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).
A previous meta-analysis has confirmed that treatment of hypogonadal patients with testosterone improves erections compared to placebo (Jain et al 2000). A number of studies have investigated the effect of testosterone levels on erectile dysfunction in normal young men by inducing a hypogonadal state, for example by using a GnRH analogue, and then replacing testosterone at varying doses to produce levels ranging from low-normal to high (Buena et al 1993; Hirshkowitz et al 1997). These studies have shown no significant effects of testosterone on erectile function. These findings contrast with a similar study conducted in healthy men aged 60–75, showing that free testosterone levels achieved with treatment during the study correlate with overall sexual function, including morning erections, spontaneous erections and libido (Gray et al 2005). This suggests that the men in this older age group are particularly likely to suffer sexual symptoms if their testosterone is low. Furthermore, the severity of erectile dysfunction positively correlates with lower testosterone levels in men with type 2 diabetes (Kapoor, Clarke et al 2007).
Men's levels of testosterone, a hormone known to affect men's mating behaviour, changes depending on whether they are exposed to an ovulating or nonovulating woman's body odour. Men who are exposed to scents of ovulating women maintained a stable testosterone level that was higher than the testosterone level of men exposed to nonovulation cues. Testosterone levels and sexual arousal in men are heavily aware of hormone cycles in females.[46] This may be linked to the ovulatory shift hypothesis,[47] where males are adapted to respond to the ovulation cycles of females by sensing when they are most fertile and whereby females look for preferred male mates when they are the most fertile; both actions may be driven by hormones.

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.
Two of the immediate metabolites of testosterone, 5α-DHT and estradiol, are biologically important and can be formed both in the liver and in extrahepatic tissues.[151] Approximately 5 to 7% of testosterone is converted by 5α-reductase into 5α-DHT, with circulating levels of 5α-DHT about 10% of those of testosterone, and approximately 0.3% of testosterone is converted into estradiol by aromatase.[2][151][157][158] 5α-Reductase is highly expressed in the male reproductive organs (including the prostate gland, seminal vesicles, and epididymides),[159] skin, hair follicles, and brain[160] and aromatase is highly expressed in adipose tissue, bone, and the brain.[161][162] As much as 90% of testosterone is converted into 5α-DHT in so-called androgenic tissues with high 5α-reductase expression,[152] and due to the several-fold greater potency of 5α-DHT as an AR agonist relative to testosterone,[163] it has been estimated that the effects of testosterone are potentiated 2- to 3-fold in such tissues.[164]

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.
In accordance with sperm competition theory, testosterone levels are shown to increase as a response to previously neutral stimuli when conditioned to become sexual in male rats.[40] This reaction engages penile reflexes (such as erection and ejaculation) that aid in sperm competition when more than one male is present in mating encounters, allowing for more production of successful sperm and a higher chance of reproduction.
^ Butenandt A, Hanisch G (1935). "Umwandlung des Dehydroandrosterons in Androstendiol und Testosterone; ein Weg zur Darstellung des Testosterons aus Cholestrin" [About Testosterone. Conversion of Dehydro-androsterons into androstendiol and testosterone; a way for the structure assignment of testosterone from cholesterol]. Hoppe-Seyler's Z Physiol Chem (in German). 237 (2): 89–97. doi:10.1515/bchm2.1935.237.1-3.89.

Try diet and exercise changes as your health permits. Losing weight, eating the right foods, and getting more exercise are great ways to naturally increase testosterone while also improving your overall health. While mild to moderate changes are likely safe in most teenage boys, you should consult your doctor before making any significant changes to make sure those changes will be right for your specific health needs.
In addition to weight training, combining this with interval training like burst training is the best overall combo to increase HGH. In fact, Burst training has been proven to not only boost T-levels, it helps keeps your testosterone elevated and can prevent its decline. Burst training involves exercising at 90–100 percent of your maximum effort for a short interval in order to burn your body’s stored sugar (glycogen), followed by a period of low impact for recovery.
Imagine if there was a pill that would transform your dick into an unstoppable orgasm machine; A pill that gave you the confidence to talk to any girl, because you knew one night with you and she would be begging for your cock. Women are attracted to men that can make them climax. The most PATHETIC trait a man can have is being bad at sex. But the exact opposite is also true.
I know the experiment didn’t simply bring me back to my pre-August levels because of the fact that when I learned that the original test I took can sometimes overestimate your T levels, I took a more accurate test around four months after the start of the experiment (I’ve continued the lifestyle changes made during the experiment) and my total T had gone up again to 826.9 ng/dL.
Yeah, you could do expensive hormone replacement. Or you could take a synthetic test booster. But at the end of the day, neither of these compare to being able to boost testosterone naturally. Nature didn’t intend for you to inject yourself with hormones. Somewhere along the line something went wrong. At your natural level, you are designed to flourish. And the world has everything available for you and your testosterone levels to do so.

