Coconut Oil In Health: Monolaurin’s Potential As Cure For HIV/AIDS

Dr. Conrado S. Dayrit

The coconut is called the tree of life for it has been providing us, humans, food and drink,

materials for housing, fuel and many industrial uses. And its medicinal uses are many and varied. The latest medical potential of products of the coconut first identified by Jon Kabara and others in the 70s, is the anti-bacterial, anti-viral and anti-fungal activity of its medium chain fatty acids, particularly lauric acid (C12:0) in its monoglyceride form (monolaurin or ML).

The first clinical trial ever of ML was on 15 HIV-infected patients reporting regularly at the San

Lazaro Hospital, Manila who, never having received any anti-HIV medication, were randomly

assigned to 3 treatment groups: 7.2 g ML, 2.4 g ML and 50 ML of coconut oil daily for 6 months.

The San Lazaro Hospital Team was led by Eric Tayag.

Viral, CD4 and CDS counts, complete blood counts, blood lipids and tests for liver and kidney

functions were done at the beginning of the study and after 3 and 6 months of treatment. In one patient, the viral load was too low to count.

By the 3rd month, 7 of the patients (50%) showed reduced viral load and by the 6th month 8

patients (2 receiving 7.2h ML, 4 receiving 2.4 g ML and 3 receiving, coconut oil had a lowered viral count. The CD4/CD8 counts showed a favorable increase in 5 patients. There were no serious side effects observed.

Three patients developed AIDS on 3rd month of therapy when their CD4 count dropped below

200. One of these three, who was in the coconut oil group. died 2 weeks after the study. The two other AIDS patients were in the 2.4 g ML group; one recovered fully on the 6th month and the other showed a rapid return towards normal CD4 and CD8 counts.



Folkloric and Ayurvedic writings are replete with accounts of the efficacy of the coconut for

many ailments -from the cure of wounds, bums, ulcers, lice infestations to dissolution of kidney

stones(l) and treatment of choleraic dysenteries(2). The people of South Asia and the Pacific also look to the coconut as an important provider of food, drink and fuel, not to mention its many uses in industry. Hence, it has been called the tree of life.


More recently, Lim-Sylianco et al demonstrated in animals a powerful protecting effect of

coconut oil against six powerful muta-carcinogenic chemicals, (such as benzpyrine, azaserine and nitrosamines). The protection was observed not only when coconut oil was given with the diet for several days before the mutacarcinogen but also when it was given in one bolus or dose with the mutacarcinogen(J.4). In both experiments, coconut oil gave a significantly higher protection than soybean oil. In another animal study by Lim-Navarro, et al (5), evidence for another protectant effect of coconut oil was obtained, i.e. significant prevention against shock in rats injected with E. coli endotoxin. The mechanism for these anti-inflammatory, antitoxic, antimutacarcinogenic actions are still not known.


Anti-Infective Action

In a series of papers published in the 70s, Jon J Kabara et al (6-10) and other workers studied

the anti-microbial activity of various fatty acids. They found that the medium chain fatty acids

(MCF A) with 6 to 12 carbons, possessed significant activity against gram positive bacteria, but not against gram negatives; they were also active against lipid coated viruses as well as fungi and

protozoa. Saturated fatty acids, longer than 14 carbons long had no such activity. And of the MCFA, lauric acid (CI2:0) was most potent, particularly in its monoglyceride form (monolaurin); it was more active than caprilic acid (C-8) caprie acid (C-I0) or myristic acid (C-14). The dilaurin and trilaurin (di and triglycerides) had no activity. This finding has found use in the incorporation of monolaurin in cosmetic products and mouth washes; but although classified by the USFDA as GRAS (Generally Regarded as Safe), its oral use for systemic inflections has not been tried.


HIV-AIDS Patients and the Coconut

According to Mary Enig(11), the AIDS organization, Keep Hope Alive, has documented several

HIV -AIDS patients whose viral load fell to as low as undetectable levels, when they took coconut oil or ate coconut (half a coconut a day) or when they added coconut to their anti-HIV medication (anti protease and/or antiretrovirals) that had previously not been effective. The amount of coconut oil consumed (50 ml or 3 1/2 tablespoonfuls) or half of a coconut, would contain 20-25 grams of lauric acid, which indicates that the oil is metabolized in the body to release lauric acid and/or monolaurin.


The Monolaurin Trial on HIV-AIDS

The first clinical trial (pilot study) using Monolaurin for 6 months as monotherapy on 15 mv

patients was just completed (12). These 15 patients (Table 1) ages 21 to 38 years, 5 males and 10

females, were all regularly reporting to San Lazaro Hospital, the hospital for infectious disease of

the Department of Health. None of them could afford’ or ever received anti-HIV treatment. The

males averaged 58 k in weight (49 to 68 k) and the females, 54k (39 to 65 k). Seven showed

elevated liver enzymes (ALT and AST) and 12 had unexplained eosinophilia. Two patients had

high serum cholesterol and one had elevated triglyceride. No one had renal dysfunction. Their viral load ranged from 1,960 to 1,190,000 except for one patient (#94-022B) whose load was too low to 3 count (below 400). This fact unfortunately was not determined before the random assignment of the patients to the 3 treatment groups. The monolaurin used was 95% pure. It was given in capsules, each containing 800 mg ML. The coconut oil was administered by tablespoonfuls.


