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I'm curious if any of you have supplement regimens for "Methylation" support. I've been prophylactically taking 1mg of methyl-b12 and 800mcg of methyl-folate for a few years after learning of my +/+ C677T polymorphism (among others.) More recently, I've tacked on B1, B2, and B6 (P5P.) I've been thinking about readdressing this stack and pulling back on everything but the b12 & b9, then maybe experimenting with trimethylglycine. I did come across this article: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4262445/ Would TMG be more likely to ferment to TMAO or promote cardiovascular disease, or might this be a health-promoting cardio-protective supplement? Have you experimented with dialing in an ideal b-vitamin complex to address things like C677T?
All, In another apparent micronutrient synergy involving DHA for improved brain health (see Curcumin Elevates DHA in the Brain thread for the other), this new randomized control trial  found that supplementing for two years with three B-vitamins (folic acid, B6 and B12) slowed the cognitive decline that often leads from mild cognitive impairment (MCI) to Alzheimer's Disease (AD), but only if the person had "high normal" levels of serum DHA at baseline: When omega-3 fatty acid concentrations are low, B vitamin treatment has no effect on cognitive decline in MCI, but when omega-3 levels are in the upper normal range, B vitamins interact to slow cognitive decline. A clinical trial of B vitamins combined with omega-3 fatty acids is needed to see whether it is possible to slow the conversion from MCI to AD. Michael warns against CRers supplementing with DHA, but for brain health it seems that adequate DHA may be important. Curcumin might help increase DHA in the brain by boosting ALA->DHA conversion, but he's also dissed curcumin, so I'm wondering what he thinks of all this... --Dean ----------  J Alzheimers Dis. 2016 Jan 6. [Epub ahead of print] Omega-3 Fatty Acid Status Enhances the Prevention of Cognitive Decline by B Vitamins in Mild Cognitive Impairment. Oulhaj A(1), Jernerén F(2), Refsum H(2,)(3), David Smith A(2), de Jager CA(4). Free full text: http://content.iospress.com/articles/journal-of-alzheimers-disease/jad150777 A randomized trial (VITACOG) in people with mild cognitive impairment (MCI) found that B vitamin treatment to lower homocysteine slowed the rate of cognitive and clinical decline. We have used data from this trial to see whether baseline omega-3 fatty acid status interacts with the effects of B vitamin treatment. 266 participants with MCI aged ≥70 years were randomized to B vitamins (folic acid, vitamins B6 and B12) or placebo for 2 years. Baseline cognitive test performance, clinical dementia rating (CDR) scale, and plasma concentrations of total homocysteine, total docosahexaenoic and eicosapentaenoic acids (omega-3 fatty acids) were measured. Final scores for verbal delayed recall, global cognition, and CDR sum-of-boxes were better in the B vitamin-treated group according to increasing baseline concentrations of omega-3 fatty acids, whereas scores in the placebo group were similar across these concentrations. Among those with good omega-3 status, 33% of those on B vitamin treatment had global CDR scores >0 compared with 59% among those on placebo. For all three outcome measures, higher concentrations of docosahexaenoic acid alone significantly enhanced the cognitive effects of B vitamins, while eicosapentaenoic acid appeared less effective. When omega-3 fatty acid concentrations are low, B vitamin treatment has no effect on cognitive decline in MCI, but when omega-3 levels are in the upper normal range, B vitamins interact to slow cognitive decline. A clinical trial of B vitamins combined with omega-3 fatty acids is needed to see whether it is possible to slow the conversion from MCI to AD. PMID: 26757190