This article will propose that humans have an adaptive vulnerability to certain forms of mental retardation, specifically, neuropathological disorders that cause decreased energy expenditure in the hippocampus and the cerebral cortex. This hypothesis will be analyzed in terms of the thrifty phenotype paradigm according to which adverse prenatal events can cause differential gene expression resulting in a phenotype that is better suited, metabolically, for a deprived environment. For example, a malnourished mother has an increased propensity to give birth to offspring that feature a "thrifty phenotype" which permits highly efficient calorie utilization, increased fat deposition and a sedentary nature. This article interprets several prenatal occurrences, including maternal malnourishment, low birth weight, multiparity, short birth interval, advanced maternal age and maternal stress--which are currently identified by the epidemiological literature as risk factors for neuropathology--to be environmental cues that communicate to the fetus that, because it will be neglected of maternal investment, developing a metabolically conservative brain will be the most effective ecological strategy. Success in hunting and foraging in mammals, primates and especially humans is known to be dependent on prolonged maternal investment. Low levels of maternal care are known to result in low survivorship of offspring, largely because the offspring are forced to subsist using simple, low-yield foraging strategies. A predictive, adaptive response, marked by cerebral hypometabolism, may produce a level of metabolic conservancy that mitigates the risks associated with low levels of maternal care. This article will suggest that certain, human neuropathological phenotypes would have been well suited for an ecological niche that closely resembled the less skill-intensive niche of our less encephalized, primate ancestors. The forms of congenital neuropathology discussed in this article do not cause damage to vital homeostatic systems; most simply decrease the size and energy expenditure of the cerebral cortex and the hippocampus, the two structures known to show plasticity during changes in ecological rigor in vertebrates. Also, many disorders that present comorbidly with neuropathology, such as tendency toward obesity, decrement in anabolic hormones, hypotonic musculature, up-regulation of the hypothalamic-pituitary-adrenal axis, and decreased thyroid output are associated with energy conservancy and the thrifty phenotype, further implicating neuropathology in an ecological strategy. Determining the relative impact of evolutionary causation on neuropathological disease should prove informative for medical and gene therapeutic treatment modalities. Furthermore, use of the maternal deprivation paradigm presented here may help researchers more precisely identify the risk factors that determine cognitive trajectory.

译文

:本文将建议人类对某些形式的智力低下,特别是导致海马和大脑皮层能量消耗减少的神经病理性疾病具有适应性脆弱性。将根据节俭的表型范式分析该假设,根据该节制,产前不良事件可引起差异基因表达,从而导致表型在代谢上更适合于缺乏的环境。例如,营养不良的母亲生育后代的倾向增加,其后代具有“节俭表型”,可以高效利用热量,增加脂肪沉积和久坐。本文解释了几种产前事件,包括孕产妇营养不良,低出生体重,多胎性,出生间隔短,产妇高龄和产妇压力-这些在流行病学文献中目前被确定为神经病理学的危险因素-是可以传达信息的环境提示对胎儿而言,开发新陈代谢的保守大脑将是最有效的生态策略,因为它将被忽略对母亲的投资。已知在哺乳动物,灵长类动物尤其是人类中成功进行狩猎和觅食取决于长期的母体投资。众所周知,低水平的产妇护理会导致后代的存活率较低,这在很大程度上是因为使用简单,低产的觅食策略迫使后代生存。以脑代谢不足为特征的预测性,适应性反应可能会产生一定程度的代谢保守性,从而减轻与低水平孕产妇保健相关的风险。本文将建议某些人类神经病理学表型非常适合于生态位,该位生态位与我们脑部较少的灵长类祖先的技术强度较低的位十分相似。本文讨论的先天性神经病理学形式不会对重要的稳态系统造成损害;最简单的方法是减少大脑皮层和海马体的大小和能量消耗,这两个结构在脊椎动物的生态严谨性变化过程中表现出可塑性。同样,许多与神经病理学同时出现的疾病,例如肥胖倾向,合成代谢激素的减少,低渗性肌肉组织,下丘脑-垂体-肾上腺轴的上调以及甲状腺输出的减少,都与能量守恒和节俭的表型有关,进一步将神经病理学牵涉到生态策略中。确定进化因果关系对神经病理学疾病的相对影响,应为医学和基因治疗方法提供参考。此外,此处介绍的孕产剥夺范式的使用可能有助于研究人员更准确地确定决定认知轨迹的风险因素。

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