It is important not to use any DHEA product without the supervision of a professional. Find a qualified health care provider who will monitor your hormone levels and determine if you require supplementation. Rather than using an oral hormone supplementation, I recommend trans-mucosal (vagina or rectum) application. Skin application may not be wise, as it makes it difficult to measure the dosage you receive. This may cause you to end up receiving more than what your body requires.
In addition to conjugation and the 17-ketosteroid pathway, testosterone can also be hydroxylated and oxidized in the liver by cytochrome P450 enzymes, including CYP3A4, CYP3A5, CYP2C9, CYP2C19, and CYP2D6.[155] 6β-Hydroxylation and to a lesser extent 16β-hydroxylation are the major transformations.[155] The 6β-hydroxylation of testosterone is catalyzed mainly by CYP3A4 and to a lesser extent CYP3A5 and is responsible for 75 to 80% of cytochrome P450-mediated testosterone metabolism.[155] In addition to 6β- and 16β-hydroxytestosterone, 1β-, 2α/β-, 11β-, and 15β-hydroxytestosterone are also formed as minor metabolites.[155][156] Certain cytochrome P450 enzymes such as CYP2C9 and CYP2C19 can also oxidize testosterone at the C17 position to form androstenedione.[155]
The reasons for considering such therapy become evident from the many associations, indicated above, that reduced testosterone has with a variety of both physiological functions (bone metabolism, muscle mass, cognitive function, libido, erectile function) and pathophysiological states (metabolic syndrome, diabetes mellitus, obesity, insulin resistance, autoimmune disease). Although a definitive long-term, large scale placebo-controlled double-blind study of testosterone therapy in the aging male has not yet been carried out, multiple shorter-term trials have suggested improvement by testosterone with a resultant enhancement of muscle mass, bone density, libido, erectile function, mood, motivation and general sense of well-being.
Likewise, the amino acids in a protein-rich diet play a big role in both testosterone and muscle growth. As Chris Lockwood, Ph.D., explains, "When combined with training, which increases the sensitivity of androgen receptors, and the consumption of essential amino acids necessary to support protein synthesis, the effects of testosterone on muscle and performance is significantly amplified."[3,4]
That testosterone decreases with age has been clearly established by many studies over many years in several different populations of men (Harman et al 2001; Feldman et al 2002; Araujo et al 2004; Kaufman and Vermeulen 2005). Of even greater significance is the steeper fall of the most biologically active fraction of total testosterone, non-sex hormone binding globulin (SHBG)- bound testosterone, or bioavailable testosterone (bio-T). The classical, but not the only approach to measuring bio-T, is to precipitate out SHBG (and hence the testosterone which is strongly bound to it as well) and measure the remainder as total testosterone (Tremblay 2003). Vermeulen et al (1999) have devised a less tedious and less expensive method of measuring a surrogate for bio-T, namely calculated bio-T, inserting total T, albumin, SHBG and a constant into a mathematical formulation. There is a strong correlation between actual bio-T and calculated bio-T (Emadi-Konjin et al 2003).

“I have seen them work for people,” says GP and hormonal therapy expert at Omniya London, Dr Sohere Roked. “I think sometimes people feel that it’s not a good thing to do or they’re just wasting their time taking it, but I have seen people who combine that with a good diet and exercise and have noticed a change in their physique, their energy, their mood, and the sort of things that testosterone would naturally help.”


In the U.S., where millions watch the Super Bowl simply to see the clever and costly commercials, and where pharmaceuticals with potentially deadly side effects are pushed on the public at every turn, it's probably not surprising that ads for "Low T" are now splayed across billboards in Florida, with its huge number of older residents, or that a chain of "Low T Centers" has sprung up in Texas and around the heartland.

