Critical periods in human growth and their relationship to diseases of aging
Critical periods in human growth and their relationship to diseases of aging
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DOI：
10.1002/ajpa.10183
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发表时间：
2002-01-01
期刊：
影响因子：
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通讯作者：
Demerath, EW
中科院分区：
文献类型：
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作者：
Cameron, N;Demerath, EW
长期以来，人们已经认识到，在哺乳动物发育过程中存在“关键时期”，此时需要暴露于特定的环境刺激，以引起特定解剖结构的正常发育或其正常功能。生物体对这些刺激的反应取决于解剖成熟的特定水平和快速解剖和/或功能变化的状态。对生长关键期的讨论并不局限于狭义的发展时间框架的经典定义，在这一定义中，必须存在特定的环境阈值或限制，才能保证正常的生长和功能。使用生长学和流行病学的方法，我们提出了一个寿命的角度来看，其中包括积累和相互作用的风险，从产前生活中表现出来。通过了解生长和发育的过程，并通过仔细观察生长过程，可以识别导致后期疾病的早期变异。在这里，我们回顾了大量的证据表明，在成长过程中的暴露，后来的发病率和死亡率。胎儿似乎响应侮辱在产前期间通过“编程”的过程中，这有短期的生存优势，但可能有一个长期的缺点，因为它与心血管疾病，高血压，II型糖尿病，和后来的肥胖。出生体重低加上婴儿期出生后快速生长似乎也与儿童期和成人期葡萄糖耐量和肥胖症后遗症有关。与出生体重无关，儿童中期肥胖反弹的时间也预示着以后的肥胖。青少年生长和成熟的时间、幅度和持续时间与关键的身体组成变化相关，包括身体脂肪和骨矿化的正常获得。特别是，获得适当的峰值骨量对于确定骨质疏松症的后期风险至关重要。讨论了通过端粒磨损将早期生长变化与后期慢性疾病风险联系起来的假定因果机制。端粒DNA随每次细胞分裂的强制性丢失充当有丝分裂时钟，并标记细胞中的生长和修复过程的速率。虽然还需要更多的工作，但现有的研究支持这样一种观点，即端粒缩短不仅是细胞分裂的时钟，而且标志着相对生长速度，并通过其对细胞衰老的影响促进常见的衰老退行性过程。Yrbk Phys Anthropol 45：159-184，2002. (C)2002 Wiley-Liss，Inc.
It has long been recognized that there are "critical periods" during mammalian development when exposure to specific environmental stimuli are required in order to elicit the normal development of particular anatomical structures or their normal functioning. The responses of the organism to these stimuli depend on a specific level of anatomical maturation and a state of rapid anatomical and/or functional change. This discussion of critical periods in growth is not confined to the classic definition of a narrow time frame of development during which a particular environmental threshold or limit must exist for normal growth and function to ensue. Using both auxological and epidemiological approaches, we suggest a lifespan perspective which encompasses accumulating and interacting risks that are manifest from prenatal life onward. By understanding the process of growth and development, and by scrutinizing the growth process, early variations that lead to later disease can be identified. Here we review a significant amount of the evidence that links exposure during growth to later morbidity and mortality.The fetus appears to respond to insults during the prenatal period through the process of "programming," which has short-term survival advantages but may have a longterm disadvantage in that it is associated with cardiovascular disease, hypertension, type II diabetes, and later obesity. Low birth weight combined with rapid postnatal growth during infancy also appears to be associated, for instance, with later childhood and adult sequelae in terms of glucose tolerance and obesity. Independent of birth weight, the timing of adiposity rebound during mid-childhood also predicts later obesity. The timing, magnitude, and duration of adolescent growth and maturation are associated with critical body composition changes, including the normal acquisition of body fat and bone mineralization. In particular, the acquisition of appropriate peak bone mass is critical in determining the later risk of osteoporosis.A putative causal mechanism linking early growth variation to later chronic disease risk through telomeric attrition is discussed. The obligatory loss of telomeric DNA with each cell division serves as a mitotic clock and marks the rate of growth and repair processes in the cell. Although much more work is required, existing studies support the notion that telomere shortening is not only a clock of cellular division, but also marks relative growth rate, as well as contributing to common degenerative processes of aging through its impact on cellular senescence. Yrbk Phys Anthropol 45:159-184, 2002. (C) 2002 Wiley-Liss, Inc.