Libido and hormones.

Libido is the drive to have a sexual activity. Gonadal hormones play a major role in activating and maintaining libido in both men and women. Other hormones, though, interact with them in influencing sexuality, such as prolactin and also brain neurotransmitters. The role of hormones declines with age and sexuality becomes more mind-induced. Nevertheless, some aspects of sexuality remain linked to hormones. For example, a reduction of central arousability is typical of hypogonadal state. However, it is not clear at what level of androgen deficiency the loss of libido begins and if adequate external stimuli can overcome a partial deficiency.

Differential dynamic responses of luteinizing hormone to gonadotropin releasing hormone in patients affected by bulimia nervosa-purging versus non-purging type.

OBJECTIVE: Aim of the study was to investigate the presence of underlying abnormalities affecting the hypothalamus-pituitary-gonadal axis in 13 normal weight eumenhorreic bulimics as expressed by a different gonadotropin response to gonadotropin releasing hormone (GnRH), comparing patients with (n = 6) and without (n = 7) purging behaviours to controls (n = 5). METHOD: Subjects were administered an intravenous GnRH infusion for four hours, with an additional bolus at first and third hour. RESULTS: Non-purging bulimics showed a significantly reduced luteinizing hormone (LH) response to GnRH compared to controls; purging bulimics, following the second bolus, demonstrated a statistically reduced peak, in comparison to both controls and non-purging bulimics. DISCUSSION: even in the absence of overt menstrual disturbances, an altered LH secretion elicited by pulsatile stimulation of endogenous GnRH was found, with a more severe impairment in purging than in non-purging bulimics, possibly related to their greater psychopathological and physical burden.

Environmental and occupational exposure to benzene by analysis of breath and blood.

Benzene exposure of chemical workers was studied, during the entire workshift, by continuous monitoring of workplace benzene concentration, and 16 hours after the end of the workshift by the measurement of alveolar and blood benzene concentrations and excretion of urinary phenol. Exposure of hospital staff was studied by measuring benzene concentrations in the alveolar and blood samples collected during the hospital workshift. Instantaneous environmental air samples were also collected, at the moment of the biological sampling, for all the subjects tested. A group of 34 chemical workers showed an eight hour exposure to benzene, as a geometric mean, of 1.12 micrograms/l which corresponded, 16 hours after the end of the workshift, to a geometric mean benzene concentration of 70 ng/l in the alveolar air and 597 ng/l in the blood. Another group of 27 chemical workers (group A) turned out to be exposed to an indeterminable eight hour exposure to benzene that corresponded, the morning after, to a geometric mean benzene concentration of 28 ng/l in the alveolar air and 256 ng/l in the blood. The group of hospital staff (group B) had a benzene concentration of 14 ng/l in the alveolar air and 269 ng/l in the blood. Instantaneous environmental samples showed that in the infirmaries the geometric mean benzene concentration was 58 ng/l during the examination of the 34 chemical workers, 36 ng/l during the examination of the 27 chemical workers (group A), and 5 ng/l during the examination of the 19 subjects of the hospital staff (group B). Statistical analysis showed that the alveolar and blood benzene concentrations in the 34 workers exposed to 1.12 microgram/l of benzene differed significantly from those in groups A and B. It was found, moreover, that the alveolar and blood benzene concentrations were higher in the smokers in groups A and B but not in the smokers in the group of 34 chemical workers. The slope of the linear correlation between the alveolar and the instantaneous environmental benzene concentrations suggested a benzene alveolar retention of about 55%. Blood and alveolar benzene concentrations showed a highly significant correlation and the blood/air partition coefficient, obtained from the slope of the regression line, was 7.4. In the group of the 34 chemical workers no correlation was found between the TWA benzene exposure and the urinary phenol excretion.