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).
Hacking your testosterone influences everything from body composition to energy levels to mood. It’s easy to eat more butter; it’s hard to visit a doctor and get tested, but that’s what I recommend: know your levels. If you’re 25, you’ll know what your target is when you’re 35. By the time you’ve noticed symptoms of low testosterone, it’s too late to get your “normal” measurements!

Dr. Shiel received a Bachelor of Science degree with honors from the University of Notre Dame. There he was involved in research in radiation biology and received the Huisking Scholarship. After graduating from St. Louis University School of Medicine, he completed his Internal Medicine residency and Rheumatology fellowship at the University of California, Irvine. He is board-certified in Internal Medicine and Rheumatology.
In a recent study of male workers, men with low testosterone levels had an increased chance of severe erectile dysfunction (Kratzik et al 2005), although such a link had not been found previously (Rhoden et al 2002). Certainly erectile dysfunction is considered part of the clinical syndrome of hypogonadism, and questions regarding erectile dysfunction form part of the clinical assessment of patients with hypogonadism (Morley et al 2000; Moore et al 2004).
^ Jump up to: a b Lazaridis I, Charalampopoulos I, Alexaki VI, Avlonitis N, Pediaditakis I, Efstathopoulos P, Calogeropoulou T, Castanas E, Gravanis A (2011). "Neurosteroid dehydroepiandrosterone interacts with nerve growth factor (NGF) receptors, preventing neuronal apoptosis". PLoS Biol. 9 (4): e1001051. doi:10.1371/journal.pbio.1001051. PMC 3082517. PMID 21541365.
When many people think of someone with a high level of testosterone, they may picture a man loaded with strength, sexual prowess, and machismo. But while high-T has been correlated with all those things, it’s also been correlated with aggression, sexual misconduct, and violence. One of testosterone’s most common uses—as a performance-enhancing steroid—illustrates both sides of the hormone. Injecting steroids can be a quick way for athletes to dramatically improve performance, but the side effects can also be extreme, and can include excessive body hair growth, sexual dysfunction, and the hard-to-corral anger known as “roid rage.”

Once a complete sexual and medical history has been completed, appropriate laboratory studies should be conducted. In the initial evaluation of ED, sophisticated laboratory testing is rarely necessary. For example, serum testosterone (and sometimes prolactin) is typically only useful when the patient demonstrates hypogonadal features or testicular atrophy, or when clinical history is suggestive. Additional hormonal evaluation may include thyroid stimulating hormone in those with a clinical suspicion of hypothyroidism or appropriate diabetes screening in those presenting with a concern for impaired glucose metabolism. If the patient has not been evaluated with a lipid panel and hyperlipidemia is suspected, measurement and appropriate referral to internal medicine or cardiology is recommended. In most cases, a tentative diagnosis can be established with a complete sexual and medical history, physical examination, and limited or no laboratory testing.
The information provided does not constitute a diagnosis of your condition. You should consult a medical practitioner or other appropriate health care professional for a physical exmanication, diagnosis and formal advice. Health24 and the expert accept no responsibility or liability for any damage or personal harm you may suffer resulting from making use of this content.

Performance anxiety can be another cause of impotence. If a person wasn’t able to achieve an erection in the past, he may fear he won’t be able to achieve an erection in the future. A person may also find he can’t achieve an erection with a certain partner. Someone with ED related to performance anxiety may be able to have full erections when masturbating or when sleeping, yet he isn’t able to maintain an erection during intercourse.
