Free and bioavailable fractions of sex steroids may influence bones in young men, depending on age and oestradiol level.

INTRODUCTION: Longitudinal bone growth ceases by the end of puberty, and it is thought to be a result, in both sexes, of increased pubertal oestrogen serum concentrations. Since peak bone mass is achieved by the third decade of life or later, the aim of this study was to relate sex steroid hormones and sex hormone binding globulin (SHBG) levels to bone quality in men during their third and fourth decades of life. MATERIAL AND METHODS: Eighty men, healthy volunteers aged between 18 and 39 years, were subjected to an interviewer-administered questionnaire, body mass index (BMI) measurement, blood sample and calcaneal quantitative ultrasound (QUS) (Hologic-SAHARA). Blood was assessed for testosterone (T), oestradiol (E2), dehydroepiandrosterone sulfate (DHEAS), SHBG, luteinising hormone (LH) and follicle stimulating hormone (FSH). Free and bioavailable T and E2 levels were calculated knowing SHBG and albumin levels. RESULTS: While T, E2, DHEAS, LH and FSH levels were not related, free and bioavailable fractions of T and E2 were positively associated with QUS readings. SHBG level was associated negatively. After dichotomisation for age, the associations remained significant only for younger subjects (18-30 years, n = 47). After adjustment for other co-variants, only SHBG in younger subjects retained its negative association with QUS. Older subjects (31-39 years, n = 33) revealed higher BMI and lower serum concentrations of total (-17 %), free (-18.5%) and bioavailable (-22.5%) levels of E2 than younger subjects. CONCLUSION: Free and bioavailable fractions of sex steroids may influence bones in young men, depending on age and E2 level.

[Physiological significance of estrogens in men--breakthrough in endocrinology]. / Znaczenie fizjologiczne estrogenów u mezczyzn--przelom w endokrynologii.

Estradiol (E2) is traditionally recognised as the female sex hormone. It has been believed for 40 years, that E2 didn't exert any influence or caused impairment of the gonadal function in men. The main source of E2 in men is adipose tissue and the brain. E2 is also produced in adrenals, liver, mammary glands, hair and in male gonad. Daily production and the level of E2 in the blood in men are higher than those in postmenopausal women. At the end of the 80-ties we were first reporting that during sexual maturation E2 can be the important hormonal signal for the initiation of spermatogenesis. The traditional view about unimportant or inhibitory role of E2 in male physiology was finally refuted thanks to discovering estrogen receptors in males. In the 90-ties, transgenic mice with the lack of estrogen receptor (ER) or gene encoding enzyme aromatase, that enable the conversion of testosterone into E2, were also produced. Observations of men with inherited mutations of these genes, considerably extended our knowledge about E2 in men in stroma bones formation, inhibition of their growing, lipids metabolism and sexual maturation, the effects that were attributed to testosterone action until today. New data also points at important role of estrogens and ER in the function of the cardio-vascular system and in counteracting coronary disease in men.

[Important functions of estrogens in men--breakthrough in contemporary medicine]. / Wazne funkcje estrogenów u mezczyzn--przelom we wspóczesnej medycynie.

Estradiol (E2) is traditionally recognised as the female sex hormone. Since discovery of estrogens in the early forties of XX century it has been believed, that these hormones caused impairment of the gonadal function in men or didn't exert any influence. New studies are contradictory, but indicate also a possible involvement of estrogens in the pathogenesis of some systemic diseases of men. The main source of E2 in men is adipose tissue and the brain. E2 is also produced in adrenals, liver, mammary glands, hair and in male gonads. Daily production and blood level of E2 in men are higher than those in postmenopausal women. In 1988 we were the first to demonstrate that E2 is an important hormonal signal for initiation of spermatogenesis. The traditional view about unimportant or inhibitory role of E2 in male physiology was finally refuted thanks to discovery of the estrogen receptors in males. In the middle 90ties transgenic mice with the lack of estrogen receptor (ER knockout) or enzyme aromatase, that enable the conversion of testosterone into E2, were produced. Observations of men with inherited mutations of these genes, considerably extended our knowledge about stimulatory role of E2 in men in the formation of bone stroma, inhibition of their linear growth, lipids metabolism and sexual maturation, the effects that were attributed to testosterone action until today. New data indicate role of estrogens and ER in the function of the cardio-vascular system. Their link with development of arteriosclerosis seems, however, to be bipolar. In single reported cases of men with the inactivating mutations of ERalpha or aromatase genes, a precocious arteriosclerosis is noted. From the other site, men homozygous for the most common variant of ERalpha gene (ESR1c.454-397cc) have a significantly increased risk of myocardial infraction. Estrogens are the risk factors in prostatic cancer and their local tissue increase in autoimmune diseases is connected with aggravation of the proliferative complications of these disorders.

Sex steroids and heart rate variability in patients after myocardial infarction.

BACKGROUND: Although the relationship between sex steroid levels and coronary artery disease (CAD) has been the subject of many studies there are still controversies concerning the role of sex steroids in CAD. In patients with CAD, especially after a myocardial infarction, there is evidence for autonomic nervous system dysfunction. However, there is no data detailing the relationship between sex steroids and cicardian autonomic activity in patients with CAD. The aim of the study was to evaluate the association between sex steroids and heart rate variability (HRV) parameters in postinfarction patients. METHODS: In 88 postinfarction men (aged 36-73, average 53 years), 24-hour Holter monitoring was performed to assess HRV parameters: SDNN, SDNNI, SDANN, rMSSD, pNN50, and levels of the following hormones were measured: testosterone, estradiol, free testosterone index, and estradiol/testosterone ratio. Univariate and multivariate regression analyses were used to investigate the relationship between HRV parameters and levels of tested hormones. RESULTS: Increased testosterone levels were associated with increased SDNN (r = 0.38, P = 0.03), increased rMSSD (r = 0.51, P = 0.002), and increased pNN50 (r = 0.45, P = 0.007). These associations remained significance after adjustment for age, ejection fraction, and other relevant clinical covariates. There was no significant association between estradiol and HRV parameters. CONCLUSION: In men with a history of myocardial infarction, higher levels of testosterone are associated with higher HRV measures of parasympathetic activity. These findings suggest that testosterone beneficially influences autonomic regulation of the heart.

[Sex steroids and heart rate variability in men with coronary artery disease after myocardial infarction]. / Steroidy plciowe a zmiennosc rytmu serca u mezczyzn z choroba wiencowa po zawale serca.

The role of sex steroids in coronary artery disease (CAD) has been studied for years. In patients after myocardial infarction autonomic nervous system dysfunction has been described. Heart rate variability (HRV) analysis is one of the method of autonomic nervous system evaluation. The aim of the study was to evaluate correlations between sex steroids and HRV in 88 men (aged 36-73, av. 53 yrs), with the history of MI, with angiographically documented CAD. In all the patients 24-hour Holter monitoring was performed to assess HRV time domain parameters: SDNN, SDNNI, SDANN, rMSSD, pNN50. Levels of testosterone and estradiol were measured in two subsequent blood samples, taken with 30 min interval. Free testosterone index as well as estradiol/testosterone ratio were assessed. For statistics r-Spearman test was used. Positive correlations were found between testosterone and SDNN (r = 0.38, p = 0.03), testosterone and rMSSD (r = 0.51, p = 0.002) and between testosterone and pNN50 (r = 0.45, p = 0.007). Since rMSSD and pNN50 are parameters describing parasympathetic activity, our results suggest that in CAD men with the history of myocardial infarction, testosterone may influences the function of autonomic nervous system promoting parasympathetic dominance. It can be favorable for the circulatory system function.