Heart Diet Also Saves Brain

 
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Each year about one million Americans are diagnosed with Alzheimer’s disease (AD). AD accounts for about 2/3 of all dementia cases in US. Most other dementia cases are attributed to vascular disease in the brain. The primary cause of AD appears to be the build-up of plaques composed largely of a small protein (amyloid). These amyloid protein clumps accumulate in the brain and eventually cause so much damage that cognitive function is greatly diminished, with memory and executive cognitive function usually the most impacted. Most of the dementia not attributed primarily to AD is caused by damage to the brain’s vascular structure, which has long been known to be promoted by hypertension, elevated serum cholesterol, obesity, insulin resistance, and type 2 diabetes. Elevated homocysteine levels have been linked to more CVD and even more strongly with a greater risk of developing both AD and vascular dementias.

While CVD is primarily associated with the buildup of cholesterol-rich plaques in the artery wall and AD is primarily associated with the buildup of amyloid plaques in the brain, it is increasingly clear that both AD and CVD have many similar risk factors. Another link between AD and CVD comes from a genetic factor long associated with heightened AD risk. People who inherit the apoE4 allele (a protein involved in the transport of cholesterol and other lipid substances) are known to be much more likely to develop both AD and CVD than those who inherit the apoE2 or apoE3 alleles. Sadly, the medical treatment of AD is known to be minimally effective at treating symptoms and does nothing to slow the progression of this disease. So it is clear that preventing or slowing the accumulation of these amyloid plaques and the damage they cause in the brain is crucial. For now, the only viable way to reduce the growing burden that AD and vascular dementia places on individuals, their families, and American society is major changes in what we eat coupled with more activity/exercise, and perhaps some cognitive training too.

Finnish Geriatric Intervention Study (FINGER)  

Over the past several years, data from the FINGER Study have helped clarify the important roles of diet and lifestyle factors (which have long been linked to CVD risk factors) to the development of dementia and the loss of cognitive function over time. Lifestyle-related CVD risk factors have increasingly been associated with dementia risk in observational studies. The FINGER Study was a proof-of-concept randomized controlled trial (RCT), designed to assess the efficacy of altering known and suspected AD risk factors to help prevent the loss of cognitive function in a group of elderly Finnish people at risk of developing AD.

The FINGER Study enrolled 1260 men and women aged 60-77 years who had taken part in previous Finnish national surveys. Inclusion criteria for FINGER were the presence of CVD risk factors, older age, and dementia. Initial cognition function tests showed that they had average or slightly lower than expected scores for their age. Over the next 2 years, the intervention group (N=631) were encouraged to follow a heart-healthy diet and exhorted to exercise. They also received cognitive training and had their CVD risk factors monitored. The primary outcome was a change of cognition function as measured through a comprehensive neuropsychological battery of tests. The 629 subjects in the control group received only general health information.

About 95% of both groups had at least one post-baseline assessment and were included in the modified intention-to-treat analysis. Findings from this large, long-term, RCT trial suggest that lifestyle interventions could improve (or at least help maintain) cognitive functioning in at-risk elderly people from the general population.

A more recent paper from the FINGER study group examined secondary measures of cognitive function including memory, executive functioning, and processing speed and whether these changes correlated with any change in leukocyte DNA. The length of their DNA’s telomere was examined initially and again after 2 years in 775 participants (392 controls, 383 intervention). The shortening of the subjects telomeres is a biomarker of faster aging. The goal was to assess whether baseline telomere length was associated with better cognitive function seen in the initial FINGER study. Since older age is the greatest AD risk factor, the researchers wanted to see if telomere length was impacted by the heart-healthy diet, exercise, and cognitive training. Intervention and control groups did not significantly differ at baseline. The researchers observed that shorter telomeres were related to a less healthful baseline lifestyle. The intervention benefits of a healthy diet, exercise, and cognitive training on executive functioning were more pronounced among those whose initial telomere measurements were shorter (suggesting more advanced biological age). This suggests that lifestyle intervention was especially beneficial among subjects who were initially at a higher-risk of dementia. The results showed that after 2 years the heart-healthy diet and lifestyle intervention program was associated with significantly less loss of cognitive function.

