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It is estimated that men in their 70s have mean T levels 35% lower than younger men . A progressive decline in testosterone (T) is seen with male aging, estimated at 0.4% to 2.0% decline per year after age 30 . Good TRT care is not just about chasing a particular hormone level.
In 2003, a small RCT study reported that the mean Hamilton score (21.8) in younger men (mean age 46.9 years) with hypogonadism and major depressive disorder refractory to antidepressant medications decreased by ~ 60% when their total testosterone levels were increased from 293 to 789 ng/dl (10.16–27.36 nmol/L SI units) by TRT compared to placebo treatment . Three early interventional studies of TRT using testosterone gel or intramuscular testosterone undecanoate in men with hypogonadism based on mean total testosterone levels ranging from 230 to 300 ng/dl (7.97–10.40 SI units) reported a significant reduction in depressive symptoms 80–82. In the Testosterone Trials cohort of hypogonadal men were characterized as having two morning total testosterone levels less than 275 ng/dl (9.53 nmol/L SI units), sexual dysfunction, and diminished physical functioning including low vitality. ADT involves treatment with a gonadotrophin-releasing hormone (GnRH) superagonist to desensitize and downregulate pituitary GnRH receptors, thereby depleting testosterone 45, 46. In addition to being a prospective study, another strength of the HIMS study was measuring total testosterone levels using LC–MS/MS mass spectrometry, which is a critical methodology for accurately measuring hypogonadal testosterone levels . This study also reported that low levels of dihydrotestosterone, estradiol, and free testosterone (calculated) did not confer risk for developing incident depression. In 2018, the Endocrine Society Clinical Practice Guideline established criteria for hypogonadism requiring that two morning serum testosterone levels are below 280–300 ng/dl (9.7–10.4 nmol/L SI units) .
Currently, there is evidence that leptin not only indirectly affects the steroidogenesis in Leydig cells through the regulation of the HPG axis but is also capable of directly affecting the activity of steroidogenesis system 3, 8. GnRH and NPY increase the leptin expression by pituitary gonadotrophs, while the gastrointestinal hormone ghrelin, the regulator of food intake and the functional antagonist of leptin, on the contrary, suppresses the ob gene expression 69, 72. In rats the pituitary leptin level varies significantly during the postnatal development, and in female rats it changes at the different stages of the estrous cycle and during pregnancy . The functions of the autonomous leptin system in the pituitary, its participation in gonadotropins production and the relationship between the activity of this system and the physiological state of the HPG axis are supported by the following facts. At the same time, under conditions of prolonged administration of leptin, an increase in LH level or lack of leptin effect on LH secretion were detected, which may be assumed to be due to varying degrees of leptin resistance in the case of long-term action of leptin on hypothalamic neurons. This review presents the comprehensive analysis of the involvement of leptin, adiponectin, resistin and visfatin in the regulation of the male HPG axis and steroidogenesis, as well as of the possible mechanisms of this regulation. Some adipokines can also directly affect the functions of Leydig cells, as indicated by a high level of adipokines expression in the testes, as well as detection of the main components of the adipokine signaling, including adipokine-specific receptors, in testicular cells, including Leydig cells 16, 17, 18, 19.
Should we be looking at other pituitary hormones given my symptoms, or is this an isolated finding in an otherwise stable picture? These symptoms could point to a structural issue, such as a pituitary adenoma, that exists independently of hormone therapy. For a man who is not using any form of exogenous testosterone or other hormone therapy, low or undetectable LH and FSH deserve closer attention. When a lab reports a value at zero, it generally means the hormone level is too low for the specific test to measure, not necessarily that there is a literal absence of every molecule in the bloodstream. The hypothalamus detects elevated circulating testosterone and concludes there is no need to keep signaling the pituitary. This entire feedback loop is called the hypothalamic-pituitary-gonadal axis, or HPG axis, and it is one of the most elegantly self-regulating systems in the body.
