Pathogens may have assisted the evolution of endothermy by restricting its reversibility

Endothermy is an important trait in the biology of several (extant and extinct) groups of amniotes. Despite its distinct benefits, it is an extremely expensive trait, and the drivers for its emergence and evolutionary success are debated. I offer a hypothesis complementary to current theories, linking endotherms' capacity for thermogenesis with the need to increase body temperature during pathogen infection ("fever", present in both endotherms and ectotherms). I do not propose this as a primary driver of endothermy; rather, the emergence of efficient fever prevented the secondary loss of endothermy. After endothermy has evolved in a given lineage, the stabler host temperature, coupled with higher direct transmission due to incubation and parental care, would lead to the propagation and specialization of pathogens in the population. Hence, although ectothermy carries no inherent disadvantage, reverting from endothermy to ectothermy faces the obstacle of an already-high pathogen load. Reduced heat production would increase the gap from normal to fever temperature, impairing the reliability of the response and increasing its cost, when pathogen load in the population is already higher and more specialized as enabled by endothermy. This factor may be enough to outweigh selective pressures against the energetic cost of endothermy. This hypothesis, though anecdotally supported by the intriguing fact that endothermy is very rarely lost (and is often retained even when homeothermy is not), is merely a conceptual framework and must be tested further.