The sex hormone testosterone is far more than just the stuff of the alpha male's swagger. Though it plays a more significant role in the life of the biological male, it is actually present in both sexes to some degree. Despite popular perceptions that testosterone primarily controls aggression and sex drive—although it does play a role in both of those things—research has shown that individual levels of testosterone are also correlated with our language skills and cognitive abilities. Testosterone occurs in the body naturally, but can be administered as a medication, too: its most common uses are in the treatment of hypogonadism and breast cancer, as well as in hormone therapy for transgender men.
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.
Phthalates are found to cause poor testosterone synthesis by disrupting an enzyme required to create the male hormone. Women with high levels of DEHP and DBP (two types of phthalates) in their system during pregnancy were found to have sons that had feminine characteristics Phthalates are found in vinyl flooring, detergents, automotive plastics, soaps and shampoos, deodorants, perfumes, hair sprays, plastic bags and food packaging, among a long list of common products. Aside from phthalates, other chemicals that possess gender-bending traits are:
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]
However, some of these signs and symptoms can be caused by factors other than low testosterone, including medication side effects, thyroid problems, depression and excessive alcohol use. There are also conditions, such as obstructive sleep apnea, that might affect testosterone levels. Once these conditions are identified and treated, testosterone typically will return to a normal level.
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.
We do note that Beast Sports’ supplemental magnesium level is fairly low — 26 mg per serving, up to 52 mg per day. If your diet is not particularly rich in magnesium (found in leafy greens, nuts, and whole grains), Beast Sports may not give you enough to meet the daily recommended dose. However, if you’re taking other multi-vitamins or supplements with magnesium, you’re less likely to cross that 350mg daily upper limit.
The first period occurs between 4 and 6 weeks of the gestation. Examples include genital virilisation such as midline fusion, phallic urethra, scrotal thinning and rugation, and phallic enlargement; although the role of testosterone is far smaller than that of dihydrotestosterone. There is also development of the prostate gland and seminal vesicles.
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).

If a man's testosterone looks below the normal range, there is a good chance he could end up on hormone supplements—often indefinitely. "There is a bit of a testosterone trap," Dr. Pallais says. "Men get started on testosterone replacement and they feel better, but then it's hard to come off of it. On treatment, the body stops making testosterone. Men can often feel a big difference when they stop therapy because their body's testosterone production has not yet recovered."

If your levels are indeed low, there are a number of synthetic and bioidentical testosterone products on the market, as well as DHEA, which is the most abundant androgen precursor prohormone in the human body, meaning that it is the largest raw material your body uses to produce other vital hormones, including testosterone in men and estrogen in women.

Low testosterone levels may contribute to decreased sex drive, erectile dysfunction, fragile bones, and other health issues. Having low testosterone levels may also indicate an underlying medical condition. See your doctor if you suspect you have low testosterone. A simple blood test is all it takes to check if your testosterone falls within the normal range.
I recommend using a trans-mucosal DHEA cream. Applying it to the rectum or if you are a a woman, your vagina, will allow the mucous epithelial membranes that line your mucosa to perform effective absorption. These membranes regulate absorption and inhibit the production of unwanted metabolites of DHEA. I personally apply 50 milligrams of trans-rectal DHEA cream twice a day – this has improved my own testosterone levels significantly. However, please note that I do NOT recommend prolonged supplementation of hormones. Doing so can trick your body into halting its own DHEA production and may cause your adrenals to become seriously impaired down.
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Magnesium comes with a strict upper cap. Excess magnesium is hard on your kidneys, and can lead to kidney failure. The NIH recommends that men consume 400-420 mg of magnesium daily, but that they should not exceed 350 mg of supplemental magnesium per day. Because while it’s rare for people to chronically overdose on magnesium through diet (you’d have to eat a lot of almonds and spinach, for example), overdose by supplement is far more common.
Testosterone fluctuates according to age and life circumstance, often plummeting at the onset of parenthood, and spiking (for some) during moments of triumph. Romantic relationships, too, can impact a person’s testosterone production; though the reasons are still not fully understood, entering a relationship tends to increase women’s testosterone levels, while decreasing men’s. Since males produce significantly more testosterone than females—about 20 times more each day—females can be more sensitive to these fluctuations. High levels of testosterone, particularly in men, have been correlated with a greater likelihood of getting divorced or engaging in extramarital affairs, though a causal link has not been established.
Does the diminution that age brings with it in both total and bioavailable T have any clinical significance? This question leads us to the theme of this paper, “The Many Faces of Testosterone”. If testosterone were simply a “sex hormone” involved only with sexual desire and arousal we might tend to dismiss testosterone treatment in the aging man as merely a “life-style” therapy without any substantive basis for broad physiological necessity. The fact is, however, that the sexual attributes of testosterone are the least of its physiological necessities and that testosterone has a broad spectrum of demonstrated physiological functions as well as a wide variety of physiological and pathophysiological associations about which we are just learning.
The chemical synthesis of testosterone from cholesterol was achieved in August that year by Butenandt and Hanisch.[183] Only a week later, the Ciba group in Zurich, Leopold Ruzicka (1887–1976) and A. Wettstein, published their synthesis of testosterone.[184] These independent partial syntheses of testosterone from a cholesterol base earned both Butenandt and Ruzicka the joint 1939 Nobel Prize in Chemistry.[182][185] Testosterone was identified as 17β-hydroxyandrost-4-en-3-one (C19H28O2), a solid polycyclic alcohol with a hydroxyl group at the 17th carbon atom. This also made it obvious that additional modifications on the synthesized testosterone could be made, i.e., esterification and alkylation.
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