alzheimer’s has progressed to hallucinations and childlike cognition. She and her family are wealthy and have come together to support him, yet the “best care around” from medical doctors has been medication that apparently calms down the agitation that started when he got sick. In other words, the best that mainstream medicine has to offer for Alzheimer’s, even to the wealthy, is a tranquilizer as the brain continues to deteriorate.

The woman was shocked and excited when I told her about the possible aid of coconut oil for dementia patients. I informed her of the news story that circulated in 2012 about the neurologist, Dr. Mary Newport, who fed coconut oil to her husband with severe Alzheimer’s, and saw a rapid and sustained improvement in his symptoms.

Alzheimer’s has increasingly been called “diabetes of the brain”, or “type 3 diabetes”, since brain cells in dementia patients are insulin-resistant and therefore unable to utilize glucose (Monte and Wands, 2008). 

The ketones supplied by the medium-chain triglycerides (MCTs) in coconut oil are said to be the reason it helps, acting as an alternate cellular energy source to glucose, and indeed coconut oil is even medicinal during type 1-diabetic hypoglycemia (Page, et al., 2009), but there are several more therapeutic constituents in coconut oil with unrelated yet possibly equally important roles as the ketones.

There are several species of fungi in the brains of Alzheimer’s patients, particularly in the frontal cortex (the “higher-thinking” brain region), the hippocampus (the center of memory and emotional regulation), and throughout the blood vessels (Pisa, et al., 2015). The bacteria that cause gingivitis, porphyromonas gingivalis, are found in the brains of Alzheimer’s patients (Dominy, et al., 2019). Coconut oil possesses the potent antibacterial, antifungal MCTs, caprylic acid, capic acid, and lauric acid, which inhibit oral and intestinal porphyromonas gingivalis (Dewi, et al., 2017), while protecting intestinal epithelium integrity, which would reasonably help prevent the migration of pathogenic bacteria into the brain in the first place, since a leaky gut creates a leaky brain (Obrenovich, 2018).

Coconut oil suppresses pain and edema, mainly through lauric acid’s inhibition of the inflammatory mediators, histamine, serotonin, prostaglandins, and kinin peptides at localized tissue injury (Intahphuak, et al., 2010)

Coconut oil, along with virgin olive oil, successfully treated atopic dermatitis in a double-blind, placebo-controlled trial. Coconut oil performed better than olive oil at killing the staphylococcus aureus bacteria (Verallo-Rowell, et al., 2008). This is another example of lauric acid’s potent, broad-spectrum antipathogenic properties.

The medium-chain triglycerides, by upregulating mitochondrial-synthesis genes, increase our ability to use glucose for energy while also providing energy as ketones. This metabolic upregulation increases skeletal-muscular exercise endurance. In a high-temperature endurance test, mice fed MCTs ran over two times longer than mice fed a normal diet (Wang, et al., 2018).

Mitochondrial function is a determinant of an organism’s ability to thrive socially and experience pleasure (Hollis, et al., 2015). Anxious, subordinate rats have reduced mitochondrial proteins and respiratory capacity, less ATP, and more free radicals in their nucleus accumbens, compared to low-anxiety rats. When anxious rats are fed MCTs for just one week, their anxiety goes down and their social ability goes up. Interestingly, their nucleus accumbens didn’t seem to change, but instead the energy efficiency of the medial prefrontal cortex, the “higher-thinking”, executive function brain region, did (Hollis, et al., 2018).

Mango and Coconut Still Life (2019) by Youqing Wang

Coconut oil against cancer and inflammation

Coconut oil’s anticancer cell effect ranges from mild to extreme depending on which formulation of coconut oil contacts which cancer cell type. Virgin coconut oil inhibits the liver cancer-derived HepG2 cancer cells whereas refined and distilled coconut oils inhibit cervical cancer-derived HeLa cells (Verma, et al., 2019). 

Cancer cells preferentially exploit aerobic glycolysis, “stealing” glucose for energy and using up to 10x more glucose than normal cells, but they can’t efficiently use ketones for energy, and the presence of blood ketones interferes with their glucose metabolism, so ketones and ketogenic diets can be viable adjunctive therapies against cancer (Poff, et al., 2014). 

