Published by Medical Hypotheses 2006
Reser, J. 2006. Evolutionary Neuropathology and Congenital Mental Retardation: Environmental cues predictive of maternal deprivation influence the fetus to minimize cerebral metabolism in order to express bioenergetic thrift. Medical Hypotheses, Volume 67, Issue 3, 529-544.
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.