Can DHA as found in fish oil and algae protect the brain from Alzheimer’s?
One of the major news stories on brain health and prevention coming out of Sunday’s oral presentations at the International Conference on Alzheimer’s Disease (ICAD) in Vienna, were the reports on the effectiveness of DHA, an Omega-3 fatty acid, present in fish oil and algae. Last year a major study looking at fish oil’s affect in arresting Alzheimer’s was disappointing. I reported yesterday on a minor study investigating the value of DHA for prevention in an animal study. But on Sunday, the 2nd day into the conference, long awaited results (I’ve personally been looking for this since March) were finally presented on two major well designed multi-center studies of DHA – one conducted in part here in Salt Lake City.

In the first MIDAS (Memory Improvement with DHA Study) researchers looked at the Effects of DHA on Physiological and Safety Parameters in Age-Related Cognitive Decline. This was a randomized, double-blind, placebo-controlled, multi-center, six month study to determine the effects of 900mg/d DHA on improving cognitive functions in healthy elderly with ARCD (Age Related Cognitive Decline). Safety and tolerability were also assessed. 485 subjects, some from Utah, were involved in this study.

Results showed significantly fewer errors made on a visuospatial memory test with DHA versus placebo at six months compared to baseline (diff. score -1.63±0.76, p<0.03). A significant decrease in heart rate (DHA change from baseline of -3.2 vs. -1BPM, p<0.03) occurred and highly correlated with week 24 plasma levels (p<0.01).

Conclusions: Six month supplementation with DHA (900mg/d) improves memory function and decreases heart rate in healthy older adults with ARCD. DHA also exhibited an excellent safety profile in this older population.

Those results were good, but expected (see my article on Omega-3 and DHA under the diet and nutrition section of this website). The second study was or greater interest for those concerned about AD (Alzheimer’s Disease). It was a clinical trial of DHA (docosahexanoic acid) for the treatment of Alzheimer’s disease. This study was also a double blind, randomized, placebo-controlled clinical trial comparing DHA and placebo in AD patients. It was conducted by the National Institute on Aging Alzheimer’s Disease Cooperative Study Unit. Fifty one sites in the United States enrolled 402 subjects between February and November 2007. Subjects had a diagnosis of probable AD with Mini-mental state exam score (MMSE) 14-26, and dietary DHA intake of ≤ 200 mg per day.

Subjects in this study were treated with DHA or placebo at a dose of 2 grams per day for 18 months, [that’s a lot of DHA] with the final subjects completing clinical activity in May 2009. Co-primary outcomes were rate of change on Alzheimer’s disease assessment scale-cognitive (ADAS-cog) and rate of change on Clinical Dementia Scale-sum of the boxes (CDR-SOB).

Results:
The study population was 52.2% female with a mean age of 76 ± 8.7 years, mean education of 14.3± 2.8 years, and mean MMSE=20.7 ± 3.6, with 59% ApoE4 positive and 41% ApoE4 negative. Mean plasma DHA at baseline was 3.15±1.12 weight percent.

Conclusions:
Unfortunately they found no significant difference over the 18 month period in thinking or memory abilities, nor on subjects abilities to perform activities of daily living. Although there was some difference in behavioral symptoms, like sleep, anxiety etc, favoring those on the DHA. However, they did find that in those who did not have the APOe4 Alzheimer’s gene, DHA supplementation did appear to have some protective value.

What is the take-home from these two studies? While DHA was not shown to significantly impact the course of Alzheimer’s in later stages, it may help to prevent the development of dementia symptoms if sufficient amounts are taken early enough. And it may be of some value in reducing anxiety and sleep related problems for some with dementia

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Another study of note was an Italian study which found that the incidents of AD appears to be rising in Western countries for those over the age of 80.

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Of interest to Utah residents was The Cache County Dementia Progression Study conducted at Utah State University. In this study they looked at the Interaction between C-Reactive Protein level (a bio marker for inflammation) and APOE genotype in predicting rate of progression in Alzheimer’s disease. First they noted that chronic inflammation has been implicated in the development of Alzheimer’s Disease (AD). Elevated levels of C-reactive protein (CRP) and interleukin-6 have been associated with increased risk for incident AD and more rapid cognitive decline in elderly individuals without dementia. In their study they looked at 187 individuals in the Cache County Memory Study (62% females) with possible/probable AD. What they found was neither CRP nor APOE alone predicted progression on the Mini Mental State Exam (MMSE) (p=0.3). However, in models controlling for dementia duration, there was a significant interaction between CRP, APOE and time (p=0.026). APOE E4 carriers with high CRP levels declined 0.2 times more rapidly on the MMSE than non-carriers with normal-average CRP levels.

Conclusions:
High baseline CRP levels interacted with APOE genotype to predict cognitive but not functional progression in AD. Future studies will examine the effects of CRP in relation to anti-inflammatory treatments and other health conditions on dementia progression.

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In a U of Connecticut study of well educated adults awareness of risk factors for Alzheimer’s disease, they found more than 500 respondents from the US, England, Canada and Ireland, generally showed a lack of awareness of the importance of obesity, high blood pressure, and stress as risk factors for Alzheimer’s and a less than expected awareness of the value of exercise as a protective factor, to reduce the risk for AD.

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A Wake Forest, NC study also looked at modifiable risk factors for dementia. In this 6 year study researchers found those who consumed a moderate amount of alcohol (8-14 drinks per week/ 1-2 per day) appeared to have a somewhat lower risk of developing dementia than abstainers. In cognitively normal individuals the moderate drinkers has 37% less risk of developing dementia than those who abstained. Mild consumption also had a protective effect. However, in older adults with mild cognitive impairment alcohol was not protective, in fact in this population drinking increased the risk, and the more they drank the faster their dementia progressed.

So while moderate drinking appears to have some protective effect, for those without memory problems, once dementia gets started continued alcohol consumption only appears to accelerates that decline.

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Dr. Yaffe from the University of San Francisco talked about the relationship between PTSD (Post Traumatic Stress Disorder) and dementia. She noted that PTSD has been shown to reduce hippocampus (the primary organ of memory) volume, and prolonged stress increases cortisol which over time can cause brain damage (see “Stress Depression and Dementia” under Stress and Depression Management on this site).

In their review of the files of more than 50,000 veterans, some with PTSD some without, after adjusting for other things they found those with PTSD had more than double the risk of developing all dementias, as veterans who did not suffer from PTSD. (See our article on Stress and Depression for ideas on how to control stress.)

There were more than 200 studies presented on Sunday and Monday. Obviously this is only a small sample. Stay tuned to this site www.4abettermemory.com for more information to come.

 

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