Diet and Healthy Aging

Max Planck Institute for Biology of Aging, Cologne, Germany.
New England Journal of Medicine (Impact Factor: 55.87). 12/2012; 367(26):2550-1. DOI: 10.1056/NEJMcibr1210447
Source: PubMed

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    • "However, another long-term study conducted by the National Institute of Aging (NIA) in caloricrestricted rhesus monkeys did not show an increase in lifespan (Mattison et al., 2012). This different outcome could be because in the NIA study, the control group food rations had a different dietary composition or because the control group was not fed ad libitum and as a consequence was also subjected to a minor form of caloric restriction (Partridge, 2012). This latter explanation is supported by the fact that the control monkeys in the NIA study weighted substantially less than the national average for body weight in the same age groups (Colman et al., 2014). "
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    ABSTRACT: Many diets and nutritional advice are circulating, often based on short- or medium-term clinical trials and primary outcomes, like changes in LDL cholesterol or weight. It remains difficult to assess which dietary interventions can be effective in the long term to reduce the risk of aging-related disease and increase the (healthy) lifespan. At the same time, the scientific discipline that studies the aging process has identified some important nutrient-sensing pathways that modulate the aging process, such as the mTOR and the insulin/insulin-like growth factor signaling pathway. A thorough understanding of the aging process can help assessing the efficacy of dietary interventions aimed at reducing the risk of aging-related diseases. To come to these insights, a synthesis of biogerontological, nutritional, and medical knowledge is needed, which can be framed in a new discipline called 'nutrigerontology'. © 2014 The Authors. Aging Cell published by the Anatomical Society and John Wiley & Sons Ltd.
    Full-text · Article · Dec 2014 · Aging cell
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    • "The evidence that CR is capable to extend lifespan in non-human primates was not confirmed in the National Institute of Aging study, which showed that old-onset CR was beneficial on several measures of metabolic health and overall function, and afforded protection against age-associated sarcopenia and neurodegeneration, but did not improve survival outcomes (Mattison et al., 2012; Cava and Fontana, 2013). Besides, the impact on human life span is difficult to study due to the scarce long-term compliance to CR (Roth and Polotsky, 2012; Niccoli and Partridge 2011; Partridge, 2012). Restriction of caloric intake is known to reduce blood sugar and insulin levels and to lower resistance to insulin of peripheral tissues. "
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    ABSTRACT: Adult tissue stem cells have the ability to adjust to environmental changes and affect also the proliferation of neighboring cells, with important consequences on tissue maintenance and regeneration. Stem cell renewal and proliferation is strongly regulated during aging of the organism. Caloric restriction is the most powerful anti-aging strategy conserved throughout evolution in the animal kingdom. Recent studies relate the properties of caloric restriction to its ability in reprogramming stem-like cell states and in prolonging the capacity of stem cells to self-renew, proliferate, differentiate, and replace cells in several adult tissues. However this general paradigm presents with exceptions. The scope of this review is to highlight how caloric restriction impacts on diverse stem cell compartments and, by doing so, might differentially delay aging in the tissues of lower and higher organisms.
    Full-text · Article · Nov 2013 · Experimental gerontology
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    • "Physical activity and nutritional habits are variables in lifestyle that decrease the incidence of some age-related diseases (Pekkanen et al., 1987; Blair et al., 1995), which have been positively associated with longevity. Also, in the last 80 years, caloric restriction (CR) has been demonstrated to increase the maximum life span in yeast, worms, flies, and rodents (Partridge, 2012). As previous studies in centenarians have shown (Tietz et al., 1992; Chan et al., 1999), overall liver function under normal physiological conditions is not dramatically impaired with aging. "
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    ABSTRACT: The liver is the only internal human organ capable of natural regeneration of lost tissue; as little as 25% of a liver can regenerate into a whole liver. The process of aging predisposes to hepatic functional and structural impairment and metabolic risk. Therefore, understanding how aging could affect the molecular pathology of liver diseases is particularly important, and few studies to date have tackled this complex process. The most common liver disease, affecting one third of the overall population, is non-alcoholic fatty liver disease (NAFLD), characterized by an intrahepatic accumulation of lipids. NAFLD can evolve into non-alcoholic steatohepatitis (NASH) in the presence of oxidative stress and inflammation. NASH is a serious risk factor for disabling and deadly liver diseases such as cirrhosis and hepatocellular carcinoma (HCC). Old age seems to favor NAFLD, NASH and ultimately HCC, in agreement with the inflamm-aging theory, according to which aging accrues inflammation. However, the incidence of HCC drops significantly in the very elderly (individuals aged more than 70) and the relationship between the progression of NAFLD/NASH/HCC and very old age is obscure. In this review, we discuss the literature and we argue that there might be an age window in which the liver becomes resistant to the development of injury; this needs to be studied to understand fully the interaction between age and liver diseases from a therapeutic perspective. This article is protected by copyright. All rights reserved.
    Full-text · Article · Jul 2013 · Aging cell
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