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Wuppertal, Germany

Haider A.,Private Practice | Saad F.,Bayer Pharma | Saad F.,Gulf Medical University | Doros G.,Boston University | Gooren L.,Emeritus Medical Center
Obesity Research and Clinical Practice | Year: 2014

Background Treatment of obesity with diet and exercise may have short-term success but longer-term maintenance of weight loss is less successful. Obesity is associated with a reduction of serum testosterone, and, vice versa, a reduction in serum testosterone is associated with obesity and features of the metabolic syndrome. Objective To investigate whether restoring serum testosterone to normal in hypo-gonadal obese men is beneficial with regard to weight loss and improvement of the metabolic syndrome. Methods A prospective registry accumulated to 181 men over five years (mean serum testosterone 10.06 ± 1.3 nmol/L (N > 12.1), body mass index (BMI) ≥30 kg/m 2. Of these men, 72 had diabetes mellitus type 2. All received parenteral testosterone undecanoate 1000 mg/12 weeks for up to five years. Results Waist circumference (cm) decreased from 111.2 ± 7.54 to 100.46 ± 7.1, weight (kg) from 114.71 ± 11.59 to 93.2 ± 8.49, BMI (kg/m2) from 36.72 ± 3.72 to 30.2 ± 2.59 (all variables statistically significant vs. baseline (p < 0.0001) and each year compared to the previous year (p < 0.0001)). In the 72 diabetic men, waist circumference (cm) decreased from 112.93 ± 7.16 to 101.48 ± 7.24, weight (kg) from 116.94 ± 11.62 to 94.42 ± 9.42, BMI (kg/m 2) from 37.71 ± 3.5 to 30.95 ± 2.69 (all variables statistically significant vs. baseline (p < 0.0001) and each year compared to the previous year (p < 0.0001)). In all men serum glucose, HbA1c, lipid profiles and blood pressure improved significantly. Testosterone treatment as assessed by hemoglobin, hematocrit, serum prostate specific antigen (PSA) and occurrence of prostate cancer was acceptably safe. Conclusions Normalizing serum testosterone in obese hypogonadal men, also in those with diabetes type 2, improved their metabolic state. © 2013 Asian Oceanian Association for the Study of Obesity. Published by Elsevier Ltd. All rights reserved. Source

Saad F.,Bayer Pharma | Saad F.,Gulf Medical University
Asian Journal of Andrology | Year: 2015

It is no exaggeration to say that our conceptualization of the (patho-) physiological functions of testosterone has undergone a revolutionary development over the last three decades. The traditional thinking was that the biological functions of testosterone were restricted mainly to the area of reproduction and male sexuality. However, scientific research has clearly demonstrated that testosterone is a multi-system hormone serving a wide range of hitherto unsuspected biological functions. Source

Haider A.,Private Practice | Meergans U.,Wesermuende Hospital | Traish A.,Boston University | Saad F.,Bayer Pharma | And 4 more authors.
International Journal of Endocrinology | Year: 2014

Testosterone deficiency leads to bone loss and testosterone treatment has a beneficial effect. This study investigated the effects of normalizing serum testosterone on bone mineral density in 45 men with osteoporosis, diagnosed with testosterone deficiency (serum testosterone levels <12.1 nmol/L, T-scores: (mean ± SD) -3.12 ± 0.45, minimum: -4.10, and maximum: -2.60). In a cumulative, prospective, registry study of hypogonadal men (mean age: 53 ± 7 years) they received parenteral testosterone undecanoate of 1000 mg/12 weeks for up to six years. After one year 44 men were included in the registry, after two years 36 men, after three years 32 men, after four years 25 men, after five years 10 men and after six years 4 men. The declining numbers do not reflect drop-out rates but are a result of the registry design. Over the 6 year period there was a significant and progressive improvement of the T-scores in these men. Normalizing of serum testosterone leads to an improvement of bone mineral density and this improvement was progressive with the time period of testosterone administration. In this study of 6-years many men with testosterone deficiency suffered from classical diagnoses (Klinefelter's syndrome and testicular pathology) hitherto undiagnosed. © 2014 Ahmad Haider et al. Source

Saad F.,Bayer Pharma | Saad F.,Gulf Medical University | Gooren L.J.,VU University Amsterdam
Maturitas | Year: 2014

Some men between the ages 45 and 60 years develop complaints and symptoms reminiscent of menopausal complaints in women. So, parallels were sought between the changes in female and male endocrinology during that period of life. Indeed, men do show a decline of serum testosterone from age 40 to 50 years onwards but it is a slow decline of 1-2% per year and over time it may amount to hypogonadism. The mechanism of a decline in serum testosterone in men does not resemble the menopause; it is partially an aging neuroendocrine system with a less efficient testosterone production but equally or more important, the result of inhibition of testosterone production by metabolic factors in relation to visceral obesity. These effects are in part reversible with weight loss. A hypogonadal state in aging men has deleterious effects. Mortality of all causes is highest in men with low testosterone impacting on their metabolic state leading to diabetes mellitus, cardiovascular disease, osteoporosis, and sexual dysfunction. Normalization of testosterone in aging hypogonadal men has a beneficial effect on the above pathologies. The fear that testosterone treatment of elderly men would lead to prostate disease has not been substantiated in studies. So, while men do not have a 'menopause', testosterone deficiency in old age deserves serious attention. © 2014 Elsevier Ireland Ltd. Source

Westphal C.,Charite - Medical University of Berlin | Westphal C.,Center for Cardiovascular Research | Schubert C.,Charite - Medical University of Berlin | Schubert C.,Center for Cardiovascular Research | And 7 more authors.
PLoS ONE | Year: 2012

The aim of this study was to investigate the effects of 17β-estradiol (E2), the selective ERα agonist 16α-LE2, and the selective estrogen receptor modulator (SERM) raloxifene on remodeling processes during the development of myocardial hypertrophy (MH) in a mouse model of pressure overload. Myocardial hypertrophy in ovariectomized female C57Bl/6J mice was induced by transverse aortic constriction (TAC). Two weeks after TAC, placebo treated mice developed left ventricular hypertrophy and mild systolic dysfunction. Estrogen treatment, but not 16α-LE2 or raloxifene reduced TAC induced MH compared to placebo. E2, 16α-LE2 and raloxifene supported maintenance of cardiac function in comparison with placebo. Nine weeks after induction of pressure overload, MH was present in all TAC groups, most pronounced in the raloxifene treated group. Ejection fraction (EF) was decreased in all animals. However, 16α-LE2 treated animals showed a smaller reduction of EF than animals treated with placebo. E2 and 16α-LE2, but not raloxifene diminished the development of fibrosis and reduced the TGFβ and CTGF gene expression. Treatment with E2 or 16α-LE2 but not with raloxifene reduced survival rate after TAC significantly in comparison with placebo treatment. In conclusion, E2 and 16α-LE2 slowed down the progression of MH and reduced systolic dysfunction after nine weeks of pressure overload. Raloxifene did not reduce MH but improved cardiac function two weeks after TAC. However, raloxifene was not able to maintain EF in the long term period. © 2012 Westphal et al. Source

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