The brain is also affected by this sexual differentiation;[13] the enzyme aromatase converts testosterone into estradiol that is responsible for masculinization of the brain in male mice. In humans, masculinization of the fetal brain appears, by observation of gender preference in patients with congenital diseases of androgen formation or androgen receptor function, to be associated with functional androgen receptors.[95]
Dr. Anthony’s Notes: DHEA is a powerful supplement for testosterone, energy, and overall well-being in our older Fit Fathers. A small dose of 25-50mg/day is enough to exert noticeable benefits. This supplement is over-the-counter. Verdict: this is one of the testosterone supplements that work. How To Take DHEA: Take 25-50mg once per day with food. Special Medical Note: DHEA is a MILD CYP3A4 inhibitor (a liver enzyme that processes MANY very common medications). This is the same isoenzyme that Grapefruit inhibits – albeit DHEA inhibits to a much weaker degree. If you’ve ever heard “don’t eat grapefruit with your Lipitor (cholesterol medication)”… this is the reason why. When we inhibit the CYP3A4 enzyme, more of the medications you're taking circulates (it’s not metabolized as fast). Check with your doctor for medication interactions before using DHEA.

Regardless of the method of testosterone treatment chosen, patients will require regular monitoring during the first year of treatment in order to monitor clinical response to testosterone, testosterone levels and adverse effects, including prostate cancer (see Table 2). It is recommended that patients should be reviewed at least every three months during this time. Once treatment has been established, less frequent review is appropriate but the care of the patient should be the responsibility of an appropriately trained specialist with sufficient experience of managing patients treated with testosterone.

^ Jump up to: a b Sapienza P, Zingales L, Maestripieri D (September 2009). "Gender differences in financial risk aversion and career choices are affected by testosterone". Proceedings of the National Academy of Sciences of the United States of America. 106 (36): 15268–73. Bibcode:2009PNAS..10615268S. doi:10.1073/pnas.0907352106. PMC 2741240. PMID 19706398.
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Reduce stress levels. Stress is ubiquitous in the modern world, particularly for teenagers who face a variety of pressures and expectations. High levels of stress triggers the release of the stress hormone cortisol, which tends to counteract the negative physiological effects of stress. That's certainly beneficial, but cortisol also blocks the effects and impact of testosterone within the body, which can cause significant problems for teenage boys.[7] As such, try to provide a low-stress, stable environment for your teenager and give him opportunities to vent his frustrations and other emotions. Exercising, playing sports and developing enjoyable hobbies are all great at reducing stress.

^ Southren AL, Gordon GG, Tochimoto S, Pinzon G, Lane DR, Stypulkowski W (May 1967). "Mean plasma concentration, metabolic clearance and basal plasma production rates of testosterone in normal young men and women using a constant infusion procedure: effect of time of day and plasma concentration on the metabolic clearance rate of testosterone". The Journal of Clinical Endocrinology and Metabolism. 27 (5): 686–94. doi:10.1210/jcem-27-5-686. PMID 6025472.
A large number of side-effects have been attributed to testosterone. In our clinical experience, the incidence of significant adverse effects with treatment producing physiological testosterone levels is low, and many side effects attributed to testosterone are mainly relevant to supraphysiological replacement. Some adverse effects are specific to a given mode of delivery and have already been described. Potential adverse effects concerning the prostate have also been discussed and require appropriate monitoring of symptoms, PSA and digital rectal examination. Other tumors which may be androgen responsive include cancer of the breast and primary liver tumors, and these are both contraindications to testosterone treatment

