https://www.cambridge.org/core/journals/british-journal-of-nutrition/article/the-role-of-dietary-coconut-for-the-prevention-and-treatment-of-alzheimers-disease-potential-mechanisms-of-action/1C610ECEA7E7D7CD3E7323A0477E6731
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- DOI: https://doi.org/10.1017/S0007114515001452
- Published online: 22 May 2015
Abstract
Coconut, Cocos nucifera L., is a tree
that is cultivated to provide a large number of products, although it is
mainly grown for its nutritional and medicinal values. Coconut oil,
derived from the coconut fruit, has been recognised historically as
containing high levels of saturated fat; however, closer scrutiny
suggests that coconut should be regarded more favourably. Unlike most
other dietary fats that are high in long-chain fatty acids, coconut oil
comprises medium-chain fatty acids (MCFA). MCFA are unique in that they
are easily absorbed and metabolised by the liver, and can be converted
to ketones. Ketone bodies are an important alternative energy source in
the brain, and may be beneficial to people developing or already with
memory impairment, as in Alzheimer's disease (AD). Coconut is classified
as a highly nutritious ‘functional food’. It is rich in dietary fibre,
vitamins and minerals; however, notably, evidence is mounting to support
the concept that coconut may be beneficial in the treatment of obesity,
dyslipidaemia, elevated LDL, insulin resistance and hypertension –
these are the risk factors for CVD and type 2 diabetes, and also for AD.
In addition, phenolic compounds and hormones (cytokinins) found in
coconut may assist in preventing the aggregation of amyloid-β peptide,
potentially inhibiting a key step in the pathogenesis of AD. The purpose
of the present review was to explore the literature related to coconut,
outlining the known mechanistic physiology, and to discuss the
potential role of coconut supplementation as a therapeutic option in the
prevention and management of AD.
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