Testosterone is an important hormone for both men and women. Even though it’s often associated with a man’s libido, testosterone occurs in both sexes from birth. In females, it plays a part in sexual drive, energy, and physical strength. In males, it stimulates the beginning of sexual development and helps maintain a man’s health throughout his life.
If you are serious about losing weight, you have got to strictly limit the amount of processed sugar in your diet, as evidence is mounting that excess sugar, and fructose in particular, is the primary driving factor in the obesity epidemic. So cutting soda from your diet is essential, as is limiting fructose found in processed foods, fruit juice, excessive fruit and so-called "healthy" sweeteners like agave.
The reliable measurement of serum free testosterone requires equilibrium dialysis. This is not appropriate for clinical use as it is very time consuming and therefore expensive. The amount of bioavailable testosterone can be measured as a percentage of the total testosterone after precipitation of the SHBG bound fraction using ammonium sulphate. The bioavailable testosterone is then calculated from the total testosterone level. This method has an excellent correlation with free testosterone (Tremblay and Dube 1974) but is not widely available for clinical use. In most clinical situations the available tests are total testosterone and SHBG which are both easily and reliably measured. Total testosterone is appropriate for the diagnosis of overt male hypogonadism where testosterone levels are very low and also in excluding hypogonadism in patients with normal/high-normal testosterone levels. With increasing age, a greater number of men have total testosterone levels just below the normal range or in the low-normal range. In these patients total testosterone can be an unreliable indicator of hypogonadal status. There are a number of formulae that calculate an estimated bioavailable or free testosterone level using the SHBG and total testosterone levels. Some of these have been shown to correlate well with laboratory measures and there is evidence that they more reliably indicate hypogonadism than total testosterone in cases of borderline biochemical hypogonadism (Vermeulen et al 1971; Morris et al 2004). It is important that such tests are validated for use in patient populations relevant to the patient under consideration.
Cross-sectional studies conducted at the time of diagnosis of BPH have failed to show consistent differences in testosterone levels between patients and controls. A prospective study also failed to demonstrate a correlation between testosterone and the development of BPH (Gann et al 1995). Clinical trials have shown that testosterone treatment of hypogonadal men does cause growth of the prostate, but only to the size seen in normal men, and also causes a small increase in prostate specific antigen (PSA) within the normal range (Rhoden and Morgentaler 2005). Despite growth of the prostate a number of studies have failed to detect any adverse effects on symptoms of urinary obstruction or physiological measurements such as flow rates and residual volumes (Snyder et al 1999; Kenny et al 2000, 2001). Despite the lack of evidence linking symptoms of BPH to testosterone treatment, it remains important to monitor for any new or deteriorating problems when commencing patients on testosterone treatment, as the small growth of prostate tissue may adversely affect a certain subset of individuals.
Cross-sectional studies have not shown raised testosterone levels at the time of diagnosis of prostate cancer, and in fact, low testosterone at the time of diagnosis has been linked with more locally aggressive and malignant tumors (Massengill et al 2003; Imamoto et al 2005; Isom-Batz et al 2005). This may reflect loss of hormone related control of the tumor or the effect of a more aggressive tumor in decreasing testosterone levels. One study found that 14% of hypogonadal men, with normal digital rectal examination and PSA levels, had histological prostate cancer on biopsy. It is possible that low androgen levels masked the usual evidence of prostate cancer in this population (Morgentaler et al 1996). Most longitudinal studies have not shown a correlation between testosterone levels and the future development of prostate cancer (Carter et al 1995; Heikkila et al 1999; Stattin et al 2004) but a recent study did find a positive association (Parsons et al 2005). Interpretation of such data requires care, as the presentation of prostate cancer could be altered or delayed in patients with lower testosterone levels.

