长寿，先天还是后天，基因还是环境使然？

在各个不同年代，不同国家，不同地域，不同种族，都有长寿老人出现，不同的研究推断，分别从遗传基因，环境，气候，饮食，心理，健身，生活习惯等多个方面出发作出了不同的结论，您的ideal又怎样呢？

Longevity varies between and within species. The existence of species-specific limit to human life-span and its partial heritability indicate the existence of genetic factors that influence the ageing process. Insight into the nature of these genetic factors is provided by evolutionary studies, notably the disposable soma theory, which suggests a central role of energy metabolism in determining life-span. Energy is important in two ways. First, the disposable soma theory indicates that the optimum energy investment in cell maintenance and repair processes will be tuned through natural selection to provide adequate, but not excessive, protection against random molecular damages (e.g. to DNA, proteins). All that is required is that the organism remains in a sound condition through its natural expectation of life in the wild environment, where accidents are the predominant cause of mortality. Secondly, energy is implicated because of the intrinsic vulnerability of mitochondria to damage that may interfere with the normal supply of energy to the cell via the oxidative phosphorylation pathways. Oxidative phosphorylation produces ATP, and as a by-product also produces highly reactive oxygen radicals that can damage many cell structures, including the mitochondria themselves. Several lines of evidence link, on the one hand, oxidative damage to cell ageing, and on the other hand, energy-dependent antioxidant defences to the preservation of cellular homeostasis, and hence, longevity. Models of cellular ageing in vitro allow direct investigation of mechanisms, such as oxidative damage, that contribute to limiting human life-span. The genetic substratum of inter-individual differences in longevity may be unraveled by a two-pronged reverse genetics approach: sibling pair analysis applied to nonagenarian and centenarian siblings, combined with association studies of centenarians, may lead to the identification of genetic influences upon human longevity. These studies have become practicable thanks to recent progress in human genome mapping, especially to the development of microsatellite markers and the integration of genetic and physical maps.

Those amazing studies linking specific genes to obesity, long life and just about everything else may be wrong.

It was big news when ffice:smarttags" />laceName w:st="on">HarvardlaceName> laceName w:st="on">MedicallaceName> laceType w:st="on">SchoollaceType> researchers four years ago zeroed in on a region of the human genome linked to exceptional longevity. The Wall Street Journal did a front-page story; Good Morning America, CNN and NPR also covered it. Two years later the researchers pinpointed a gene in that region called MTP (for microsomal transfer protein) that boosted the odds of living to 100. The discovery was, it seemed, a giant step forward in understanding the genetic component of longevity.

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A follow-up publication last spring got no media coverage. In a study of 1,039 centenarians and 550 younger control-group patients, researchers at the University Hospital in Kiel, Germany found no link whatsoever between MTP and long life. The original correlation, they concluded, was likely "artifactual," due to ethnic differences that muddied the comparison. A Danish study also failed to confirm a link between MTP and longevity.