Carbs play a big part in determining your Testosterone levels. Let's start with what to avoid. First, research shows that a large serving of sugar (75g of glucose), decreased Testosterone levels by as much as 25%! (25 & 26). I know this is a pretty extreme dosage, but you may want to avoid massive servings of sugar! Also, men who have Metabolic syndrome have lower Testosterone levels (27). Metabolic syndrome is often brought about by chronic high blood sugar which leads to insulin resistance.

Before assessing the evidence of testosterone’s action in the aging male it is important to note certain methodological considerations which are common to the interpretation of any clinical trial of testosterone replacement. Many interventional trials of the effects of testosterone on human health and disease have been conducted. There is considerable heterogenicity in terms of study design and these differences have a potential to significantly affect the results seen in various studies. Gonadal status at baseline and the testosterone level produced by testosterone treatment in the study are of particular importance because the effects of altering testosterone from subphysiological to physiological levels may be different from those of altering physiological levels to supraphysiological. Another important factor is the length of treatment. Randomised controlled trials of testosterone have ranged from one to thirty-six months in duration (Isidori et al 2005) although some uncontrolled studies have lasted up to 42 months. Many effects of testosterone are thought to fully develop in the first few months of treatment but effects on bone, for example, have been shown to continue over two years or more (Snyder et al 2000; Wang, Cunningham et al 2004).
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:
Findings that improvements in serum glucose, serum insulin, insulin resistance or glycemic control, in men treated with testosterone are accompanied by reduced measures of central obesity, are in line with other studies showing a specific effect of testosterone in reducing central or visceral obesity (Rebuffe-Scrive et al 1991; Marin, Holmang et al 1992). Furthermore, studies that have shown neutral effects of testosterone on glucose metabolism have not measured (Corrales et al 2004), or shown neutral effects (Lee et al 2005) (Tripathy et al 1998; Bhasin et al 2005) on central obesity. Given the known association of visceral obesity with insulin resistance, it is possible that testosterone treatment of hypogonadal men acts to improve insulin resistance and diabetes through an effect in reducing central obesity. This effect can be explained by the action of testosterone in inhibiting lipoprotein lipase and thereby reducing triglyceride uptake into adipocytes (Sorva et al 1988), an action which seems to occur preferentially in visceral fat (Marin et al 1995; Marin et al 1996). Visceral fat is thought to be more responsive to hormonal changes due to a greater concentration of androgen receptors and increased vascularity compared with subcutaneous fat (Bjorntorp 1996). Further explanation of the links between hypogonadism and obesity is offered by the hypogonadal-obesity-adipocytokine cycle hypothesis (see Figure 1). In this model, increases in body fat lead to increases in aromatase levels, in addition to insulin resistance, adverse lipid profiles and increased leptin levels. Increased action of aromatase in metabolizing testosterone to estrogen, reduces testosterone levels which induces further accumulation of visceral fat. Higher leptin levels and possibly other factors, act at the pituitary to suppress gonadotrophin release and exacerbate hypogonadism (Cohen 1999; Kapoor et al 2005). Leptin has also been shown to reduce testosterone secretion from rodent testes in vitro (Tena-Sempere et al 1999). A full review of the relationship between testosterone, insulin resistance and diabetes can be found elsewhere (Kapoor et al 2005; Jones 2007).
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:
For this reason I recommend doing your own research on this supplement before taking it. 5g of ground up dried powder is what was used in the studies. I recommend taking 1-2 capsules of the concentrated form from Paradise Herbs. Alternatively, the Aggressive Strength Test Booster also has MP in its formula so you may prefer to use that blend instead. 
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The maximum hormone concentration in the blood is reported immediately after the workout. And the effect lasts throughout the day. However, it’s important to ensure that your physical activity is moderate. The matter is that too much high-intensity exercise can give an undesirable result. But even if for any reason you can’t attend a gym, it’s not a problem. Just move as much as possible during the day. Even simple walking will be of great benefit.

Ok. So this product is meant to be taken continuously and without side-effects. But my question is, will there be replenishment from this product in aiding the body's natural ability to produce testosterone? In other words, will there ever be a time when I can say well I don't have to take this any more as my body is producing testosterone again on it's own and my muscle mass has been enhanced?
Testosterone has two major effects on bones: (a) through conversion to estradiol by way of the enzyme, aromatase, testosterone inhibits osteoclastic activity and hence bone resorption; and (b) through conversion to DHT via 5-α-reductase, it stimulates osteoblastic activity and so enhances the laying down of bone (Tivesten et al 2004; Davey and Morris 2005). Hypogonadal men are at risk for the development of osteopenia or osteoporosis and hence for subsequent fracture (Fink et al 2006). About one-third of all osteoporotic hip fractures occur in men and the risk of any osteoporotic fracture in men over 50 is as high as 25 percent (Seeman 1997; Adler 2006). Although treatment with testosterone in hypogonadal men increases bone mineral density (Katznelson et al 1996), it has not yet been established that this results in a reduction in fracture rate.
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.
The science backs up the soldier’s self discovery, in fact, exposure to radiation (whether it’s from an army radar or the cell phone in your pocket, or the wifi router in your house) has been shown to lower sperm quality, fertility and testosterone. This is true not only for military personnel (88, 89,90) but all males living in a modern world (91).

