The diagnosis of late-onset hypogonadism requires the combination of low serum testosterone levels with symptoms of hypogonadism. Questionnaires are available which check for the symptoms of hypogonadism. These have been validated for the assessment of aging patients with hypogonadism (Morley et al 2000; Moore et al 2004) but have a low specificity. In view of the overlap in symptoms between hypogonadism, aging and other medical conditions it is wise to use a formal method of symptom assessment which can be used to monitor the effects of testosterone replacement.
There is also a crazy case study about a Thai-male who reportedly got his DHT levels all the way to 158% above medical reference ranges after supplementing with Butea Superba (he visited the doctor and complained of too high libido), after some examination and questioning, the doctors thought it might be the supplement causing this sudden increase in androgenic hormones and they instructed him to seize the consumption. Within a week his blood serum 5-a DHT had fallen back to normal.
This supplement is not only marketed to increase sexual desire, but the manufacturer also claims this testosterone booster can accelerate muscle growth, build endurance and decrease muscle pain after workouts. The main ingredient in the product is 25 mg of zinc. Additional ingredients include a proprietary blend of ginkgo biloba, cayenne pepper, tribulis terristris and maca. Recommended dosage is three capsules taken on a daily basis as a dietary supplement.
When we face stress, our adrenal glands secrete cortisol to prepare our bodies and minds to handle the stressful situation — the primal fight-or-flight response. In small dosages, cortisol is fine and even useful, but elevated cortisol levels for prolonged periods can do some serious damage to our bodies and minds. One area that seems to take a hit when cortisol is high is our testosterone levels. Several studies have shown a link between cortisol and testosterone. When cortisol levels are high, testosterone levels are low; and when testosterone levels are high, cortisol levels are low.
Most Americans today are sleep deprived, which may be a contributing factor to declining testosterone levels in men. See, our body makes nearly all the testosterone it needs for the day while we’re sleeping. That increased level of T that we experience at night is one of the reasons we wake up with “Morning Wood.” (If you don’t have Morning Wood on a consistent basis, you might have low T).
Christopher Walker is a co-founder of UMZU and creator of the Thermo Diet. He is the first person to get a Duke Neuroscience degree in 3 years. After naturally solving his own health complications with a brain tumor as a teenager, he has devoted his life to creating all-natural products and education to help men, women, children and pets to improve their own health naturally using science-backed research.
Christopher Walker is a co-founder of UMZU and creator of the Thermo Diet. He is the first person to get a Duke Neuroscience degree in 3 years. After naturally solving his own health complications with a brain tumor as a teenager, he has devoted his life to creating all-natural products and education to help men, women, children and pets to improve their own health naturally using science-backed research.
This doesn’t mean Super Test is perfect — we take a closer look at some of its ingredients below — but it beats out the competition. Every other supplement we looked at either didn’t have all four ingredients, overdosed us on vitamins or minerals (a good way to develop kidney and liver problems), contained ingredients that would harm us, or some combination thereof.
Intracoronary artery infusion of testosterone causes significant coronary artery dilatation and not constriction as previously thought (Webb et al 1999). When degree of coronary obstruction is assessed by angiography, there is a direct relationship between degree of coronary artery narrowing and reduced testosterone levels (Phillips et al 1994). Men with low testosterone levels have been observed to have: premature atherosclerosis, increased visceral adipose tissue, hyperinsulinemia, and other risk factors for myocardial infarction (Phillips 2005). Insulin resistance has been shown to be associated with a decrease in Leydig cell secretion of testosterone (Pitteloud et al 2005). Muller and colleagues suggest that low endogenous total testosterone and SHBG levels increase the risk of metabolic syndrome in aging and aged men. They demonstrated that low levels of testosterone are related to lower insulin sensitivity and higher fasting insulin levels (Muller et al 2005). These authors speculate that testosterone might play a protective role in the development of metabolic syndrome, insulin resistance, diabetes mellitus and cardiovascular disease in aging men.
Take 250 mg of Forskolin, standardized to 10 percent, twice a day. Take one serving before training and the other with a meal. According to "Natural Anabolics," Forskolin decreased body fat and increased free testosterone levels in training individuals as compared to a placebo. Forskolin comes from the herb coleus forskohlii and is also known as Forslean.
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Levels of testosterone naturally decrease with age, but exactly what level constitutes "low T," or hypogonadism, is controversial, Harvard Medical School said. Testosterone levels vary wildly, and can even differ depending on the time of day they're measured (levels tend to be lower in the evenings). The National Institutes of Health includes the following as possible symptoms of low testosterone:
Testosterone is the main hormone associated with muscle mass, strength gains, and libido. But that's far from the only thing it does in the body. As Chris Lockwood, Ph.D., explains in the article "All About Testosterone," it impacts everything from mood and memory to bone health—but yes, to be clear, it also makes muscles bigger and stronger, and helps increase endurance and athletic performance.
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.
Some boys even develop enlarged testicles and penis, armpit or pubic hair, as well as facial hair as early as age nine! Early puberty is not something to be taken lightly because it can significantly influence physical and psychological health, including an increased risk of hormone-related cancers. Precocious sexual development may also lead to emotional and behavioral issues, such as:
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).
The second theory is similar and is known as "evolutionary neuroandrogenic (ENA) theory of male aggression".[78][79] Testosterone and other androgens have evolved to masculinize a brain in order to be competitive even to the point of risking harm to the person and others. By doing so, individuals with masculinized brains as a result of pre-natal and adult life testosterone and androgens enhance their resource acquiring abilities in order to survive, attract and copulate with mates as much as possible.[78] The masculinization of the brain is not just mediated by testosterone levels at the adult stage, but also testosterone exposure in the womb as a fetus. Higher pre-natal testosterone indicated by a low digit ratio as well as adult testosterone levels increased risk of fouls or aggression among male players in a soccer game.[80] Studies have also found higher pre-natal testosterone or lower digit ratio to be correlated with higher aggression in males.[81][82][83][84][85]
"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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