Alzheimer Disease (AD) linked to PUFA accumulation in brain

So much for the “beneficial” effects of PUFA. What makes this study particularly interesting is that it calls into question a favorite defensive maneuver of clinical nutritionists. Namely, when challenged about the known inflammatory effects of omega-6 fatty acids, most medical professionals make a desperate claim that omega-3 fatty acids are actually protective and we should try to increase the omega-3/omega-6 ratio instead of criticizing all PUFA. Well, the study below pours cold water on that claim as it found that AD is associated with a build up of all major PUFA, both omega-6 and omega-3, as well as one of the MUFA. So, those fish oil supplements we still see advertised on TV are likely worse than useless – they may directly cause AD if used for a sufficiently long period of time. In contrast, not a single saturated fatty acid was found to be associated with AD, and I think that by itself speaks volumes of who the culprit is. Perhaps just as importantly, in the lead author’s own words, the study corroborates once again the hypothesis that AD is a metabolic condition.

“…Researchers are studying late-onset Alzheimer’s in the context of age-related brain changes. A new study – published in the journal PLOS Medicinelooks at how fatty acid metabolites in the brain tissue of healthy seniors behave and affect the participants’ cognitive abilities.”

“…The researchers measured the metabolite levels of the brain regions commonly associated with Alzheimer’s: the middle frontal gyrus and the inferior temporal gyrus. They also examined metabolite levels in a brain area that is not normally affected by Alzheimer’s pathology – the cerebellum…The fatty acids shown to correlate with AD in this study were: docosahexaenoic acid, linoleic acid, arachidonic acid, linolenic acid, eicosapentaenoic acid, and oleic acid. Cristina Legido-Quigley and colleagues explain the significance of the study: “[This] work suggests that dysregulation of UFA’s metabolism plays a role in driving AD pathology and that these results provide further evidence for the metabolic basis of AD pathogenesis.”