Trials of testosterone treatment in men with type 2 diabetes have also taken place. A recent randomized controlled crossover trial assessed the effects of intramuscular testosterone replacement to achieve levels within the physiological range, compared with placebo injections in 24 men with diabetes, hypogonadism and a mean age of 64 years (Kapoor et al 2006). Ten of these men were insulin treated. Testosterone treatment led to a significant reduction in glycated hemoglobin (HbA1C) and fasting glucose compared to placebo. Testosterone also produced a significant reduction in insulin resistance, measured by the homeostatic model assessment (HOMA), in the fourteen non-insulin treated patients. It is not possible to measure insulin resistance in patients treated with insulin but five out of ten of these patients had a reduction of insulin dose during the study. Other significant changes during testosterone treatment in this trial were reduced total cholesterol, waist circumference and waist-hip ratio. Similarly, a placebo-controlled but non-blinded trial in 24 men with visceral obesity, diabetes, hypogonadism and mean age 57 years found that three months of oral testosterone treatment led to significant reductions in HbA1C, fasting glucose, post-prandial glucose, weight, fat mass and waist-hip ratio (Boyanov et al 2003). In contrast, an uncontrolled study of 150 mg intramuscular testosterone given to 10 patients, average age 64 years, with diabetes and hypogonadism found no significant change in diabetes control, fasting glucose or insulin levels (Corrales et al 2004). Another uncontrolled study showed no beneficial effect of testosterone treatment on insulin resistance, measured by HOMA and ‘minimal model’ of area under acute insulin response curves, in 11 patients with type 2 diabetes aged between 33 and 73 years (Lee et al 2005). Body mass index was within the normal range in this population and there was no change in waist-hip ratio or weight during testosterone treatment. Baseline testosterone levels were in the low-normal range and patients received a relatively small dose of 100 mg intramuscular testosterone every three weeks. A good increase in testosterone levels during the trial is described but it is not stated at which time during the three week cycle the testosterone levels were tested, so the lack of response could reflect an insufficient overall testosterone dose in the trial period.
Benefits: Maca roots originates from the mountains of Peru. For a long time, natives have been using Maca roots as not only a food supply but for it’s properties for increasing sexual potency. It has been prove to improve erectile dysfunctions, libido and sperm production. Maca roots stimulate semen volume, sperm count and sperm motility, which makes Maca a powerful Aphrodisiac.
The partial synthesis in the 1930s of abundant, potent testosterone esters permitted the characterization of the hormone's effects, so that Kochakian and Murlin (1936) were able to show that testosterone raised nitrogen retention (a mechanism central to anabolism) in the dog, after which Allan Kenyon's group was able to demonstrate both anabolic and androgenic effects of testosterone propionate in eunuchoidal men, boys, and women. The period of the early 1930s to the 1950s has been called "The Golden Age of Steroid Chemistry", and work during this period progressed quickly. Research in this golden age proved that this newly synthesized compound—testosterone—or rather family of compounds (for many derivatives were developed from 1940 to 1960), was a potent multiplier of muscle, strength, and well-being.
This paper will aim to review the current evidence of clinical effects of testosterone treatment within an aging male population. As with any other clinical intervention a decision to treat patients with testosterone requires a balance of risk versus benefit. We shall try to facilitate this by examining the effects of testosterone on the various symptoms and organs involved.
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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).
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Testosterone may prove to be an effective treatment in female sexual arousal disorders, and is available as a dermal patch. There is no FDA approved androgen preparation for the treatment of androgen insufficiency; however, it has been used off-label to treat low libido and sexual dysfunction in older women. Testosterone may be a treatment for postmenopausal women as long as they are effectively estrogenized.
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In 2002, the federally sponsored Women’s Health Initiative (WHI) stopped its hormone replacement therapy (HRT) trial (estrogen plus progestin), which included more than 16,000 women, three years early because those taking the pills had an increased risk of developing breast cancer and blood clots, and an increased risk of suffering a stroke or heart attack than those taking a placebo. The findings ran counter to the long-held belief that HRT could preserve health — and trim heart-disease risk in women.
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 have tried pellets, I went from 5 grams/day gel, to 10 grams, had little change due to work schedule and no energy made it difficult to manage daily. Levels got down to 78 at one point. Testo pellets worked great but it took 10 to make a difference and it brought me up to the 300-400 range. My body rejected 3 pellets and expelled them. Tried axiron, didn’t work, natesto, which the doc never heard off next, a Nasal spray which helped but the bottle ran out 5 days early either by my mistake or dosage problems. Back to 10 grams Testim AG ($360 after deductible) which helps if i could stay consistent but I’m 28. With a job, and health insurance, deductible issues I can not afford 800 dollars a month, 360 after deductible. Recent levels of FSH/LH are .7 and 1.2 (low). Total testosterone 114, free 18.9, and bioavalability at 39.6 (low). I had a MRI of my pituitary gland today, and get results next week. Hoping to start depo T next week as I return to work. If I can recommend anything to anyone, is make sure it’s affordable, you have the time or energy to apply/administer, and understand most people will not understand what you are going through. 2 killers of testosterone are chronic stress and lack of sleep. In 3 years of treatment I wish I came to this man’s article and others and read up prior because I’m on the brink of losing everything I’ve worked for due to hypogonadism. Wish you all results and good health, and thank you for a great article!
Testosterone does a lot more than you’d think, whether we’re talking about male or female biology. It’s the hormone that helps you burn fat, build muscle , and increase your sex drive , and its power doesn’t stop there. Keeping your testosterone levels in a normal range can make you happier, too , and testosterone can even improve your cardiovascular health and decrease your risk of mortality (from all causes!), according to a study of 83,000 older men who underwent testosterone replacement therapy .
Known as the "male hormone," testosterone is produced primarily by the testicles. "Beginning around age 30, testosterone levels begin to decline naturally and continue to do so as a man ages," says Holly Lucille, ND, RN, a naturopathic doctor, educator, and author, "sometimes leading to low testosterone symptoms such as depressed moods, decreased sex drive, erectile dysfunction, and difficulties with concentration and memory.”
Magnesium: About 60% of our (if you’re a man) testosterone is bound to Sex Hormone Binding Globulin (SHBG), which removes the anabolism of testosterone and the availability thereof, robbing the rest of the body from any testosterone. What magnesium does is it lowers the SHBG count by quite a bit, granting the free testosterone in the body to increase in a large amount.
Men who watch a sexually explicit movie have an average increase of 35% in testosterone, peaking at 60–90 minutes after the end of the film, but no increase is seen in men who watch sexually neutral films. Men who watch sexually explicit films also report increased motivation, competitiveness, and decreased exhaustion. A link has also been found between relaxation following sexual arousal and testosterone levels.