We reviewed the ingredient lists of our supplements and cut three that prescribed us an overdose of magnesium. While it’s possible to stay under the 350mg daily limit of supplemental magnesium by taking fewer pills than the manufacturer recommends, we were concerned that any manufacturer would advise you to exceed the recommended safety limit for magnesium intake by almost a third.
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Ginger has been used as medicine for centuries due to its potent antioxidant potential. It also exhibits anti-inflammatory properties which makes it best for natural therapeutics. It improves the sexual function and testosterone levels by stimulating the luteinizing hormone. It also enhances the sperm count, which makes it useful to solve infertility issues.
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).
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It is now well-established that elderly men with type 2 diabetes mellitus have reduced levels of testosterone (Barrett-Connor 1992; Betancourt-Albrecht and Cunningham 2003). It is known, however, that obese men and diabetic men have reduced levels of SHBG (Barrett-Connor 1990) which could account for the lower total testosterone levels found in diabetic men. Dhindsa et al (2004) studied 103 male patients who had type 2 diabetes mellitus using free testosterone (done by equilibrium dialysis) or calculated free testosterone which takes SHBG levels into account. Of the 103 patients, 57 had free testosterone by equilibrium dialysis and of these, 14 (25%) had a free T below 0.174 nmol/L and were considered hypogonadal. Using a total testosterone of 10.4 nmol/L (300ng/dl) as the lower limit of normal 45 patients (43%) were in the hypogonadal range. They also found that LH and FSH concentrations were significantly lower in the hypogonadal group. The authors thus concluded that hypogonadotropic hypogonadism was a common finding in type 2 diabetes irrespective of glycemic control, duration of disease or the presence of complications of diabetes or obesity.

Other Potential risks that can be caused by use of testosterone supplements are: People who take good testosterone supplements or any other kind of testosterone boosters can also experience many other side effects, including stomachache, problems with urination, dizziness, mood changes, intermittent breathing during sleep, changes in testicles, appetite loss, inflammation of gums, weight gain, nausea, painful erection, and protracted erection.
Vitamin D deficiency is a growing epidemic in the US, and is profoundly affecting men’s health. The cholesterol-derived steroid hormone vitamin D is crucial for men’s health. It plays a role in the development of the sperm cell nucleus, and helps maintain semen quality and sperm count. Vitamin D can also increase your testosterone level, helping improve your libido. Have your vitamin D levels tested using a 25(OH)D or a 25-hydroxyvitamin D test. The optimal level of vitamin D is around 50 to 70 ng/ml for adults. There are three effective sources of vitamin D:

This is because your body is really good at self-regulating your hormone levels. So if you have normal testosterone levels, boosting above your natural base level may at best give you a few hours while your body makes, and then immediately processes out, the excess testosterone. This means you might experience higher than your average testosterone levels, but not by much, and only for a little while.


Cognitive abilities differ between males and females and these differences are present from childhood. In broad terms, girls have stronger verbal skills than boys who tend to have stronger skills related to spatial ability (Linn and Petersen 1985). It is thought that the actions of sex hormones have a role in these differences. Reviewing different cognitive strengths of male versus female humans is not within the scope of this article but the idea that cognition could be altered by testosterone deserves attention.
Are you getting enough vitamin D? Vitamin D is an essential nutrient, but it can be difficult for people to know if they are getting the right amount. Some people will be able to get enough vitamin D from sunlight. Others may need to make dietary changes or take supplements. Here, we explain how to get vitamin D from sunlight, food, and supplements. Read now
Individuals with metabolic syndrome are at increased risk for developing coronary artery disease and diabetes mellitus. Predicting who might develop the metabolic syndrome would allow preventive measures to be taken in addition to weight control and other lifestyle modifications such as cessation of smoking and increased exercise. It is known that with decreasing testosterone availability in aging males there is an increase in fat mass and decrease in lean body mass (van den Beld et al 2000), there are disorders of insulin and glucose metabolism (Haffner et al 1996) and dyslipidemia (Tsai et al 2004). Kupelian and colleagues (2006) in analyzing data from the Massachusetts Male Aging Study demonstrated that men with low levels of testosterone, sex hormone-binding globulin, or clinical androgen deficiency, especially men with a BMI of greater than 25, were at increased risk of developing the metabolic syndrome and hence, diabetes mellitus and/or coronary artery disease.
A large number of side-effects have been attributed to testosterone. In our clinical experience, the incidence of significant adverse effects with treatment producing physiological testosterone levels is low, and many side effects attributed to testosterone are mainly relevant to supraphysiological replacement. Some adverse effects are specific to a given mode of delivery and have already been described. Potential adverse effects concerning the prostate have also been discussed and require appropriate monitoring of symptoms, PSA and digital rectal examination. Other tumors which may be androgen responsive include cancer of the breast and primary liver tumors, and these are both contraindications to testosterone treatment
Testosterone makes a contribution to nitric oxide formation. Nitric oxide, released from penile nerves stimulates guanylate cyclase which catalyzes the transformation of guanosine-5-triphosphate into 3′,5′-cyclic, guanosine monophosphate (cyclic GMP). Gyclic GMP causes vasodilatation and hence erection formation (Morelli et al 2005). The breakdown of cyclic GMP to GMP is mediated by the enzyme, phosphodiesterase type-5, the inhibitors of which (eg, sildenafil citrate) enhance erection formation and maintanence (Carson and Lue 2005).
If a man's testosterone looks below the normal range, there is a good chance he could end up on hormone supplements—often indefinitely. "There is a bit of a testosterone trap," Dr. Pallais says. "Men get started on testosterone replacement and they feel better, but then it's hard to come off of it. On treatment, the body stops making testosterone. Men can often feel a big difference when they stop therapy because their body's testosterone production has not yet recovered."
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