The diagnosis of late-onset hypogonadism requires the combination of low serum testosterone levels with symptoms of hypogonadism. Questionnaires are available which check for the symptoms of hypogonadism. These have been validated for the assessment of aging patients with hypogonadism (Morley et al 2000; Moore et al 2004) but have a low specificity. In view of the overlap in symptoms between hypogonadism, aging and other medical conditions it is wise to use a formal method of symptom assessment which can be used to monitor the effects of testosterone replacement.
Longjack, also known as Tongkat ali and pasak bumi, is a shrub hailing from Southeast Asia purporting to improve libido. It’s gaining traction in the scientific community for potentially increasing testosterone levels, and researchers at South Africa’s University of the Western Cape found that longjack improved testosterone levels and muscular strength in physically active seniors (a population with typically low testosterone).
On review of the patient’s history, he was found to have undergone laboratory tests before starting to use the aforementioned testosterone booster product. All blood parameters (testosterone hormone and full chemical profile) before product intake were in the normal range. A physical examination that included blood pressure and pulse assessments showed nothing out of the ordinary, and the man appeared to be in good condition before product consumption. After that medical checkup, the athlete began to consume the product for 42 continuous days divided into 2 cycles (each cycle comprised 24 days). The daily dose was a single pack of Universal Nutrition Animal Stak (ingredients are listed in Table 1), following the exact direction of the manufacturing company hoping to get the best results.

There is a polymorphic CAG repeat sequence in the androgen receptor gene, which codes for a variable number of glutamine amino acids in the part of the receptor affecting gene transcription. A receptor with a short CAG sequence produces greater activity when androgens attach, and men with shorter CAG polymorphisms exhibit androgenic traits, such as preserved bone density (Zitzmann et al 2001) and prostate growth during testosterone treatment (Zitzmann et al 2003). Indirect evidence of the importance of androgens in the development of prostate cancer is provided by case control study findings of a shorter, more active CAG repeat sequence in the androgen receptor gene of patients with prostate cancer compared with controls (Hsing et al 2000, 2002).

Lean beef, chicken, fish, and eggs are some of your options. Tofu, nuts, and seeds have protein, too. Try to get about 5 to 6 ounces per day, although the ideal amount for you depends on your age, sex, and how active you are. When you don't eat enough of these foods, your body makes more of a substance that binds with testosterone, leaving you with less T available to do its job.
In a placebo-controlled study, 27 Division II football players received either a placebo or a ZMA supplement for a total of seven weeks during their scheduled spring practice. At the end of the seven weeks, the players taking the ZMA supplement had a 30 percent increase in testosterone, while the placebo group had a 10 percent decrease. The ZMA group also saw an 11.6 percent increase in strength, compared to only 4.6 percent in the placebo group.[7]
Vitamin D supplementation may potentially boost testosterone levels, but further research is needed to determine if it really has an effect on the testosterone levels of young people and athletes. The truth is likely similar to zinc and magnesium — being in a deficient state causes your testosterone levels to drop below baseline, and supplementing it just takes you right back to baseline (but not any higher).
Erectile dysfunction is a common finding in the aging male. A prevalence of over 70% was found in men older than 70 in a recent cross-sectional study (Ponholzer et al 2005). Treatment with phosphodiesterase-5 (PDE-5) inhibitors is proven to be effective for the majority of men but some do not respond (Shabsigh and Anastasiadis 2003). The condition is multi-factorial, with contributions from emotional, vascular, neurological and pharmacological factors. The concept of erectile dysfunction as a vascular disease is particularly interesting in view of the evidence presented above, linking testosterone to atherosclerosis and describing its action as a vasodilator.
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).
Overall, few patients have a compelling contraindication to testosterone treatment. The majority of men with late onset hypogonadism can be safely treated with testosterone but all will require monitoring of prostate parameters HDL cholesterol, hematocrit and psychological state. It is also wise to monitor symptoms of sleep apnea. Other specific concerns may be raised by the mode of delivery such as local side effects from transdermal testosterone.
As blood levels of testosterone increase, this feeds back to suppress the production of gonadotrophin-releasing hormone from the hypothalamus which, in turn, suppresses production of luteinising hormone by the pituitary gland. Levels of testosterone begin to fall as a result, so negative feedback decreases and the hypothalamus resumes secretion of gonadotrophin-releasing hormone. 
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]
Smith and colleagues (2005) undertook a prospective study on the contribution of stress to coronary heart disease. Their study, which involved 2512 men aged 45 to 59 years, looked at a number of metabolic parameters. They found that an increased cortisol to testosterone ratio was associated with a high risk of coronary artery disease and that this risk was mediated by components of the insulin resistance syndrome. They reported that high cortisol and low testosterone levels are associated with a worsening of insulin resistance and that there is evidence to support the possibility of improving this pattern by treatment with testosterone.
Present in much greater levels in men than women, testosterone initiates the development of the male internal and external reproductive organs during foetal development and is essential for the production of sperm in adult life. This hormone also signals the body to make new blood cells, ensures that muscles and bones stay strong during and after puberty and enhances libido both in men and women. Testosterone is linked to many of the changes seen in boys during puberty (including an increase in height, body and pubic hair growth, enlargement of the penis, testes and prostate gland, and changes in sexual and aggressive behaviour). It also regulates the secretion of luteinising hormone and follicle stimulating hormone. To effect these changes, testosterone is often converted into another androgen called dihydrotestosterone. 
Another effect that can limit treatment is polycythemia, which occurs due to various stimulatory effects of testosterone on erythropoiesis (Zitzmann and Nieschlag 2004). Polycythemia is known to produce increased rates of cerebral ischemia and there have been reports of stroke during testosterone induced polycythaemia (Krauss et al 1991). It is necessary to monitor hematocrit during testosterone treatment, and hematocrit greater than 50% should prompt either a reduction of dose if testosterone levels are high or high-normal, or cessation of treatment if levels are low-normal. On the other hand, late onset hypogonadism frequently results in anemia which will then normalize during physiological testosterone replacement.
Since then there have been many publications documenting suppressed testosterone and gonadotropins (Daniell 2006) in men using opioid medications whether these agents were administrated orally (Daniell 2002) or intrathecally (Finch et al 2000). Not only do opioids act centrally by suppressing GnRH, they also act directly on the testes inhibiting the release of testosterone by Leydig cells during stimulation with human chorionic gonadotropin (Purohit et al 1978). Although the large majority of men (and women) receiving opioids do develop hypogonadism, about 15 percent also develop central hypocorticism and 15 percent develop growth hormone deficiency (Abs et al 2000).
Androgens may modulate the physiology of vaginal tissue and contribute to female genital sexual arousal.[48] Women's level of testosterone is higher when measured pre-intercourse vs pre-cuddling, as well as post-intercourse vs post-cuddling.[49] There is a time lag effect when testosterone is administered, on genital arousal in women. In addition, a continuous increase in vaginal sexual arousal may result in higher genital sensations and sexual appetitive behaviors.[50]