There have been case reports of development of prostate cancer in patients during treatment with testosterone, including one case series of twenty patients (Gaylis et al 2005). It is not known whether this reflects an increase in incidence, as prostate cancer is very common and because the monitoring for cancer in patients treated with testosterone is greater. Randomized controlled trials of testosterone treatment have found a low incidence of prostate cancer and they do not provide evidence of a link between testosterone treatment and the development of prostate cancer (Rhoden and Morgentaler 2004). More large scale clinical trials of longer durations of testosterone replacement are required to confirm that testosterone treatment does not cause prostate cancer. Overall, it is not known whether testosterone treatment of aging males with hypogonadism increases the risk of prostate cancer, but monitoring for the condition is clearly vital. This should take the form of PSA blood test and rectal examination every three months for the first year of treatment and yearly thereafter (Nieschlag et al 2005). Age adjusted PSA reference ranges should be used to identify men who require further assessment. The concept of PSA velocity is also important and refers to the rate of increase in PSA per year. Patients with abnormal rectal examination suggestive of prostate cancer, PSA above the age specific reference range or a PSA velocity greater than 0.75 ng/ml/yr should be referred to a urologist for consideration of prostate biopsy.


1. Go Mediterranean. Keeping up with specific types of food that you should or should not eat can be hard, especially if you don’t have a general guide. There are a number of studies that have concluded that the Mediterranean diet can indeed boost the amount of testosterone in the body, and enhance the strength of an erection as well. The Mediterranean diet contains a lot of healthy fat, like polyunsaturated fat and monounsaturated fat. Aside from being pro-testosterone, the Mediterranean diet is also the only diet that is certified to help decrease the chances of developing cancer and heart conditions. Those who are taking erection enhancement supplements can also benefit from the Mediterranean diet. This type of diet originated from the Southern part of Greece, and is composed of food groups such as nuts, whole grains, fruits, extra virgin olive oil, red wine, fats and vegetables.

Decreased testosterone production in men with rheumatoid arthritis is a common finding (Stafford et al 2000), and it is now generally recognized that androgens have the capacity to suppress both the hormonal and cellular immune response and so act as one of the body’s natural anti-inflammatory agents (Cutolo et al 2002). This known anti-inflammatory action of testosterone has led to studying the effect of testosterone therapy in men with rheumatoid disease. Although not all studies have reported positive effects of testosterone treatment (Hall et al 1996), some studies do demonstrate an improvement in both clinical and chemical markers of the immune response (Cutolo et al 1991; Cutolo 2000). This observation would go along with more recent evidence that testosterone or its metabolites protects immunity by preserving the number of regulatory T cells and the activation of CD8+ T cells (Page et al 2006).

When testosterone and endorphins in ejaculated semen meet the cervical wall after sexual intercourse, females receive a spike in testosterone, endorphin, and oxytocin levels, and males after orgasm during copulation experience an increase in endorphins and a marked increase in oxytocin levels. This adds to the hospitable physiological environment in the female internal reproductive tract for conceiving, and later for nurturing the conceptus in the pre-embryonic stages, and stimulates feelings of love, desire, and paternal care in the male (this is the only time male oxytocin levels rival a female's).[citation needed]
Testosterone makes a contribution to nitric oxide formation. Nitric oxide, released from penile nerves stimulates guanylate cyclase which catalyzes the transformation of guanosine-5-triphosphate into 3′,5′-cyclic, guanosine monophosphate (cyclic GMP). Gyclic GMP causes vasodilatation and hence erection formation (Morelli et al 2005). The breakdown of cyclic GMP to GMP is mediated by the enzyme, phosphodiesterase type-5, the inhibitors of which (eg, sildenafil citrate) enhance erection formation and maintanence (Carson and Lue 2005).
The Organon group in the Netherlands were the first to isolate the hormone, identified in a May 1935 paper "On Crystalline Male Hormone from Testicles (Testosterone)".[180] They named the hormone testosterone, from the stems of testicle and sterol, and the suffix of ketone. The structure was worked out by Schering's Adolf Butenandt, at the Chemisches Institut of Technical University in Gdańsk.[181][182]

