“I’m a retired firefighter going on 65 and noticed I was getting soft and bigger in the belly even though I do regular exercise (jogging 3-4 miles 4 to 5 times a week). Since using Andro400, I’ve lost 2 inches off my waist and 12-13 pounds. I did not diet, ate what I normally do (here in Vegas, lots of buffets). Started out with a 38 inch waist, now 36; 195 lbs., now in the 182 range.”
How is it that women for many years have had HRT available and it is common place and acceptable for them? Men are expected to just have a decline and when they start to look into this, immediately they are looked at as they just want to do steroids. This is not the case for any of the comments I have read. I too simply like having my levels where they should be and if taken for this reason should be common place just as it is for estrogen replacement in women.
If you do take DAA I recommend cycling it (i.e. 5 days on, 2 off, over 4 weeks then 4 weeks off). And taking it with an aromatase inhibitor (which ensures the aspartic acid doesn’t get converted to estrogen). Especially as more studies are coming out showing the increase in testosterone is limited to a week or two before it drops back to normal levels.
Testosterone is only one of many factors that influence aggression and the effects of previous experience and environmental stimuli have been found to correlate more strongly. A few studies indicate that the testosterone derivative estradiol (one form of estrogen) might play an important role in male aggression. Studies have also found that testosterone facilitates aggression by modulating vasopressin receptors in the hypothalamus.
Men's levels of testosterone, a hormone known to affect men's mating behaviour, changes depending on whether they are exposed to an ovulating or nonovulating woman's body odour. Men who are exposed to scents of ovulating women maintained a stable testosterone level that was higher than the testosterone level of men exposed to nonovulation cues. Testosterone levels and sexual arousal in men are heavily aware of hormone cycles in females. This may be linked to the ovulatory shift hypothesis, where males are adapted to respond to the ovulation cycles of females by sensing when they are most fertile and whereby females look for preferred male mates when they are the most fertile; both actions may be driven by hormones.
Intramuscular testosterone injections were first used around fifty years ago. Commercially available preparations contain testosterone esters in an oily vehicle. Esterification is designed to retard the release of testosterone from the depot site into the blood because the half life of unmodified testosterone would be very short. For many years intramuscular preparations were the most commonly used testosterone therapy and this is still the case in some centers. Pain can occur at injection sites, but the injections are generally well tolerated and free of major side effects. Until recently, the available intramuscular injections were designed for use at a frequency of between weekly and once every four weeks. These preparations are the cheapest mode of testosterone treatment available, but often cause supraphysiological testosterone levels in the days immediately following injection and/or low trough levels prior to the next injection during which time the symptoms of hypogonadism may return (Nieschlag et al 1976). More recently, a commercial preparation of testosterone undecanoate for intramuscular injection has become available. This has a much longer half life and produces testosterone levels in the physiological range throughout each treatment cycle (Schubert et al 2004). The usual dose frequency is once every three months. This is much more convenient for patients but does not allow prompt cessation of treatment if a contraindication to testosterone develops. The most common example of this would be prostate cancer and it has therefore been suggested that shorter acting testosterone preparations should preferably used for treating older patients (Nieschlag et al 2005). Similar considerations apply to the use of subcutaneous implants which take the form of cylindrical pellets injected under the skin of the abdominal wall and steadily release testosterone to provide physiological testosterone levels for up to six months. Problems also include pellet extrusion and infection (Handelsman et al 1997).
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).
Epidemiological evidence supports a link between testosterone and glucose metabolism. Studies in non-diabetic men have found an inverse correlation of total or free testosterone with glucose and insulin levels (Simon et al 1992; Haffner et al 1994) and studies show lower testosterone levels in patients with the metabolic syndrome (Laaksonen et al 2003; Muller et al 2005; Kupelian et al 2006) or diabetes (Barrett-Connor 1992; Andersson et al 1994; Rhoden et al 2005). A study of patients with type 2 diabetes using measurement of serum free testosterone by the gold standard method of equilibrium dialysis, found a 33% prevalence of biochemical hypogonadism (Dhindsa et al 2004). The Barnsley study demonstrated a high prevalence of clinical and biochemical hypogonadism with 19% having total testosterone levels below 8 nmol/l and a further 25% between 8–12 nmol/l (Kapoor, Aldred et al 2007). There are also a number longitudinal studies linking low serum testosterone levels to the future development of the metabolic syndrome (Laaksonen et al 2004) or type 2 diabetes (Haffner et al 1996; Tibblin et al 1996; Stellato et al 2000; Oh et al 2002; Laaksonen et al 2004), indicating a possible role of hypogonadism in the pathogenesis of type 2 diabetes in men. Alternatively, it has been postulated that obesity may be the common link between low testosterone levels and insulin resistance, diabetes and cardiovascular disease (Phillips et al 2003; Kapoor et al 2005). With regard to this hypothesis, study findings vary as to whether the association of testosterone with diabetes occurs independently of obesity (Haffner et al 1996; Laaksonen et al 2003; Rhoden et al 2005).
“We need carbs, fats, and proteins to have optimal T levels,” says Howse. A healthy amount of carbs, for example, keeps cortisol levels low (more on why this is important to come). Meanwhile, dietary fats produce cholesterol, which our body can later convert into testosterone. And, finally, protein supports body composition by enhancing muscle repair and growth and increasing satiety.
Keep more weapons in your arsenal: Occasionally use lifting methods like forced reps, negatives, and dropsets to further stress your body. Personal trainer and fitness journalist Michael Berg explains in "6 Ways to Crank Up Your Testosterone Levels" that going beyond muscular failure with these techniques has been shown to pump up T-levels in study subjects.
