As we age, the body undergoes multiple degenerative changes at multiple sites and in multiple systems. The changes of aging are inevitable and inexorable and represent the march toward ultimate death. We are mortal beings whose destiny it is to die. As we come to learn about the processes of life we can better prepare ourselves for the finality of death and on the way perhaps retard the degenerative process, or repair it (for however long we may enjoy this repair), or substitute chemical compounds that our bodies once produced in abundance, an abundance which fades with the advance of age.

Testosterone is more than a “male sex hormone”. It is an important contributor to the robust metabolic functioning of multiple bodily systems. The abuse of anabolic steroids by athletes over the years has been one of the major detractors from the investigation and treatment of clinical states that could be caused by or related to male hypogonadism. The unwarranted fear that testosterone therapy would induce prostate cancer has also deterred physicians form pursuing more aggressively the possibility of hypogonadism in symptomatic male patients. In addition to these two mythologies, many physicians believe that testosterone is bad for the male heart. The classical anabolic agents, 17-alkylated steroids, are, indeed, potentially harmful to the liver, to insulin action to lipid metabolism. These substances, however, are not testosterone, which has none of these adverse effects. The current evidence, in fact, strongly suggests that testosterone may be cardioprotective. There is virtually no evidence to implicate testosterone as a cause of prostate cancer. It may exacerbate an existing prostate cancer, although the evidence is flimsy, but it does not likely cause the cancer in the first place. Testosterone has stimulatory effects on bones, muscles, erythropoietin, libido, mood and cognition centres in the brain, penile erection. It is reduced in metabolic syndrome and diabetes and therapy with testosterone in these conditions may provide amelioration by lowering LDL cholesterol, blood sugar, glycated hemoglobin and insulin resistance. The best measure is bio-available testosterone which is the fraction of testosterone not bound to sex hormone binding globulin. Several forms of testosterone administration are available making compliance much less of an issue with testosterone replacement therapy.
In 1927, the University of Chicago's Professor of Physiologic Chemistry, Fred C. Koch, established easy access to a large source of bovine testicles — the Chicago stockyards — and recruited students willing to endure the tedious work of extracting their isolates. In that year, Koch and his student, Lemuel McGee, derived 20 mg of a substance from a supply of 40 pounds of bovine testicles that, when administered to castrated roosters, pigs and rats, remasculinized them.[179] The group of Ernst Laqueur at the University of Amsterdam purified testosterone from bovine testicles in a similar manner in 1934, but isolation of the hormone from animal tissues in amounts permitting serious study in humans was not feasible until three European pharmaceutical giants—Schering (Berlin, Germany), Organon (Oss, Netherlands) and Ciba (Basel, Switzerland)—began full-scale steroid research and development programs in the 1930s.

Cross-sectional studies have found a positive association between serum testosterone and some measures of cognitive ability in men (Barrett-Connor, Goodman-Gruen et al 1999; Yaffe et al 2002). Longitudinal studies have found that free testosterone levels correlate positively with future cognitive abilities and reduced rate of cognitive decline (Moffat et al 2002) and that, compared with controls, testosterone levels are reduced in men with Alzheimer’s disease at least 10 years prior to diagnosis (Moffat et al 2004). Studies of the effects of induced androgen deficiency in patients with prostate cancer have shown that profoundly lowering testosterone leads to worsening cognitive functions (Almeida et al 2004; Salminen et al 2004) and increased levels of serum amyloid (Gandy et al 2001; Almeida et al 2004), which is central to the pathogenesis of Alzheimer’s disease (Parihar and Hemnani 2004). Furthermore, testosterone reduces amyloid-induced hippocampal neurotoxity in vitro (Pike 2001) as well as exhibiting other neuroprotective effects (Pouliot et al 1996). The epidemiological and experimental data propose a potential role of testosterone in protecting cognitive function and preventing Alzheimer’s disease.


