In order to discuss the biochemical diagnosis of hypogonadism it is necessary to outline the usual carriage of testosterone in the blood. Total serum testosterone consists of free testosterone (2%–3%), testosterone bound to sex hormone binding globulin (SHBG) (45%) and testosterone bound to other proteins (mainly albumin −50%) (Dunn et al 1981). Testosterone binds only loosely to albumin and so this testosterone as well as free testosterone is available to tissues and is termed bioavailable testosterone. Testosterone bound to SHBG is tightly bound and is biologically inactive. Bioavailable and free testosterone are known to correlate better than total testosterone with clinical sequelae of androgenization such as bone mineral density and muscle strength (Khosla et al 1998; Roy et al 2002). There is diurnal variation in serum testosterone levels with peak levels seen in the morning following sleep, which can be maintained into the seventh decade (Diver et al 2003). Samples should always be taken in the morning before 11 am to allow for standardization.
Testosterone is everywhere playing multiple roles from intrauterine life to advanced age. Table 1, the contents of which are always undergoing change primarily because of newly observed associations, provides an overview of the bodily systemic functions and patho-physiological states in which testosterone finds itself implicated. In some of these states there is a clear physiological cause and effect relationship. In others, evidence of the physiological role is early or tenuous.
Bisphenol-A also known under the name of BPA is a chemical compound which is very widespread for manufacturing a wide spectrum of plastic items and aluminum cans. Many studies have already proven the fact that even the smallest amount of BPA is very harmful to the human health. This compound causes hormonal imbalance and even may lead to prostate cancer.
For men with low blood testosterone levels, the benefits of hormone replacement therapy usually outweigh potential risks. However, for most other men it's a shared decision with your doctor. It offers men who feel lousy a chance to feel better, but that quick fix could distract attention from unknown long-term hazards. "I can't tell you for certain that this raises your personal risk of heart problems and prostate cancer, or that it doesn't," Dr. Pallais says.
When your testosterone levels go up, so does your libido. Unfortunately, the inverse is not true — your libido levels can go up without your testosterone levels also going up. And that’s how most supposed T-boosters “work”: they make you feel ornery, leading you to think that your T levels are appreciably higher, when they actually aren’t. In rare cases, supplementation will result in a 20% testosterone increase. This kind of improvement may sound impressive, but is irrelevant for practical purposes.
Fenugreek, which is scientifically known as Trigonella foenum-graecum, is a popular medicinal herb used in India and areas of the Middle East. Studies on fenugreek suggest that it can increase testosterone levels by acting as an aromatase inhibitor. Aromatase is the enzyme responsible for converting testosterone into estrogen. Studies show that subjects supplementing fenugreek experienced a boost in testosterone as well as reduced fat loss and increased strength and muscle mass.
Cardiovascular disease, and its underlying pathological process atherosclerosis, is an important cause of morbidity and mortality in the developed and developing world. Coronary heart disease in particular is the commonest cause of death worldwide (AHA 2002; MacKay and Mensah 2004). As well as increasing with age, this disease is more common in the male versus female population internationally, which has led to interest in the potential role of sex hormones in modulating risk of development of atherosclerosis. Concerns about the potential adverse effects of testosterone treatment on cardiovascular disease have previously contributed to caution in prescribing testosterone to those who have, or who are at risk of, cardiovascular disease. Contrary to fears of the potential adverse effects of testosterone on cardiovascular disease, there are over forty epidemiological studies which have examined the relationship of testosterone levels to the presence or development of coronary heart disease, and none have shown a positive correlation. Many of these studies have found the presence of coronary heart disease to be associated with low testosterone levels (Reviews: Jones, Jones et al 2003; Jones et al 2005).
