Affective disorders, including depression, mood and schizoaffective and anxiety episodes and inflammatory conditions present close associations with both behavioral and biological contiguity with possible reciprocal determination of each other in a bidirectional loop. Depressive states facilitate inflammatory reactions whereas inflammatory conditions promote depressive onset and continuance together other neuropsychiatric affective features. Patients presenting affective disorders demonstrate all the cardinal features of inflammation, such as increased circulating levels of inflammatory inducers, activated sensors, and inflammatory mediators targeting a plethora of brain and CNS and other tissues throughout the body of the afflicted individual. It is becoming increasingly evident that the etiopathophysiology and the clinical debut and progression of these disorders are promoted by a range of inflammatory processes originating both intrinsically and extrinsically. Notably, pro-inflammatory cytokines modulate mood behavior, motivation, cognitive functioning and somatic integrity through the reduction of brain monoamine and metabolic levels, the activation neuroendocrine responses, promotion excitotoxicity (increased glutamate levels), and the impairment of brain plasticity and memory. In this context, the contributions of early-life adversity and stress trauma seem to produce the underpinnings of epigenetic misadventure than maintain the dispositions of illhealth and negative prognoses. Under a variety of circumstance, physical exercise, by itself or combined with dietary implementation, has provided substantial levels of amelioration of the affective detriments.
Prof. Dr. Trevor Archer
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