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EJ Giltay, AW Toorians, AR Sarabdjitsingh, NA de Vries, and LJ Gooren

A high scalp sensitivity to androgens is part of the pathophysiology of male-pattern baldness (MPB). Androgens affect established risk factors for coronary heart disease (CHD), and a supposedly heightened impact on these risk factors is hypothesized to explain the epidemiological association between MPB and CHD. In this retrospective, observational study we studied 81 female-to-male transsexual (F-->M) subjects, mean age 36.7 years (range 21-61), treated with testosterone esters (n=61; 250 mg i.m./2 weeks) or testosterone undecanoate (n=20; 160-240 mg/day orally). The degree of MPB was self-assessed using a 5-point scale (i.e. type I (no hair loss) to type V (complete hair loss)). Body mass index, blood pressure and levels of lipid and insulin were retrospectively assessed at the start of testosterone administration (0.5-24 years before) and between 3 and 4 months of follow-up. We found that 31 of 81 (38.3%) F-->M transsexuals had MPB type II-V. Thinning of hair was related to the duration of androgen administration and present in about 50% of F-->M transsexuals after 13 years. None of the CHD risk factors at follow-up, nor proportional changes, was associated with the degree MPB, except that there was an unexpected tendency of lower fasting glucose levels in balding subjects. Therefore, our findings do not support the idea that MPB serves as an indicator of increased CHD risk through androgenic effects on classic CHD risk factors.

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EJ Giltay, EJ Duschek, MB Katan, PL Zock, SJ Neele, and JC Netelenbos

Estrogens may affect the essential n-6 and n-3 fatty acids arachidonic acid (AA; C20:4n-6) and docosahexaenoic acid (DHA; C22:6n-3). Therefore, we investigated the long-term effects of hormone replacement therapy and raloxifene, a selective estrogen-receptor modulator, in two randomized, double-blind, placebo-controlled studies. In study I, 95 healthy, non-hysterectomized, early postmenopausal women (age range 47-59 years) received one of the following treatments: daily raloxifene 60 mg (n=24), daily raloxifene 150 mg (n=23), 0.625 mg conjugated equine estrogens (CEE) plus 2.5 mg medroxyprogesterone acetate (MPA; n=24), or placebo (n=24). In study II, 30 men (age range 60-69 years) received daily 120 mg raloxifene (n=15) or placebo (n=15). In study I, plasma cholesteryl ester fatty acids were measured at baseline and after 6, 12, and 24 months in 83 (drop out rate 13%), 73 (23%), and 70 (25%) women respectively. In study II, fatty acids were measured at baseline and after 3 months in 29 men (drop out rate 3%). In postmenopausal women, administration of 150 mg raloxifene increased AA by a mean of +6.1% (P=0.055, not significant). Administration of CEE plus MPA increased AA by +14.1% (P<0.0005). Mean changes in DHA were +22.1% (P=0.003) and +14.9% (P=0.047) respectively, as compared with placebo. In men, 120 mg raloxifene for 3 months did not significantly affect AA (-5.2%; P=0.342) or DHA (+4.0%; P=0.755), but it increased testosterone levels by +19.8% (P=0.006). Administration of raloxifene 150 mg/day as well as CEE plus MPA to postmenopausal women increases the proportion of AA and DHA in plasma cholesteryl esters during a follow-up of 2 years. Short term administration of raloxifene in elderly men did not affect AA or DHA. The synthesis of AA and DHA from precursors may be enhanced through an estrogen receptor-dependent pathway.