Today, I review, link to, and embed P4-450: VITACOG’S STUDY OF MILD COGNITIVE IMPAIRMENT–A ROAD NOT TAKEN. Richard N. Podell
First published: 01 July 2019 https://doi.org/10.1016/j.jalz.2019.06.4122
All that follows is from the above resource.
Background
In 2010 Dr. David Smith and colleagues from Oxford published potentially ground-breaking data on treating MCI. Over two years subjects taking B vitamins to lower blood homocysteine had significantly slower rates of brain atrophy and cognitive decline compared to placebo. In 2015 Vitacog showed that B vitamin treatment mainly benefited subjects whose initial homocysteine levels were high (>11.3 umol/L) and whose blood omega 3 fatty acid levels were above average. Interdependence between homocysteine and omega 3 fats is plausible because of the metabolic relations between the cycle of homocysteine to S-adenosyl methionine (SAMe); SAMe’s ability to methylate phosphatidyl ethanolamine into phosphatidyl choline (PC); PC’s ability to incorporate the omega 3, DHA, into its molecule; and PC-DHA’s potential to stabilize cell membranes.
Methods
Review of Research. Results: Given the lim-itations of treatments for MCI and MCI’s link to Alzheimer’s, onemight expect that Vitacog’s findings would have been re-testedquite soon. But this didn’t happen. Dr. Smith told me that his groupmade six funding proposals but all were rejected—probablybecause studies of homocysteine-lowering to prevent heart attacksand strokes had failed to show benefit. But none of the heart orstroke studies measured omega 3’s. Surely, a fair proportion of theirsubjects had relatively low levels of omega 3’s by Vitacog’s stan-dards. So without a 2×2 breakdown for both homocysteine andomega 3’s we can’t know whether or not the sub-group of patientswith adequate omega 3’s might have had fewer heart attacks. Andeven if lowering homocysteine plus adequate omega 3’s doesn’tprevent M.I. or stroke, there’s still reason to confirm Vitacog’s po-tential for MCI.
Results
Given the limitations of treatments for MCI and MCI’s link to Alzheimer’s, one might expect that Vitacog’s findings would have been re-tested quite soon. But this didn’t happen. Dr. Smith told me that his group made six funding proposals but all were rejected—probably because studies of homocysteine-lowering to prevent heart attacks and strokes had failed to show benefit. But none of the heart or stroke studies measured omega 3’s. Surely, a fair proportion of their subjects had relatively low levels of omega 3’s by Vitacog’s standards. So without a 2×2 breakdown for both homocysteine and omega 3’s we can’t know whether or not the sub-group of patients with adequate omega 3’s might have had fewer heart attacks. And even if lowering homocysteine plus adequate omega 3’s doesn’t prevent M.I. or stroke, there’s still reason to confirm Vitacog’s potential for MCI.
Conclusions
A very practical problem: As the Vitacog study itself fades from memory, will its clinical and scientific insights be lost? I expect they will– unless by persuasion or good luck those of our leaders who have the power to act choose to review Vitacog’s data and then judge for themselves–Does Vitacog’s path deserves to push forward?
