Male hypogonadism becomes more common with increasing age and is currently an under-treated condition. The diagnosis of hypogonadism in the aging male requires a combination of symptoms and low serum testosterone levels. The currently available testosterone preparations can produce consistent physiological testosterone levels and provide for patient preference.
"I went from 230 pounds down to 192. When my son got married, I went for the suit fitting, and I was a size 48. When I went back to do the final fitting, I was a 44! I want to keep getting it for the weight loss; I lost 4 inches around my belly, and I want to get rid of the rest of the weight around my belly. I’m 57, and my wife says I look like I’m back in my 30s. I have more energy for sure, and I’m going to participate in one of those Savage races where they have the obstacle courses with one of our kids."
Changes in body composition are seen with aging. In general terms, aging males are prone to loss of muscle mass and a gain in fat mass, especially in the form of visceral or central fat. An epidemiological study of community dwelling men aged between 24 and 85 years has confirmed that total and free testosterone levels are inversely correlated with waist circumference and that testosterone levels are specifically related to this measure of central obesity rather than general obesity (Svartberg, von Muhlen, Sundsfjord et al 2004). Prospective studies show that testosterone levels predict future development of central obesity (Khaw and Barrett-Connor 1992; Tsai et al 2000). Reductions in free testosterone also correlate with age related declines in fat free mass (muscle mass) and muscle strength (Baumgartner et al 1999; Roy et al 2002). Studies in hypogonadal men confirm an increase in fat mass and decrease in fat free mass versus comparable eugonadal men (Katznelson et al 1998). Taken together, the epidemiological data suggest that a hypogonadal state promotes loss of muscle mass and a gain in fat mass, particularly visceral fat and therefore mimics the changes of ‘normal’ aging.
More can be learned from a large, randomized, placebo-controlled trial of finasteride treatment in 18,800 men aged 55 or more. Finasteride is a 5α-reductase inhibitor which acts to prevent the metabolism of testosterone to dihydrotestosterone (DHT) – the most active androgen in the prostate. The trial showed a greater overall incidence of prostate cancer in the control group, but men treated with finasteride were more likely to have high grade tumors (Thompson et al 2003), suggesting that reduced androgen exposure of the prostate may delay the presentation of prostate cancer and/or promote advanced disease in some other way.
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 am 56 and I have been taking 100 mg of Test Cyp IM once a week for the last 4 months. My total T fluctuates between 500 and 1000 and my E2 has been staying under 30 with the help of Arimidex 0.5 mg every 3.5 days. I do not know what my free T is due to the expense but I feel much better than I did. Not great but much better so I will continue. If you are not feeling good on TRT then you should have your E2 checked because it is probably over 30 which will counteract the effects of your free T.
This post can absolutely change your life, and probably help you avoid some pitfalls. Like shrunken balls. (I am not an expert in the synthetic anabolic testosterone drugs used by bodybuilders — they carry lots of risks but pack a big punch if you want to get swole. Bulletproof is all about having massive clean energy, looking good, and living a very long time…so anabolic steroids aren’t on my roadmap.)
The most popular way is to combine with a good tasting protein powder. Advanced BCAA’s taste very bitter due to the high amount of peptides. Peptides taste very bitter. You want to use 1 tsp of Advanced BCAA’s with every serving of protein powder. This will really upgrade the quality of the protein powder by adding BCAA, AND in peptides form. If you are using a whey protein you’ll increase the overall BCAA content by over 20%
Forged Methyl EAA stands out as it has a special concentrated derivative of D-Aspartic Acid (DAA) which is touted as being 50 times more effective than normal DAA. The formula is so strong that Transform supplements had to put an estrogen blocker as when your testosterone levels get boosted very high, your body will start to convert it to estrogen. It comes with a hefty price tag but many users have considered it to be hands down the strongest on the market.
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).
If a man's testosterone looks below the normal range, there is a good chance he could end up on hormone supplements—often indefinitely. "There is a bit of a testosterone trap," Dr. Pallais says. "Men get started on testosterone replacement and they feel better, but then it's hard to come off of it. On treatment, the body stops making testosterone. Men can often feel a big difference when they stop therapy because their body's testosterone production has not yet recovered."
After various studies in animals had shown anabolic (muscle building) properties among the various Fenugreek benefits, a study was conducted on men undergoing resistance training. During the study the participants trained in a supervised manner 4 times a week for 8 weeks. Although the levels of DHT (Dihydrotestosterone) were reduced in those taking the Fenugreek supplement, other hormonal markers were not affected. Another study further supported those findings, while also reporting that those taking the supplement witnessed an additional 2kg of fat loss and 2kg more muscle mass gain over the same period. Impressive results indeed.
I’ve had low testo in the winter for the last 10 years, with the lowest values around april (live in the north). But last year (in september) I started using vitamine D (10 000 IU) and K2 (180 mcg), combined with magnesium (200 mg malate) and zinc (25 mg malate and piccolinate) every night, and since then I no longer have low testo in the winter, and is feeling like I do in the summer and have normal testo levels. This combo may work for other people as well. And the risk for dangerous side effects is probabaly neglectable. But it takes a couple of weeks before it kicks in.