Fatherhood decreases testosterone levels in men, suggesting that the emotions and behavior tied to decreased testosterone promote paternal care. In humans and other species that utilize allomaternal care, paternal investment in offspring is beneficial to said offspring's survival because it allows the parental dyad to raise multiple children simultaneously. This increases the reproductive fitness of the parents, because their offspring are more likely to survive and reproduce. Paternal care increases offspring survival due to increased access to higher quality food and reduced physical and immunological threats.[60] This is particularly beneficial for humans since offspring are dependent on parents for extended periods of time and mothers have relatively short inter-birth intervals.[61] While extent of paternal care varies between cultures, higher investment in direct child care has been seen to be correlated with lower average testosterone levels as well as temporary fluctuations.[62] For instance, fluctuation in testosterone levels when a child is in distress has been found to be indicative of fathering styles. If a father's testosterone levels decrease in response to hearing their baby cry, it is an indication of empathizing with the baby. This is associated with increased nurturing behavior and better outcomes for the infant.[63]
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.
The production of the stress hormone cortisol blocks the production and effects of testosterone. From a biological perspective, cortisol increases your “fight or flight” response, thereby lowering testosterone-associated functions such as mating, competing, and aggression. Chronic stress can take a toll on testosterone production, as well as your overall health. Therefore, stress management is equally important to a healthy diet and regular exercise. Tools you can use to stay stress-free include prayer, meditation, laughter, and yoga. Relaxation skills, such as deep breathing and visualization, can also promote your emotional health.

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.


Testosterone makes a contribution to nitric oxide formation. Nitric oxide, released from penile nerves stimulates guanylate cyclase which catalyzes the transformation of guanosine-5-triphosphate into 3′,5′-cyclic, guanosine monophosphate (cyclic GMP). Gyclic GMP causes vasodilatation and hence erection formation (Morelli et al 2005). The breakdown of cyclic GMP to GMP is mediated by the enzyme, phosphodiesterase type-5, the inhibitors of which (eg, sildenafil citrate) enhance erection formation and maintanence (Carson and Lue 2005).
It is now well-established that elderly men with type 2 diabetes mellitus have reduced levels of testosterone (Barrett-Connor 1992; Betancourt-Albrecht and Cunningham 2003). It is known, however, that obese men and diabetic men have reduced levels of SHBG (Barrett-Connor 1990) which could account for the lower total testosterone levels found in diabetic men. Dhindsa et al (2004) studied 103 male patients who had type 2 diabetes mellitus using free testosterone (done by equilibrium dialysis) or calculated free testosterone which takes SHBG levels into account. Of the 103 patients, 57 had free testosterone by equilibrium dialysis and of these, 14 (25%) had a free T below 0.174 nmol/L and were considered hypogonadal. Using a total testosterone of 10.4 nmol/L (300ng/dl) as the lower limit of normal 45 patients (43%) were in the hypogonadal range. They also found that LH and FSH concentrations were significantly lower in the hypogonadal group. The authors thus concluded that hypogonadotropic hypogonadism was a common finding in type 2 diabetes irrespective of glycemic control, duration of disease or the presence of complications of diabetes or obesity.

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).
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.

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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.


This doesn’t mean Super Test is perfect — we take a closer look at some of its ingredients below — but it beats out the competition. Every other supplement we looked at either didn’t have all four ingredients, overdosed us on vitamins or minerals (a good way to develop kidney and liver problems), contained ingredients that would harm us, or some combination thereof.

Testosterone booster products obtained from trusted sources and administered as per the recommendations of the manufacturer may still present some health risks. The present case provided weak evidence of causality between acute liver injury and a commercial testosterone booster. To guarantee an optimal outcome with no severe side effects, further research is warranted to confirm the present findings and determine whether the effects observed in this case report would be statistically significant in larger samples.
My question is in two parts, I am looking for energy and some muscle build but only do push ups and sit ups so not looking for massive results. I am diabetic and I am wanting to get a testosterone booster to have more energy for daily use not so much for help in the bedroom but I would not mind if it helps out. Would I be able to take it not just for a certain product but any testosterone booster? The other question is does it help with any form of muscle growth, again not anything big but some? I would appreciate any advice or information you can give me.

