A new study published in The Lancet found that people genetically predisposed to Alzheimer’s disease may need a much higher intake of omega-3 fatty acids, EPA and DHA, than what was  previously suggested in studies which have established a link between higher omega-3 intake and reduced incidences of Alzheimer’s disease (AD) and dementia.
 
In a group of 33 men and women above the age of 55 who were not cognitively impaired themselves but had a family history of AD, approximately half of the group carried a gene variant known as APOE4, which is linked to brain inflammation and is known to increase the risk factor of developing AD by a factor of at least four. The group adhered to a typically American lifestyle and dietary pattern, in which they were generally sedentary, and ate little to no fatty fish. Each participant had refrained from taking omega-3 capsules for at least three months prior to the study
 
Those in the treatment group were required to take omega-3 supplements containing 2,152 mg of DHA for 6 months, and were also instructed to limit their polyunsaturated fatty acid intake. The control group was instructed to take placebo capsules containing corn/soy oil. Both groups were instructed to take a vitamin B complex daily, which helps the body process omega-3s. The dose of DHA far exceeded dosages used in previous clinical trials assessing omega 3s’ preventative potential.
 
The Blood-Brain Barrier

All participants were evaluated for plasma and CSF levels of DHA and EPA at baseline, and six months following treatment. Cognitive function tests were also given at baseline and a the end of the treatment period. The treatment group had an average 200% increase in their blood plasma DHA levels compared to the placebo group, however, the DHA content in the treatment group’s cerebrospinal fluid only increased by an average of 28%, which was still better than what was previously reported in studies using lower DHA doses. It is understood that the neuroprotective effect associated with omega-3s can only occur based upon the passage of DHA through the blood-brain barrier.
 
Another noteworthy observation was that in both the plasma and CSF measurements, the percentage increase for DHA tended to be lower in the participants who carried a copy of the APOE4 gene.
 
Those in the treatment group who did not carry the APOE4 gene experienced a three-times greater increase of EPA in their cerebrospinal fluid than those who were APOE4 carriers.
 
The authors of this study believe that since variations in the ability of EPA and DHA to cross the blood-brain barrier occurred in this study, omega-3 concentrations in the blood may not be a good indicator of how much EPA and DHA is reaching the brain.
 
“Therefore, future research should strongly consider whether a dose of 2 grams daily of omega-3 is enough to find benefit for a disease like AD or whether even higher doses should be administered,” Dr. Bill Harris of OmegaQuant, the company which conducted the fatty acid analysis in this study, said. “This may be especially true for those who have known risk factors for AD, such as carrying the APOE4 gene variant. It appears that these people may be less able to transfer DHA from the blood to the brain than those who don’t carry the gene.”
 
The results of this study attracted funding for a larger trial, for which recruitment is now underway, OmegaQuant said.