In a 1995 study, several late-stage pediatric patients with astrocytoma (brain cancer) were put on a ketogenic diet with 60% of calories coming from MCTs. After just 7 days, their tumors had a 22% average loss in glucose uptake (Nebeling and Learner, 1995). That is, they were losing the ability to obtain energy whatsoever. The patients’ blood glucose stabilized at low-normal with their blood ketones at 20-30x normal. One girl remained on the diet as an outpatient and was still free of disease progression one year later (Nebeling, et al., 1995).

Ketogenic diets alone slow tumor growth and sensitize them for destruction by chemotherapy, but the addition of MCTs to a long-chain triglyceride-based ketogenic diet suppressed tumor growth ~20-30% more than ketosis alone, and ~20-40% more than chemotherapy alone, in mice with neuroblastoma. For SH-SY5Y neuroblastomas, after 36 days, 100% of the mice eating MCTs had survived, 70% for the ketosis mice, and only 60% of the chemotherapy-only mice. For SK-N-BE(2) neuroblastomas, 84% of MCT-eating mice lived, with only 42% of the ketosis mice and 22% of the chemotherapy-only mice (Aminzadeh-Gohari, et al., 2017).

In Japan, 10 patients with recurrent stage IV colon cancer were put on ketogenic diets with added MCT oil, in addition to chemotherapy. A control group receiving only chemotherapy had a 21% response rate and 64% disease control rate while the ketogenic diet group had a 60% response rate and 70% disease control rate. After one year on the diet, 5 of the 10 patients were in complete remission of colon cancer. None in the chemotherapy-only group achieved remission (Furukawa, et al., 2018).  

In guinea pigs, virgin coconut oil at a 4 g/kg dose prevents inflammation and cancerous cell growth (hyperplasia) in the lungs and airways (Vasconcelos, et al., 2020). 

In Malaysian women undergoing chemotherapy, 20 ml virgin coconut oil per day significantly improved their subjective quality-of-life, fatigue, breathing, sleep, appetite, sexual function, body image, breast pain, and future outlook, compared to the control group (Law, et al., 2014).

Coconut oil restores the antioxidant capacity of animals with chronic allergic lung inflammation (Vasconcelos, et al., 2020).

Rats that eat enough heated palm oil develop high blood pressure, raising systolic BP by +15, by raising the heart’s angiotensin-converting enzyme (ACE) and causing hypertrophy of the myocardium (heart muscles). The heated palm oil also raised thiobarbituric acid reactive substances (TBARS), byproducts of lipid peroxidation, which is inflammatory and pro-aging degradation of the polyunsaturated fat in palm oil. Virgin coconut oil completely reversed the systolic BP increase, even lowering it 10 points under baseline, as well as remodeling the anatomical changes caused by the oxidative damage (Kamisah, et al., 2015).

Like coffee and tea, coconut oil is high in the antioxidative polyphenols and tocotrienols. Virgin coconut oil polyphenols preserve cells and glutathione against oxidative stress (Illam, et al., 2017) and tocotrienols protect stem cells from radiation exposure (Singh, et al., 2013).

Weight loss, cravings, and digestion

In a study at the Vellalar College for Women, 1 tablespoon of coconut oil fed daily to 100 obese adolescent girls reduced their serum cholesterol and improved their digestion, while 1 tbsp applied daily to their skin and hair reduced dandruff and improved skin texture (Anuradha and Sugumar, 2009). 20 obese Malaysian subjects fed virgin coconut oil for 6 weeks lost an average of 3 cm in waist circumference with no alteration in their lipid profile (Liau, et al., 2011).

In men, 2.5 grams of lauric acid reduced food cravings without affecting sexual or financial desires (Zhao, et al., 2020).

In China, 112 people with elevated blood triglycerides had 2 daily tablespoons of MCT oil added to their diet. Without any change in caloric intake or exercise, after 8 weeks, they showed significant decreases in all measures of body weight, body fat, and blood triglycerides (Xue, et al., 2009).

Coconut water, the coconut’s “liquid endosperm” that exists to nourish the developing embryo, contains flavonoids with significant anti-inflammatory properties. 

The juice’s unique composition of kinetin and micronutrients lend to its antioxidant effect. It’s a general antihistaminergic, suppressing inflammation and allergies, although I think some may have issues with the salicylates inducing a histamine reaction regardless. 

