Scheme of the hypothesis integrating the circadian control, brown adipose tissue activity, and mood. Rapid changes in ambient temperature (cold nights, warm days) which are typical at temperate latitudes during the late-spring activate brown adipose tissue, once being activated it will not cool down easily and remains therefore prone to over-activation. Because of a genetic effect (CRY2 gene mutations or common variants which compromise the function of CRY2 proteins) or abnormalities in the post-translational control of CRY2, brown adipose tissue is over-activated easily. It is currently not known, whether this kind of over-activation of brown adipose tissue, hypothesized to lead to the increased cold tolerance but to cause defect in tolerance to heat, characterizes mood disorders and anxiety disorders, and whether it contributes to the seasonal peaks in their occurrence and mortality rates for deaths from suicide, but it needs to be tested against experiments and observations.