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There is increasing interest in the group of patients who fail to respond to treatment with PDE-5 inhibitors and have low serum testosterone levels. Evidence from placebo-controlled trials in this group of men shows that testosterone treatment added to PDE-5 inhibitors improves erectile function compared to PDE-5 inhibitors alone (Aversa et al 2003; Shabsigh et al 2004).
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).
These "disease-awareness" campaigns—ostensibly a public service intended to educate those potentially at risk about a condition they may not even have heard of but "could" have—are subtle, even insidious. They may not mention a specific product, but a bit of sleuthing reveals that their sponsors are usually pharmaceutical companies that "just happen" to manufacture products used to treat the real (or at least alleged) condition.
"The Journal of Clinical Endocrinology and Metabolism" published that males who switched from a high-fat diet to a low-fat diet also saw a decrease in their testosterone levels. If you want to put some fat back into your diet without fearing cardiac implications, plant-based saturated fat like coconut is just the ticket. Meat-based fat is also acceptable if kept to less than 10% of your dietary fat intake.

There is increasing interest in the group of patients who fail to respond to treatment with PDE-5 inhibitors and have low serum testosterone levels. Evidence from placebo-controlled trials in this group of men shows that testosterone treatment added to PDE-5 inhibitors improves erectile function compared to PDE-5 inhibitors alone (Aversa et al 2003; Shabsigh et al 2004).
Why bother with such common micronutrients? Because it's not uncommon for athletes to suffer from zinc and magnesium deficiencies, partly due to inadequate replenishing of levels after intense bouts of exercise. Deficiencies in these key minerals can lead to a poor anabolic hormone profile, impaired immune function, and increased cortisol, ultimately leading to decreases in strength and performance.[6]
Visit your doctor if you’re experiencing symptoms for the first time. Low testosterone levels cause similar symptoms to other conditions, so it’s best to get a diagnosis from a doctor. During your appointment, talk to your doctor about any medications you are taking, as well as any recent life changes, as there may be an easy-to-treat underlying cause for your low hormones.[19] Here are the most common symptoms of low testosterone:[20]
A loophole in FDA regulations allows pharmaceutical marketers to urge men to talk to their doctors if they have certain "possible signs" of testosterone deficiency. "Virtually everybody asks about this now because the direct-to-consumer marketing is so aggressive," says Dr. Michael O'Leary, a urologist at Harvard-affiliated Brigham and Women's Hospital. "Tons of men who would never have asked me about it before started to do so when they saw ads that say 'Do you feel tired?'"
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