Ashwagandha: One of the hottest herbs out there right now, this adaptogen packs a one-two punch. First, it helps the body fight off stress: According to one Indian Journal of Psychological Medicine study, ashwagandha has a cortisol-lowering effect—a major benefit to anyone who wants their body to be more T-friendly. And, second, it can also support your T-boosting training efforts. One Journal of the International Society of Sports Nutrition study, for example, found that men who supplemented with ashwagandha saw significantly greater strength and T gains after eight weeks of resistance training than those who took a placebo.
Anabolic–androgenic steroids (AASs) are synthetic derivatives of testosterone that are commonly used among athletes aged 18–40 years, but many reports have demonstrated the presence of numerous toxic and hormonal effects as a result of long-term use of an AAS.[9] Testosterone-foods act as natural libido boosters. Due to the growing interest in herbal ingredients and other dietary supplements worldwide, the use of testosterone boosters is becoming more and more mainstream among athletes, but several side effects were documented. Hence, this study established to help in the assessment of the side effects and health risks which could occur among athletes consuming testosterone boosters.
Testosterone decreases body fat. Testosterone plays an important role in regulating insulin, glucose, and fat metabolism. As our T levels decrease, our body’s ability to regulate insulin, glucose, and fat metabolism decreases, which in turn causes adipose tissue (i.e. fat) to begin accumulating. To add insult to injury, that increased adipose tissue may also contribute to further decreasing testosterone levels because it converts testosterone into estrogen.

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.[155] 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][155][161][162] 5α-Reductase is highly expressed in the male reproductive organs (including the prostate gland, seminal vesicles, and epididymides),[163] skin, hair follicles, and brain[164] and aromatase is highly expressed in adipose tissue, bone, and the brain.[165][166] As much as 90% of testosterone is converted into 5α-DHT in so-called androgenic tissues with high 5α-reductase expression,[156] and due to the several-fold greater potency of 5α-DHT as an AR agonist relative to testosterone,[167] it has been estimated that the effects of testosterone are potentiated 2- to 3-fold in such tissues.[168]

“I'm having great results. Everybody is seeing a difference. People say, “You look good! Did you lose weight? What are you taking?” I'm 59, and I'm bringing my belt down a couple different notches. I couldn't break 180 lbs for nothing, no matter what I tried. Now it's 175 lbs. and she's going from there. I was just doing it for the belly -- no matter what I just couldn't get rid of the belly (until now). And I'm not as tired as I used to be.“
Testosterone is an androgen hormone produced by the adrenal cortex, the testes (in men), and the ovaries (in women). It is often considered the primary male sex hormone. Testosterone stimulates the development of male secondary sex characteristics (like body hair and muscle growth) and is essential in the production of sperm. In women, testosterone plays a role in egg development and ovulation.
In summary it’s important to know that this topic is still hotly debated, and there are a lot of inconsistencies in the data. We do know that soy contains phytoestrogens and does seem to have a lot of affects on the body, including some studies that show decreased Testosterone levels. For that reason (and the fact that it tastes like ass) I avoid it, and I recommend you also avoid it (in particular soy isolates!) if you’re seeking higher testosterone.
We required all of our testosterone boosters to have magnesium, but gave preference to magnesium aspartate, citrate, lactate, and chloride. These forms have been found to be more easily absorbed than magnesium oxide and sulfate. (On the other hand, it didn’t count if the supplement had magnesium stearate, which is used to make pills not stick together.)
“This study establishes testosterone levels at which various physiological functions start to become impaired, which may help provide a rationale for determining which men should be treated with testosterone supplements,” Finkelstein says. “But the biggest surprise was that some of the symptoms routinely attributed to testosterone deficiency are actually partially or almost exclusively caused by the decline in estrogens that is an inseparable result of lower testosterone levels.”
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).
I’ve been on testosterone replacement for over 3 years and at first I did the shots and my mood swings were ridiculous, my skin broke out on my chest and shoulders, and my henatocrit went to 55%. I finally got fed up with doing shots every two weeks and switched to Gel and it’s been so much better. It actually increases my levels which is rare for most men. I do 12.5 mg, three pumps a day, and this keeps My level between 500 and 600. My hematocrit is 48.5 and no mood swings.

The T Trials will serve as a prelude to lengthier and more robust trials in the future. More results from the T Trials are now coming in and overall results were mixed, with testosterone replacement associated with some benefits and some risks. More research needs to be done to figure out the balance of these potential benefits and risks as well as the precise clinical utility of testosterone treatment.
"A lot of the symptoms are mirrored by other medical problems," Hedges says. "And for a long time, we were not attributing them to low testosterone, but to diabetes, depression, high blood pressure, and coronary artery disease. But awareness and appreciation of low testosterone has risen. We recognize now that low testosterone may be at the root of problems."
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