For men with low blood testosterone levels, the benefits of hormone replacement therapy usually outweigh potential risks. However, for most other men it's a shared decision with your doctor. It offers men who feel lousy a chance to feel better, but that quick fix could distract attention from unknown long-term hazards. "I can't tell you for certain that this raises your personal risk of heart problems and prostate cancer, or that it doesn't," Dr. Pallais says.
In the hepatic 17-ketosteroid pathway of testosterone metabolism, testosterone is converted in the liver by 5α-reductase and 5β-reductase into 5α-DHT and the inactive 5β-DHT, respectively.[1][151] Then, 5α-DHT and 5β-DHT are converted by 3α-HSD into 3α-androstanediol and 3α-etiocholanediol, respectively.[1][151] Subsequently, 3α-androstanediol and 3α-etiocholanediol are converted by 17β-HSD into androsterone and etiocholanolone, which is followed by their conjugation and excretion.[1][151] 3β-Androstanediol and 3β-etiocholanediol can also be formed in this pathway when 5α-DHT and 5β-DHT are acted upon by 3β-HSD instead of 3α-HSD, respectively, and they can then be transformed into epiandrosterone and epietiocholanolone, respectively.[153][154] A small portion of approximately 3% of testosterone is reversibly converted in the liver into androstenedione by 17β-HSD.[152]
In summary, low testosterone levels are linked to the presence of numerous cardiovascular risk factors. Testosterone treatment acts to improve some of these factors, but effects may vary according to pre- and post-treatment testosterone levels, as well as other factors. There is little data from trials specific to aging males. Appropriately-powered randomized controlled trials, with cardiovascular disease primary endpoints, are needed to clarify the situation, but in the meantime the balance of evidence is that testosterone has either neutral or beneficial effects on the risk of cardiovascular disease in men. It is particularly important to define the effect of testosterone treatment on cardiovascular disease in view of its potential use as an anti-anginal agent.
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.
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.
In general, the normal range in males is about 270 to 1070 ng/dL with an average level of 679 ng/dL. A normal male testosterone level peaks at about age 20, and then it slowly declines. Testosterone levels above or below the normal range are considered by many to be out of balance. Moreover, some researchers suggest that the healthiest men have testosterone levels between 400 - 600 ng/dL.
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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Researchers found that the simple act ‘expressing power through open, expansive postures’ (i.e. standing up straight and proud) can increase Testosterone and decrease cortisol (58), along with improving feelings of power and tolerance for risk. Easy! Your mother was right – don’t slouch. This could be a handy trick before making a speech or going on a date!
In the hepatic 17-ketosteroid pathway of testosterone metabolism, testosterone is converted in the liver by 5α-reductase and 5β-reductase into 5α-DHT and the inactive 5β-DHT, respectively.[1][151] Then, 5α-DHT and 5β-DHT are converted by 3α-HSD into 3α-androstanediol and 3α-etiocholanediol, respectively.[1][151] Subsequently, 3α-androstanediol and 3α-etiocholanediol are converted by 17β-HSD into androsterone and etiocholanolone, which is followed by their conjugation and excretion.[1][151] 3β-Androstanediol and 3β-etiocholanediol can also be formed in this pathway when 5α-DHT and 5β-DHT are acted upon by 3β-HSD instead of 3α-HSD, respectively, and they can then be transformed into epiandrosterone and epietiocholanolone, respectively.[153][154] A small portion of approximately 3% of testosterone is reversibly converted in the liver into androstenedione by 17β-HSD.[152]
Testosterone has several positive effects on sexual function, but its most significant effect is on libido, sexual interest and arousal. Boys going through puberty develop an enhanced interest in sex (thoughts, fantasies, masturbation, intercourse) as a consequence of rising levels of testosterone. Hypogonadal men usually have a significant improvement in libido when TRT is initiated (Wang et al 2000; Morley and Perry 2003).
Conflicting results have been obtained concerning the importance of testosterone in maintaining cardiovascular health.[29][30] Nevertheless, maintaining normal testosterone levels in elderly men has been shown to improve many parameters that are thought to reduce cardiovascular disease risk, such as increased lean body mass, decreased visceral fat mass, decreased total cholesterol, and glycemic control.[31]
Exercise is one of the most effective ways to prevent many lifestyle-related diseases. Interestingly, it can also boost your testosterone. A large review study found that people who exercised regularly had higher testosterone levels. In the elderly, exercise increases testosterone levels, fitness and reaction time. New research in obese men suggests that increased physical activity was even more beneficial than a weight loss diet for increasing testosterone levels. Resistance training, such as weight lifting, is the best type of exercise to boost testosterone in both the short- and long-term. High-intensity interval training (HIIT) can also be very effective, although all types of exercise should work to some extent. Taking caffeine and creatine monohydrate as supplements may further boost your levels when combined with a training program.
There are studies that show Soy consumption in humans leads to lower sperm count, but unfortunately they did not look at testosterone levels in the study (40). This (41) particular study compared the estrogen production of men drinking soy protein to those drinking whey. After two weeks they found the estradiol levels were equal, however soy drinkers had LOWER Testosterone levels and HIGHER cortisol levels (both bad).