Recognized risk factors for ED include cardiovascular disease (CVD) (hypertension, atherosclerosis, and hyperlipidemia), diabetes, depression, alcohol use, smoking, pelvic/perineal surgery or trauma, neurologic disease, obesity, pelvic radiation, and Peyronie’s disease. One study suggested that the relationship between arterial disease and ED is very strong, with 49% (147 of 300) of patients with coronary artery disease noted on cardiac catheterization reporting significant erectile dysfunction.6 Endothelial dysfunction has been indicated as the pathophysiologic mechanism responsible for both CVD and ED.7 The Boston Area Community Health survey demonstrated a dose-response between smoking and incidence of erectile dysfunction.8 Animal studies have demonstrated both smooth-muscle disruption and decreased production of neural nitric oxide synthase in cigarette-exposed animals.9
The association between low testosterone and ED is not entirely clear. Although these 2 processes certainly overlap in some instances, they are distinct entities. Some 2-21% of men have both hypogonadism and ED; however, it is unclear to what degree treating the former will improve erectile function. [17] About 35-40% of men with low testosterone see an improvement in their erections with testosterone replacement; however, almost 65% of these men see no improvement. [15]
Trials of testosterone treatment in men with type 2 diabetes have also taken place. A recent randomized controlled crossover trial assessed the effects of intramuscular testosterone replacement to achieve levels within the physiological range, compared with placebo injections in 24 men with diabetes, hypogonadism and a mean age of 64 years (Kapoor et al 2006). Ten of these men were insulin treated. Testosterone treatment led to a significant reduction in glycated hemoglobin (HbA1C) and fasting glucose compared to placebo. Testosterone also produced a significant reduction in insulin resistance, measured by the homeostatic model assessment (HOMA), in the fourteen non-insulin treated patients. It is not possible to measure insulin resistance in patients treated with insulin but five out of ten of these patients had a reduction of insulin dose during the study. Other significant changes during testosterone treatment in this trial were reduced total cholesterol, waist circumference and waist-hip ratio. Similarly, a placebo-controlled but non-blinded trial in 24 men with visceral obesity, diabetes, hypogonadism and mean age 57 years found that three months of oral testosterone treatment led to significant reductions in HbA1C, fasting glucose, post-prandial glucose, weight, fat mass and waist-hip ratio (Boyanov et al 2003). In contrast, an uncontrolled study of 150 mg intramuscular testosterone given to 10 patients, average age 64 years, with diabetes and hypogonadism found no significant change in diabetes control, fasting glucose or insulin levels (Corrales et al 2004). Another uncontrolled study showed no beneficial effect of testosterone treatment on insulin resistance, measured by HOMA and ‘minimal model’ of area under acute insulin response curves, in 11 patients with type 2 diabetes aged between 33 and 73 years (Lee et al 2005). Body mass index was within the normal range in this population and there was no change in waist-hip ratio or weight during testosterone treatment. Baseline testosterone levels were in the low-normal range and patients received a relatively small dose of 100 mg intramuscular testosterone every three weeks. A good increase in testosterone levels during the trial is described but it is not stated at which time during the three week cycle the testosterone levels were tested, so the lack of response could reflect an insufficient overall testosterone dose in the trial period.
Capogrosso, P., Colicchia, M., Ventimiglia, E., Castagna, G., Clementi, M. C., Suardi, N., ... Salonia, A. (2013, July). One patient out of four with newly diagnosed erectile dysfunction is a young man — worrisome picture from the everyday clinical practice. The journal of sexual medicine. 10(7), 1833–1841. Retrieved from https://onlinelibrary.wiley.com/doi/full/10.1111/jsm.12179
Testosterone levels generally peak during adolescence and early adulthood. As you get older, your testosterone level gradually declines — typically about 1 percent a year after age 30 or 40. It is important to determine in older men if a low testosterone level is simply due to the decline of normal aging or if it is due to a disease (hypogonadism).
Camacho EM1, Huhtaniemi IT, O'Neill TW, Finn JD, Pye SR, Lee DM, Tajar A, Bartfai G, Boonen S, Casanueva FF, Forti G, Giwercman A, Han TS, Kula K, Keevil B, Lean ME, Pendleton N, Punab M, Vanderschueren D, Wu FC; EMAS Group. “Age-associated changes in hypothalamic-pituitary-testicular function in middle-aged and older men are modified by weight change and lifestyle factors: longitudinal results from the European Male Ageing Study.” Eur J Endocrinol. 2013 Feb 20;168(3):445-55. doi: 10.1530/EJE-12-0890. Print 2013 Mar.
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.
Conditions associated with reduced nerve and endothelium function (eg, aging, hypertension, smoking, hypercholesterolemia, and diabetes) alter the balance between contraction and relaxation factors (see Pathophysiology). These conditions cause circulatory and structural changes in penile tissues, resulting in arterial insufficiency and defective smooth muscle relaxation. In some patients, sexual dysfunction may be the presenting symptom of these disorders.
