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SUBJECT: Special issue: Why we age! From nutrition investigator Roc

WHY WE AGE - Science 4 Dec 2015 special issue
Pg 1191 - Healthy Aging: Key questions for strategies to delay aging: 1)Is it relatively easy to implement? 2) Can it be effective when started in mid-life or later? 3) Do benefits outweigh the risks?

Box 1: Geroscience interventions with translational potential.
Dietary restriction: Dietary restriction (DR) is the most studied intervention for delaying aging (16). Although not universally effective, a majority of studies have documented significant increases in both life span and health span when DR is applied in laboratory models, including nonhuman primates (17). Limited studies also indicate important health benefits, including reversal of disease risk factors (16), in people who practice DR. Although DR is not a viable translational approach at the population level, research in this area has incited the search for alternative dietary modifications (e.g., low-protein diets) or small-molecule DR mimetics (e.g., mTOR inhibitors, see below) that can provide the health benefits of DR without requiring reduced food consumption.
Exercise: A large body of literature provides evidence that the health benefits of exercise are consistent with the enhancement of health span (1819). However, poor compliance, especially in the elderly population, makes this intervention challenging to apply. Thus, there is high interest in developing pharmacologic interventions that would synergize with lower levels of exercise.
mTOR inhibitors: Rapamycin extends life span and promotes health span in mice, as well as in simpler organisms. Treatment beginning late in life is sufficient to extend life span, reverse cardiac decline, and improve immune function in mice (20). A recent study also reported that a rapamycin derivative significantly boosts immune function in elderly people (10).
Metformin and acarbose: Metformin and acarbose are widely used antidiabetes drugs. Metformin improves health span in mice and may slightly extend life span (21), whereas acarbose markedly extends life span in male mice and modestly extends life span in female mice (22). In a nonrandomized retrospective analysis, diabetic patients taking metformin have reduced mortality compared with diabetic patients not receiving metformin, and they may live longer than nondiabetics not receiving metformin (23).
NAD precursors and sirtuin activators: As discussed by Verdin in a companion Review (24), nicotinamide adenine dinucleotide (NAD) precursors such as nicotinamide riboside and nicotinamide mononucleotide have been reported to improve health span in mouse models of muscle aging and cognitive decline. The mechanism of action is not clear, but it may involve activation of sirtuin NAD-dependent protein deacetylases, along with enhanced mitochondrial function (25). Other, possibly more specific, sirtuin activators also improve health span and slightly extend life span in mice (26).
Modifiers of senescence and telomere dysfunction: Senescent cells accumulate during aging and secrete factors that promote inflammation and cancer (27). As discussed in the companion Review by Blackburn et al. (28), telomere dysfunction is a major cause of cell senescence, and strategies to enhance telomerase function offer promise for improving health span (29), although the possibility of increased cancer risk must be addressed. Likewise, genetic and pharmacological strategies to target and kill senescent cells enhance both life span and markers of health in short-lived mice with high levels of senescent cells (3031).
Hormonal and circulating factors: Age-related changes in important hormones (including sex-steroids, growth hormone, and insulin-like growth factor 1) are well documented; however, the risks and benefits of hormone supplementation in aging remain largely controversial (32). As discussed in the companion Review by Goodell and Rando (33), heterochronic parabiosis experiments in which the circulatory system of an aged mouse is shared with that of a young mouse suggest that additional, more subtle humoral factors affect age-associated declines in several tissues, including the brain, muscle, liver, and heart (34). Some progress has been made toward defining these factors (35), and an effort is under way to determine whether transfusion of young plasma can delay Alzheimer’s disease (36).
Mitochondrial-targeted therapeutics: As discussed in the companion Review by Wang and Hekimi (37), mitochondrial dysfunction is a major contributor to aging and age-related diseases, although the mechanisms are more complex than initially suggested by the Harman’s free radical theory of aging (38). Attention is now being directed to interventions that augment mitochondrial function, energetics, and biogenesis, including mitochondrial-targeted antioxidants and NAD precursors (39).

SUMMARIES AND LINKS to J Nutrition Dec, 2015

Okay for infants to gain weight - Promotion of weight gain in children between 12.0–17.9 mo of age was not associated with higher metabolic risk 15 y later. On the contrary, there was some evidence of reduced metabolic risk in the intervention group.

Data have shown that healthy children and adolescents have an inadequate intake of zinc, an essential nutrient for growth. Our data suggest that 4 wk of zinc supplementation increases bone formation in premenarcheal girls.

Over one-half the adult US population consumes nutritional supplements, and over one-quarter consumes supplemental chromium. The odds of having Type 2 Diabetes were 27% lower in those who, in the previous 30 d, had consumed supplements containing chromium

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