by Brian Shilhavy
Editor, Health Impact News
For more than a decade now, we have been publishing research and testimonials from people who have had success in reversing Alzheimer’s Disease with coconut oil. The research and testimonials are published on CoconutOil.com, part of the Health Impact News network.
During this same time period, we have seen the pharmaceutical industry fail over and over again to develop a drug that is effective in treating Alzheimer’s Disease.
Researchers in Australia are now studying coconut oil, and its unique composition of medium chain fatty acids, as a way to prevent and treat Alzheimer’s Disease.
Starting from the basis that Alzheimer’s Disease is a form of diabetes, referred to in the past as a “Type 3” form of diabetes, or what the Australian researchers refer to as “brain glucose hypometabolism,” the research focuses on providing an alternative form of energy to the brain in the form of “ketone bodies.”
The title of their study is: Potential of coconut oil and medium chain triglycerides in the prevention and treatment of Alzheimer’s disease, published in the March 2020 edition of the journal Mechanisms of Ageing and Development.
It is an exhaustive look at the current literature on this topic, with hundreds of references.
Abstract
Alzheimer’s disease (AD) is the most common form of dementia. Currently, there is no effective medication for the prevention or treatment of AD. This has led to the search for alternative therapeutic strategies.
Coconut oil(CO) has a unique fatty acid composition that is rich in medium chain fatty acids(MCFA), a major portion of which directly reaches the liver via the portal vein, thereby bypassing the lymphatic system.
Given that brain glucose hypometabolism is a major early hallmark of AD, detectable well before the onset of symptoms, ketone bodies from MCFA metabolism can potentially serve as an alternative energy source to compensate for lack of glucose utilisation in the brain.
Additionally, neuroprotective antioxidant properties of CO have been attributed to its polyphenolic content. This review discusses how the metabolism of CO and MCFA may aid in compensating the glucose hypometabolism observed in the AD brain.
Furthermore, we present the current evidence of the neuroprotective properties of CO on cognition, amyloid-β pathogenicity, inflammation and oxidative stress.
The current review addresses the influence of CO/MCFA on other chronic disorders that are risk factors for AD, and addresses existing gaps in the literature regarding the use of CO/MCFA as a potential treatment for AD.
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