Directions — SUGGESTED USE: As a dietary supplement take 3 capsules daily, preferably with a meal, or as directed by a healthcare professional. — Take two capsules with a meal twice a day. On days that you are not training, take two capsules in the morning and two capsules at night. On days that you train, take two capsules about an hour before workouts and take two capsules in the morning or at night depending on when you train.
Longitudinal studies in male aging studies have shown that serum testosterone levels decline with age (Harman et al 2001; Feldman et al 2002). Total testosterone levels fall at an average of 1.6% per year whilst free and bioavailable levels fall by 2%–3% per year. The reduction in free and bioavailable testosterone levels is larger because aging is also associated with increases in SHBG levels (Feldman et al 2002). Cross-sectional data supports these trends but has usually shown smaller reductions in testosterone levels with aging (Feldman et al 2002). This is likely to reflect strict entry criteria to cross-sectional studies so that young healthy men are compared to older healthy men. During the course of longitudinal studies some men may develop pathologies which accentuate decreases in testosterone levels.
A number of research groups have tried to further define the relationship of testosterone and body composition by artificial alteration of testosterone levels in eugonadal populations. Induction of a hypogonadal state in healthy men (Mauras et al 1998) or men with prostate cancer (Smith et al 2001) using a gonadotrophin-releasing-hormone (GnRH) analogue was shown to produce increases in fat mass and decreased fat free mass. Another experimental approach in healthy men featured suppression of endogenous testosterone production with a GnRH analogue, followed by treatment with different doses of weekly intramuscular testosterone esters for 20 weeks. Initially the experiments involved men aged 18–35 years (Bhasin et al 2001) but subsequently the study was repeated with a similar protocol in men aged 60–75 years (Bhasin et al 2005). The different doses given were shown to produce a range of serum concentrations from subphysiological to supraphysiological (Bhasin et al 2001). A given testosterone dose produced higher serum concentrations of testosterone in the older age group (Bhasin et al 2005). Subphysiological dosing of testosterone produced a gain in fat mass and loss of fat free mass during the study. There were sequential decreases in fat mass and increases in fat free mass with each increase of testosterone dose. These changes in body composition were seen in physiological and supraphysiological treatment doses. The trend was similar in younger versus older men but the gain of fat mass at the lowest testosterone dose was less prominent in older patients (Bhasin et al 2001; Bhasin et al 2005). With regard to muscle function, the investigators showed dose dependent increases in leg strength and power with testosterone treatment in young and older men but there was no improvement in fatigability (Storer et al 2003; Bhasin et al 2005).
Dobs and colleagues found that men with an increased body mass index had both reduced testosterone and reduced high density lipoprotein (HDL) levels. Treatment with testosterone increased the levels of HDL (Dobs et al 2001). Rising levels of HDL are not a consistent finding with TRT. More often, however, one finds reduced total cholesterol, low density lipoprotein (LDL) cholesterol and triglyceride levels with TRT (Zgliczynski et al 1996; Whitsel et al 2001).
I bought most of the ingredients for my Testosterone Salad at Whole Foods. For those curious, I added up all the ingredients and divided by six (I typically ate six of these salads in a week). The cost per salad was roughly $5. That’s about the price many folks pay every day for a crappy fast food meal. If you’re on a budget, I’m sure you could get the ingredients at Walmart and bring the cost per salad down even more.
Your first step should be to see your doctor. If you think you have low testosterone, we cannot stress enough that you should proceed with caution and talk to a medical professional — taking a booster can definitely do more harm than good. Low testosterone can be a symptom of more serious problems, like a pituitary disorder or a side-effect of medication, and a booster can mask the root cause. A doctor will be able to evaluate your testosterone levels with a simple blood test, and if you both decide a booster is the way to go, give the ingredients of any supplement a once-over to make sure that they’re not at risk of making your personal health situation worse.

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.
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.
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).
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.
One study looking at alcohol consumption found that increasing alcohol consumption led to a higher level of free & total testosterone compared to a non-drinking control group (20). Drinking did however lower SHBG testosterone levels, though this type of testosterone is bound to a protein meaning our bodies cannot use it to build muscle or increase our mood.
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Testosterone may prove to be an effective treatment in female sexual arousal disorders,[52] and is available as a dermal patch. There is no FDA approved androgen preparation for the treatment of androgen insufficiency; however, it has been used off-label to treat low libido and sexual dysfunction in older women. Testosterone may be a treatment for postmenopausal women as long as they are effectively estrogenized.[52]
The effect excess testosterone has on the body depends on both age and sex. It is unlikely that adult men will develop a disorder in which they produce too much testosterone and it is often difficult to spot that an adult male has too much testosterone. More obviously, young children with too much testosterone may enter a false growth spurt and show signs of early puberty and young girls may experience abnormal changes to their genitalia. In both males and females, too much testosterone can lead to precocious puberty and result in infertility. 
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