ABSTRACT
The hypothesis put forward here attempts to explain how the efficacy of venlafaxine against climacteric symptoms, including sweating, can be reconciled with the fact that this medication is known to cause sweating as an adverse side-effect. Peripherally, the sweating function is regulated noradrenergically by the sympathetic nervous system, central noradrenergic signal transmission being subject partly to inhibitory, partly to excitatory influences by serotonin (5-HT). Theoretically, sweating can be both initiated and inhibited by the activity of selective 5-HT reuptake inhibitors (SSRIs), so that the noradrenergic "tone" resulting from the interaction of noradrenergic and serotonergic neurons in the various regions of the brain probably determines the degree of sweating. Venlafaxine can counteract sweating at low doses as a result of its serotonergic effect, while it can increase sweating at higher doses with an increasing noradrenergic active component. At daily doses of up to 75 mg venlafaxine, sweating is largely avoided as a concomitant effect.
Subject(s)
Cyclohexanols/therapeutic use , Selective Serotonin Reuptake Inhibitors/therapeutic use , Sweat , Humans , Models, Biological , Models, Theoretical , Norepinephrine/metabolism , Serotonin/metabolism , Sympathetic Nervous System/drug effects , Synaptic Transmission/drug effects , Venlafaxine HydrochlorideABSTRACT
Elevated plasma homocysteine levels have been found in different psychiatric disorders, including major depression and eating disorders. The aim of the present study was to evaluate whether presence of depression or depressive symptoms is associated with elevated homocysteine levels in patients with eating disorders. Total plasma homocysteine levels were assessed in 44 females with anorexia nervosa (n = 21) or bulimia nervosa (n = 23). Comorbid major depressive disorder (MDD) was diagnosed according to DSM-IV criteria using a semi-structured interview (SCID-I). Furthermore, depressive symptoms were assessed using Beck's depression inventory (BDI). Presence of MDD was not associated with elevated homocysteine levels (t-test: T = 0.42; df = 42; P = 0.68). However, self-rated presence of clinically relevant depressive symptoms (BDI score18) was associated with elevated homocysteine (T = -2.8; df = 42; P = 0.008). Presence of depressive symptoms may explain elevated homocysteine levels previously reported in patients with eating disorders or vice versa. Longitudinal studies are needed to unravel this hen or egg problem.
