The measurable physiological and psychological outcomes resulting from specific hormones and neurosteroids that serve to reduce anxiety and promote a state of calm. These effects are mediated through direct interaction with neurotransmitter systems in the brain, particularly those regulating emotional processing and stress reactivity. Understanding these effects is paramount for clinically addressing mood disorders rooted in endocrine imbalances.
Origin
This term is a fusion of ‘Anxiolytic,’ derived from the Greek words ‘anxio’ (anxiety) and ‘lysis’ (to loosen or dissolve), and ‘Hormone Effects,’ denoting the action of endocrine signaling molecules. The clinical recognition of sex and adrenal steroids influencing anxiety predates modern endocrinology. The precise molecular understanding of this interaction is a contemporary development.
Mechanism
Key hormones like allopregnanolone and dehydroepiandrosterone (DHEA) sulfate exert their anxiolytic action by enhancing the inhibitory function of Gamma-Aminobutyric Acid (GABA) receptors. This augmentation hyperpolarizes neurons, decreasing overall neural excitability in regions like the amygdala, which processes fear and stress. Proper hormonal balance supports this natural dampening mechanism, promoting resilience against psychological stressors.
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