The mediterranean diet: Good for the heart = good for the brain?

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    The Mediterranean Diet: Good for theHeart Good for the Brain?

    T he prevalence of Alzheimer disease (AD) and otherdementias is expected to nearly quadruple worldwideover the next 40 years if a prevention or cure is not

    developed.1 Currently available dementia medications

    have been shown to have relatively small effect sizes in

    clinical trials and do not clearly modify the disease

    course.2 In addition, several agents have recently failed in

    phase III clinical trials.35 There is growing awareness

    that treatment at the time patients develop AD symp-

    toms may be too late, as these symptoms likely reflect

    the end stage of a neurodegenerative process that has

    occurred over many years or even decades. Therefore, the

    field has begun to shift away from treatment and toward

    prevention efforts.Dietary factors have been identified as 1 of the

    more promising strategies for dementia prevention.6

    Some observational studies have found that individualswho consume diets higher in folate, fish, omega-3 fattyacids, or antioxidants have a decreased risk of developingdementia.7 However, randomized controlled trials(RCTs) of specific dietary componentsincluding folicacid with or without other B vitamins, docosahexaenoicacid, eicosapentaenoic acid,7 and vitamins C, E, or beta-carotene8,9have yielded disappointing results to date.This has led some to suggest that the overall diet may bemore important than a single component.6

    The Mediterranean diet (MeDi) is a particularlypromising dietary pattern for lowering dementia risk.MeDi is characterized by high consumption of fruits,vegetables, legumes, and complex carbohydrates; moder-ate consumption of fish; olive oil as the primary sourceof fat; and low-to-moderate alcohol consumption (

  • examining the association between MeDi and neurodege-nerative outcomes has been performed using the WHI-CAP cohort, which raises concern regarding the general-izability of the findings. Although this study populationis ethnically diverse, it is restricted to a small geographicregion in New York, and the dietary patterns in thisregion may not reflect the full range of dietary patternsin other regions. For example, a recent study in Francefound that greater MeDi adherence was associated withslower cognitive decline but not lower dementia inci-dence.19 Moving forward, it will be critical to examinethe association between MeDi and neurodegenerativeoutcomes in other cohorts.

    Ultimately, RCTs will be needed to determinewhether the association between MeDi and AD is causaland whether dietary intervention in high-risk elders canprevent or delay onset of AD. However, it is encouragingthat RCTs that have examined MeDi in other settingshave yielded promising results, particularly for improvingcardiovascular and metabolic profiles. A recent RCT inindividuals with a high cardiovascular disease risk foundthat MeDi was more effective than a low-fat diet forimproving plasma glucose, systolic blood pressure, andcholesterol levels.20 Another trial of individuals withnewly diagnosed type II diabetes found that MeDi wasassociated with greater weight loss, greater improvementsin glycemic control and coronary risk measures, and lessmedication use compared to a low-fat diet.21 MeDi alsohas been associated with greater ability to reverse meta-bolic syndrome status22 and lower diabetes incidence23,24

    compared with a low-fat diet. However, several otherRCTs have found that MeDi is equivalent to otherhealthy diets. An RCT in individuals who had had theirfirst myocardial infarction found that low-fat and MeDidiets were both associated with an approximately 70%reduction in subsequent cardiovascular events or mortal-ity compared with a matched usual care control group.25

    Another trial found that low-fat, MeDi, and low-carbo-hydrate diets were associated with similar improvementsin carotid atherosclerosis.26 Nonetheless, these trials dem-onstrate that dietary modifications do affect cardiovascu-lar risk and metabolic status and raise hope that, over thelong term, dietary changes could lead to lower incidenceof AD.

    For a dementia prevention strategy to be feasible, itmust first do no harm. Many individuals considered tobe at high risk for ADeven those with high levels ofAD biomarkers or evidence of AD neuropathologywillnever develop dementia symptoms in their lifetimes.Therefore, it is crucial that prevention interventions tar-geting these individuals have low side effect profiles. Oneof the appealing aspects of lifestyle interventions such asMeDi is that they are exceptionally low risk with a highpotential for gain. In addition, they are relatively inex-pensive and have the potential to reduce other diseasessuch as cardiovascular disease and metabolic disorders.

    Although neurologists should not be expected to play therole of dietary counselors, recommendation of MeDi tohigh-risk patients may be an option for AD preventionwhere pharmaceutical interventions have so far beenineffective.

    Potential Conflicts of Interest

    Nothing to report.

    Deborah E. Barnes, PhD, MPH

    Department of Psychiatry

    University of California, San Francisco

    and San Francisco Veterans Affairs Medical Center

    San Francisco, CA

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    DOI: 10.1002/ana.22376

    ANNALS of Neurology

    228 Volume 69, No. 2