Medscape: Which foods or dietary patterns were associated with an increased or decreased risk for dementia?
Dr. Isaacson: Although the full results of our work are not yet finalized, we reviewed many dozens of studies, including randomized controlled trials (RCTs) and prospective cohort studies, that evaluated various dietary interventions in normal, nondemented persons; patients with MCI; and patients with AD. The interventions included the Mediterranean diet, omega-3 fatty acids, antioxidants, B vitamins, and low-carbohydrate diets.
On the basis of our preliminary review, a combination of B vitamins (folic acid, B6, and B12) probably improves cognitive impairment in MCI, whereas a Mediterranean diet may improve cognitive function in AD and probably decreases the risk for AD in both MCI patients and nondemented persons.
We also found some promising potential interventions for cognitively normal persons and MCI patients. We found that, for example, specific omega-3 fatty acids are likely to decrease cognitive impairment in MCI, and flavonoids (eg, regular intake of at least 8 oz per week of blueberries and strawberries) may delay symptoms.
On the other hand, there is strong evidence that beta-carotene does not decrease the risk for AD in nondemented patients. There is weak to moderately strong evidence against vitamin E as helpful in nondemented persons and MCI patients; however, a recent RCT found that 2000 IU resulted in slower functional decline and decreased caregiver burden.
Although there is insufficient evidence for a low-carbohydrate diet, one small RCT demonstrated cognitive improvements with a very low-carbohydrate diet, as well as beneficial effect on a number of relevant biomarkers. In addition, preliminary evidence suggests that dietary ketosis may lead to cognitive benefits in a subset of AD patients, although further studies are necessary.
Medscape: On the basis of your findings, what would your take-home message be for clinicians?
Dr. Glazer: AD starts in the brain 20-30 years before the first symptoms of memory loss, and several nutritional approaches, as well as other lifestyle interventions, may be among the most appropriate strategies for managing AD risk that we have today. Dietary interventions should be considered in the management of patients at risk for AD, and probably also in the earliest stages. Aside from being low-risk, these strategies may have other health-promoting benefits (eg, prevention of cardiovascular disease and the metabolic syndrome).
Because currently available pharmacologic interventions may have limited efficacy in some patients, it is necessary to take a more comprehensive, multimodal approach toward AD care. Although our conclusions are based on a preliminary review of the evidence, physicians should consider recommending a Mediterranean diet across the spectrum of AD (stages 1-3), specific omega-3 fatty acids for MCI patients, and flavonoids and B vitamins to those with MCI, as well as to those at risk.
There is less robust evidence toward improving clinical outcomes in dementia due to AD, but this may be attributed to use relatively too late to more meaningfully modify the disease process. As such, dietary interventions may be more helpful in normal, preclinical AD and MCI patients, before they begin to develop functional impairment and dementia.
Our group is currently studying the most effective methods to teach people about these brain-healthy dietary strategies in an effort to understand which methods work best. For busy clinicians who do not have the time or who may not be comfortable with nutritional counseling, we would suggest referral to a registered dietitian, or inviting their patients to participate in an online education research study led by investigators at Weill Cornell Medical College (www.AlzU.org), which uses an online AD nutrition tracking system to longitudinally study outcomes.
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