Based on early-20th century births (before electric illumination), studies of schizophrenia (SCZ) found a disease-incidence excess among people born around late-Feb and an equally significant deficit among those born six-months later around late-Aug. In pursuit of this phenomenon, we previously found the same birth seasonality in 1) failures of neural-tube closure (NTDs), 2) cerebral laterality deficits (CADs) (from studies of month-of-birth and hand or visual-field preferences among professional baseball players), 3) creativity (from studies of pre-modern American visual, performing and literary artists) and 4) mathematical gift (from studies of American and earlier European scientists). Given that SCZ, creativity and mathematical gift were all three found associated with reduced left-hemisphere dominance, the findings suggested CADs as a single, primary effect. Left-right brain differentiation occurs in the neurulating, early-fourth-week embryo concomitantly with and via similar cellular processes as those responsible for neural-tube closure. Those stages are sharply coincident with the summer-solstice in late-Feb borns and the winter-solstice in late-Aug borns. This suggested a “solstitial hypothesis” that, based on an earlier “premature-differentiation” hypothesis of NTDs, implicated pro-oxidant sunlight actions on the maternal blood. At the summer-solstice, a pro-oxidant peak of the maternal blood would prematurely trigger the all-important and free-radical dependent (see later) embryonic switch from cellular proliferation to differentiation. This would curtail a narrow time-window during which the left cerebral hemisphere normally grows more cells that the right hemisphere. The opposite of this would occur at the winter-solstice. An analogous, free-radical based hypothesis would also explain a more recently found set of seasonalities involving Nov-vs-May birthrate peaks and early-fifth-month fetal stages of male-female differentiation. Maternal oxidant stress would again be involved here given that sexually-dimorphic neurogenesis is critically dependent on apoptotic cell death, a switch that, like the proliferationàdifferentiation switch, is also triggered by a sudden drop in the cellular redox potential.