I thought you guys might find this study interesting. I’ve have an issue where 1000IU of HCG twice a week alone turns me into walking wood but T+250IU HCG+AI=zero libido. Great labs and gym results but still zero libido. I’m going to switch over to HCG monotherapy and ginnie pig that long term. (I’m well aware of the risk of desensitization and I’ve read enough from endo studies to feel confident in my dose.)
Anyway enjoy and comment.
Comparison of the efficacy of long-term self-administration of subcutaneous human chorionic gonadotrophin with intramuscular exogenous testosterone (Sustanon) in male hypogonadism
SJ Caddy1 & TH Jones1,2
1Academic Unit of Endocrinology, Division of Genomic Medicine, University of Sheffield Medical School, Sheffield, UK; 2Centre for Diabetes and Endocrinology, Barnsley District General Hospital, Barnsley, UK.
Male hypogonadism can occur either due to disorders at the hypothalamic or pituitary levels or as a result of primary testicular failure. Conventionally, testosterone is replaced by depot intramuscular injections of testoterone esters or as implants producing non-physiological levels of serum testosterone. Human chorionic gonadotrophin (hCG) given twice-weekly s.c., stimulates endogenous testosterone secretion through its LH like action resulting in physiological serum testosterone levels (1). This treatment is only suitable for patients with hypogonadotrophic hypogonadism.
Twenty-one male hypogonadal patients were recruited. Eleven, (mean age 31.8; range 22-43), were treated with hCG. Seven had idiopathic isolated hypogonadotrophic hypogonadism (IHH), two Kallman’s syndrome, one secondary hypogonadism and one panhypopituitarism. Of ten patients treated with exogenous testosterone (Sustanon), (mean age 47.0; range 23-59), four had primary hypogonadism, two IHH, two panhypopituitarism and two acromegaly. Mean total serum testosterone, sex hormone binding globulin, free androgen index and oestradiol were recorded. Each patient completed two validated questionnaires: The Health Status (SF-36) Questionnaire and The ADAM Male Hypogonadal Questionnaire.
The mean serum testosterone (hCG-15.06nmol/l: Sustanon-15.65nmol/l: P=0.843), FAI (hCG-8.82units: Sustanon-9.33units: P=0.841) and oestradiol (hCG-5.11pmol/l: Sustanon-9.00pmol/l: P=0.223) showed no significant difference between the two therapies. The mean hypogonadal scores (a higher score equates to more symptoms; a score of 3 or less indicates no hypogonadal symptoms, if positive responses to loss of libido and less strong erections are negative) differed to a statistically significant degree (hCG-1.72: Sustanon-5.90: P=0.002). The hypogonadal scores negatively correlated with the general health questionnaire indicating higher hypogonadal scores to be associated with a diminished quality of life. In conclusion, a single measurement of serum testosterone does not equate to an effective evaluation of therapeutic response as assessed by the validated questionnaires. Hypogonadal patients prescribed hCG treatment regimes, as apposed to exogenous testosterone, experience fewer residual hypogonadal symptoms and also enjoy, on average, a better quality of life.
(1) Jones TH et al. Eur J Endocrinol 1994, 131;173-178
Endocrine Abstracts 3 P246