Side note, insurance rarely will cover it and cause a long paper trail to even approve it which is unfortunate and disheartening. Especially when it is done out of network. Currently I have found a place to supply all of the aboue sent to my house at approximately $200.00 per month. Still an unfortunate cost for a medical reason that the insurance companies don’t approve. Best of luck to all of you.

There is a polymorphic CAG repeat sequence in the androgen receptor gene, which codes for a variable number of glutamine amino acids in the part of the receptor affecting gene transcription. A receptor with a short CAG sequence produces greater activity when androgens attach, and men with shorter CAG polymorphisms exhibit androgenic traits, such as preserved bone density (Zitzmann et al 2001) and prostate growth during testosterone treatment (Zitzmann et al 2003). Indirect evidence of the importance of androgens in the development of prostate cancer is provided by case control study findings of a shorter, more active CAG repeat sequence in the androgen receptor gene of patients with prostate cancer compared with controls (Hsing et al 2000, 2002).
I noticed that you say that those that have prostate cancer should not have testosterone replacement therapy, Why-in light of the studies that say that there is no danger from testosterone therapy to one that had/has prostate cancer? If this is your opinion do you have any suggestions as to what I should do about my symptoms? Does testosterone replacement therapy actually do anything?
I’m a 49yr old who had a testosterone level of below 300 . I have been on AndroGel for over one year now. The first three months my levels were running between 500 and 600.in the fourth month my level spiked to over 1200 and cut my doctor cut my dosage back to half. my levels fell back to below normal and have since remained that way even though I have been put on the normal dosage again. It seems as though my body has stopped responding to the andro gel.
The largest amounts of testosterone (>95%) are produced by the testes in men,[2] while the adrenal glands account for most of the remainder. Testosterone is also synthesized in far smaller total quantities in women by the adrenal glands, thecal cells of the ovaries, and, during pregnancy, by the placenta.[130] In the testes, testosterone is produced by the Leydig cells.[131] The male generative glands also contain Sertoli cells, which require testosterone for spermatogenesis. Like most hormones, testosterone is supplied to target tissues in the blood where much of it is transported bound to a specific plasma protein, sex hormone-binding globulin (SHBG).
Sexual dysfunction and low libido are among the most easily reversible symptoms of hypogonadism. Systematic reviews of randomized, placebo-controlled clinical trials of testosterone in men, including older men (aged 60 years and over) and middle-aged men, with sexual dysfunction and hypogonadism have shown large favourable effects on libido and moderate effects on satisfaction with erectile function.1-5 In men who do not respond sufficiently to testosterone therapy alone, the combination of phosphodiesterase 5-inhibitors and testosterone may be indicated, as there are suggestions that the combination may be synergistic.1

^ Butenandt A, Hanisch G (1935). "Umwandlung des Dehydroandrosterons in Androstendiol und Testosterone; ein Weg zur Darstellung des Testosterons aus Cholestrin" [About Testosterone. Conversion of Dehydro-androsterons into androstendiol and testosterone; a way for the structure assignment of testosterone from cholesterol]. Hoppe-Seyler's Z Physiol Chem (in German). 237 (2): 89–97. doi:10.1515/bchm2.1935.237.1-3.89.
There are a lot of test booster blends out there. A lot of them are junk. I have tried to cover the most effective herbs above. As always, I recommend doing your own research and experiment to see if you notice an effect. If you would like one easy herbal solution I recommend starting with Mike Mahlers Aggressive Strength product purely because I have solid anecdotal evidence of its effectiveness. But again, supplements should be seen purely as that - a supplement to a healthy diet, plenty of sleep, hard training with adequate rest.
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Findings that improvements in serum glucose, serum insulin, insulin resistance or glycemic control, in men treated with testosterone are accompanied by reduced measures of central obesity, are in line with other studies showing a specific effect of testosterone in reducing central or visceral obesity (Rebuffe-Scrive et al 1991; Marin, Holmang et al 1992). Furthermore, studies that have shown neutral effects of testosterone on glucose metabolism have not measured (Corrales et al 2004), or shown neutral effects (Lee et al 2005) (Tripathy et al 1998; Bhasin et al 2005) on central obesity. Given the known association of visceral obesity with insulin resistance, it is possible that testosterone treatment of hypogonadal men acts to improve insulin resistance and diabetes through an effect in reducing central obesity. This effect can be explained by the action of testosterone in inhibiting lipoprotein lipase and thereby reducing triglyceride uptake into adipocytes (Sorva et al 1988), an action which seems to occur preferentially in visceral fat (Marin et al 1995; Marin et al 1996). Visceral fat is thought to be more responsive to hormonal changes due to a greater concentration of androgen receptors and increased vascularity compared with subcutaneous fat (Bjorntorp 1996). Further explanation of the links between hypogonadism and obesity is offered by the hypogonadal-obesity-adipocytokine cycle hypothesis (see Figure 1). In this model, increases in body fat lead to increases in aromatase levels, in addition to insulin resistance, adverse lipid profiles and increased leptin levels. Increased action of aromatase in metabolizing testosterone to estrogen, reduces testosterone levels which induces further accumulation of visceral fat. Higher leptin levels and possibly other factors, act at the pituitary to suppress gonadotrophin release and exacerbate hypogonadism (Cohen 1999; Kapoor et al 2005). Leptin has also been shown to reduce testosterone secretion from rodent testes in vitro (Tena-Sempere et al 1999). A full review of the relationship between testosterone, insulin resistance and diabetes can be found elsewhere (Kapoor et al 2005; Jones 2007).
Cross-sectional studies have found a positive association between serum testosterone and some measures of cognitive ability in men (Barrett-Connor, Goodman-Gruen et al 1999; Yaffe et al 2002). Longitudinal studies have found that free testosterone levels correlate positively with future cognitive abilities and reduced rate of cognitive decline (Moffat et al 2002) and that, compared with controls, testosterone levels are reduced in men with Alzheimer’s disease at least 10 years prior to diagnosis (Moffat et al 2004). Studies of the effects of induced androgen deficiency in patients with prostate cancer have shown that profoundly lowering testosterone leads to worsening cognitive functions (Almeida et al 2004; Salminen et al 2004) and increased levels of serum amyloid (Gandy et al 2001; Almeida et al 2004), which is central to the pathogenesis of Alzheimer’s disease (Parihar and Hemnani 2004). Furthermore, testosterone reduces amyloid-induced hippocampal neurotoxity in vitro (Pike 2001) as well as exhibiting other neuroprotective effects (Pouliot et al 1996). The epidemiological and experimental data propose a potential role of testosterone in protecting cognitive function and preventing Alzheimer’s disease.
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Well, this is another area of confusion and great debate, but I don’t think it’s as confusing as it appears to be in the literature. When most doctors learned about testosterone in medical school, they learned about total testosterone, or all the testosterone in the body. But about half of the testosterone that’s circulating in the bloodstream is not available to the cells. It’s tightly bound to a carrier molecule called sex hormone–binding globulin, which we abbreviate as SHBG.