Boron, a mineral, keeps the cell walls of plants strong. Eating dried fruits and nuts gives you abundant amounts of boron. You can also take boron supplements. It's important to keep your daily boron intake at less than 20 mg, however, according to a current factsheet available from the U.S. National Library of Medicine. High doses of boron can cause serious side effects such as skin inflammation and peeling, irritability, tremors or depression.
As with cognitive effects, previous studies examining CVD changes following testosterone treatment have been conflicting and inconclusive. Dr. Budoff and his research team used coronary computed tomographic angiography (CCTA) to assess 138 men, including 73 treated with testosterone and 65 receiving placebo, for changes in coronary artery plaque volume after 1 year.
There are positive correlations between positive orgasm experience in women and testosterone levels where relaxation was a key perception of the experience. There is no correlation between testosterone and men's perceptions of their orgasm experience, and also no correlation between higher testosterone levels and greater sexual assertiveness in either sex.
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.
Type 2 diabetes is an important condition in terms of morbidity and mortality, and the prevalence is increasing in the developed and developing world. The prevalence also increases with age. Insulin resistance is a primary pathological feature of type 2 diabetes and predates the onset of diabetes by many years, during which time raised serum insulin levels compensate and maintain normoglycemia. Insulin resistance and/or impaired glucose tolerance are also part of the metabolic syndrome which also comprises an abnormal serum lipid profile, central obesity and hypertension. The metabolic syndrome can be considered to be a pre-diabetic condition and is itself linked to cardiovascular mortality. Table 1 shows the three commonly used definitions of the metabolic syndrome as per WHO, NCEPIII and IDF respectively (WHO 1999; NCEPIII 2001; Zimmet et al 2005).
Two of the immediate metabolites of testosterone, 5α-DHT and estradiol, are biologically important and can be formed both in the liver and in extrahepatic tissues. Approximately 5 to 7% of testosterone is converted by 5α-reductase into 5α-DHT, with circulating levels of 5α-DHT about 10% of those of testosterone, and approximately 0.3% of testosterone is converted into estradiol by aromatase. 5α-Reductase is highly expressed in the male reproductive organs (including the prostate gland, seminal vesicles, and epididymides), skin, hair follicles, and brain and aromatase is highly expressed in adipose tissue, bone, and the brain. As much as 90% of testosterone is converted into 5α-DHT in so-called androgenic tissues with high 5α-reductase expression, and due to the several-fold greater potency of 5α-DHT as an AR agonist relative to testosterone, it has been estimated that the effects of testosterone are potentiated 2- to 3-fold in such tissues.
Another point I’d like to make for people worried about a link between high testosterone and prostate cancer is that it just doesn’t make sense. Prostate cancer becomes more prevalent in men as they age, and that’s also when their testosterone levels decline. We almost never see it in men in their peak testosterone years, in their 20s for instance. We know from autopsy studies that 8% of men in their 20s already have tiny prostate cancers, so if testosterone really made prostate cancer grow so rapidly — we used to talk about it like it was pouring gasoline on a fire — we should see some appreciable rate of prostate cancer in men in their 20s. We don’t. So, I’m no longer worried that giving testosterone to men will make their hidden cancer grow, because I’m convinced that it doesn’t happen.
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Vitamin D is arguably the most important vitamin when it comes to testosterone. A study published in the Journal of Clinical Endocrinology examined the relationship between vitamin D supplementation and testosterone levels in men. The authors found that participants with higher levels of vitamin D had significantly higher levels of free testosterone compared to those with insufficient levels of vitamin D.8 Based on these study results, it appears vitamin D has a strong relationship with testosterone levels.
A previous meta-analysis has confirmed that treatment of hypogonadal patients with testosterone improves erections compared to placebo (Jain et al 2000). A number of studies have investigated the effect of testosterone levels on erectile dysfunction in normal young men by inducing a hypogonadal state, for example by using a GnRH analogue, and then replacing testosterone at varying doses to produce levels ranging from low-normal to high (Buena et al 1993; Hirshkowitz et al 1997). These studies have shown no significant effects of testosterone on erectile function. These findings contrast with a similar study conducted in healthy men aged 60–75, showing that free testosterone levels achieved with treatment during the study correlate with overall sexual function, including morning erections, spontaneous erections and libido (Gray et al 2005). This suggests that the men in this older age group are particularly likely to suffer sexual symptoms if their testosterone is low. Furthermore, the severity of erectile dysfunction positively correlates with lower testosterone levels in men with type 2 diabetes (Kapoor, Clarke et al 2007).
It’s perhaps no coincidence that Giacomo Casanova, who was said to eat 50 oysters for breakfast each morning, reportedly bed half of Europe. After all, oysters are brimming with zinc, a mineral that elevates testosterone while simultaneously boosting growth factor hormone—both of which enhance muscle growth and physical performance (in and out of the bedroom).
Why is there no information on the increase of estrogen when on Testosterone replacement therapy? I have been on t replacement for about 2 years and over that time my balls have gotten to the size of a large grape. I have fatty tissue on my chest and my estrogen level is over 400. There needs to be a study created to test all of these side effects and posable treatments like estrogen lowering drugs and HCG for maintaining Testicle size.
One study showed that six months of zinc supplementation among slightly zinc-deficient elderly men doubled serum levels of testosterone. And another eight-week trial found that college football players who took a nightly zinc supplement showed increased T-levels and increased leg strength that was 250 percent greater than a placebo! Holy quads, Batman! Research has also shown deficiencies in zinc to be a risk factor for infertility caused by low testosterone levels.
Natural remedies for treating erectile dysfunction Erectile dysfunction has many causes, can affect any male, and is often distressing? Some people advocate several different natural remedies, mostly herbs and other plants. Here, we look at their merits and side effects, plus lifestyle changes, and alternative therapies that may bring relief for erectile dysfunction. Read now