Chronic exposure to addictive drugs in substance use disorders and stressors in mood disorders render the brain more vulnerable to inflammation. Inflammation in the brain, or neuroinflammation, is characterized by gliosis, microglial activation, and sustained release of cytokines, chemokines, and pro-inflammatory factors compromising the permeability of the blood-brain barrier. There is increased curiosity in understanding how substance misuse and/or repeated stress exposure affect inflammation and contribute to abnormal neuronal activity, altered neuroplasticity, and impaired cognitive control, which eventually promote compulsive drug-use behaviors and worsen mood disorders. This review will emphasize human imaging studies to explore the link between brain function and peripheral markers of inflammation in substance use disorders and mood disorders.

Whilst it is well recognized that progesterone is involved in the elevation of body temperature following ovulation, the mechanism for this process has not been determined. In this study 87 patients undergoing in-vitro fertilization recorded their basal body temperature during one treatment cycle. Exogenous gonadotrophin therapy administered to induce multiple folliculogenesis considerably elevated periovulatory oestrogen levels and early luteal phase progesterone. Body temperature rapidly rose to plateau 48 h after follicular aspiration in all patients. The amplitude of the temperature rise was independent of the progesterone concentration and the type of hormonal stimulation. There was no correlation between the degree of elevation of progesterone and the amplitude of the rise in body temperature over the first 4 days of the luteal phase. It is postulated that serum progesterone levels do not directly control body temperature, but that an oestrogen-progesterone synergism may be involved.

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