Ghlissi, Z., Atheymen, R., Boujbiha, M. A., Sahnoun, Z., Makni Ayedi, F., Zeghal, K., ... Hakim, A. (2013, December). Antioxidant and androgenic effects of dietary ginger on reproductive function of male diabetic rats [Abstract]. International Journal of Food Sciences and Nutrition, 64 (8), 974–978. Retrieved from https://www.ncbi.nlm.nih.gov/pubmed/23862759
VI-PEX or Vasodilator Ingredients with Penile Expansion is a highly-potent combination of blood flow-boosting ingredients which prolong and intensify the vasodilation properties of Male UltraCore, resulting in an undeniable improvement in size and hardness during penile erection. VI-PEX technology works hand-in-hand with STEM technology to leverage sexual arousal as a size-boosting factor during penile erection.
In order to discuss the biochemical diagnosis of hypogonadism it is necessary to outline the usual carriage of testosterone in the blood. Total serum testosterone consists of free testosterone (2%–3%), testosterone bound to sex hormone binding globulin (SHBG) (45%) and testosterone bound to other proteins (mainly albumin −50%) (Dunn et al 1981). Testosterone binds only loosely to albumin and so this testosterone as well as free testosterone is available to tissues and is termed bioavailable testosterone. Testosterone bound to SHBG is tightly bound and is biologically inactive. Bioavailable and free testosterone are known to correlate better than total testosterone with clinical sequelae of androgenization such as bone mineral density and muscle strength (Khosla et al 1998; Roy et al 2002). There is diurnal variation in serum testosterone levels with peak levels seen in the morning following sleep, which can be maintained into the seventh decade (Diver et al 2003). Samples should always be taken in the morning before 11 am to allow for standardization.
Testosterone replacement therapy is currently only FDA approved for men who have been diagnosed with hypogonadism, but it’s also prescribed off-label for older men who take it in hopes that it will improve their libido. The use of testosterone therapy is increasingly common in the United States, with more than 2 million men receiving the therapy. Not every man benefits from taking testosterone supplements. Testosterone is available in different forms, including topicals such as gels, creams, and patches; injections; and pellets that are surgically placed directly beneath the skin. (7)
Consume enough zinc. Zinc is a mineral needed for many body functions including healthy immune function, bone strength and the production of testosterone. In fact, low levels of zinc are correlated to low levels of testosterone in men and teenage boys.[8] Mild zinc deficiency is now fairly common among Americans, so there's a good chance your teenage boy (particularly if he isn't a healthy eater) may be deficient. Ask your doctor for a blood test to get a better idea, but in the meantime, focus on serving and eating foods that are rich in zinc, such as meats, fish, low-fat milk, hard cheeses, beans and some nuts and seeds.

