Inaccurate or misinterpreted test results can either falsely diagnose or miss a case of testosterone deficiency. Your testosterone level should be measured between 7 am and 10 am, when it's at its peak. Confirm a low reading with a second test on a different day. It may require multiple measurements and careful interpretation to establish bioavailable testosterone, or the amount of the hormone that is able to have effects on the body. Consider getting a second opinion from an endocrinologist.
Among my favorite stress management tools is the Emotional Freedom Technique (EFT), a method similar to acupuncture but without the use of needles. EFT is known to eliminate negative behavior and instill a positive mentality. Always bear in mind that your emotional health is strongly linked to your physical health, and you have to pay attention to your negative feelings as much as you do to the foods you eat.
For people who are worried about low or high testosterone, a doctor may perform a blood test to measure the amount of the hormone in the patient's blood. When doctors find low-T, they may prescribe testosterone therapy, in which the patient takes an artificial version of the hormone. This is available in the following forms: a gel to be applied to the upper arms, shoulders or abdomen daily; a skin patch put on the body or scrotum twice a day; a solution applied to the armpit; injections every two or three weeks; a patch put on the gums twice a day; or implants that last four to six months.
Before the ready availability of non-injectible testosterone preparations, and because of their ease of administration by the oral route, 17-alkylated steroids were popular surrogate agents for testosterone. These substances, however, were capable of inducing several risk factors for coronary artery disease (Kopera 1993; Hall and Hall 2005) and as a consequence, particularly after the revelations of extensive 17-alkylated anabolic steroid abuse by athletes, testosterone, became unjustly incriminated. The evidence, however, tends to suggest just the opposite; testosterone may even be cardioprotective. Dunajska and colleagues have demonstrated that when compared to controls, men with coronary artery disease tend to have: lower total testosterone levels and free androgen indices, more abdominal fat, higher blood sugar and insulin levels (Dunajska et al 2004).
The normal development of the prostate gland is dependent on the action of testosterone via the androgen receptor, and abnormal biosynthesis of the hormone or inactivating mutations of the androgen receptor are associated with a rudimentary prostate gland. Testosterone also requires conversion to dihydrotestosterone in the prostate gland for full activity. In view of this link between testosterone and prostate development, it is important to consider the impact that testosterone replacement may have on the prevalence and morbidity associated with benign prostatic hypertrophy (BPH) and prostate cancer, which are the common conditions related to pathological growth of the prostate gland.
A number of epidemiological studies have found that bone mineral density in the aging male population is positively associated with endogenous androgen levels (Murphy et al 1993; Ongphiphadhanakul et al 1995; Rucker et al 2004). Testosterone levels in young men have been shown to correlate with bone size, indicating a role in determination of peak bone mass and protection from future osteoporosis (Lorentzon et al 2005). Male hypogonadism has been shown to be a risk factor for hip fracture (Jackson et al 1992) and a recent study showed a high prevalence of hypogonadism in a group of male patients with average age 75 years presenting with minimal trauma fractures compared to stroke victims who acted as controls (Leifke et al 2005). Estrogen is a well known determinant of bone density in women and some investigators have found serum estrogen to be a strong determinant of male bone density (Khosla et al 1998; Khosla et al 2001). Serum estrogen was also found to correlate better than testosterone with peak bone mass (Khosla et al 2001) but this is in contradiction of a more recent study showing a negative correlation of estrogen with peak bone size (Lorentzon et al 2005). Men with aromatase deficiency (Carani et al 1997) or defunctioning estrogen receptor mutations (Smith et al 1994) have been found to have abnormally low bone density despite normal or high testosterone levels which further emphasizes the important influence of estrogen on male bone density.
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