Testosterone is a male hormone. Hormones are chemical messengers that are secreted by the brain directly into the blood, which carries them to organs and tissues of the body to perform their functions. Testosterone is produced by the testicles, two oval organs that produce sperm in men. Dietary supplements help with increasing the levels of hormones if we have low levels in the body. In men, testosterone plays a key role in the development of male reproductive organs. In addition, it helps with increasing muscle mass, bone mass, and the growth of body hair. It is also good for general health and well-being. It also prevents loss of bone mass and density. Testosterone also helps maintain the sex drive and energy levels. Moreover, it helps with production of sperm and red blood cells. Testosterone levels start to fall with age. As a result, some men who have low testosterone levels may benefit from testosterone prescribed by their doctor. Testosterone booster supplements may also help.
The Organon group in the Netherlands were the first to isolate the hormone, identified in a May 1935 paper "On Crystalline Male Hormone from Testicles (Testosterone)". They named the hormone testosterone, from the stems of testicle and sterol, and the suffix of ketone. The structure was worked out by Schering's Adolf Butenandt, at the Chemisches Institut of Technical University in Gdańsk.
At the present time, it is suggested that androgen replacement should take the form of natural testosterone. Some of the effects of testosterone are mediated after conversion to estrogen or dihydrotestosterone by the enzymes aromatase and 5a-reductase enzymes respectively. Other effects occur independently of the traditional action of testosterone via the classical androgen receptor- for example, its action as a vasodilator via a cell membrane action as described previously. It is therefore important that the androgen used to treat hypogonadism is amenable to the action of these metabolizing enzymes and can also mediate the non-androgen receptor actions of testosterone. Use of natural testosterone ensures this and reduces the chance of non-testosterone mediated adverse effects. There are now a number of testosterone preparations which can meet these recommendations and the main factor in deciding between them is patient choice.
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.
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).
It's not enough just to increase the testosterone your body produces, because as we age, the testosterone we naturally produce is often bound by SHBG (sex hormone binding globulin) thus becoming unavailable for use in the body. It’s imperative that your testosterone remains unbound or “free” if you want to enjoy all the wonderful benefits testosterone provides.
The reliable measurement of serum free testosterone requires equilibrium dialysis. This is not appropriate for clinical use as it is very time consuming and therefore expensive. The amount of bioavailable testosterone can be measured as a percentage of the total testosterone after precipitation of the SHBG bound fraction using ammonium sulphate. The bioavailable testosterone is then calculated from the total testosterone level. This method has an excellent correlation with free testosterone (Tremblay and Dube 1974) but is not widely available for clinical use. In most clinical situations the available tests are total testosterone and SHBG which are both easily and reliably measured. Total testosterone is appropriate for the diagnosis of overt male hypogonadism where testosterone levels are very low and also in excluding hypogonadism in patients with normal/high-normal testosterone levels. With increasing age, a greater number of men have total testosterone levels just below the normal range or in the low-normal range. In these patients total testosterone can be an unreliable indicator of hypogonadal status. There are a number of formulae that calculate an estimated bioavailable or free testosterone level using the SHBG and total testosterone levels. Some of these have been shown to correlate well with laboratory measures and there is evidence that they more reliably indicate hypogonadism than total testosterone in cases of borderline biochemical hypogonadism (Vermeulen et al 1971; Morris et al 2004). It is important that such tests are validated for use in patient populations relevant to the patient under consideration.
While researchers in Brisbane, Australia, found that while Testofen (“a standardized [fenugreek] extract and mineral formulation”) significantly improved the sexual arousal, orgasm, and the general quality of life of participants, it did not remarkably increase testosterone above normal levels. Participants who took Testofen were more satisfied with their energy, well-being, and muscle strength than those who took the placebo.
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One study found that men who took 3,332 international units (IU) of vitamin D daily for one year significantly increased their testosterone levels. But vitamin D supplements may only work for men who are severely deficient in this specific vitamin. Another study found that men without a vitamin D deficiency had no increase in testosterone levels after taking vitamin D.
This over-the-counter supplement is intended to increase your body's level of testosterone to its highest. The manufacturer also advertises the positive effect that the drug can have on your sex life and achieving muscle growth. As a supplement, you are instructed to take four capsules each night before bed. On training days, recommended dosage is two capsules before you workout. Ingredients found in the product include tribulis terristris, long jack, maca root and epimedium.
