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Dopaminergic pathways are similarly affected, with reduced tyrosine hydroxylase activity leading to diminished dopamine in the basal ganglia and prefrontal cortex, manifesting as anhedonia, reduced motivation, and psychomotor retardation (73, 74)

evidence largely from GH-deficient populations but physiologically plausible in somatopause A note on evidence grading: most CJC-1295 human data comes from short-term pharmacokinetic trials rather than long-term outcome studies

No statistical method was used to calculate sample size in animal experiments

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