Aging is accompanied by a gradual decline in core body temperature, a phenomenon consistently observed across populations but most often interpreted as a passive marker of metabolic slowdown. In this article, we propose a complementary perspective: that age-related cooling is not only a consequence of aging but may also act as an active contributor to structural tissue changes that further accelerate physiological decline. We review evidence showing that older adults exhibit reduced metabolic heat production, impaired thermoregulatory control, thinning of the skin, and loss of subcutaneous adipose tissue with concurrent redistribution of fat toward visceral depots. We integrate these findings into a novel conceptual framework in which declining body temperature promotes skin thinning and subcutaneous fat loss through reduced tissue perfusion, slowed cellular and enzymatic activity, altered hormonal signaling, and impaired regenerative capacity. These tissue changes, in turn, increase heat loss, establishing a self-reinforcing feedback loop that amplifies thermal instability and systemic aging. We further discuss the physiological consequences of increased heat loss in later life, including slowed metabolism, impaired immune function, hormonal dysregulation, and increased frailty. Importantly, we distinguish pathological age-related heat loss from adaptive, regulated reductions in body temperature observed in longevity-promoting contexts such as caloric restriction, highlighting the role of thermal control versus uncontrolled thermal leakage. Finally, we outline testable predictions and experimental approaches—ranging from longitudinal human studies and thermal interventions to animal and cellular models—that could validate or refute this hypothesis. By reframing aging as a progressive loss of thermal integrity, this work suggests that maintaining stable tissue temperature and minimizing chronic heat loss may represent an underexplored avenue for preserving tissue function and healthspan in aging populations.