Human Nutrition Research Centre, Centre for Brain Ageing and Vitality, Institute for Ageing and Health, Newcastle University, Campus for Ageing and Vitality, Newcastle upon Tyne NE4 5PL, UK.
Proc Nutr Soc. 2013 May;72(2):246-50. doi: 10.1017/S0029665112003023. Epub 2013 Jan 14.
Over the past two centuries human life expectancy has increased by nearly 50 years. Genetic factors account for about one-third of the variation in life expectancy so that most of the inter-individual variation in lifespan is explained by stochastic and environmental factors, including diet. In some model organisms, dietary (energy) restriction is a potent, and highly reproducible, means of increasing lifespan and of reducing the risk of age-related dysfunction although whether this strategy is effective in human subjects is unknown. This is ample evidence that the ageing process is plastic and research demonstrates that ageing is driven by the accumulation of molecular damage, which causes the changes in cell and tissue function that characterise the ageing phenotype. This cellular, tissue and organ damage results in the development of age-related frailty, disabilities and diseases. There are compelling observational data showing links between eating patterns, e.g., the Mediterranean dietary pattern, and ageing. In contrast, there is little empirical evidence that dietary changes can prolong healthy lifespan and there is even less information about the intervention modalities that can produce such sustainable dietary behaviour changes. In conclusion, current research needs include (1) a better understanding of the causal biological pathways linking diet with the ageing trajectory, (2) the development of lifestyle-based interventions, including dietary changes, which are effective in preventing age-related disease and disability and (3) the development of robust markers of healthy ageing, which can be used as surrogate outcome measures in the development and testing of dietary interventions designed to enhance health and well-being long into old age.
在过去的两个世纪中,人类的预期寿命增加了近 50 年。遗传因素约占预期寿命变化的三分之一,因此,寿命的个体间大部分差异是由随机因素和环境因素(包括饮食)解释的。在一些模式生物中,饮食(能量)限制是一种增强寿命和降低与年龄相关的功能障碍风险的有效且高度可重复的方法,尽管这种策略在人类中的有效性尚不清楚。这充分证明了衰老过程是具有可塑性的,研究表明,衰老受分子损伤的积累所驱动,这些损伤会导致细胞和组织功能的变化,从而形成衰老表型。这种细胞、组织和器官的损伤导致与年龄相关的虚弱、残疾和疾病的发展。有令人信服的观察性数据表明,饮食模式(例如地中海饮食模式)与衰老之间存在联系。相比之下,几乎没有经验证据表明饮食变化可以延长健康寿命,甚至更少的信息表明可以采取哪些干预方式来产生这种可持续的饮食行为改变。总之,目前的研究需求包括:(1)更好地理解饮食与衰老轨迹之间的因果生物学途径;(2)制定基于生活方式的干预措施,包括饮食变化,以有效预防与年龄相关的疾病和残疾;(3)开发健康衰老的稳健标志物,可作为开发和测试旨在增强健康和幸福感的饮食干预措施的替代终点。