Sleep occurs in close relation to changes in body temperature. Both the monophasic sleep period in humans and the polyphasic sleep periods in rodents tend to be initiated when core body temperature is declining. This decline is mainly due to an increase in skin blood flow, and consequently skin warming and heat loss. We have proposed that these intrinsically occurring changes in core and skin temperature could modulate neuronal activity in sleep regulating brain areas (48). We here provide results compatible with this hypothesis. We obtained 144 sleep onset latencies (SOL) while directly manipulating core and skin temperatures within the comfortable range in 8 healthy subjects under controlled conditions. The induction of a proximal skin temperature difference of only 0.78±0.03°C (mean±s.e.m.) around a mean of 35.13±0.11°C changed SOL by 26% (3.09 (95% confidence interval [CI], 1.91 to 4.28) minutes around a mean of 11.85 minutes (CI, 9.74 to 14.41)), with faster sleep onsets when the proximal skin was warmed. The reduction in SOL occurred in spite of a small but significant decrease in subjective comfort during proximal skin warming. The induction of changes in core temperature (=0.20±0.02°C) and distal skin temperature (=0.74±0.05°C) were ineffective. Previous studies have demonstrated correlations between skin temperature and SOL. Also, sleep disruption by ambient temperatures that activate thermoregulatory defense mechanisms have been shown. The present study is the first to experimentally demonstrate a causal contribution to sleep onset latency of skin temperature manipulations within the range of its normal nocturnal fluctuations. Circadian and sleep-appetitive behavior induced variations in skin temperature might act as an input signal to sleep-regulating systems.