One of The Strongest Alzheimer’s Preventions

A broad group of lifestyle and behavioral factors have been associated with the risk of developing Alzheimer’s disease including diet, stress, exercise and others.  A new study has increased the importance of one that has been previously known, educational attainment.

The study, CoSTREAM, looked at genetic patterns that have been previously shown to highly correlate with the likelihood of educational attainment. This gene pattern was also highly associated with a reduced likelihood of developing Alzheimer’s.  For every year of educational completion the risk of Alzheimer’s was reduced 11%.  If education included the completion of college, risk was further reduced 26%.

The researchers commented that this association is consistent with the reducing rate of Alzheimer’s disease in the United Kingdom which contrasts to the sharply increasing rate in the United States.  Along with greater emphasis on diet, exercise, and smoking reduction the UK has increased educational emphasis.

The effect is thought to relate to the development of "cognitive reserve". Just as physical exercise causes muscle to build up decreasing the risk of injury and age-related muscle loss, education builds up brain structure and offsets age related brain loss.

While recent losses in financial support for higher education in the US have occurred

 based on “costs”, this may be short-sighted given the staggering cost projections associated with Alzheimer’s disease over the next 30 years.  Saving a dollar now but costing hundreds more in the near future is never a winning strategy.

The best plan is for each individual to do everything to facilitate their own higher education and to continue “brain exercise” with life-long learning.

Larsson et al.  Modifiable pathways in Alzheimer’s disease: Mendelian randomisation analysis.  BMJ 2017; 359.

Alzheimer’s Genetic Risk Factor Requires Careful Management of Omega-3 Fatty Acid Levels

Some of the risk of developing Alzheimer’s disease is mediated by genetic variation.  The most common and involved variation is a variant of the gene that makes the apoprotein apoE.  This apoprotein is involved in many processes in brain cells including the removal of the toxic protein β amyloid which causes tissue damage if it builds up in excess.

Risk of the disease is greatly increased in those with the variant form of the gene called apoE4.  Nine percent of adults have the apoE4 variant and their disease risk is increased between 3 and 10-fold depending on the presence of 1 or 2 copies of the gene variant.

While the presence of apoE4 increases the disease risk, the final triggering of the disease requires the presence of different environment triggers such as chronic inflammation or insulin resistance.  Both of these processes are worsened by low cell levels of omega-3 fatty acids which must come from diet.  New study has found that this relationship is compounded by the fact that it requires higher amounts of omega-3 FA intake to maintain cell levels in those with the apoE4 gene variant.

The study looked at blood and brain cell omega-3 FA levels in rats that share the traits of development of Alzheimer’s with humans.  The levels were significantly lower in those animals with the apoE4 variant.  The lower levels of omega-3 FAs correlated with cognitive and behavioral deficits typical to human Alzheimer’s.  The lower levels of omega-3 FAs appears to come from increased “catabolism” or breakdown of these fatty acids.  The solution is that those with the apoE4 variant require higher levels of dietary and supplemental omega-3 FAs to maintain cell levels and prevent cognitive decline.

The difficulty in managing omega-3 FA levels is that there is wide variation of intake levels from person to person required to maintain adequate cell levels.  This can be managed by actually measuring cell levels and adjusting supplementation until these levels are adequate.  This is done with a red blood cell test.  Blood cell levels have been correlated with levels in brain cells validating this testing.  The test above shows a low omega-3 FA cell level at 3.72%.  Levels need to be 10% or greater for optimal brain protection.  

The test at the left shows an ideally managed omega-3 FA level at 11%.  The dietary levels required to maintain these levels varies from person to person so supplementation levels should be managed by cell level testing rather than by using an arbitrary consumption level. 

There are several risk factors that have to be managed more carefully in persons with the apoE4 gene variant.  Omega-3 FA levels is clearly one of them.  If someone is genetically predisposed to Alzheimer’s disease, development of it is not a given and it can be prevented with careful lifestyle management.

Nock et al.  Carriers of an apolipoprotein E epsilon 4 allele are more vulnerable to a dietary deficiency in omega-3 fatty acids and cognitive decline.  Molecular and Cell Biology of Lipids, 2017:1862;1068–1078.