The 3 treatment groups to which the 15 patients were randomly assigned were {Table II):

a) High Dose Monolaurin (HML): 7.2 grams (9 capsules) ML 3 time daily or about

22 grams daily

b) Low Dose Monolaurin (LML): 2.4 grams (3 capsules) ML 3 times daily or 7.2

grams daily.

c) Coconut oil (CNO): 15 ml 3 times daily or 45 ml daily. The ML content of this

dose is about the same as HML.

All patients were observed daily for any side effects. Baseline, 3-month and 6-month laboratory

examinations included: viral load (by PCR method), CD4 and CD8 counts (by-flow-cytometric

method), complete blood count, tests for liver function (ALT, AST), renal function (urea N and

creatinine), blood lipids (cholesterol, triglycerides, HDL) and body weight (k). Treatment benefit

was defmed as reduction in viral load and increase in CD4 count.

Tables II and III summarize the effects of the 3 treatment groups on the viral load, CD4 and

CD8 counts. On the 3rd month, 2 showed decreased viral count with HML, 2 with LML and 3 with CNO for a total of 7 patients benefited. The other patients all had increased viral load. Patient #94- 022A continued to have undeterminable viral load and was excluded from the computation. On the 6th month, and end of the study. 8 of the 14 patients had decreased viral count, (2 of the 4 given HML, 4 of the 5 given LML and 3 of the 5 given CNO). The decrease in viral count was, however, significant only in 3 patients using the log Baseline-log 6th month ~ 0.5 criterion. Two of these significant decreases were in the CNO group and one in the LML group. The CD4. and CD8 counts (Table III) increased only in 5 patients and did not quite correlate with the fall in viral load, decreasing even when the viral load fell and increasing when the viral load rose. Patient #93006 had a steady viral load during the first 3 months but suffered a severe secondary infection in the 5th and 6th month, which caused the HIV infection to worsen despite fairly good CD4/CD8 response.


AIDS (CD4 less than 200) developed in 3 patients on the 3ni month of LML therapy (2 patients)

and CNO therapy (1 patient). The last mentioned patient (#86-001) died 2 weeks after the termination of the study. The patient under LML, however, fared better; one (# 93028) recovered by the 6th month. and the other (#95052) was showing improvement of both CD4 and CD8 counts at the end of the study.

Eleven (11) subjects gained weight -from 1 k to 23 k -including the 2 who developed AIDS and

were recovering. The single AIDS fatality lost 6 k. The other 3 who failed to gain weight had

decreasing viral and rising CD4 counts.


About one-half of the subjects in this study complained of feeling of warmth and a greenish

hue to their urine (Table IV A), Both occurred at the beginning of the study and did not interfere

with its continuation. Another 3 subjects had flaring up of their acne.

There were 11 subjects with eosinophilia at the start and 7 subjects with some liver dysfunction

(Table 1). The treatment caused a rise of the eosinophilia in 7 of the II, and a rise in ALT/AST in 3 of the 7 (Table IVA).

The patients with normal liver and kidney functions showed no effect from the treatments.

At the beginning, 2 subjects had elevated cholesterol and another one had high serum triglyceride (Table !VB). After 6 months, 4 patients had abnormal cholesterol and triglyceride, 3 had high cholesterol only and 2 had high triglyceride only.


Conclusion from the Study

This initial trial confirmed the anecdotal reports that coconut oil does have an anti-viral effect

and can beneficially reduce the viral load of HIV patients. The positive anti-viral action was seen

not only with the monoglyceride of lauric acid but with coconut oil itself. This indicates that coconut

oil is metabolized to monoglyceride forms of C-8, C-IO, C- 12 to which it must owe its antipathogenic

activity. More and longer therapies using monolaurin will have to be designed and done before the defmitive role of such coco products can be determined. With such products, the outlook for more efficacious and cheaper anti HIV therapy is improved.


Anti-pathogen Mechanism of Monotriglycerides of MCT

The fact dlat monolaurin’s activity is limited to lipid coated organisms (gram positive bacteria,

enveloped viruses) suggests strongly that the relatively short C-12, C-IO or C-8 [Icelandic scientists have recently reported on the effectiveness of monocaprin (C-IO) against HIV virus] probably exert their action on the lipid-layered coat or plasma membrane to destabilize it or even to cause its  rupture. If this mechanism proves correct, monolaurin (and monocaprin and monocapryliu) could be bactericidal and could act synergistically with the present anti-HIV agents (the antiretrovirals and protease inhibitors).



With all the opprobrium cast against it, it bears repeating again and again that no evidence has

ever been presented to prove that coconut oil causes coronary heart disease in humans. All the

evidences presented have been in various species of animals who were given coconut oil alone

without the necessary dose of essential fats or PUFA that should be given, just like the essential

vitamins and minerals. On the contrary, the human epidemiologic evidence proves that coconut oil

is safe. Coconut eating peoples like the Polynesians (Table V) and Filipinos (Fig. I) have low

cholesterol, on the average, and very low incidence of heart disease.