Individuals with metabolic syndrome are at increased risk for developing coronary artery disease and diabetes mellitus. Predicting who might develop the metabolic syndrome would allow preventive measures to be taken in addition to weight control and other lifestyle modifications such as cessation of smoking and increased exercise. It is known that with decreasing testosterone availability in aging males there is an increase in fat mass and decrease in lean body mass (van den Beld et al 2000), there are disorders of insulin and glucose metabolism (Haffner et al 1996) and dyslipidemia (Tsai et al 2004). Kupelian and colleagues (2006) in analyzing data from the Massachusetts Male Aging Study demonstrated that men with low levels of testosterone, sex hormone-binding globulin, or clinical androgen deficiency, especially men with a BMI of greater than 25, were at increased risk of developing the metabolic syndrome and hence, diabetes mellitus and/or coronary artery disease.
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).
In addition to weight training, combining this with interval training like burst training is the best overall combo to increase HGH. In fact, Burst training has been proven to not only boost T-levels, it helps keeps your testosterone elevated and can prevent its decline. Burst training involves exercising at 90–100 percent of your maximum effort for a short interval in order to burn your body’s stored sugar (glycogen), followed by a period of low impact for recovery.
I didn't feel bad before, even when I wouldn't have a good night's rest. I just felt stronger and more willing to workout. I didn't realize what was going on until one day before bed; as usual I was taking my ZMA. I thought back on how the research said ZMA was a testosterone booster, and then it hit me. This stuff is what was helping me out in terms of increased male hormone drive.
Cognitive abilities differ between males and females and these differences are present from childhood. In broad terms, girls have stronger verbal skills than boys who tend to have stronger skills related to spatial ability (Linn and Petersen 1985). It is thought that the actions of sex hormones have a role in these differences. Reviewing different cognitive strengths of male versus female humans is not within the scope of this article but the idea that cognition could be altered by testosterone deserves attention.
Testosterone is significantly correlated with aggression and competitive behaviour and is directly facilitated by the latter. There are two theories on the role of testosterone in aggression and competition. The first one is the challenge hypothesis which states that testosterone would increase during puberty thus facilitating reproductive and competitive behaviour which would include aggression. Thus it is the challenge of competition among males of the species that facilitates aggression and violence. Studies conducted have found direct correlation between testosterone and dominance especially among the most violent criminals in prison who had the highest testosterone levels. The same research also found fathers (those outside competitive environments) had the lowest testosterone levels compared to other males.
D-Aspartic acid is a natural amino acid involved in the synthesis and release of testosterone, which research shows can be used as a testosterone booster for infertile men. One 90-day study gave D-Aspartic acid to men with impaired sperm production, and found their sperm count rose from 8.2 million sperm per ml to 16.5 million sperm per ml, more than a 100 per cent increase.
Every vitamin, mineral, and ingredient that affects the human body can be taken in enough quantities that they are harmful, or toxic, even the ones that — at lower levels — are beneficial or necessary. Unfortunately, testosterone boosters contain a lot of ingredients that are not well understood. This means in addition to not being able to confirm whether certain ingredients increase testosterone, the scientific and medical communities also don’t know at what levels many ingredients become toxic. On the up side, you might need to eat several pounds of a particular leafy plant before it becomes harmful. On the down side, it could be significantly less that pushes you over your body’s limit. We simply don’t know how little or how much the human body can tolerate. We recommend keeping your doctor in the loop when you add any supplement with unproven ingredients into your diet — they’ll be able to help you find and track any undesired side-effects that these ingredients might cause.
Testosterone is observed in most vertebrates. Testosterone and the classical nuclear androgen receptor first appeared in gnathostomes (jawed vertebrates). Agnathans (jawless vertebrates) such as lampreys do not produce testosterone but instead use androstenedione as a male sex hormone. Fish make a slightly different form called 11-ketotestosterone. Its counterpart in insects is ecdysone. The presence of these ubiquitous steroids in a wide range of animals suggest that sex hormones have an ancient evolutionary history.
Testosterone levels generally peak during adolescence and early adulthood. As you get older, your testosterone level gradually declines — typically about 1 percent a year after age 30 or 40. It is important to determine in older men if a low testosterone level is simply due to the decline of normal aging or if it is due to a disease (hypogonadism).