Gender differences and environmental inputs
In the comments section of my first post, commenter JB remarks
It is hard to fathom that well-to-do black women neglect to take doctor-recommended prenatal vitamins (which include magnesium). And that’s when vitamins are most important, no?
To which I reply:
I’d be willing to accept that genetic differences related to biochemical processing may also potentiate any environmental affects related to vitamin processing and blood-lead levels. Perhaps blacks simply have more difficulty utilizing vitamins and maintaining them in their bloodstream or removing toxins like lead for that matter?
My overall premise is that: Different groups may be more sensitive to certain environmental inputs than others.
While sex differences are more pronounced than racial differences, below I show a study on the effects of “social stressors” on pubertal and adult mice. Female mice exposed to pubertal or adult stress show significantly more sensitivity to amphetamines and nicotine, while males did not:
The present findings indicate that chronic social stressors alter HPA stress responses and locomotor responses to psychostimulants in females, and not in males, depending upon the age at which the animals underwent the social stressors procedure: Females stressed in adolescence showed enhanced behavioral sensitivity amphetamine, and females stressed in adulthood showed heightened corticosterone release in response to a new stressor.
[McCormick CM, Robarts D, Kopeikina K, et al. Long-lasting, sex- and age-specific effects of social stressors on corticosterone responses to restraint and on locomotor responses to psychostimulants in rats. Horm Behav. 2005;48:64-74.]
Human studies also show females are very negatively affected by stress in ways that males are not. This has societal implications as females will very soon outnumber males among medical school matriculates.
In contrast, prenatal exposure to nicotine appears to affect the blood pressure of male mice, but not female mice:
Prenatal nicotine had no effect on baseline BP but significantly increased Ang II–stimulated BP in male but not female offspring. The baroreflex sensitivity was significantly decreased in both male and female offspring. Prenatal nicotine significantly increased arterial media thickness in male but not female offspring. In male offspring, nicotine exposure significantly increased Ang II–induced contractions of aortas and mesenteric arteries. These responses were not affected by inhibition of endothelial NO synthase activity.
[Xiao D, Xu Z, Huang X, et al. Prenatal gender-related nicotine exposure increases blood pressure response to angiotensin II in adult offspring. Hypertension. 2008;51:1239-47.]