The Atherosclerosis Risk in Communities (ARIC) study, which was published in April 2017 in JAMA, examined a subgroup of 322 subjects who were an average of 52 years old at the beginning of the study 20 years ago. These subjects underwent PET scans between 2011 and 2013 and were assessed for several cardiovascular risk factors. Dr. Gottesman’s group showed an increased late-brain amyloid load with several CVD risk factors. Elevated midlife body mass index (odds ratio [OR], 2.06), having one CVD risk factor at midlife (OR, 1.88) and having two CVD risk factors at midlife (OR, 2.88) all significantly increased the risk of loss of cognitive function. These findings indicate that CVD risk factors long known to promote atherosclerotic plaques in arteries are now also seen as risk factors for amyloid deposition and plaque development in the brain, which leads to AD.

The American Heart Association and American Stroke Association recently released an advisory on ways to preserve cognitive function and reduce the risk of developing dementia. They identified seven strategies that research indicates will help prevent cognitive decline and dementia. These include (1) do not smoke, (2) engage in regular physical activity, (3) adopt and maintain a heart-healthy diet, (4) maintain a body mass index of less than 25 kg/m2, (5) maintain an untreated systolic blood pressure below 120 mm Hg, (6) maintain an untreated total serum cholesterol level of less than 200mg/dl, and (7) maintain a normal fasting blood glucose level of less than 100 mg/dL.

Bottom Line: It is becoming increasingly clear that the adoption of a heart-healthy diet long promoted to reduce the risk of heart disease may also be the best way to protect the brain from not only stroke but also dementia.

By James J. Kenney, PhD, FACN

References:

  1.  http://www.bmj.com/content/349/bmj.g4433/rr/761349
  2.  http://stroke.ahajournals.org/content/30/8/1548
  3.  Ngandu T; Lehtisalo J; Solomon A, et. al.  A 2-year multidomain intervention of diet, exercise, cognitive training, and vascular risk monitoring versus control to prevent cognitive decline in at-risk elderly people (FINGER): a randomized controlled trial. Lancet 2015;385(9984) :2255-63.
  4.  Sindi S; Ngandu T; Hovatta I; et. al. Baseline Telomere Length and Effects of a Multidomain Lifestyle Intervention on Cognition: The FINGER Randomized Controlled Trial. J. Alzheimers Dis 2017;59(4);1459-70.
  5.  Gottesman RF; Schneider AL; Zhou Y; et. al. Association Between Midlife Vascular Risk Factors and Estimated Brain Amyloid Deposition. JAMA;317(14):1443-50.
  6.  http://stroke.ahajournals.org/content/48/10/e284

A Note About the AHA’s Simple Seven

I applaud the American Heart Association for their “life’s simple seven.” I do have some minor issues with three of their points. One of them is achieving a BMI of 25 for someone who has a BMI chronically elevated above 40, for instance is virtually impossible. They should “achieve a normal weight if overweight or achieve and maintain over 10% weight reduction from baseline if obese” so that the criteria is not untenable. 
Regarding a fasting glucose of less than 100, we both know that that is only half the story. Ideally, it could be modified to say “a fasting glucose less than 100 with a concomitantly measured fasting of 5 or less and an A1c of <5.5. Or, if diabetic, optimal blood sugar control on the least amount of medications necessary and no other outward signs of insulin resistance or metabolic syndrome.”
Lastly, we both know that a untreated cholesterol of 200 is not horrible. But it is far from what would be currently considered truly optimal on an individual basis. The life’s simple seven may be a reasonable public health guide to all, but if we are guiding people from an optimal perspective, then we would certainly use non-HDL as the most practical goal – which I would say should be, untreated, less than 120 in most cases if not less than 100 (unless we’re talking about secondary prevention where the level might be even less).

By Tom Rifai MD FACP, Reality Meets Science® LLC, President, RealityMeetsScience.com

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