It's not enough just to increase the testosterone your body produces, because as we age, the testosterone we naturally produce is often bound by SHBG (sex hormone binding globulin) thus becoming unavailable for use in the body. It’s imperative that your testosterone remains unbound or “free” if you want to enjoy all the wonderful benefits testosterone provides.
Both men and women with Alzheimer’s Disease were found to have an increased concentration of SHBG and decreased free androgen index when compared with controls (Paoletti et al 2004). In a prospective study of 574 men whose baseline age span was 32–87 years and who were followed for a mean of 19.1 years (range, 4–37), the risk of developing Alzheimers’ Disease decreased 26 percent for each 10 unit increase in free testosterone index. The authors concluded that testosterone may be important for the prevention and treatment of AD (Moffat et al 2004).
Researchers at Ball State University found that “strength training can induce growth hormone and testosterone release.” (6) Another study from the University of Nebraska Medical Center researched the acute effects of weight lifting on serum testosterone levels. (7) The results concluded that even moderate weight lifting and light weightlifting increased serum testosterone levels in participants.
This over-the-counter supplement is intended to increase your body's level of testosterone to its highest. The manufacturer also advertises the positive effect that the drug can have on your sex life and achieving muscle growth. As a supplement, you are instructed to take four capsules each night before bed. On training days, recommended dosage is two capsules before you workout. Ingredients found in the product include tribulis terristris, long jack, maca root and epimedium.
Vitamin D is a fat-soluble vitamin and is obtained from sunlight. In the active form, it acts as a steroid hormone in the body. These days many people suffer from vitamin D deficiency because lacking exposure to sunlight, but taking vitamin D supplements to improve the weakness. Low vitamin D levels also lower the testosterone levels, but with intake of vitamin D, the testosterone levels boost. In typical cases, vitamin D doesn’t show the significant result in testosterone levels but people who are vitamin D deficient shows an increase in testosterone levels.
There is no definite age to recommend when is appropriate to start using a Testosterone Booster. It depends on the age in which you initially hit puberty, and how long your body produces testosterone at its peak level. If you feel as though your Testosterone levels have started to decline, usually characterised through a decrease in strength, energy, libido and ability to build size, then these are usually good determinants that it may be time to commence using a Natural Testosterone booster. The Typical age range is between 21- 25, however this is highly variable depending on your own genetics, training and diet.
Testosterone is a stimulant of hematopoiesis in the bone marrow and consequently, increases the hematocrit (Shahidi 1973). Men with unexplained anemia should have their testosterone measured and if reduced, these men should be treated with testosterone. Because of the erythropoietin stimulating effect of testosterone, one of the parameters to be monitored during testosterone treatment is hematocrit since a small percent of testosterone-treated men develop polycythemia.
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).
On the average, you need to sleep at least 8 hours per night to stay healthy. If you want a night sleep to contribute to the maximum testosterone production, it’s important to make your sleep comfortable. Thus, the bedroom temperature shouldn’t exceed 21°C. In addition, you should ventilate your bedroom thoroughly before sleeping. Furthermore, before going to bed, don’t overload your stomach with fatty foods, as well as don’t drink alcohol and caffeinated beverages. Finally, you have to avoid intense physical activity before bedtime.6
While I do have a pretty manly mustache, I’m not a doctor or a medical expert. I’m a guy with a law degree he’s never used who blogs about manliness. What I’m about to share shouldn’t be taken as a substitute for qualified medical expertise. It’s simply my experience and views on the subject. Before you make any changes in lifestyle or diet, talk to your doctor or healthcare provider. Be smart.
Popular through the centuries in Ayurvedic healing (a traditional practice of medicine in India) ashwagandha is what is known as an "adaptogen." This means the body may be able to use it to help adapt to stressors. While many people supplement with it for reducing cortisol, anxiety, and fatigue levels, ashwagandha also holds relevance for us here with potential testosterone boosting benefits.
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).