How diet boosts brain power: the science

Still not good enough, we need EXACT amounts. When will your doctor provide that?

How diet boosts brain power: the science

 

Annabel and I read hundreds of research articles each month to keep up to date with the latest findings on healthy longevity. We’ve learned to decode the different methodologies to understand which are the most meaningful, and relevant, to The Age-Well Project. There’s such a broad span of research methods, from investigating the insides of petri dishes to investigating the insides of real people. Many of the best studies on lifestyle review the habits of large groups of people over a long time. As The Age-Well Project is all about the correlation of healthy lifestyle and longevity, it makes sense that these studies are the ones we focus on.
There’s an obvious flaw with many of these large-scale epidemiological studies, however. They rely on the memory (and honesty!) of the participants. Can you remember what you ate last week? I can’t. And if I was being questioned by a health researcher, I might forget those left-over-from-Christmas chocolates I polished off or the ‘may-as-well-finish-the-bottle’ glass of wine I imbibed.
As many of you know, my mother and grandmother spent years living with severe dementia so I’m always really grateful for quality research with genuinely useful findings. This week I came across a fascinating study on the power of diet to boost brain power in older people which – ironically – didn’t rely on memory.  What grabbed my attention was that the research fused two disciplines, applying methods from nutritional epidemiology and cognitive neuroscience together. Instead of relying on participants’ recall of what they’d eaten, the study focussed on ‘biomarkers’ in the blood by testing levels of specific nutrients. And instead of just using cognitive tests to assess brain health, the research team also deployed MRI scans to evaluate the efficiency of brain function. 116 people aged 65-75 were tested and you can read the paper here.
The results revealed that several specific nutrients were associated with better cognitive performance: polyunsaturated fatty acids (omega-3 and omega-6), lycopene, carotenoids plus vitamins B12 and D. These nutrients appeared to work together in different ‘equations’ to boost brain health.

• Omega-3 + Omega-6 + carotenes = more efficient communication between the neural networks in the brain.
• Omega-3 + Omega-6 = better performance of the fronto-parietal network (related to our attention span) and improvement in general intelligence
• Omega-3 + Omega-6 + lycopene =  moderation of the dorsal attention network (which helps us focus) and executive function.

Thankfully, these nutrients are abundant in some of our favourite Age-Well foods. Omega-3 fatty acids are found in oily fish, walnuts and chia seeds, omega-6 fatty acids in flaxseed, pumpkin seeds, pine nuts and pistachios (although few of us are deficient in Omega-6 as it is found in most seed oils used in commercial food production). Lycopene gives tomatoes, watermelon and red peppers their vivid red colour; carotenoids deliver the orange hue of sweet potatoes and carrots. Vitamin B12 is found in meat and dairy (vegans need to supplement). As we’ve said many times before, we get most of our Vitamin D from sunlight so if, like us, you’re in the middle of a northern winter you need a supplement for this too.

World Renowned Heart Surgeon Speaks Out On What Really Causes Heart Disease

This enumerates a lot about why cholesterol is not the problem, inflammation is the problem.

World Renowned Heart Surgeon Speaks Out On What Really Causes Heart Disease

Circulating omega-6 polyunsaturated fatty acids and total and cause-specific mortality: the Cardiovascular Health Study

Since this seems helpful the next obvious step is to create a stroke protocol for how to get Omega-6 PFAs to the helpful level in your bloodstream. Do not do this on your own. This is a job for that great stroke association in the sky, that doesn't exist yet. You're fucking screwed because we have no one putting all this research together into a coherent whole for stroke prevention and rehabilitation. The answers are out there, we just need a couple dozen geniuses to put this all together. This won't happen in our lifetimes because everyone in the stroke world is JUST WAITING FOR SOMEONE ELSE TO SOLVE THE PROBLEM!
I dare you to prove me wrong and that you have taken up this challenge.
Matt Lopez, president of the NSA?

Dr. Mariel Jessup, president of the ASA?
WSO President - Steve Davis (Australia)?   
Circulating omega-6 polyunsaturated fatty acids and total and cause-specific mortality: the Cardiovascular Health Study

Wu JH¹, Lemaitre RN², King IB², Song X², Psaty BM², Siscovick DS², Mozaffarian D².

Author information

Abstract

BACKGROUND:

Although omega-6 polyunsaturated fatty acids (n-6 PUFA) have been recommended to reduce coronary heart disease (CHD), controversy remains about benefits versus harms, including concerns over theorized proinflammatory effects of n-6 PUFA. We investigated associations of circulating n-6 PUFA including linoleic acid (the major dietary PUFA), γ-linolenic acid, dihomo-γ-linolenic acid, and arachidonic acid, with total and cause-specific mortality in the Cardiovascular Health Study, a community-based U.S. cohort.

METHODS AND RESULTS:

Among 2792 participants(aged ≥65 years) free of cardiovascular disease at baseline, plasma phospholipid n-6 PUFA were measured at baseline using standardized methods. All-cause and cause-specific mortality, and total incident CHD and stroke, were assessed and adjudicated centrally. Associations of PUFA with risk were assessed by Cox regression. During 34 291 person-years of follow-up (1992-2010), 1994 deaths occurred (678 cardiovascular deaths), with 427 fatal and 418 nonfatal CHD, and 154 fatal and 399 nonfatal strokes. In multivariable models, higher linoleic acid was associated with lower total mortality, with extreme-quintile hazard ratio =0.87 (P trend=0.005). Lower death was largely attributable to cardiovascular disease causes, especially nonarrhythmic CHD mortality (hazard ratio, 0.51; 95% confidence interval, 0.32-0.82; P trend=0.001). Circulating γ-linolenic acid, dihomo-γ-linolenic acid, and arachidonic acid were not significantly associated with total or cause-specific mortality (eg, for arachidonic acid and CHD death, the extreme-quintile hazard ratio was 0.97; 95% confidence interval, 0.70-1.34; P trend=0.87). Evaluated semiparametrically, linoleic acid showed graded inverse associations with total mortality (P=0.005). There was little evidence that associations of n-6 PUFA with total mortality varied by age, sex, race, or plasma n-3 PUFA. Evaluating both n-6 and n-3 PUFA, lowest risk was evident with highest levels of both.

CONCLUSIONS:

High circulating linoleic acid, but not other n-6 PUFA, was inversely associated with total and CHD mortality in older adults.
Inversely meaning high levels of linoleic acid are associated with lower mortality.