On the basis of this PoOO hypothesis, we suggest that male experimental animals exposed to dioxin, when mated with unexposed females, will experience early loss of male-biased conceptuses, resulting in a reduced number of progeny that are female-biased.
We hypothesize that the intricate connections between equal gender proportions and optimal conceptions at the core of the fertile window of the menstrual cycle and between disproportionate rates of male-biased and pathologic conceptuses outside of it are due to periovulatory hormone modulation, which simultaneously affects cervical liquefaction and oocyte maturation (8,9).
We hypothesize that determination of both male sex and pathology of the progeny by PrOO will initially cause a positive male-biased dose response, which, after having reached a threshold, will be followed by a negative one due to disproportional loss of male-specific conceptuses and sublethal X-linked genes (21).
Male-biased loss of pathologic conceptuses entails reversal of the secondary sex ratio (SSR) at birth; male-biased loss of children and adults affects the decline of the tertiary sex ratio during life, causing the increasing "gender gap.
The intricate connections between either equal proportions of each sex and optimal conceptions at the core of the fertile window of the menstrual cycle, or between disproportionate rates of male-biased and pathologic conceptuses outside of this window are due to periovulatory hormone variation, which simultaneously modulates cervical liquefaction and oocyte maturation.