There are the testosterone deficiency signs, such as loss of sexual desire, erectile dysfunction, impaired fertility, chronic fatigue, etc. But it’s not always possible to understand which medical condition caused the decrease in testosterone levels. For example, if you always feel exhausted and have no sexual desire, it may provide evidence of depression.
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.
The Sharks had said that these miracle testosterone pills were designed to increased men's size, and that’s exactly what happened with my hubby! I still find it hard to believe that this stuff turned him into a long, strong, wild beast in bed — and all for the price of a movie ticket and without any expensive prescription. I find the results to be worth every penny (I already ordered three more packs) — life is too valuable, and I’m not the kind of girl that skimps on pleasures.
A large number of trials have demonstrated a positive effect of testosterone treatment on bone mineral density (Katznelson et al 1996; Behre et al 1997; Leifke et al 1998; Snyder et al 2000; Zacharin et al 2003; Wang, Cunningham et al 2004; Aminorroaya et al 2005; Benito et al 2005) and bone architecture (Benito et al 2005). These effects are often more impressive in longer trials, which have shown that adequate replacement will lead to near normal bone density but that the full effects may take two years or more (Snyder et al 2000; Wang, Cunningham et al 2004; Aminorroaya et al 2005). Three randomized placebo-controlled trials of testosterone treatment in aging males have been conducted (Snyder et al 1999; Kenny et al 2001; Amory et al 2004). One of these studies concerned men with a mean age of 71 years with two serum testosterone levels less than 12.1nmol/l. After 36 months of intramuscular testosterone treatment or placebo, there were significant increases in vertebral and hip bone mineral density. In this study, there was also a significant decrease in the bone resorption marker urinary deoxypyridinoline with testosterone treatment (Amory et al 2004). The second study contained men with low bioavailable testosterone levels and an average age of 76 years. Testosterone treatment in the form of transdermal patches was given for 1 year. During this trial there was a significant preservation of hip bone mineral density with testosterone treatment but testosterone had no effect on bone mineral density at other sites including the vertebrae. There were no significant alterations in bone turnover markers during testosterone treatment (Kenny et al 2001). The remaining study contained men of average age 73 years. Men were eligible for the study if their serum total testosterone levels were less than 16.5 nmol/L, meaning that the study contained men who would usually be considered eugonadal. The beneficial effects of testosterone on bone density were confined to the men who had lower serum testosterone levels at baseline and were seen only in the vertebrae. There were no significant changes in bone turnover markers. Testosterone in the trial was given via scrotal patches for a 36 month duration (Snyder et al 1999). A recent meta-analysis of the effects on bone density of testosterone treatment in men included data from these studies and two other randomized controlled trials. The findings were that testosterone produces a significant increase of 2.7% in the bone mineral density at the lumber spine but no overall change at the hip (Isidori et al 2005). These results from randomized controlled trials in aging men show much smaller benefits of testosterone treatment on bone density than have been seen in other trials. This could be due to the trials including patients who are not hypogonadal and being too short to allow for the maximal effects of testosterone. The meta-analysis also assessed the data concerning changes of bone formation and resorption markers during testosterone treatment. There was a significant decrease in bone resorption markers but no change in markers of bone formation suggesting that reduction of bone resorption may be the primary mode of action of testosterone in improving bone density (Isidori et al 2005).
Other stereotypical "macho" behaviors can affect testosterone in women, according to a 2015 report in the Proceedings of the National Academy of Sciences. For example, posing in a powerful way increases testosterone in both women and men. The 2015 report showed that having women role-play a position of power — acting like a boss — had the same effect.
As crazy as it seems, it has lately been proven that there is a no relation between cholesterol intake and heart attack as doctors once thought (and many still do). This is slowly becoming common knowledge, regardless of pharmaceutical companies wishes. (Trust me, this billion dollar industry does not want you to know this. You don;t have to be a conspiracy theorist to see this.)

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).
Currently available testosterone preparations in common use include intramuscular injections, subcutaneous pellets, buccal tablets, transdermal gels and patches (see Table 2). Oral testosterone is not widely used. Unmodified testosterone taken orally is largely subject to first-pass metabolism by the liver. Oral doses 100 fold greater than physiological testosterone production can be given to achieve adequate serum levels. Methyl testosterone esters have been associated with hepatotoxicity. There has been some use of testosterone undecanoate, which is an esterified derivative of testosterone that is absorbed via the lymphatic system and bypasses the liver. Unfortunately, it produces unpredictable testosterone levels and increases testosterone levels for only a short period after each oral dose (Schurmeyer et al 1983).
Get plenty of vitamin D. Vitamin D is a very important nutrient when it comes to testosterone production. This makes sense when you realize that vitamin D acts more like a steroidal hormone than it does like any typical vitamin. A 2010 study looked at the relationship between vitamin D supplementation and testosterone levels in men and found that those with higher levels of the vitamin also had higher levels of testosterone in their blood.[12] Vitamin D is made by human skin in response to intense summer sunshine, but a lack of going outdoors has triggered near epidemic levels of deficiency in American teenagers. Compounding this problem is that most northern states don't get enough sunshine to trigger vitamin D production for many months of the year.
Are you getting enough vitamin D? Vitamin D is an essential nutrient, but it can be difficult for people to know if they are getting the right amount. Some people will be able to get enough vitamin D from sunlight. Others may need to make dietary changes or take supplements. Here, we explain how to get vitamin D from sunlight, food, and supplements. Read now

Hypogonadism is a disease in which the body is unable to produce normal amounts of testosterone due to a problem with the testicles or with the pituitary gland that controls the testicles. Testosterone replacement therapy can improve the signs and symptoms of low testosterone in these men. Doctors may prescribe testosterone as injections, pellets, patches or gels.
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