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As most people age, they show a gradual decline in mental ability, particularly in short-term memory and processing speed. For many people, however, this decline is more serious, progressing to mild cognitive impairment or various types of dementia. The definition of "mild cognitive impairment" is evolving, but the term typically refers to impairment that does not interfere with functioning, but can be detected by other people and by tests of cognitive function "Dementia" refers to progressive global decline in multiple areas of cognitive function and is often defined as a deficit in memory and in at least 1 other domain, such as attention, language, or problem-solving, that is severe enough to interfere with daily life. The prevalence of dementia varies from about 1%-2% among people aged 65-74 years and increases to approximately 30% among people aged 85 years or older.
Numerous observational studies have assessed the relationship between cognitive decline and various risk factors, including medical disorders, medications, genetic factors, lifestyle choices, physical activity, and nutrition. Recent systematic reviews of this research noted that an increased risk for cognitive decline was associated with diabetes, current smoking, depressive symptoms, the metabolic syndrome, and the genetic allele apolipoprotein E epsilon-4 (ApoE4).
A lower risk for cognitive decline was associated with involvement in cognitive, physical, or other leisure activities and with some dietary factors, such as omega-3 fatty acid intake, vegetable consumption, and following a Mediterranean diet
Only a small number of randomized controlled trials testing the effect of dietary interventions on cognitive function have been done, and in these trials, cognitive measures were usually secondary outcomes. In randomized controlled trials, 2 factors have been found to be associated with reducing the risk for cognitive decline: physical activity and cognitive engagement. For all other tested factors, there was either no association with cognitive decline or the results of the trials were inconsistent
This article reviews the data on the relationship between dietary factors and cognitive decline in older adults.
These factors include omega-3 fatty acids, B vitamins and folate, and antioxidants (vitamin C, vitamin E, and beta-carotene).
Polyunsaturated fatty acids are an important component of neuronal membranes and are required for the development and function of the brain; DHA is the primary long-chain polyunsaturated fatty acid in the brain. The omega-3 fatty acids -- alpha-linolenic acid (ALA), eicosapentaenoic acid (EPA), and docosahexaenoic acid (DHA) -- also have anti-inflammatory properties. Dietary sources of ALA include nuts and vegetable oils; however, ALA is poorly converted to DHA in humans. The main dietary sources of EPA and DHA are fatty fish, which derive DHA from dietary microalgae. Algal DHA supplements take DHA directly from microalgae. Several epidemiologic studies have found that regular fish consumption is associated with lower risk for cognitive decline or dementia. Observational studies have also found that polyunsaturated fatty acids were associated with lower risk for cognitive decline. Recent controlled trials have yielded conflicting results
In a randomized, double-blind, placebo-controlled clinical study, the effects of algal DHA supplementation on cognitive function were determined in healthy older adults with age-related cognitive decline. A total of 485 healthy persons aged 55 years or older who had a Mini-Mental State Examination score greater than 26 and a Logical Memory (Wechsler Memory Scale III) baseline score 1 or more standard deviations below those of younger adults were randomly assigned to receive oral algal DHA, 900 mg/day, or matching placebo for 24 weeks. The primary outcome was the CANTAB® Paired Associates Learning (PAL), a visuospatial learning and episodic memory test. The study found that compared with participants receiving placebo, those who received algal DHA had significantly fewer PAL 6-pattern errors at 24 weeks. This 2-fold reduction in the number of PAL errors indicates a benefit roughly equivalent to having learning and memory skills of someone 3 years younger on this memory task. Algal DHA supplementation was also associated with improved immediate and delayed verbal recognition memory scores but not working memory or executive function test scores. Plasma DHA levels doubled and were correlated with improved PAL scores in the DHA group. Supplementation with DHA for 24 weeks improved learning and memory in this population.
In another recent study, 402 people with mild-to-moderate Alzheimer disease (AD) were randomly assigned, and 295 participants completed the trial while taking study medication (171 in the algal DHA group and 124 in the placebo group). The main outcome measures were change in the cognitive subscale of the Alzheimer’s Disease Assessment Scale (ADAS-cog) and change in the Clinical Dementia Rating (CDR) sum of boxes. The rate of brain atrophy was also determined by volumetric magnetic resonance imaging in a subsample of 102 participants. Supplementation with algal DHA had no beneficial effect on rate of change on ADAS-cog score. The CDR sum of boxes score improved slightly for the algal DHA group and the placebo group and did not significantly differ between these groups. In the subsample of participants who had magnetic resonance imaging, algal DHA did not affect the rate of brain atrophy. However, in a subgroup of participants without the ApoE4 gene, significantly less decline was seen on the ADAS-cog with algal DHA treatment, suggesting that further research in specific subpopulations is needed.
The range of impairment among participants differed in these 2 studies, which may have contributed to differences in cognitive responses. Moreover, the tools used to measure the cognitive changes also differed. Cognitive impairment was greater in persons with AD versus those with age-related memory loss. The results suggest, however, that DHA supplementation may ameliorate early memory and learning deficits associated with aging. Larger studies of similar populations and of longer duration are needed to confirm this association.
