Programs of the Public Health Service.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to D E Price.
Explore the source record for details and available documents.
Androgen deficiency may contribute to female sexual dysfunction and loss of libido. The role of the active metabolite of testosterone, dihydrotestosterone (DHT), in these conditions is uncertain. The aim of this study was to determine the role of androgens and DHT in the etiology of loss of libido in healthy women. We studied 29 premenopausal women with reduced libido (subjects) and 12 healthy females (controls). They were aged 18 to 45 years and in a stable heterosexual relationship. At 9 a.m. we took venous blood in the follicular phase for serum estradiol, total testosterone, and DHT, dehydroepiandrosterone sulfate (DHEAS), and SHBG levels. Subjects were interviewed by a psychosexual counsellor. Using the modified Wilson's sexual fantasy questionnaire (Baumgartner, Scalora, & Huss, 2002) and sexual satisfaction by Golombok-Rust Inventory of Sexual Satisfaction (GRISS Rust & Golombok, 1985, 1986) we assessed sexual drive. The total testosterone and DHT levels (mean +/- SD) were respectively 0.97 +/- 0.38 mmol/L and 0.76 +/- 0.37 nmol/L in subjects and 0.97 +/- 0.41 mmol/L and 0.77 +/- 0.15 nmol/L in controls. The SHBG and DHEAS were respectively 65 +/- 42 mmol/L and 3.76 +/- 1.0 umol/L in subjects and 65 +/- 29 mmol/L and 3.67 +/- 2.6 in controls. The scores of the Wilson questionnaire and GRISS were respectively 21 +/- 14.1 and 5 +/- 2.1 in subjects and 35 +/- 14.8 & 2 +/- 1.2 in controls. Subjects were more likely than controls to have low income (48% versus 8%, p < 0.02), a minor illnesses (57% versus 17%, p < 0.02), a history of depression (57% versus 8%, p = 0.025) and to report sexual problems in their partners (24% versus 0%, p = 0.053). Loss of libido in otherwise healthy women may be related to relationship problem, depression, psychosocial factors, and sexual dysfunction in the partner but do not appear to be related to androgen status.
The red cell sorbitol concentration has been suggested as a measure of polyol pathway activity. Red cell sorbitol levels were higher in 53 patients having insulin-dependent diabetes mellitus (IDDM) than in 16 control subjects. Six patients having IDDM underwent hyperglycaemic 'clamp' studies; the red cell sorbitol level returned to the normal range when the blood glucose was clamped at 5 mmol/l for 1 h and rapidly increased when it was clamped at 15 and 25 mmol/l for a further hour at each level. Seven patients with IDDM were rendered hypoglycaemic; red cell sorbitol levels rapidly fell to a level less than, but not significantly different from normal. The results of these studies suggest that in IDDM red cell sorbitol levels are a reflection of prevailing blood glucose concentration and do not indicate long-term sorbitol accumulation in other tissues.
A patient developed proliferative retinopathy after more than 60 years of complication-free diabetes. This may have been precipitated by an episode of ketosis or by cataract extraction, and emphasizes the need for persistent vigilance in examination for retinopathy.