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).
[quote]You see there is a difference between your free testosterone levels and your total testosterone levels. As testosterone flows through your blood, free testosterone is chemically active and available for your body to use as it will. While other testosterone is floating around bound to SHGB (Sex Hormone Binding Globulin). This testosterone is inactive and unable to be used by your body because the SHGB renders it inert. So while you may have a high amount of “total testosterone,” much of it may be unavailable to be used by your body. So it is really the amount of free testosterone in your body that you should be concerned with.”[/quote]

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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).
A diagnosis of low testosterone is typically made if a man’s free testosterone hormone level is below 300 ng/dL. But as a doctor specializing in sexual health, I typically consider optimized male testosterone levels somewhere between 600 to 800 ng/dL—rarely above or below those numbers. The tests that I routinely recommend to my male clients can be found in this test panel and include biomarkers associated with testosterone, free and total (this includes sex-hormone binding globulin [SHBG]), estradiol, estrogen (total and serum), cortisol, DHEAs, thyroid-stimulating hormone (TSH), hemoglobin A1C, and vitamin D.
The real danger comes when you eat a diet high in sugars and carbohydrates (90% of Americans). The sugar binds to LDL (So-called bad cholesterol – PS: It’s not even cholesterol, it’s a protein) and renders it inert. When inert, the LDL cannot pull good cholesterol (HDL) into your cells. This is bad. So what you need to do in conduction with your high fat diet is take in a lot of cruciferous vegetables, limit your carb intake, don’t touch toxic sugars. And exercise regularly.
Although some men believe that taking testosterone medications may help them feel younger and more vigorous as they age, few rigorous studies have examined testosterone therapy in men who have healthy testosterone levels. And some small studies have revealed mixed results. For example, in one study healthy men who took testosterone medications increased muscle mass but didn't gain strength.
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