If you're completely inactive, or if you're completely burned out from overly intense training, neither one is going to help your T-levels. And when it comes to nutrition, eating enough—and getting adequate dietary fats—are both essential for healthy testosterone levels, and for general health.[2] In "All About Testosterone," Chris Lockwood, Ph.D., notes that extreme low-calorie dieting and fasting will hinder testosterone levels from staying at their peak, along with better-known villains like chronic stress.
Testosterone is everywhere playing multiple roles from intrauterine life to advanced age. Table 1, the contents of which are always undergoing change primarily because of newly observed associations, provides an overview of the bodily systemic functions and patho-physiological states in which testosterone finds itself implicated. In some of these states there is a clear physiological cause and effect relationship. In others, evidence of the physiological role is early or tenuous.
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).
Free testosterone (T) is transported into the cytoplasm of target tissue cells, where it can bind to the androgen receptor, or can be reduced to 5α-dihydrotestosterone (DHT) by the cytoplasmic enzyme 5α-reductase. DHT binds to the same androgen receptor even more strongly than testosterone, so that its androgenic potency is about 5 times that of T.[114] The T-receptor or DHT-receptor complex undergoes a structural change that allows it to move into the cell nucleus and bind directly to specific nucleotide sequences of the chromosomal DNA. The areas of binding are called hormone response elements (HREs), and influence transcriptional activity of certain genes, producing the androgen effects.
Men who watch a sexually explicit movie have an average increase of 35% in testosterone, peaking at 60–90 minutes after the end of the film, but no increase is seen in men who watch sexually neutral films.[43] Men who watch sexually explicit films also report increased motivation, competitiveness, and decreased exhaustion.[44] A link has also been found between relaxation following sexual arousal and testosterone levels.[45]
Pregnant or nursing women who are exposed to EDCs can transfer these chemicals to their child. Exposure to EDCs during pregnancy affects the development of male fetuses. Fewer boys have been born in the United States and Japan in the last three decades. The more women are exposed to these hormone-disrupting substances, the greater the chance that their sons will have smaller genitals and incomplete testicular descent, leading to poor reproductive health in the long term. EDCs are also a threat to male fertility, as they contribute to testicular cancer and lower sperm count. All of these birth defects and abnormalities, collectively referred to as Testicular Dysgenesis Syndrome (TDS), are linked to the impaired production of testosterone.5
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:
The mechanism of age related decreases in serum testosterone levels has also been the subject of investigation. Metabolic clearance declines with age but this effect is less pronounced than a reduction in testosterone production, so the overall effect is to reduce serum testosterone levels. Gonadotrophin levels rise during aging (Feldman et al 2002) and testicular secretory responses to recombinant human chorionic gonadotrophin (hCG) are reduced (Mulligan et al 1999, 2001). This implies that the reduced production may be caused by primary testicular failure but in fact these changes are not adequate to fully explain the fall in testosterone levels. There are changes in the lutenising hormone (LH) production which consist of decreased LH pulse frequency and amplitude, (Veldhuis et al 1992; Pincus et al 1997) although pituitary production of LH in response to pharmacological stimulation with exogenous GnRH analogues is preserved (Mulligan et al 1999). It therefore seems likely that there are changes in endogenous production of GnRH which underlie the changes in LH secretion and have a role in the age related decline in testosterone. Thus the decreases in testosterone levels with aging seem to reflect changes at all levels of the hypothalamic-pituitary-testicular axis. With advancing age there is also a reduction in androgen receptor concentration in some target tissues and this may contribute to the clinical syndrome of LOH (Ono et al 1988; Gallon et al 1989).

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).


Your diet is the best source of zinc; along with protein-rich foods like meats and fish, other good dietary sources of zinc include raw milk, raw cheese, beans, and yogurt or kefir made from raw milk. It can be difficult to obtain enough dietary zinc if you're a vegetarian, and also for meat-eaters as well, largely because of conventional farming methods that rely heavily on chemical fertilizers and pesticides. These chemicals deplete the soil of nutrients ... nutrients like zinc that must be absorbed by plants in order to be passed on to you.

To get your levels into the healthy range, sun exposure is the BEST way to optimize your vitamin D levels; exposing a large amount of your skin until it turns the lightest shade of pink, as near to solar noon as possible, is typically necessary to achieve adequate vitamin D production. If sun exposure is not an option, a safe tanning bed (with electronic ballasts rather than magnetic ballasts, to avoid unnecessary exposure to EMF fields) can be used.


