For men with low blood testosterone levels, the benefits of hormone replacement therapy usually outweigh potential risks. However, for most other men it's a shared decision with your doctor. It offers men who feel lousy a chance to feel better, but that quick fix could distract attention from unknown long-term hazards. "I can't tell you for certain that this raises your personal risk of heart problems and prostate cancer, or that it doesn't," Dr. Pallais says.
In the hepatic 17-ketosteroid pathway of testosterone metabolism, testosterone is converted in the liver by 5α-reductase and 5β-reductase into 5α-DHT and the inactive 5β-DHT, respectively.[1][155] Then, 5α-DHT and 5β-DHT are converted by 3α-HSD into 3α-androstanediol and 3α-etiocholanediol, respectively.[1][155] Subsequently, 3α-androstanediol and 3α-etiocholanediol are converted by 17β-HSD into androsterone and etiocholanolone, which is followed by their conjugation and excretion.[1][155] 3β-Androstanediol and 3β-etiocholanediol can also be formed in this pathway when 5α-DHT and 5β-DHT are acted upon by 3β-HSD instead of 3α-HSD, respectively, and they can then be transformed into epiandrosterone and epietiocholanolone, respectively.[157][158] A small portion of approximately 3% of testosterone is reversibly converted in the liver into androstenedione by 17β-HSD.[156]
Some foods, vitamins, and herbs can help boost your testosterone levels. Be sure to talk to your doctor, if you’re concerned about low testosterone. These alternative and natural treatments aren’t proven to be more, or as, effective as traditional testosterone therapy. Some may also interact with any medications you may be taking and cause unintended side effects.
Testoshred stands out as a muscle hardening testosterone booster as it first combines 3 clinically studied and effective testosterone boosting agents with the powerful estrogen reducer Arimistane. The addition of Arimistane helps to prevent the conversion of testosterone to estrogen resulting in higher testosterone levels, while increasing muscle hardness and reducing body fat.
The mineral zinc is important for testosterone production, and supplementing your diet for as little as six weeks has been shown to cause a marked improvement in testosterone among men with low levels.1 Likewise, research has shown that restricting dietary sources of zinc leads to a significant decrease in testosterone, while zinc supplementation increases it2 -- and even protects men from exercised-induced reductions in testosterone levels.3
In essence, there are two types of testosterone boosters, namely natural and synthetic supplements. Anabolic steroids which are under the synthetic category are known to deliver positive results as well as nasty side effects. It is due to this reason that an increasing number of bodybuilders and athletes are now utilizing safer testosterone boosters.

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).
What is your opinion of using depo-testosterone injections on women? I am 44 and have had a complete hyserectomy. My OB/GYN was injecting the hormone when I complained of low libido. Unfortunately, the doctor was asked to leave the practice and his replacement refuses to use the injections on me. Any thoughts or suggestions would be greatly appreciated.
BCAA peptides are the building blocks of muscle.  Your body cannot make BCAA’s.  You have to eat them.  One easy way of course is food and things like whey protein powder.  That is why whey protein works so well because it contains BCAA’s at high levels.  Advanced BCAA is 50% BCAA in peptide form!!  Peptides are digested faster and more efficiently than whole foods and normal protein powders.  This means more muscle building and recovery support!!
The evidence shows that testosterone treatment does not change the strength or rate of urine flow, does not change the ability to empty the bladder, and does not change other symptoms such as frequency or urgency of urination, as assessed by the American Urological Association Symptom Score or the International Prostate Symptom Score. I’ve had a couple of patients over the years who had some worsening of urinary symptoms with testosterone, but that’s rare, even with long-term use.
Inaccurate or misinterpreted test results can either falsely diagnose or miss a case of testosterone deficiency. Your testosterone level should be measured between 7 am and 10 am, when it's at its peak. Confirm a low reading with a second test on a different day. It may require multiple measurements and careful interpretation to establish bioavailable testosterone, or the amount of the hormone that is able to have effects on the body. Consider getting a second opinion from an endocrinologist.
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).
Benefits: Maca roots originates from the mountains of Peru. For a long time, natives have been using Maca roots as not only a food supply but for it’s properties for increasing sexual potency. It has been prove to improve erectile dysfunctions, libido and sperm production. Maca roots stimulate semen volume, sperm count and sperm motility, which makes Maca a powerful Aphrodisiac.
The normal development of the prostate gland is dependent on the action of testosterone via the androgen receptor, and abnormal biosynthesis of the hormone or inactivating mutations of the androgen receptor are associated with a rudimentary prostate gland. Testosterone also requires conversion to dihydrotestosterone in the prostate gland for full activity. In view of this link between testosterone and prostate development, it is important to consider the impact that testosterone replacement may have on the prevalence and morbidity associated with benign prostatic hypertrophy (BPH) and prostate cancer, which are the common conditions related to pathological growth of the prostate gland.
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).
When the body cannot produce enough testosterone on its own, the term is called hypogonadism.  Testosterone boosters do not give the user actual testosterone (like with steroids), rather, they kickstart the production of this very important hormone.  For that reason, it’s important to find a potent formulation that has one or multiple key ingredients in it.
Note that DHT is what causes male pattern baldness so it stands to reason that fenugreek may delay the balding process.  A quick Google search of “fenugreek and baldness” reveals that I am not the only genius struck with this idea.  There are sites out there that claim that a fenugreek+saw palmetto concoction or applying a fenugreek paste can help prevent Mr. Cleanitis.
i have been on T therapy for 32 years now after being diagnosed with Klinefelters. Recently my pharmacy had been non responsive to my request to refill and they flat out refused/declined the request from my doctor which was T powder mixed with a cream base that you place on the shoulder. I asked if I could purchase it with cash and they told me that the FDA is not approving this usage anymore but did not provide an option. Completely out now for close to a week and have been working for five weeks trying to get again. Now what to do, I’m having all kinds of weird feelings including anxiety to the max, nervous, irritable, muscle cramps/pains … I guess they just don’t care that we cannot get something our bodies have adjusted too for many years. Strange thing is I think I have found a compounding pharmacy in Houston Texas that will fill this Rx. I’m not sure how one can do this and another cannot especially if they have compounding capabilities. Now I’m wondering if I can get thru this and stop taking it alltogether however I already know I’m seeing signs of being forgetful, lack of energy and foggy brain. I wonder if this will ever stop. The really bad thing is that I’m traveling for work and cannot get into my doctor’s office. This whole process is not great. I can only imagine what a person must feel taking hard drugs then not getting any all at once.
"Some say it's just a part of aging, but that's a misconception," says Jason Hedges, MD, PhD, a urologist at Oregon Health and Science University in Portland. A gradual decline in testosterone can't explain a near-total lack of interest in sex, for example. And for Hedges' patients who are in their 20s, 30s, and early 40s and having erectile problems, other health problems may be a bigger issue than aging.
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