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Health
See other Health Articles

Title: Is Coconut Oil Effective for Alzheimer Disease?
Source: [None]
URL Source: http://www.medscape.com/viewarticle/764495
Published: May 31, 2012
Author: Gayle Nicholas Scott, PharmD
Post Date: 2012-05-31 01:44:21 by Tatarewicz
Keywords: None
Views: 15

Response from Gayle Nicholas Scott, PharmD Assistant Professor, Eastern Virginia Medical School, Norfolk, Virginia; Clinical Pharmacist, Chesapeake Regional Medical Center, Chesapeake, Virginia

Coconut oil and a related medical food, Axona® (Accera, Inc; Broomfield, Colorado), are being promoted as treatments for Alzheimer disease (AD). Obtained from the kernel of the coconut palm (Cocos nucifera),[1] coconut oil contains medium-chain fatty acids, predominately lauric acid but also caprylic, myristic, and palmitic acids. Medium-chain triglycerides are the esterified form of medium-chain fatty acids; the terms are often used interchangeably.[2] The active ingredient of Axona is caprylic triglyceride. In the published research available, the product is called AC-1202.[3-5]

Proponents claim that coconut oil and Axona provide ketones as an alternative to glucose for cerebral metabolic processes. Advocates of these treatments describe AD as "diabetes of the brain" and contend that the AD brain is better able to use ketones than glucose.[6] This theory is not widely accepted among AD clinicians and researchers,[7] but some speculate that ketogenesis might improve free radical-mediated pathologies associated with AD.[8]

Normally, metabolic energy comes from glucose. When glucose availability is reduced, the liver produces ketone bodies (primarily acetoacetate and beta-hydroxybutyric acid [beta-OHB]) as energy sources. Unlike the heart and skeletal muscle, the brain cannot use fatty acids as an energy source because it requires glucose or ketone bodies.[8]

Medium-chain triglycerides are more ketogenic than long-chain triglycerides, such as those in animal fat. Ketogenic diets, which are diets high in fat and low in carbohydrates and proteins, have been used since the time of Hippocrates for treatment of epilepsy; the mechanism is still unknown.[8] Ketogenic diets are still used in refractory epilepsy, but poor tolerance of the gastrointestinal side effects and dislike for the diet limit effectiveness.[9] Medium-chain triglyceride diets are better tolerated than classic ketogenic diets, which include more long-chain triglycerides. Because medium-chain triglycerides are highly ketogenic, patients can consume more carbohydrates, making the diet more palatable.[8]

Several theories have been proposed for beneficial effects of ketones in AD, including prevention of amyloid plaques, reduction of proinflammatory mediators associated with neurodegeneration, and a neurotrophic effect of cerebral ketone metabolism.[10] Studies with encouraging results using ketogenic diets in AD have been published.[10-13] In a 6-week clinical study of 23 elderly patients with mild cognitive dysfunction, a diet very low in carbohydrates, which increased ketone levels, improved memory function better than a high-carbohydrate diet.[10] In another preliminary clinical study of 20 persons with AD or mild cognitive impairment, administration of a medium-chain triglyceride beverage was associated with improvement on some cognitive measurements in response to acute elevation of beta-OHB levels 90 minutes after treatment in 2 single-dose study visits, but only in patients without the apolipoprotein E gene (n = 9).[14]

A literature search for coconut oil and AD revealed no clinical studies. A search for the medical food Axona yielded 1 manufacturer-sponsored study and 2 substudies.[3-5] In a 90-day, randomized, double-blind phase 2 study, 152 persons diagnosed with mild to moderate AD received Axona10-20 g/daily or placebo. The primary endpoint was improvement on the AD Assessment Scale-Cognitive subscale (ADAS-Cog). At 45 days, patients receiving the study drug showed improvement on the ADAS-Cog, as noted in company advertising. However, scores were similar in both groups at day 90 and after a 2-week washout period on day 104. In patients without the apolipoprotein E gene, Axona was superior to placebo at both time points.[3]

According to the Alzheimer's Association, the manufacturer of Axona elected to market the product as a medical food rather than conducting phase 3 studies in a larger population to prove effectiveness. Medical foods do not require phase 3 studies.[15]

Both coconut oil and Axona are high in calories and saturated fat, but some research suggests that coconut oil neither increases weight nor adversely affects lipid levels.[2,16,17] Gastrointestinal adverse effects, particularly diarrhea, were frequent causes of discontinuation in the phase 2 study.[3] Coconut oil costs about $12 for 16 oz. Axona costs about $85 per month.

Currently, neither coconut oil nor Axona can be recommended for AD due to lack of credible effectiveness research. For patients or family members who insist on these products, suggest starting with a low dose and gradually increasing the dose to avoid adverse gastrointestinal effects. Healthcare providers should monitor for adverse effects and effectiveness and possibly increased lipid levels.

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