In a placebo-controlled study, 27 Division II football players received either a placebo or a ZMA supplement for a total of seven weeks during their scheduled spring practice. At the end of the seven weeks, the players taking the ZMA supplement had a 30 percent increase in testosterone, while the placebo group had a 10 percent decrease. The ZMA group also saw an 11.6 percent increase in strength, compared to only 4.6 percent in the placebo group.
Ten healthy men aged around 24 years old spent 1 week sleeping for 8 hours per night at home, they then spent the next 11 nights in a lab. They slept for 10 hours per night for 3 nights, followed by 8 nights of restricted sleep, when they slept for only 5 hours. Doctors checked their blood every 15 to 30 minutes during the last night that they slept 10 hours, as well as on the sleep-restricted session.
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).
Workouts lasting longer than about an hour may begin to spike cortisol levels and subsequently decrease testosterone. Additionally, research has demonstrated that a shorter rest period between sets (1 minute versus 3 minutes) elicited higher acute hormonal responses following a bout of resistance training.11 To maximize your testosterone response, keep your rest periods short and total workout time to 60 minutes or fewer.
Vitamin D, a steroid hormone, is essential for the healthy development of the nucleus of the sperm cell, and helps maintain semen quality and sperm count. Vitamin D also increases levels of testosterone, which may boost libido. In one study, overweight men who were given vitamin D supplements had a significant increase in testosterone levels after one year.5
Testosterone is included in the World Health Organization's list of essential medicines, which are the most important medications needed in a basic health system. It is available as a generic medication. The price depends on the form of testosterone used. It can be administered as a cream or transdermal patch that is applied to the skin, by injection into a muscle, as a tablet that is placed in the cheek, or by ingestion.
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, showed no improvement with testosterone treatment. Many times, other health problems play a role in erectile difficulties. These can include:
Vitamin D is arguably the most important vitamin when it comes to testosterone. A study published in the Journal of Clinical Endocrinology examined the relationship between vitamin D supplementation and testosterone levels in men. The authors found that participants with higher levels of vitamin D had significantly higher levels of free testosterone compared to those with insufficient levels of vitamin D.8 Based on these study results, it appears vitamin D has a strong relationship with testosterone levels.
On review of the patient’s history, he was found to have undergone laboratory tests before starting to use the aforementioned testosterone booster product. All blood parameters (testosterone hormone and full chemical profile) before product intake were in the normal range. A physical examination that included blood pressure and pulse assessments showed nothing out of the ordinary, and the man appeared to be in good condition before product consumption. After that medical checkup, the athlete began to consume the product for 42 continuous days divided into 2 cycles (each cycle comprised 24 days). The daily dose was a single pack of Universal Nutrition Animal Stak (ingredients are listed in Table 1), following the exact direction of the manufacturing company hoping to get the best results.
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Like other steroid hormones, testosterone is derived from cholesterol (see figure). The first step in the biosynthesis involves the oxidative cleavage of the side-chain of cholesterol by cholesterol side-chain cleavage enzyme (P450scc, CYP11A1), a mitochondrial cytochrome P450 oxidase with the loss of six carbon atoms to give pregnenolone. In the next step, two additional carbon atoms are removed by the CYP17A1 (17α-hydroxylase/17,20-lyase) enzyme in the endoplasmic reticulum to yield a variety of C19 steroids. In addition, the 3β-hydroxyl group is oxidized by 3β-hydroxysteroid dehydrogenase to produce androstenedione. In the final and rate limiting step, the C17 keto group androstenedione is reduced by 17β-hydroxysteroid dehydrogenase to yield testosterone.
This herb, used for centuries in foods, even poultices, was reported in the International Journal of Sport Nutrition and Exercise Metabolism to have reduced body fat and improved total testosterone levels versus a placebo in a double-blind trial. Fenugreek may also be helpful if you feel your sex drive is on the wane, as other research has found it can boost libido. You can get it in curries (it’s used to flavor them) and teas, or as a supplement in TestroVax, by Novex Biotech, which promises to boost testosterone levels 42% in 12 days. (novexbiotech.com)
Why niacinamide could positively impact 5-a reduced androgens? It’s complex, but simply put, its a crucial part of this compound called NADPH (Nicotinamide adenine dinucleotide phosphate). And NADPH is a co-factor in many anabolic/androgenic reactions of the body, including both testosterone and dihydrotestosterone production (NADPH is needed for the production of 5-ar enzyme).
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.