The AdipoR2 was located on the surface of Leydig cells, while AdipoR1 was found in the epithelium of the seminiferous tubules. The production of adiponectin in the testes of hypophysectomized rats is significantly reduced, but is completely restored after their treatment with hCG. These facts suggest that the main, if not the only, source of adiponectin in the semen is adiponectin, coming from the bloodstream. The concentration of adiponectin in the seminal fluid of healthy men is 100 times lower than in the bloodstream. Three transcripts of the Adiponectin gene, 2.5, 1.8 and 1.2 kb, were detected in the adipose tissue, while in Leydig cells were only two transcripts, 1.2 and 17. Adiponectin inhibits both the basal and GnRH-stimulated LH secretion, and its effect is detected even after a short exposure with gonadotrophs 14, 144.|In obesity, which was characterized by the reduced plasma level of adiponectin 134, 136, 137, its concentration in the brain areas was also decreased . In addition, a large number of adiponectin receptors and the components of adiponectin-regulated signaling pathways have been identified in the ARC and paraventricular nuclei of the hypothalamus 131, 132, 133, 134 and in other brain areas . It is suggested that the receptor-mediated transport of adiponectin through the BBB can be carried out through the AdipoR1 and AdipoR2 receptors located on the endothelium of cerebral vessels (Figure 2). To interact with hypothalamic neurons, the main target of adiponectin in the CNS, it is necessary to transport adiponectin into the brain through the BBB.|It is unclear why companies would include components in their supplements that have no evidence to support their use. For 24.8%, or 27 out of 109 individual supplements, there was data showing an increase in T with supplementation. Only 5.5% of supplements had more than two studies looking at their effect on T.|Total levels of testosterone in the body have been reported as 264 to 916 ng/dL (nanograms per deciliter) in non-obese European and American men age 19 to 39 years, while mean testosterone levels in adult men have been reported as 630 ng/dL. Finally, increasing levels of testosterone through a negative feedback loop act on the hypothalamus and pituitary to inhibit the release of GnRH and FSH/LH, respectively. Androgen receptors occur in many different vertebrate body system tissues, and both males and females respond similarly to similar levels. The areas of binding are called hormone response elements (HREs), and influence transcriptional activity of certain genes, producing the androgen effects. Free testosterone (T) is transported into the cytoplasm of target tissue cells, where it can bind to the androgen receptor, or can be reduced to 5α-dihydrotestosterone (5α-DHT) by the cytoplasmic enzyme 5α-reductase. Only the free amount of testosterone can bind to an androgenic receptor, which means it has biological activity.}
In accordance with sperm competition theory, testosterone levels are shown to increase as a response to previously neutral stimuli when conditioned to become sexual in male rats. Studies have shown small or inconsistent correlations between testosterone levels and male orgasm experience, as well as sexual assertiveness in both sexes. This is known as hormone replacement therapy (HRT) or testosterone replacement therapy (TRT), which maintains serum testosterone levels in the normal range. Some of these effects may decline as testosterone levels might decrease in the later decades of adult life. have been undertaken on the relationship between more general aggressive behavior, and feelings, and testosterone. Nearly all studies of juvenile delinquency and testosterone are not significant.}
As FSH levels drop, the surrounding follicles develop a more androgen-rich environment. FSH stimulates aromatase activity in granulosa cells, converting androgens to estrogen. This increase in inhibin B, along with rising estrogen levels, contributes to the suppression of FSH secretion, which is critical for the selection of a single dominant follicle. As previously stated, during the follicular phase, estrogen and LH levels rise, and entry into the luteal phase does not occur unless a surge in these hormones occurs up to a certain threshold. Additionally, the effects of these hormones on GnRH secretion can vary depending on the stage of the estrous cycle, nutritional status, and other physiological factors.
The effects of leptin on the male HPG axis can be carried out at the level of hypothalamic neurons, pituitary gonadotrophs and testicular cells. This latter finding suggests that men with an androgen receptor having higher sensitivity and transcription activity due to shorter CAG repeats is more strongly impacted by higher testosterone levels and will be more responsive to testosterone replacement therapy. However, a study using a logistic regression analysis with stratification for AR CAG repeat length found that the risk for depression was significantly lower in men with a highly sensitive androgen receptor due to short CAG repeats if their testosterone levels were high . A genetically informed precision medicine approach using genes regulating testosterone levels and androgen receptor sensitivity will likely be essential in gaining critical insight into the role of testosterone in depression. The regulatory effects of adiponectin circulating in the blood and adiponectin synthesized in the pituitary and testes on the activity of the male HPG axis and the testosterone production.
Dysregulation of the hypothalamic-pituitary–gonadal (HPG) axis has been observed in patients with major depressive episodes. In 2006, a Canadian study reported that total and bioavailable testosterone were significantly lower in middle-aged depressed men (40–65 years) who had considerably higher BDI and Hamilton depression scores than men enrolled in the Rancho Bernardo Study . Preclinical research has provided further evidence that androgens may reduce the risk of depression in men due to their antidepressant and neuroprotective actions in the hippocampus, limbic system, and other brain regions regulating mood 12, 13. - http://8.138.187.132:3000/thaliaallred75/thalia2000/wiki/The-Guys%27-Guide-to-Carbohydrates-and-TRT