The Latin term impotentia coeundi describes simple inability to insert the penis into the vagina; it is now mostly replaced by more precise terms, such as erectile dysfunction (ED). The study of ED within medicine is covered by andrology, a sub-field within urology. Research indicates that ED is common, and it is suggested that approximately 40% of males experience symptoms compatible with ED, at least occasionally.[38] The condition is also on occasion called phallic impotence.[39] Its antonym, or opposite condition, is priapism.[40][41]
After bombarding consumers with advertising, and massaging physicians with free meals and medical "information," the stage is set to seal the deal. "The fat guy has been seeing the ads on TV," said Fugh-Berman. "The doc has just come from a medical meeting where they were talking about how using testosterone can fight depression, etc., and they are being primed in a different way."
The association between low testosterone and ED is not entirely clear. Although these 2 processes certainly overlap in some instances, they are distinct entities. Some 2-21% of men have both hypogonadism and ED; however, it is unclear to what degree treating the former will improve erectile function. [17] About 35-40% of men with low testosterone see an improvement in their erections with testosterone replacement; however, almost 65% of these men see no improvement. [15]
While testosterone stimulates a man’s sex drive, it also aids in achieving and maintaining an erection. Testosterone alone doesn’t cause an erection, but it stimulates receptors in the brain to produce nitric oxide. Nitric oxide is a molecule that helps trigger a series of chemical reactions necessary for an erection to occur. When testosterone levels are too low, a man may have difficulty achieving an erection prior to sex or having spontaneous erections (for example, during sleep).
The researchers found that the dose of testosterone required to produce different effects in the body varied widely. The influence of testosterone and estradiol also differed. As the testosterone gel dose was reduced, the scientists showed, reductions in lean mass, muscle size, and leg-press strength resulted from decreases in testosterone itself. In contrast, increases in body fat were due to the related declines in estradiol. Both testosterone and estradiol levels were associated with libido and erectile function.
However, testosterone is only one of many factors that aid in adequate erections. Research is inconclusive regarding the role of testosterone replacement in the treatment of erectile dysfunction. In a review of studies that looked at the benefit of testosterone in men with erection difficulties, nearly half showed no improvement with testosterone treatment. Many times, other health problems play a role in erectile difficulties. These can include:
This paper will aim to review the current evidence of clinical effects of testosterone treatment within an aging male population. As with any other clinical intervention a decision to treat patients with testosterone requires a balance of risk versus benefit. We shall try to facilitate this by examining the effects of testosterone on the various symptoms and organs involved.
If you have symptoms of ED, it’s important to check with your doctor before trying any treatments on your own. This is because ED can be a sign of other health problems. For instance, heart disease or high cholesterol could cause ED symptoms. With a diagnosis, your doctor could recommend a number of steps that would likely improve both your heart health and your ED. These steps include lowering your cholesterol, reducing your weight, or taking medications to unclog your blood vessels.
show that total testosterone levels increase after exercising, especially after resistance training. Low testosterone levels can affect your sex drive and your mood. The good news is that exercise improves mood and stimulates brain chemicals to help you feel happier and more confident. Exercise also boosts energy and endurance, and helps you to sleep better. Fitness experts recommend 30 minutes of exercise every day.
Barbara Mintzes, at the University of British Columbia, said in a Skype interview, "Androgel was approved for a real condition—men who have a number of clinical or acquired conditions that affect testosterone, either through the testes or pituitary gland. So testosterone replacement therapy makes sense, and producing it in a gel makes sense. Where there is an actual need for the product, there's nothing wrong with that." But, she added, "When this gets marketed for what is essentially healthy aging, the antennas go up."
