Brain atrophy in cognitively impaired elderly: the importance of long-chain ω-3 fatty acids and B vitamin status in a randomized controlled trial

What is your doctor doing to stop brain atrophy in their stroke survivors? With all this earlier research available for years your doctor has absolutely no excuse for not having a stroke protocol to prevent brain atrophy. Do not self treat yourself, your doctor has to do this even if they know nothing about it.

From June, 2013;

Low Diastolic Pressure Linked to Brain Atrophy

And this from November, 2012:

Relationship between Physical Activity and Brain Atrophy Progression.

And from September, 2014: 

Lack of sleep may shrink your brain

From June, 2013:

Preventing Alzheimer’s disease-related gray matter atrophy by B-vitamin treatment

The latest here: 

Brain atrophy in cognitively impaired elderly: the importance of long-chain ω-3 fatty acids and B vitamin status in a randomized controlled trial

1. 1. 1. Fredrik Jernerén³,*,
      2. Amany K Elshorbagy³,⁴,
      3. Abderrahim Oulhaj⁵,
      4. Stephen M Smith⁶,
      5. Helga Refsum³,⁷, and
      6. A David Smith³

      + Author Affiliations

      1. ³From the Oxford Project to Investigate Memory and Ageing (OPTIMA), Department of Pharmacology, University of Oxford, Oxford, United Kingdom;
      2. ⁴Department of Physiology, Faculty of Medicine, University of Alexandria, Alexandria, Egypt;
      3. ⁵Institute of Public Health, College of Medicine and Health Sciences, United Arab Emirates University, Al Ain, United Arab Emirates;
      4. ⁶Functional Magnetic Resonance Imaging of the Brain Centre, Nuffield Department of Clinical Neurosciences, University of Oxford, John Radcliffe Hospital, Oxford, United Kingdom; and
      5. ⁷Department of Nutrition, Institute of Basic Medical Sciences, Faculty of Medicine, University of Oslo, Oslo, Norway

      + Author Notes

      • ↵1 Supported by grants from the Charles Wolfson Charitable Trust, The Medical Research Council, Norwegian Research Council, Norman Collisson Foundation, Alzheimer's Research UK, Henry Smith Charity, John Coates Charitable Trust, Thames Valley Dementias and Neurodegenerative Diseases Research Network of the National Institute for Health Research, the Sidney and Elizabeth Corob Charitable Trust, and Meda AB/Recip AB.
      • ↵2 Supplemental Tables 1–3 and Supplemental Figure 1 are available from the “Supplemental data” link in the online posting of the article and from the same link in the online table of contents at http://ajcn.nutrition.org.

      1. ↵*To whom correspondence should be addressed. E-mail: fredrik.jerneren@pharm.ox.ac.uk.

      Abstract

      Background: Increased brain atrophy rates are common in older people with cognitive impairment, particularly in those who eventually convert to Alzheimer disease. Plasma concentrations of omega-3 (ω-3) fatty acids and homocysteine are associated with the development of brain atrophy and dementia.

      Objective: We investigated whether plasma ω-3 fatty acid concentrations (eicosapentaenoic acid and docosahexaenoic acid) modify the treatment effect of homocysteine-lowering B vitamins on brain atrophy rates in a placebo-controlled trial (VITACOG).

      Design: This retrospective analysis included 168 elderly people (≥70 y) with mild cognitive impairment, randomly assigned either to placebo (n = 83) or to daily high-dose B vitamin supplementation (folic acid, 0.8 mg; vitamin B-6, 20 mg; vitamin B-12, 0.5 mg) (n = 85). The subjects underwent cranial magnetic resonance imaging scans at baseline and 2 y later. The effect of the intervention was analyzed according to tertiles of baseline ω-3 fatty acid concentrations.

      Results: There was a significant interaction (P = 0.024) between B vitamin treatment and plasma combined ω-3 fatty acids (eicosapentaenoic acid and docosahexaenoic acid) on brain atrophy rates. In subjects with high baseline ω-3 fatty acids (>590 μmol/L), B vitamin treatment slowed the mean atrophy rate by 40.0% compared with placebo (P = 0.023). B vitamin treatment had no significant effect on the rate of atrophy among subjects with low baseline ω-3 fatty acids (<390 μmol/L). High baseline ω-3 fatty acids were associated with a slower rate of brain atrophy in the B vitamin group but not in the placebo group.

      Conclusions: The beneficial effect of B vitamin treatment on brain atrophy was observed only in subjects with high plasma ω-3 fatty acids. It is also suggested that the beneficial effect of ω-3 fatty acids on brain atrophy may be confined to subjects with good B vitamin status. The results highlight the importance of identifying subgroups likely to benefit in clinical trials. This trial was registered at www.controlled-trials.com as ISRCTN94410159.
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