A: If a health insurance company is providing coverage for a medication, including testosterone replacement therapy, they determine the final cost of the product. Costs will vary from one health insurance plan to another. To determine the costs of the testosterone replacement options, the health insurance plan should be contacted. There are various options for testosterone replacement therapy including gels, injections, patches, and tablets that dissolve under the lip. All of the formulations can be effective and each has advantages and disadvantages. The most appropriate testosterone replacement therapy depends on a variety of factors, including cost, patient preference, and tolerability. Testosterone replacement gels, such as AndroGel and Testim, are very effective and easy to administer. AndroGel and Testim can be easily applied to the skin once daily. However, the gels can be irritating to the skin and AndroGel and Testim are typically quite expensive. Testosterone replacement injections, such as Depo-Testosterone (testosterone cypionate) and Delatestryl (testosterone enanthate), are usually inexpensive. The injections are given only once every one to two weeks. The major disadvantage with injectable testosterone is that testosterone levels may be difficult to control. Levels may be too high after an injection and too low before the following injection. A testosterone replacement patch, such as Androderm, is applied every night and left on for 24 hours. Androderm can be applied to the arm, back or stomach, in an area without too much hair. Androderm can cause irritation of the skin. A testosterone tablet, Striant, is placed under the upper lip against the gums and replaced every 12 hours. Striant molds to the upper gum so that eating and drinking can occur normally. The testosterone tablet can irritate the gums and cause a bitter taste and toothache. People with low testosterone should work with their doctor or healthcare provider to find a safe, effective, and affordable testosterone replacement option for them. For more specific information, consult with your doctor or pharmacist for guidance based on your health status and current medications, particularly before taking any action. Derek Dore, PharmD
When you’re under stress (be it from lack of sleep, workplace stress, emotional stress, stress from a bad diet, overtraining etc.), your body releases cortisol. Cortisol blunts the effects of testosterone (47), which makes sense from an evolutionary point of view – if we were stressed as cavemen chances are it was a life or death situation – not running late to a meeting - in this state (i.e. running from a lion) the body wouldn’t care if you couldn’t get it up, there was more to worry about!
In accordance with sperm competition theory, testosterone levels are shown to increase as a response to previously neutral stimuli when conditioned to become sexual in male rats.[40] This reaction engages penile reflexes (such as erection and ejaculation) that aid in sperm competition when more than one male is present in mating encounters, allowing for more production of successful sperm and a higher chance of reproduction.
Directions — SUGGESTED USE: As a dietary supplement take 3 capsules daily, preferably with a meal, or as directed by a healthcare professional. — Take two capsules with a meal twice a day. On days that you are not training, take two capsules in the morning and two capsules at night. On days that you train, take two capsules about an hour before workouts and take two capsules in the morning or at night depending on when you train.
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).

Phthalates are found to cause poor testosterone synthesis by disrupting an enzyme required to create the male hormone. Women with high levels of DEHP and DBP (two types of phthalates) in their system during pregnancy were found to have sons that had feminine characteristics Phthalates are found in vinyl flooring, detergents, automotive plastics, soaps and shampoos, deodorants, perfumes, hair sprays, plastic bags and food packaging, among a long list of common products. Aside from phthalates, other chemicals that possess gender-bending traits are:


Studies have demonstrated reduced testosterone levels in men with heart failure as well as other endocrine changes (Tappler and Katz 1979; Kontoleon et al 2003). Treatment of cardiac failure with chronic mechanical circulatory support normalizes many of these changes, including testosterone levels (Noirhomme et al 1999). More recently, two double-blind randomized controlled trials of testosterone treatment for men with low or low-normal serum testosterone levels and heart failure have shown improvements in exercise capacity and symptoms (Pugh et al 2004; Malkin et al 2006). The mechanism of these benefits is currently unclear, although a study of the acute effects of buccal testosterone given to men with chronic cardiac failure under invasive monitoring showed that testosterone increased cardiac index and reduced systemic vascular resistance (Pugh et al 2003). Testosterone may prove useful in the management of cardiac failure but further research is needed.
If in a 46 XY individual testosterone is either not produced in adequate concentrations as in gonadal dysgenesis (MacLaughlin and Donahue 2004), or in the absence of the enzyme 17 alpha-hydroxylase so that testosterone is not produced (Ergun-Longmire et al 2006), or testosterone androgen receptors are absent as in the androgen insensitivity syndrome (Hughes and Deeb 2006), phenotypic females will result.
Millions of American men use a prescription testosterone gel or injection to restore normal levels of the manly hormone. The ongoing pharmaceutical marketing blitz promises that treating "low T" this way can make men feel more alert, energetic, mentally sharp, and sexually functional. However, legitimate safety concerns linger. For example, some older men on testosterone could face higher cardiac risks.
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