Background: Elevated plasma homocysteine is a risk factor for Alzheimer disease, but the relevance of homocysteine lowering to slow the rate of cognitive aging is uncertain.Objective: The aim was to assess the effects of treatment with B vitamins compared with placebo, when administered for several years, on composite domains of cognitive function, global cognitive function, and cognitive aging.Design: A meta-analysis was conducted by using data combined from 11 large trials in 22,000 participants. Domain-based z scores (for memory, speed, and executive function and a domain-composite score for global cognitive function) were available before and after treatment (mean duration: 2.3 y) in the 4 cognitive-domain trials (1340 individuals); Mini-Mental State Examination (MMSE)–type tests were available at the end of treatment (mean duration: 5 y) in the 7 global cognition trials (20,431 individuals).Results: The domain-composite and MMSE-type global cognitive function z scores both decreased with age (mean ± SE: −0.054 ± 0.004 and −0.036 ± 0.001/y, respectively). Allocation to B vitamins lowered homocysteine concentrations by 28% in the cognitive-domain trials but had no significant effects on the z score differences from baseline for individual domains or for global cognitive function (z score difference: 0.00; 95% CI: −0.05, 0.06). Likewise, allocation to B vitamins lowered homocysteine by 26% in the global cognition trials but also had no significant effect on end-treatment MMSE-type global cognitive function (z score difference: −0.01; 95% CI: −0.03, 0.02). Overall, the effect of a 25% reduction in homocysteine equated to 0.02 y (95% CI: −0.10, 0.13 y) of cognitive aging per year and excluded reductions of >1 mo per year of treatment.Conclusion: Homocysteine lowering by using B vitamins had no significant effect on individual cognitive domains or global cognitive function or on cognitive aging.

Objectives: To determine the extent to which plasma antioxidant concentrations in people with habitual low intake of fruit and vegetables respond to increased intakes of these foods. To examine whether advice to increase fruit and vegetables will result in reduction of concentrations of total and low density lipoprotein cholesterol. Design: Randomised controlled trial in which intervention and control groups were followed up for eight weeks. The intervention group was asked to consume eight servings of fruit and vegetables a day. Setting: Dunedin, New Zealand.

Objective: To compare two low fat diets one rich in walnuts on parameters of lipid metabolism in a group of hyperlipidaemic subjects. Design: A randomised cross over study. Setting: Department of Human Nutrition, University of Otago, Dunedin, New Zealand Subjects: Twenty one men with mean (s.d) levels of total and LDL cholesterol of 6.58 (0.60) and 4.63 (0.58) respectively. Interventions: For two periods of four weeks subjects were asked to consume two low fat diets (fat 30% total energy), one containing, on average, 78 gad walnuts. Walnuts obtained through Lincoln University and the Walnut Growers Group (South Canterbury). Results: Participants reported a higher total fat intake on the walnut diet (38% compared with 30% on the low fat diet P`0.01) The most consistent change in fatty acid pro®le of triacylglycerol, phospholipid and cholesterol ester on the walnut diet was a signi®cant (P`0.01) increase in linoleic acid. Triacylglycerol linolenate also increased signi®cantly (P`0.01). Total and LDL cholesterol were lower on both experimental diets than at baseline, 0.25 mmolal and 0.36 mmolal respectively on the walnut diet and 0.13 mmolal and 0.20 mmolal respectively on the low fat diet. High density lipoprotein cholesterol was higher on both the walnut and low fat diets when compared to baseline (0.15 mmolal and 0.12 mmolal, respectively). When comparing the walnut and low fat diets only apo B was signi®cantly lower (P`0.05) on the walnut diet. Conclusions: Despite an unintended increase in the total fat intake on the walnut diet, fatty acid pro®le of the major lipid fractions showed changes which might be expected to reduce risk of cardiovascular disease. The reduction of apolipoprotein B suggests a reduction in lipoprotein mediated risk, the relatively low myristic acid content of both diets perhaps explaining the absence of more extensive differences in lipoprotein levels on the two diets.

These data suggest that cholesterol synthesis is lower during diets rich in coconut fat and safflower oil compared with diets rich in butter and might be associated with lower production rates of apoB-containing lipoproteins.

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