There is an increased incidence of hypogonadism in men with rheumatoid arthritis. Tengstrand et al (2002) studied hormonal levels in 104 men with rheumatoid arthritis and 99 age-matched healthy men. They divided their subjects into 3 age groups: 30–49, 40–59, 60–69. Mean non-sex hormone binding globulin-bound testosterone (bioavailable testosterone) was lower in men with rheumatoid arthritis for each of the three groups. LH was also found to be lower in the patients with rheumatoid arthritis suggesting a hypothalamic-pituitary cause of the reduced bioavailable testosterone. Of the 104 men with rheumatoid arthritis, 33 had hypogonadism compared to 7 of the 99 healthy controls.
If you want to naturally boost testosterone and HGH then combining weight training with HIIT workouts (high intensity interval training). Go to the gym at least three days a week, ideally at least three days a week, and lift heavy weights. Lifting heavy weights 6–12 reps with larger muscle groups like your quadriceps, hamstrings, back, shoulders and chest will help your body pack on the maximum amount of muscle. Specifically, lifting at least 30 minutes up to as long as an hour or so can be very, very beneficial boost low testosterone levels.
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“This study establishes testosterone levels at which various physiological functions start to become impaired, which may help provide a rationale for determining which men should be treated with testosterone supplements,” Finkelstein says. “But the biggest surprise was that some of the symptoms routinely attributed to testosterone deficiency are actually partially or almost exclusively caused by the decline in estrogens that is an inseparable result of lower testosterone levels.”
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.
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Testosterone is the primary male sex hormone and an anabolic steroid. In male humans, testosterone plays a key role in the development of male reproductive tissues such as testes and prostate, as well as promoting secondary sexual characteristics such as increased muscle and bone mass, and the growth of body hair.[2] In addition, testosterone is involved in health and well-being,[3] and the prevention of osteoporosis.[4] Insufficient levels of testosterone in men may lead to abnormalities including frailty and bone loss.
As we age, the body undergoes multiple degenerative changes at multiple sites and in multiple systems. The changes of aging are inevitable and inexorable and represent the march toward ultimate death. We are mortal beings whose destiny it is to die. As we come to learn about the processes of life we can better prepare ourselves for the finality of death and on the way perhaps retard the degenerative process, or repair it (for however long we may enjoy this repair), or substitute chemical compounds that our bodies once produced in abundance, an abundance which fades with the advance of age.
Other side effects include increased risk of heart problems in older men with poor mobility, according to a 2009 study at Boston Medical Center. A 2017 study published in JAMA found that treatments increase coronary artery plaque volume. Additionally, the Food and Drug Administration (FDA) requires manufactures to include a notice on the labeling that states taking testosterone treatments can lead to possible increased risk of heart attacks and strokes. The FDA recommends that patients using testosterone should seek medical attention right away if they have these symptoms:
Yeah a lot of information has come out in the last decade or so proving that cholesterol is in fact good for you, and actually has no correlation to heart disease. But I think it will be a few more years until the world will shift such a strong belief that cholesterol is the enemy. If you are interested in this you should read grain brain. It talks all about (and proves) how high carbohydrates are actually the reason for “high cholesterol” and a high fat low carb diet is great for your body, and more importantly your brain.
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]
Testosterone is necessary for normal sperm development. It activates genes in Sertoli cells, which promote differentiation of spermatogonia. It regulates acute HPA (hypothalamic–pituitary–adrenal axis) response under dominance challenge.[22] Androgen including testosterone enhances muscle growth. Testosterone also regulates the population of thromboxane A2 receptors on megakaryocytes and platelets and hence platelet aggregation in humans.[23][24]
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.
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.

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DHEA (dehydroepiandrosterone) extract - this is a chemical that used in your body which a ‘hormone precursor’. This means it’s the chemical used by the body to create hormones like oestrogen or testosterone. When taken as supplement it is believed to boost testosterone levels, but DHEA has not been shown to increase testosterone in men. DHEA comes in two form:
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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