Does photoperiodism involve a seasonal and non-pathological Warburg effect?

The precise means whereby mammals recognize and respond to changing day length so as to adjust their physiology to the seasons (photoperiodism) remains enigmatic. We present a new hypothesis according to which aerobic glycolysis (AG) within selected astrocytic syncytia plays a central role in photoperiodism. We focus on the response of the mammal breeding in longer days (LD) to the shorter days (SD) of autumn. It is posited that AG in the brain of the SD organism is activated within a specified circuitry and temporal window. The circuitry involves regions targeted by the medullary norepinephrine (NE) system including but not limited to the anterior bed nucleus of the stria terminalis; the temporal window in question is defined by the autumnal extension of darkness into a segment of the organism's circadian activity cycle that was illuminated on the previous day. Lactate generated from glucose during SD serves primarily as a signaling entity as opposed to a fuel, instructing astrocytes, for example, gradually to replace the LD genome with one specific to SD. The requirement to provision glucose to the brain for AG through SD accounts for the frequent findings of mild autumnal hyperglycemia and elevated carbohydrate appetite across many different mammalian species including human beings. So long as the sidereal environment enveloping life on earth featured its extraordinarily predictable pattern of photoperiodic change, the dangers of exposing the organism to augmented glucose and lactate within a strictly delimited window were easily outweighed by the benefits of a precision mechanism ensuring the alignment of the animal's reproductive cycle with the seasonal one. With "light pollution," that delicate balance may now be at risk.