The abscisic acid in coconut water activates the peroxisome proliferator-activated receptor-gamma protein, which inhibits the inflammatory protein complex NF-kappa B and monocyte migration (Rao and Najam, 2016). 

The salicylic acid decreases as the water ages, explaining a possible variability in reactions to different coconut water products among sensitive individuals.

In rodent’s, young coconut water has a significant antidepressant effect, seemingly through its ability to support monoamine neurotransmitter homeostasis (Rao and Najam, 2016)

The Conundrum: Caveats, warnings, possible side-effects

Too much of a good thing can turn and bite you. MCTs can be extremely medicinal in certain contexts, as seen above, but they increase adaptive immunity, which can become problematic in autoimmune disease. We need a proper ratio of regulatory T (Treg) cells to Th-17 cells to balance tolerance vs. inflammation. Getting too many LCTs or MCTs relative to short-chain fatty acids (SCFAs) can create Th17 dominance, which is already a problem in chronic inflammation and autoimmunity. SCFAs lead to more Treg cells, calming the immune system. Susceptible people eating too many calories as LCTs or MCTs, or not enough calories as SCFA while eating LCTs or MCTs, may experience adverse effects and should pay attention.

SCFAs are obtained most amply by our gut bacteria fermenting the fructooligosaccharides in vegetables like onions, lettuce, garlic, and carrots. On a 2500 calorie diet, 2 tablespoons of coconut oil may be enough to exacerbate autoimmunity, even cause neurological symptoms, if you’re SCFA-deficient (Greenfield, 2015). In mice with multiple sclerosis, excessive lauric acid worsened their symptoms by changing their gut bacteria which raised Th-17 cells, but the addition of the SCFA propionic acid prevented and reversed the multiple sclerosis symptoms via Treg cells (Haghikia, et al., 2015). In extremely dire conditions, a fine balance and attention are needed.

A high intake of saturated fat without enough polyunsaturated fat in the diet can accelerate Essential Fatty Acid (EFA) deficiency, which can manifest as many diseases, because an EFA-deficient organism, lacking the polyunsaturated fatty acids necessary for proper cell membrane fluidity, can’t properly create new cells. Proper metabolism of saturated fats like coconut oil requires EFAs, so saturated fat consumption during EFA deficiency makes coconut oil detrimental rather than beneficial. Rats who ate coconut oil as their only fat source experienced stunted growth and reduced metabolism, but adding polyunsaturated fatty acids as just 0.5-1% of their calories restored their growth and metabolism (Peifer and Holman, 1959).

Coconut oil is high in salicylates (salicylic acid; hydrolyzed aspirin) and the medium-chain triglycerides within it are histaminergic and can prove problematic for those intolerant to histamine or salicylates. One of salicylate’s metabolic cofactors is glycine (Bijay, 2006), supplementation of which seems to remedy salicylate sensitivity in some people. Glycine can be taken as an isolate or found in collagen, such as in bone broth or Great Lakes Hydrolyzed Collagen.

It seems the hydrogenation process for hydrogenated coconut oil, called the Raney catalyst, causes aluminum nanoparticles to contaminate and remain in the highly viscous end product (Travis, 2018). Rats who were fed hydrogenated coconut oil showed accelerated neuronal death mirroring the pathology of dementia. For this reason, I avoid hydrogenated coconut oil and would not recommend its consumption.

Coconut and Mango Still Life (2015) by Yuqing Wang

Recommended coconut products

Unrefined virgin coconut oil retains more potentially beneficial compounds, but also potentially allergenic coconut proteins and starches, and has a strong flavor and smell which can be unpleasant to some, in which case refined (not hydrogenated) coconut oil might be preferable, since it’s deflavored and deodorized, stores longer, and withstands higher temperatures.

Works Cited

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Aminzadeh-Gohari, Sepideh, et al. “A Ketogenic Diet Supplemented with Medium-Chain Triglycerides Enhances the Anti-Tumor and Anti-Angiogenic Efficacy of Chemotherapy on Neuroblastoma Xenografts in a CD1-Nu Mouse Model.” Oncotarget, vol. 8, no. 39, 2017, pp. 64728–64744., doi:10.18632/oncotarget.20041.

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5 thoughts on “A Review of Coconut’s Health Benefits, 2020: on Cancer, Dementia, Metabolism, Mitochondria (or: The Coconut Oil Conundrum)

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