Trials of testosterone treatment in men with type 2 diabetes have also taken place. A recent randomized controlled crossover trial assessed the effects of intramuscular testosterone replacement to achieve levels within the physiological range, compared with placebo injections in 24 men with diabetes, hypogonadism and a mean age of 64 years (Kapoor et al 2006). Ten of these men were insulin treated. Testosterone treatment led to a significant reduction in glycated hemoglobin (HbA1C) and fasting glucose compared to placebo. Testosterone also produced a significant reduction in insulin resistance, measured by the homeostatic model assessment (HOMA), in the fourteen non-insulin treated patients. It is not possible to measure insulin resistance in patients treated with insulin but five out of ten of these patients had a reduction of insulin dose during the study. Other significant changes during testosterone treatment in this trial were reduced total cholesterol, waist circumference and waist-hip ratio. Similarly, a placebo-controlled but non-blinded trial in 24 men with visceral obesity, diabetes, hypogonadism and mean age 57 years found that three months of oral testosterone treatment led to significant reductions in HbA1C, fasting glucose, post-prandial glucose, weight, fat mass and waist-hip ratio (Boyanov et al 2003). In contrast, an uncontrolled study of 150 mg intramuscular testosterone given to 10 patients, average age 64 years, with diabetes and hypogonadism found no significant change in diabetes control, fasting glucose or insulin levels (Corrales et al 2004). Another uncontrolled study showed no beneficial effect of testosterone treatment on insulin resistance, measured by HOMA and ‘minimal model’ of area under acute insulin response curves, in 11 patients with type 2 diabetes aged between 33 and 73 years (Lee et al 2005). Body mass index was within the normal range in this population and there was no change in waist-hip ratio or weight during testosterone treatment. Baseline testosterone levels were in the low-normal range and patients received a relatively small dose of 100 mg intramuscular testosterone every three weeks. A good increase in testosterone levels during the trial is described but it is not stated at which time during the three week cycle the testosterone levels were tested, so the lack of response could reflect an insufficient overall testosterone dose in the trial period.
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][151] Then, 5α-DHT and 5β-DHT are converted by 3α-HSD into 3α-androstanediol and 3α-etiocholanediol, respectively.[1][151] Subsequently, 3α-androstanediol and 3α-etiocholanediol are converted by 17β-HSD into androsterone and etiocholanolone, which is followed by their conjugation and excretion.[1][151] 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.[153][154] A small portion of approximately 3% of testosterone is reversibly converted in the liver into androstenedione by 17β-HSD.[152]

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).

Increase testosterone if you’re an adult with abnormally low levels. Under most circumstances, adults who have been medically diagnosed with low testosterone levels can safely increase their levels, and natural methods can be some of the healthiest ways to do so. That being said, you should avoid intentionally increasing your testosterone if you are still an adolescent or if you’re an adult with normal or undiagnosed levels.


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Instead of turning to some drug that can only ameliorate symptoms and cause additional complications, I recommend using a natural saw palmetto supplement. Dr. Moerck says that there are about 100 clinical studies on the benefits of saw palmetto, one of them being a contributed to decreased prostate cancer risk. When choosing a saw palmetto supplement, you should be wary of the brand, as there are those that use an inactive form of the plant.
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.
If you are serious about losing weight, you have got to strictly limit the amount of processed sugar in your diet, as evidence is mounting that excess sugar, and fructose in particular, is the primary driving factor in the obesity epidemic. So cutting soda from your diet is essential, as is limiting fructose found in processed foods, fruit juice, excessive fruit and so-called "healthy" sweeteners like agave.
Testosterone boosters are used by many athletes worldwide to achieve a significant muscle mass increase within a short period of time.[1] However; one cannot be completely confident in terms of the quality and efficacy of such products because of several reasons, such as the possibility of bad storage conditions and originating from an unreliable source. Over the years, some consumers of testosterone boosters have complained of kidney and liver abnormalities that could be linked to their use of boosters.[10] Cases of erroneous product administration have occurred in the past as athletes may not follow the instructions on the label fully, which can lead to many side effects.[11] In the present case, a man was admitted to a hospital because of a severe abdominal pain. The pain was later found to be caused by liver injury. The diagnosis confirmed that the levels of the key hepatic enzymes were markedly elevated. The medical complications observed were found to have occurred following the consumption of two courses of a commercial testosterone booster. According to researchers based in the US, about 13% of the annual cases of acute liver failure are attributable to idiosyncratic drug- and/or supplement-induced liver injury.[12] Marked increase in the levels of ALT, AST, and gamma-glutamyl transferase was observed after consuming the first course of the commercial testosterone booster, and they started to decline after the 2nd and 3rd course. This abruptly increases the levels of liver enzymes after the first course may be attributed to the interruption effect of commercial testosterone booster on liver function as a result of the effects of its ingredients.
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 regular intake of testosterone boosters is known for the high level of safety comparing to the hormone injections and the use of illegal steroids. But still to protect yourself against any possible adverse reactions, you should remember that the supplementation can’t be continuous. The breaks from time to time are required. Such an approach to the use of boosters is healthy and best-working if you aspire to enhance own hormone production without any harm.