Deficiencies in vitamin B12, vitamin B6, and folate result in a high concentration of homocysteine, which, at concentrations higher than normal physiologic levels, is neurotoxic in cell culture and experimental mouse models Vitamin B12 deficiency is common in elderly persons because of gastric conditions that restrict absorption the relationship between dementia and vitamin B12 deficiency was established more than 50 years ago. In a recent study, higher serum methylmalonic acid concentrations (a marker of vitamin B12 deficiency) were predictive of faster rates of cognitive decline, and higher serum vitamin B12 concentrations were associated with slower rates of cognitive decline. But is this dementia reversible with vitamin B12 supplementation?
Recent systematic reviews identified trials studying the effects of supplementation with vitamin B6, vitamin B12, and folate, alone or in combination.The reviews differed in their selection criteria and therefore evaluated overlapping sets of clinical trials, but they all found that the studies were small and of short duration. For example, in a review of 4 trials of folate supplementation,3 studies found improvement in some outcome measures. These 3 studies, however, involved a total of only 39 persons receiving folate. Six trials examined supplementation with various combinations of folate and B vitamins, but no improvements were found in cognitive function in any of the trials. Another systematic review of 3 studies of supplementation with vitamin B6 and 6 studies of supplementation with vitamin B12 found no effect on cognitive function. Large, well-planned studies of longer duration are needed to determine the effects of vitamin B6, vitamin B12, and folate on cognitive function.
Oxidative stress, the accumulation of reactive oxygen species, may trigger apoptosis even at moderate levels, and more severe oxidative stress can cause cell death. Numerous studies have suggested that oxidative stress may play a role in cognitive decline and dementia. Antioxidants, such as vitamins E and C and beta-carotene, may inhibit the production of reactive oxygen species and therefore may limit neuronal damage.
Observational studies of dietary antioxidants have yielded inconsistent results. Of 6 studies evaluating the effect of antioxidants ingested in food, 5 studies found that higher consumption of foods high in antioxidants was associated with lower risk for cognitive decline and dementia. Among studies in which participants were given vitamin C and vitamin E supplements, most did not find a beneficial effect associated with the supplements. A study of carotenoids found that low plasma levels of 2 specific carotenoids, lycopene and zeaxanthin, were associated with poor cognitive function.
Three randomized controlled trials have demonstrated no benefit from vitamin E supplementation. For example, in 1 double-blind study,769 participants with the amnestic subtype of mild cognitive impairment were randomly assigned to receive 2000 IU of vitamin E daily, 10 mg of donepezil daily, or placebo for 3 years. The primary outcome was clinically possible or probable AD; secondary outcomes were cognition and function. Possible or probable AD developed in 212 participants. Over the 3 years of the study, the probability of progression to AD did not differ significantly among the 3 groups. Vitamin E had no benefit in these patients with mild cognitive impairment.
Of note, antioxidant supplementation may be harmful. A recent meta-analysis found that treatment with beta-carotene, vitamin A, and vitamin E was associated with higher mortality. Further studies will be necessary to confirm this relationship, but on the basis of these data, these supplements should be used cautiously.
Research on the effect of vitamin D on cognitive decline is very limited. A recent systematic review identified 9 trials, only 1 of which was a prospective study; most of the studies were small and cross-sectional. Seven of the studies found that participants with vitamin D deficiency were at greater risk for cognitive decline; the remaining 2 studies found no association. A recently published prospective population-based study followed 858 adults aged 65 years or older for 6 years and found that low levels of vitamin D were associated with significant cognitive decline.
In general, research on dietary effects on cognitive decline in older adults has found no association or the studies have conflicting results. Many studies are small or of short duration, or the measures of cognitive decline were secondary measures, in some cases added after the study had begun.
The strongest evidence for a beneficial effect on cognitive decline is seen in the observational studies with polyunsaturated fatty acids and in a large randomized controlled trial of algal DHA in healthy, aging adults with mild memory symptoms. However, 3 randomized controlled trials of DHA plus EPA in various populations have failed to confirm this relationship. The antioxidant data demonstrate a similar and intriguing inconsistency, in that results differ on the basis of the source of the antioxidants and whether they are obtained from food or given as supplements.
Some of the inconsistencies may be a function of the considerable variation in study methodology. For example, researchers have used different definitions of "cognitive decline." In some studies, cognitive decline was based on a change in performance on a single test of cognitive function, usually a brief test of general function. In other studies, participants were tested on multiple domains of cognitive function; the domains chosen varied across the studies but generally included assessments of global function, verbal memory, visual memory, verbal fluency, naming, processing speed, attention, executive function, working memory, and reasoning. Studies also varied in the populations studied (older age is a risk factor for cognitive decline), tools used to assess diet, and statistical controls for confounding factors (including living arrangements, social factors, education, and socioeconomic status).[5,6]
New data are emerging, and although much of the research is inconclusive, DHA has recently been shown to improve memory and learning in age-related cognitive decline, suggesting that earlier intervention may be a key factor. Additional nutritional studies of longer duration and with larger samples will be required to answer the remaining questions.
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