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      The Role of Nutrients in Reducing the Risk for Noncommunicable Diseases during Aging

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          Abstract

          An increasing aging population worldwide accounts for a growing share of noncommunicable diseases (NCDs) of the overall social and economic burden. Dietary and nutritional approaches are of paramount importance in the management of NCDs. As a result, nutrition programs are increasingly integrated into public health policies. At present, programs aimed at reducing the burden of NCDs have focused mostly on the excess of unhealthy nutrient intakes whereas the importance of optimizing adequate essential and semi-essential nutrient intakes and nutrient-rich diets has received less attention. Surveys indicate that nutrient intakes of the aging population are insufficient to optimally support healthy aging. Vitamin and mineral deficiencies in older adults are related to increased risk of NCDs including fatigue, cardiovascular disease, and cognitive and neuromuscular function impairments. Reviewed literature demonstrates that improving intake for certain nutrients may be important in reducing progress of NCDs such as musculoskeletal disorders, dementia, loss of vision, and cardiometabolic diseases during aging. Current knowledge concerning improving individual nutrient intakes to reduce progression of chronic disease is still emerging with varying effect sizes and levels of evidence. Most pronounced benefits of nutrients were found in participants who had low nutrient intake or status at baseline or who had increased genetic and metabolic needs for that nutrient. Authorities should implement ways to optimize essential nutrient intake as an integral part of their strategies to address NCDs.

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          Most cited references 101

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          Vitamin B12, folic acid, and the nervous system.

          There are many reasons for reviewing the neurology of vitamin-B12 and folic-acid deficiencies together, including the intimate relation between the metabolism of the two vitamins, their morphologically indistinguishable megaloblastic anaemias, and their overlapping neuropsychiatric syndromes and neuropathology, including their related inborn errors of metabolism. Folates and vitamin B12 have fundamental roles in CNS function at all ages, especially the methionine-synthase mediated conversion of homocysteine to methionine, which is essential for nucleotide synthesis and genomic and non-genomic methylation. Folic acid and vitamin B12 may have roles in the prevention of disorders of CNS development, mood disorders, and dementias, including Alzheimer's disease and vascular dementia in elderly people.
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            Preventing Alzheimer's disease-related gray matter atrophy by B-vitamin treatment.

            Is it possible to prevent atrophy of key brain regions related to cognitive decline and Alzheimer's disease (AD)? One approach is to modify nongenetic risk factors, for instance by lowering elevated plasma homocysteine using B vitamins. In an initial, randomized controlled study on elderly subjects with increased dementia risk (mild cognitive impairment according to 2004 Petersen criteria), we showed that high-dose B-vitamin treatment (folic acid 0.8 mg, vitamin B6 20 mg, vitamin B12 0.5 mg) slowed shrinkage of the whole brain volume over 2 y. Here, we go further by demonstrating that B-vitamin treatment reduces, by as much as seven fold, the cerebral atrophy in those gray matter (GM) regions specifically vulnerable to the AD process, including the medial temporal lobe. In the placebo group, higher homocysteine levels at baseline are associated with faster GM atrophy, but this deleterious effect is largely prevented by B-vitamin treatment. We additionally show that the beneficial effect of B vitamins is confined to participants with high homocysteine (above the median, 11 µmol/L) and that, in these participants, a causal Bayesian network analysis indicates the following chain of events: B vitamins lower homocysteine, which directly leads to a decrease in GM atrophy, thereby slowing cognitive decline. Our results show that B-vitamin supplementation can slow the atrophy of specific brain regions that are a key component of the AD process and that are associated with cognitive decline. Further B-vitamin supplementation trials focusing on elderly subjets with high homocysteine levels are warranted to see if progression to dementia can be prevented.
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              Secondary analyses of the effects of lutein/zeaxanthin on age-related macular degeneration progression: AREDS2 report No. 3.

              The Age-Related Eye Disease Study (AREDS) formulation for the treatment of age-related macular degeneration (AMD) contains vitamin C, vitamin E, beta carotene, and zinc with copper. The Age-Related Eye Disease Study 2 (AREDS2) assessed the value of substituting lutein/zeaxanthin in the AREDS formulation because of the demonstrated risk for lung cancer from beta carotene in smokers and former smokers and because lutein and zeaxanthin are important components in the retina. To further examine the effect of lutein/zeaxanthin supplementation on progression to late AMD. The Age-Related Eye Disease Study 2 is a multicenter, double-masked randomized trial of 4203 participants, aged 50 to 85 years, at risk for developing late AMD; 66% of patients had bilateral large drusen and 34% had large drusen and late AMD in 1 eye. In addition to taking the original or a variation of the AREDS supplement, participants were randomly assigned in a factorial design to 1 of the following 4 groups: placebo; lutein/zeaxanthin, 10 mg/2 mg; omega-3 long-chain polyunsaturated fatty 3 acids, 1.0 g; or the combination. S Documented development of late AMD by central, masked grading of annual retinal photographs or by treatment history. RESULTS In exploratory analysis of lutein/zeaxanthin vs no lutein/zeaxanthin, the hazard ratio of the development of late AMD was 0.90 (95% CI, 0.82-0.99; P = .04). Exploratory analyses of direct comparison of lutein/zeaxanthin vs beta carotene showed hazard ratios of 0.82 (95% CI, 0.69-0.96; P = .02) for development of late AMD, 0.78 (95% CI, 0.64-0.94; P = .01) for development of neovascular AMD, and 0.94 (95% CI, 0.70-1.26; P = .67) for development of central geographic atrophy. In analyses restricted to eyes with bilateral large drusen at baseline, the direct comparison of lutein/zeaxanthin vs beta carotene showed hazard ratios of 0.76 (95% CI, 0.61-0.96; P = .02) for progression to late AMD, 0.65 (95% CI, 0.49-0.85; P = .002) for neovascular AMD, and 0.98 (95% CI, 0.69-1.39; P = .91) for central geographic atrophy. The totality of evidence on beneficial and adverse effects from AREDS2 and other studies suggests that lutein/zeaxanthin could be more appropriate than beta carotene in the AREDS-type supplements. clinicaltrials.gov Identifier: NCT00345176.
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                Author and article information

                Journal
                Nutrients
                Nutrients
                nutrients
                Nutrients
                MDPI
                2072-6643
                04 January 2019
                January 2019
                : 11
                : 1
                Affiliations
                [1 ]Nutrition Science & Advocacy, DSM Nutritional Products, CH-4303 Kaiseraugst, Switzerland; peter.van-dael@ 123456dsm.com
                [2 ]University Medical Center Groningen, 9713 GZ Groningen, The Netherlands; m.l.eggersdorfer@ 123456rug.nl
                Author notes
                [* ]Correspondence: maaike.bruins@ 123456dsm.com ; Tel.: +41-618-158-761
                Article
                nutrients-11-00085
                10.3390/nu11010085
                6356205
                30621135
                c75b591c-5398-4e09-ba3b-f474f7ef2163
                © 2019 by the authors.

                Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( http://creativecommons.org/licenses/by/4.0/).

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