Does improves high -dose oral DHA dementia?

reference

Arellanes I, Choe N, Solomon V, et al. Delivery of additional docosahexaenoic acid (DHA) to the brain: a randomized placebo -controlled clinical study. ebiomedicine . 2020; 59: 102883.

Study goal

This study was structured to assess whether high oral doses of Docosahexaenoic acid (DHA) would improve the cognitive function.

study design

randomized, placebo-controlled study

participant

A total of 33 participants were either randomized to the armed for noise (n = 18; 8 goods apoe4 carrier) or placeboot (n = 15; 7 were apoe4 support). After the departure of 4 participants, a total of 15 participants (at the age of 58–90 years) remained in the intervention group and 14 participants (at the age of 58–79 years). All participants were female, with the exception of 6 men who all non- apoe4 carrier (placebo group, n = 4; intervention group, n = 2).

racial characteristics of each arm: The intervention group consisted of 61 % white (non-hiSpaniards), 33 % Hispano-Americans, 6 % black and 0 % Asian. The placebo group consisted of 47 % white (non-Hispanic), 33 % Hispano-Americans, 13 % Asians, 7 % other and 0 % blacks.

All participants were residents of the Los Angeles area, which were recruited between 2016 and 2018. Everyone was not cognitively affected, but had at least 1 first degree in the history of dementia.

The exclusion criteria included current smokers, history of cardiovascular diseases, kidney failure or blindness, a cancer diagnosis in the past 6 months, uncontrolled thyroid function (hyper or hypo), taking coagulation medication, regular physical activity (> 150 minutes of aerobic training per week). ), drink strong (> 30 units per week) and consumption of omega-3 fatty acids (polyunsaturated fatty acids [Pufa]) capsules in the past 3 months.

Intervention

Both groups received strong doses of B vitamins: B 12 1 mg, folic acid 800 McG and B 6 100 mg together with trimethylglycin 2 g and pyridoxal-5 ′-phosphate. The treatment group also received oral omega-3 fatty acids for 6 months, which mainly contained DHA (60 %, with a DHA content of 2,152 mg). This capsule essentially contained no EPA.

Primary result measurements

The primary endpoint was every change in the DHA mirror after 6 months compared to the starting value. The secondary endpoints include changes in cerebrospinal fluid (CSF), EICOSAPENTAESON (EPA) and magnetic resonance imaging (MRI) image changes (hippocampus volume and thickness of the ENORORHINAL CORTEX). The exploratory results included Montreal Cognitive Assessment (evaluation of global cognition), Craft Stories and California verbal Learning Test 2 (evaluation of verbal memory) as well as trail making Tests A and B (evaluation of speed and executive functions).

important knowledge

There was an increase in DHA and EPA in the liquor (this is already interesting, since the participants did not add an EPA) of the treatment group. In the treatment group there was a 28 % increase in the CSF-DHA (medium difference for DHA [95 % CI]: 0.08 mg/ml [0.05, 0.10], p <0.0001); and a 43 %increase in the CSF-EPA in the treatment group (medium difference for EPA: 0.008 mg/ml [0.004, 0.011], p <0.0001).

After 6 months there was no indication that DHA improved the cognitive function or delayed the beginning of dementia.

Participants who do not increase their CSF EPA values ​​by three times apoe4 carrier.

practice implications

What my interest in this article aroused was the wording of the title: "Brain Delivery of Supplemental DHA". I imagined that the researchers would actually put the DHA directly into the brain, like an intrathecal injection. They may laugh at this idea, but I remember that I read something about the intracerebral use of gamma-linolenic acid for the treatment of human gliomas about 25 years ago. So I thought that this study would build on it. Unfortunately not. This was an oral supplementation. In short, the results of this study show that this intervention does not make sense at least for a short time (6 months) as a sole instrument for delay or treatment of dementia.

This study leaves as many questions as it gives answers. The study proves that they can increase CSF DHA by giving high doses. It also indicates that DHA can be converted into EPA. However, the aim of the study was to see whether the administration of high -dose DHA could improve the cognitive function and reduce the risk of dementia. At the end of the study (6 months) there was no improvement for these 2 end points. This should not surprise us because 6 months are a relatively short time in the life of a 55-year-old brain.

silver balls rarely hit your goal, regardless of whether it is conventional or natural interventions.

The main question that remains open is: If you give high -dose DHA over a longer period of time, will it have the desired benefit? There is indications that high-dose DHA should prevent dementia, ^{3.4 Especially for people who are not homozygot for those apoe4 gen, which is "selectively" for early Alzheimer's disease. (An important note: The DHA used in these studies was the molecular form found in fish, not the deconstructed fatty acid form, which can be found in many nutritional supplements.)}

My frustration about this article is that it is assumed that there will be a nutrient that will be the answer to the Alzheimer's/dementia puzzle. Silver balls rarely hit their goal, regardless of whether it is conventional or natural interventions. Chronic diseases are multifactorial and require multifactorial interventions. Various studies have pointed out various factors that contribute to this discouraging state and solve it, such as: B. Problems with the sugar metabolism of the central nervous system (ZNS), 5,6 Exercise, 7 sleep, 8 Virus infections, ^{9 Nutrition defects, 10.11 Alcohol consumption, 12 Medicine intake, 13 and more. It would be wonderful, but extremely unlikely if there was a single nutrient that would be the solution to prevent and treat this disease.}