Finally, we looked at the proprietary blends of our remaining boosters, and dug into their ingredient lists. Supplements frequently include ingredients known for their “folk-lore” value; they’re believed to work, even when there isn’t any scientific background to prove it. Though we didn’t ding points if an ingredient wasn’t proven to be good (just so long as it wasn’t proven to be bad), we didn’t want to include any ingredient with evidence of causing harm.
Important future developments will include selective androgen receptor modulators (SARMs). These drugs will be able to produce isolated effects of testosterone at androgen receptors. They are likely to become useful clinical drugs, but their initial worth may lie in facilitating research into the relative importance of testosterone’s action at the androgen receptor compared to at other sites or after conversion to other hormones. Testosterone will remain the treatment of choice for late onset hypogonadism for some time to come.
These results have been echoed in clinical trials. A meta-analysis of 24 RCTs looked at weight loss caused by diet or bariatric surgery:[22] In the diet studies, the average 9.8% weight loss was linked to a testosterone increase of 2.9 nmol/L (84 ng/dL). In the bariatric-surgery studies, the average 32% weight loss was linked to a testosterone increase of 8.7 nmol/L (251 ng/dL).

Stick to protocols that stress large degrees of muscle mass and are moderate- to high-intensity. Additionally, more seasoned gym-goers may want to incorporate forced repetitions periodically into their programs, as testosterone increases have been observed with this type of training.14 Incorporating other post-failure training techniques such as dropsets or partials may similarly be associated with higher T production.
Ginger has been used as medicine for centuries due to its potent antioxidant potential. It also exhibits anti-inflammatory properties which makes it best for natural therapeutics. It improves the sexual function and testosterone levels by stimulating the luteinizing hormone. It also enhances the sperm count, which makes it useful to solve infertility issues.
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.

Many studies demonstrate an improvement in mood of hypogonadal men treated with testosterone (Wang et al 1996; Azad et al 2003). The relationship between testosterone status and mood, particularly depression, remains unresolved. Using Beck’s Depression Inventory, Barrett-Connor and colleagues found that the depression score worsened as men aged, exactly at a time when testosterone levels are decreasing (Barrett-Connor et al 1999). Pope and colleagues found that testosterone treatment in men with refractory depression lowered the Hamilton Depression rating scale and the Clinical Global Impression severity rating (Pope et al 2003). The Beck Depression Inventory remained unchanged in Pope’s study.

In many of the studies we found, those who saw the most improvement in health, testosterone, or muscle gain were those with existing nutrient or vitamin deficiencies. This means that some gains may be due more to dietary changes and generally restoring nutrient and vitamin levels than any one magic ingredient, but also that making sure your diet includes healthy amounts of nutrients should be your first step.
According to British Medical Journal (BMJ), the European Male Ageing Study has provided the best estimate of the prevalence of low T—defined as a combination of sexual symptoms and measured testosterone level—finding that only 0.1 percent of men in their forties, 0.6 percent in their fifties, 3.2 percent in their sixties, and 5.1 percent of men in their seventies would meet the criteria for the diagnosis.
Dr. Anthony’s Notes: Vitamin D has about 100 other beneficial body functions outside of it's impact on testosterone. Make sure you take the active Vitamin D3 (not D2 – from plant sources!) It’s also advisable to get 20 minutes of sunshine daily (weather permitting) – without sunscreen. Verdict: this is one of the natural testosterone supplements that work. Best Food Sources of Vitamin D3: Wild Alaskan Salmon (#1), Sardines, Eggs How To Take Vitamin D3: Using 3000-5000IU of Vitamin D3 per day is a good safe, research supported dose. Your physician can also test your blood for D3 levels for more precise monitoring.
Steven Doerr, MD, is a U.S. board-certified Emergency Medicine Physician. Dr. Doerr received his undergraduate degree in Spanish from the University of Colorado at Boulder. He graduated with his Medical Degree from the University Of Colorado Health Sciences Center in Denver, Colorado in 1998 and completed his residency training in Emergency Medicine from Denver Health Medical Center in Denver, Colorado in 2002, where he also served as Chief Resident.
Grape seed extract is another ingredient with not enough research to suggest a dosage. Grape seed extract can interact with drugs like “blood thinners, NSAID painkillers (like aspirin, Advil, and Aleve), certain heart medicines, cancer treatments, and others.” If this sounds like you (or if you ever pop an Advil to clear off a headache), you’ll need to speak with a doctor to make sure this supplement is safe to take.

Total levels of testosterone in the body are 264 to 916 ng/dL in men age 19 to 39 years,[165] while mean testosterone levels in adult men have been reported as 630 ng/dL.[166] Levels of testosterone in men decline with age.[165] In women, mean levels of total testosterone have been reported to be 32.6 ng/dL.[167][168] In women with hyperandrogenism, mean levels of total testosterone have been reported to be 62.1 ng/dL.[167][168]

Testosterone is a stimulant of hematopoiesis in the bone marrow and consequently, increases the hematocrit (Shahidi 1973). Men with unexplained anemia should have their testosterone measured and if reduced, these men should be treated with testosterone. Because of the erythropoietin stimulating effect of testosterone, one of the parameters to be monitored during testosterone treatment is hematocrit since a small percent of testosterone-treated men develop polycythemia.


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.
Instead of turning to some drug that can only ameliorate symptoms and cause additional complications, I recommend using a natural saw palmetto supplement. Dr. Moerck says that there are about 100 clinical studies on the benefits of saw palmetto, one of them being a contributed to decreased prostate cancer risk. When choosing a saw palmetto supplement, you should be wary of the brand, as there are those that use an inactive form of the plant.
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