Because of the mass production, conventional pigs are fed with GMO soy and corn, and they’re living in such horrid conditions that they’re pumped full of antibiotics to ensure that the pigs won’t get any inflammatory diseases, and then they’re fed & injected with ridiculous amounts of estrogen and growth hormone to make the pigs fatter and bigger in record times.
Dr. Anthony's Notes: When evaluating the efficacy of a product, it’s tough to balance the currently available human research with thousands of years of anecdotal evidence of efficacy. Tongkat Ali is a perfect example. All of the current studies are on animal models (not humans) – this DOES NOT mean that Tongkat Ali doesn’t work with humans. It simply means more research is needed. Personally, the strong experience of thousands of men (myself included) using this herb can confirm it’s libido enhancing effects. Also, this herb is DAMN BITTER. It makes Maca powder seem like a walk in the park. Hide in a smoothie or you will be sorry haha! How To Take Tongkat Ali: 200-300mg (of a 100:1 extract) 1-2 times per day. If you are using the raw powder (recommended below) that is NOT encapsulated, definitely hide the powder in a fat burning smoothie like the “Fit Father Fat Burning Shake Recipe” we recommend in FF30X. Again, I cannot understand how damn nasty this powder tastes. Beware!
A number of epidemiological studies have found that bone mineral density in the aging male population is positively associated with endogenous androgen levels (Murphy et al 1993; Ongphiphadhanakul et al 1995; Rucker et al 2004). Testosterone levels in young men have been shown to correlate with bone size, indicating a role in determination of peak bone mass and protection from future osteoporosis (Lorentzon et al 2005). Male hypogonadism has been shown to be a risk factor for hip fracture (Jackson et al 1992) and a recent study showed a high prevalence of hypogonadism in a group of male patients with average age 75 years presenting with minimal trauma fractures compared to stroke victims who acted as controls (Leifke et al 2005). Estrogen is a well known determinant of bone density in women and some investigators have found serum estrogen to be a strong determinant of male bone density (Khosla et al 1998; Khosla et al 2001). Serum estrogen was also found to correlate better than testosterone with peak bone mass (Khosla et al 2001) but this is in contradiction of a more recent study showing a negative correlation of estrogen with peak bone size (Lorentzon et al 2005). Men with aromatase deficiency (Carani et al 1997) or defunctioning estrogen receptor mutations (Smith et al 1994) have been found to have abnormally low bone density despite normal or high testosterone levels which further emphasizes the important influence of estrogen on male bone density.
There is increasing interest in the group of patients who fail to respond to treatment with PDE-5 inhibitors and have low serum testosterone levels. Evidence from placebo-controlled trials in this group of men shows that testosterone treatment added to PDE-5 inhibitors improves erectile function compared to PDE-5 inhibitors alone (Aversa et al 2003; Shabsigh et al 2004).
Opioid substances are in common use both licit and illicit. Opiates are potent analgesics but they are also highly addictive. They are frequently prescribed for both acute and chronic pain and when used chronically, often induce opiate dependence in the user. Pain clinics regularly use narcotic agents in many of their patients. Methadone, in particular, is regularly prescribed to opiate addicts who have entered a program aimed at reducing narcotic dosage and ultimately weaning the patient off it altogether. Most men who are on chronic high doses of an opiate become hypogonadal. This was first recognized in the 1970’s when heroin addicts were found to have suppressed levels of testosterone (Brambilla et al 1977). Also suppressed were LH and FSH pointing to a probable inhibition of GnRH release.
During the second trimester, androgen level is associated with sex formation.[13] This period affects the femininization or masculinization of the fetus and can be a better predictor of feminine or masculine behaviours such as sex typed behaviour than an adult's own levels. A mother's testosterone level during pregnancy is correlated with her daughter's sex-typical behavior as an adult, and the correlation is even stronger than with the daughter's own adult testosterone level.[14]
Millions of American men use a prescription testosterone gel or injection to restore normal levels of the manly hormone. The ongoing pharmaceutical marketing blitz promises that treating "low T" this way can make men feel more alert, energetic, mentally sharp, and sexually functional. However, legitimate safety concerns linger. For example, some older men on testosterone could face higher cardiac risks.
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