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http://www.hptaxis.com/technology_aih.htm
Hypogonadism is a disturbance of HPTA homeostasis. Hypogonadism is inadequate gonadal function, as manifested by deficiencies in spermatogenesis and/or the secretion of testosterone. The definitions of hypogonadism are consistent by using either reproductive capacity, infertility, and/or biochemically by testosterone and luteinizing hormone levels. The confirmation of the state of hypogonadism is exhibited either by reproductive or biochemical parameters.
Laboratory studies are the gateway to a proper diagnosis. The laboratory performing the assay defines the normal reference range for serum sex hormones. Similarly, infertility definitions encompass spermatozoa density, number, and quality. Testosterone is the initial screening laboratory study. Gonadotropins, luteinizing hormone (LH) and follicle-stimulating hormone (FSH), classify disorder. A total testosterone value <300-ng/dL (10.4-nmol/L) suggests hypogonadism while a total testosterone value <200-ng/dL is highly correlative of hypogonadism.
In primary hypogonadism, the defect is either in the testicles, absent or decreased spermatogenesis and/or the secretion of testosterone with elevated gonadotropin levels. In secondary hypogonadism (hypogonadotropic hypogonadism), the centers in the brain that control the gonads (hypothalamus and pituitary) do not function properly, resulting in absent or decreased spermatogenesis and/or the secretion of testosterone resulting from a decrease in follicle-stimulating hormone (FSH) and/or luteinizing hormone (LH), respectively.
Hypogonadism is a disease with potentially serious consequences that include but are not limited to adverse body composition changes (decrease muscle mass and increased adiposity), decreased muscle strength, bone loss, increase in cardiovascular risk, adverse psychological effects (depression, low self esteem, guilt, increased stress, and anhedonia), sexual dysfunction (decreased libido, decreased spontaneous erections, decreased ejaculate, erection dysfunction, decreased sexual fantasies, and anorgasmia), decreased cognitive testing, sleep disturbances, infertility, and constitutional symptoms (general fatigue, agitation/motor dyskinesia, and decreased appetite).
Androgen administration or use of GnRH analogues results in a form of induced hypogonadism, functional hypogonadotropic hypogonadism. Androgen, nonsteroidal, administration is currently in the research and investigational stages. These studies indicate that their clinical use will also result in androgen-induced hypogonadism after cessation by their effects on gonadotropin levels.
Androgen induced hypogonadism (AIH) is the functional incompetence of the testes with subnormal or impaired production of testosterone or spermatozoa due to administration of androgens or anabolic steroids. AIH results from an abnormality in the normal functioning of the hypothalamic-pituitary-testicular axis (HPTA), from a negative feedback inhibition of one of the hormone secreting glands, causing a cascading unbalance in the rest of the axis. To date, all compounds classified as androgens whether prescribed clinically or from illicit use cause a negative feedback inhibition of the hypothalamic pituitary testicular axis, suppress endogenous gonadotropin secretion, and as a consequence serum testosterone.
Case controlled and observational studies from licit and illicit anabolic/androgen steroid (AAS) administration demonstrate a hypogonadal state after their cessation. AAS, including testosterone, licit and illicit, administration induce a state of hypogonadism that continues after their cessation. This state is present during their administration but typically becomes symptomatic or manifest after AAS cessation.
For over fifty years, published literature demonstrates hypogonadism occurring after AAS cessation (AIH). AIH occurs in one-hundred percent of individuals upon AAS cessation. There is not a single study within the peer-reviewed literature demonstrating an immediate return of HPTA homeostasis upon AAS cessation. AAS, licit and illicit, induce a state of hypogonadism that continues after their cessation. The only variable is the duration and severity of AIH.
Countless publications study the use of testosterone as a male contraceptive agent. The simplistic reason for this is that exogenous administration will cause HPTA suppression, a decrease of sex hormones that includes endogenous testosterone production and the gonadotropins, both follicle-stimulating hormone (FSH) and/or luteinizing hormone (LH).
The absence of FSH leads to infertility, contraception, or diminished spermatogenesis. This is an induced state of hypogonadism, infertility. The absent or decreased testicular testosterone production is replaced by its external administration. The individual does not experience the adverse effects of hypogonadism secondary to decreased serum testosterone because of exogenous testosterone administration. This does not take away from the fact that the patient is in a state of induced hypogonadism for the express purpose of contraception.
Birth control studies with testosterone administration in physiological as well as subphysiological doses demonstrate HPTA suppression. Studies conducted by World Health Organization have demonstrated complete recovery of the hypothalamic pituitary testicular axis (HPTA) after administration of supraphysiologic doses of testosterone for a year. The "complete recovery" referred to is spermatogenesis and not serum testosterone. The median time to recovery to the subject’s own geometric mean baseline sperm concentration is a range of 4.0-13.9 months. Thus, the data from the study affirm that the return of normal spermatogenesis may take over a year.
Male contraception studies with 19-nortestosterone, nandrolone, demonstrate the continued suppression of serum testosterone from control levels for greater than 15 weeks after nandrolone cessation. Other data available from the development of nandrolone decanoate for male contraception indicate that reversal of effects can take more than twelve months after discontinuation of the drugs.
The salient point is that after AAS cessation there is a period of recovery for HPTA normalization of gonadotropins (FSH and LH) and sex hormones (testosterone). This period is of an unknown duration and severity. This period of hypogonadism exposes the individual to the signs and symptoms of hypogonadism, specifically both adverse body composition changes and/or decreased muscle strength. Studies demonstrate the improvements in body composition obtained during AAS administration, are lost after AAS cessation.
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