Miller Richard A
University of Michigan, USA.
Milbank Q. 2002;80(1):155-74. doi: 10.1111/1468-0009.00006.
Aging can be slowed in laboratory rodents by low-calorie diets, and changes in single genes can extend mouse life span by 40 percent or more. Therefore, despite its surface complexity and effects on multiple cells and intercellular systems, aging in mammals might also be retarded by both genetic and nongenetic means. If human aging could be slowed pharmacologically to the extent now possible in rodents, the effect on healthy life expectancy would exceed that of abolishing cancer, cardiovascular disease, and adult-onset diabetes. Why, then, is research on the biological control of aging and longevity poorly funded and shunned by both most scientists and those setting national research priorities? Economic disincentives, disease-specific lobby groups, scientific careerism, and ineffective nostrums, together with gerontologiphobia, must be overcome before such research can improve public health.
在实验室啮齿动物中，低热量饮食可以减缓衰老，单个基因的改变能使小鼠寿命延长40%或更多。因此，尽管衰老表面上很复杂，且会对多种细胞和细胞间系统产生影响，但哺乳动物的衰老或许也能通过基因和非基因手段得到延缓。如果人类衰老能够在药理学上减缓到目前啮齿动物所能达到的程度，那么对健康预期寿命的影响将超过消除癌症、心血管疾病和成年型糖尿病的影响。那么，为什么衰老和长寿的生物控制研究资金匮乏，且遭到大多数科学家以及那些设定国家研究重点的人的回避呢？在这类研究能够改善公众健康之前，必须克服经济上的不利因素、特定疾病的游说团体、科研功利主义、无效的疗法以及对老年医学的恐惧。
