In this review, the effects of cannabinoids in the regulation of the following endocrine systems are discussed: the hypothalamic-pituitary-gonadal axis and hypothalamic-pituitary-adrenal cortex axis. Cannabis users have reduced levels of gonadotropins, reduced prolactin and growth hormone. Cannabis affects corticotropin-releasing hormone-, thyrotropin-releasing hormone-, vasopressin-, and oxytocin-expressing neurons. Therefore, our findings reveal a mechanism of rapid glucocorticoid feedback inhibition of hypothalamic hormone secretion via endocannabinoid release in the paraventricular nucleus of the hypothalamus and provide a link between the actions of glucocorticoids and cannabinoids in the hypothalamus that regulate stress and energy homeostasis. Glucocorticoid negative feedback in the brain controls stress, feeding, and neural-immune interactions by regulating the hypothalamic-pituitary-adrenal axis. Cannabis increases dopamine which decreases prolactin. Cannabis decreases oxytocin, thyroid hormone and growth hormone, and disrupts the hypothalamic-pituitary-adrenal axis. Cannabinoids suppress fertility via reducing hypothalamic gonadotropin- releasing hormone output. γ-Aminobutyric acid (GABA)(A) receptor (GABA(A)-R)-mediated transmission is a major input to gonadotropin releasing hormone cells that can be excitatory. Cannabinoids act via inhibiting GABAergic input. Cannabis disregulates the hypothalamic-pituitary-adrenal axis circadian rhythm. Cannabis decreases serum concentrations of pituitary gonadotropins. Cannabis raises cortisol and ACTH which increases cortisol which uses up progesterone reducing testosterone and estrogen. Cannabis lowers testosterone in men by inhibiting testosterone secretion and impairs fertility in males through alteration in the testicular endocannabinoid system. Cannabis suppresses copulatory behavior even when testosterone levels are maintained. It decreases sperm concentration, causes defective sperm function or alteration of sperm morphology. Endocannabinoids control male reproduction acting at central and local level via cannabinoid receptors. The cannabinoid receptor CB1 has been characterized in the testis, in somatic and germ cells of mammalian and non-mammalian animal models, and its activity related to Leydig cell differentiation, steroidogenesis, spermiogenesis, sperm quality, and maturation. Testicular degeneration and necrosis is induced by chronic administration of cannabis. In both ovulating and menopausal women, cannabis can alter pituitary gonadotropin release and alter metabolism or target tissue response to gonadal steroids, leading to reduced estrogen and progesterone production and anovulatory menstrual cycles. Cannabis presents abnormal longer ovulatory cycle lengths in females. Cannabis suppresses luteinizing hormone when sex hormones are initially high, but, chronic cannabis lowers progesterone and testosterone in men, and lowers estrogen and progesterone in women, so luteinizing hormone significantly increases which raises night time core temperature for disrupted sleep. Cannabis increases hypothalamic nitric oxide which inhibits oxytocin. Cannabis is detrimental for lactating moms. Cannabis decreases maternal care, decreases aggressive instinctual behaviors for protection of young, suppresses maternal anxiolysis, decreases plasma oxytocin levels and milk consumption and decreases activation of oxytocinergic neurons in hypothalamic nuclei. Changes in the behavioral responses of lactating mothers treated with cannabis can be related to disruption in the neuroendocrine control of oxytocin secretion. Cannabis causes impairment of glucocorticoid feedback which either enhances or decreases performance on various tasks. Cannibis can cause a decrease in thyroid which negatively affects cerebellar development and motor performance involved in adult brain function. It induces consistent behavioral changes in adults, leading to severe anxiety and morphological changes in the hippocampus, however, it shows improvements for schizophrenia: improvement in cognitive function and reduction of antipsychotic-side. Cannabis and Δ(9) -THC are anticonvulsant in most animal models but can be proconvulsant in some healthy animals. The simultaneous rapid stimulation of nitric oxide and endocannabinoid synthesis by glucocorticoids has important implications for the impact of stress on the brain as well as on neural-immune interactions in the hypothalamus. Cannabis has implications for psychosis. There are blunted psychotomimetic and amnestic effects with cannabis. Lithium increases oxytocin and helps in cannabis withdrawal, and pregnenolone/progesterone help in cannabis withdrawal as estrogen generally increases and progesterone decreases sensitivity to marijuana.
CBD does not appear to have any psychotropic ("high") effects such as those caused by ∆9-THC in marijuana, but may have anti-anxiety and anti-psychotic effects. As the legal landscape and understanding about the differences in medical cannabinoids unfolds, it will be increasingly important to distinguish "medical marijuana" (with varying degrees of psychotropic effects and deficits in executive function) – from "medical CBD therapies” which would commonly present as having a reduced or non-psychoactive side effect profile.
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