One thing that is often overlooked when it comes to testosterone boosters is the dosing. Test boosters aren’t like other supplements where you can just take the one dosing per day and forget about until the next day. As with any supplement, it only stays in your system for 4-8 hours. This means you need to be taking more than one dose per day. 2 doses are better but it still is not enough. If you want to keep your test levels up all day you will need to be taking at least 3 and preferably 4 doses per day to keep your testosterone levels high throughout the day and to keep them from dropping between doses. You should also be sure to take them every day and try to not miss any doses to get the most out of them.
Men can experience a range of symptoms if testosterone decreases more than it should. Low testosterone, or low T, is diagnosed when levels fall below 300 nanograms per deciliter (ng/dL). A normal range is typically 300–1000 ng/dL, according to the U.S. Food and Drug Administration. A blood test called a serum testosterone test is used to determine your level of circulating testosterone.

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I am now 65 & have had Low-T problems since I was about 60. I took topical Testosterone for a few years until insurance stopped covering it. Then I took injections at a Men's Health-Low-T Clinic. Then I was diagnosed with Prostate Cancer & was told to stop taking Testosterone. I underwent radiation treatment to cure the Prostate cancer, but since there is a theory that taking Testosterone can lead to Prostate cancer, I have chosen not to resume taking it. While I am glad to be free of the cancer, I have been feeling extremely fatigued & tired all the time to the point that doing much of anything like a little yard work would leave me exhausted for days.
The one side effect that no one talks about is psychological for me. Because I am 67 years old and suddenly look, feel and act 37 I only want to be around younger people. I have no use associating with people my own age. I have nothing in common and even look different. This year at my class reunion was a glaring example…..no doubt I looked younger than anyone, but it is sooo much more than just very that. My customers are young, all my girlfriends and associates. This all has a large effect on my mind. It’s hard to grasp suddenly looking and acting 30 years younger than your friends. My mind is so confused about how old I really am. I do a lot of adrenalin sports for my age snow ski, wake-surf, wake-board, scuba dive and it is no doubt just a matter of time till I get hurt doing these wild sports. In my mind I’m 37 so I think it’s all normal. This whole experience has been incredible and very positive with the only one psychological effect and no other physical side effect.
Male hypogonadism is a clinical syndrome caused by a lack of androgens or their action. Causes of hypogonadism may reflect abnormalities of the hypothalamus, pituitary, testes or target tissues. Increases in the amount of testosterone converted to estrogen under the action of the enzyme aromatase may also contribute to hypogonadism. Most aspects of the clinical syndrome are unrelated to the location of the cause. A greater factor in the production of a clinical syndrome is the age of onset. The development of hypogonadism with aging is known as late-onset hypogonadism and is characterised by loss of vitality, fatigue, loss of libido, erectile dysfunction, somnolence, depression and poor concentration. Hypogonadal ageing men also gain fat mass and lose bone mass, muscle mass and strength.
"Some say it's just a part of aging, but that's a misconception," says Jason Hedges, MD, PhD, a urologist at Oregon Health and Science University in Portland. A gradual decline in testosterone can't explain a near-total lack of interest in sex, for example. And for Hedges' patients who are in their 20s, 30s, and early 40s and having erectile problems, other health problems may be a bigger issue than aging.
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