Common side effects from testosterone medication include acne, swelling, and breast enlargement in males.[10] Serious side effects may include liver toxicity, heart disease, and behavioral changes.[10] Women and children who are exposed may develop virilization.[10] It is recommended that individuals with prostate cancer not use the medication.[10] It can cause harm if used during pregnancy or breastfeeding.[10]
Surgery: If neither drugs nor the vacuum pump works, your doctor may suggest surgery. With surgery, the doctor can place a device in your penis that will cause enough hardness for intercourse. In a few cases, infections may develop after the operation, and the doctor may have to remove the device. Another operation that may help you is rebuilding the blood vessels in the penis to increase blood flow into the penis or decrease blood flow out of the penis. These procedures can help you to get and maintain an erection.
You should talk to your doctor about possible treatments. You may want to talk to other patients who have had the treatment planned for you. You also may want to seek a second doctor's opinion about surgery before making your decision. You may find it difficult to talk to your doctor about impotence. You will want to find a doctor who treats this condition and will help you feel comfortable talking about the problem and choosing the best treatment. You can also get more information by contacting your local National Kidney Foundation affiliate.

Another study compared the response of surgically and medically castrated rabbits to vardenafil with that of control rabbits. [22] Castrated rabbits did not respond to vardenafil, whereas noncastrated rabbits did respond appropriately. This result suggests that a minimum amount of testosterone is necessary for PDE5 inhibitors to produce an erection.
In a recent study of male workers, men with low testosterone levels had an increased chance of severe erectile dysfunction (Kratzik et al 2005), although such a link had not been found previously (Rhoden et al 2002). Certainly erectile dysfunction is considered part of the clinical syndrome of hypogonadism, and questions regarding erectile dysfunction form part of the clinical assessment of patients with hypogonadism (Morley et al 2000; Moore et al 2004).

The participants were seen every 4 weeks. Blood was taken to measure hormone levels, and questionnaires were given to assess physical function, health status, vitality, and sexual function. Body fat and muscle measurements were also taken at the beginning and end of the 16 weeks. The study was funded in part by NIH’s National Institute on Aging (NIA) and National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK). Results appeared in the September 12, 2013, issue of the New England Journal of Medicine.
Psychosocial problems are important and may cause erectile dysfunction by themselves or together with other causes of erectile dysfunction, such as diabetes and heart disease. Relationships are complicated and many factors cause tensions, which can affect sexual relations. For some men, these problems can become ongoing and it can help to talk through the issue with a skilled counsellor. It is important to know that the longer erectile dysfunction is left untreated, the greater the effect on relationships. This is another reason why early treatment of erectile dysfunction is important.
In a randomized double-blind, parallel, placebo-controlled trial, sildenafil plus testosterone was not superior to sildenafil plus placebo in improving erectile function in men with ED and low testosterone levels. [19] The objective of the study was to determine whether the addition of testosterone to sildenafil therapy improves erectile response in men with ED and low testosterone levels.
Lifestyle choices that impair blood circulation can contribute to ED. Smoking, excessive drinking, and drug abuse may damage the blood vessels and reduce blood flow to the penis. Smoking makes men with atherosclerosis particularly vulnerable to ED. Being overweight and getting too little exercise also contribute to ED.  Studies indicate that men who exercise regularly have a lower risk of ED.
Testosterone is the principle sex hormone responsible for the development of reproductive function in male vertebrates. Testosterone is one of the hormones referred to as androgens, which are also known of as anabolic steroids. As a steroid hormone, testosterone is derived from cholesterol and the structure of this hormone is similar across all mammals, reptiles, birds and fish.
Of particularly concern are antihypertensive medications for CVD (eg, digoxin, disopyramide [Norpace], gemfibrozil [Lopid]), anxiety, depression (eg, lithium, monoamine oxidase inhibitors, selective serotonin reuptake inhibitors, serotonin-norepinephrine reuptake inhibitors, tricyclic antidepressants), or psychosis (eg, chlorpromazine, haloperidol, pimozide [Orap], thioridazine, thiothixene). Antihypertensive drugs, such as diuretics (eg, spironolactone, thiazides) and beta blockers, may be associated with ED. Discontinuation or switching to alternative drugs, such as angiotensin-converting enzyme inhibitors or calcium channel blockers (eg, diltiazem, nifedipine, amlodipine), may reduce ED. The newer angiotensin II receptor antagonists may be less problematic with respect to ED, but long-term data is needed to evaluate this.
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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.
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