There have been case reports of development of prostate cancer in patients during treatment with testosterone, including one case series of twenty patients (Gaylis et al 2005). It is not known whether this reflects an increase in incidence, as prostate cancer is very common and because the monitoring for cancer in patients treated with testosterone is greater. Randomized controlled trials of testosterone treatment have found a low incidence of prostate cancer and they do not provide evidence of a link between testosterone treatment and the development of prostate cancer (Rhoden and Morgentaler 2004). More large scale clinical trials of longer durations of testosterone replacement are required to confirm that testosterone treatment does not cause prostate cancer. Overall, it is not known whether testosterone treatment of aging males with hypogonadism increases the risk of prostate cancer, but monitoring for the condition is clearly vital. This should take the form of PSA blood test and rectal examination every three months for the first year of treatment and yearly thereafter (Nieschlag et al 2005). Age adjusted PSA reference ranges should be used to identify men who require further assessment. The concept of PSA velocity is also important and refers to the rate of increase in PSA per year. Patients with abnormal rectal examination suggestive of prostate cancer, PSA above the age specific reference range or a PSA velocity greater than 0.75 ng/ml/yr should be referred to a urologist for consideration of prostate biopsy.
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.
Men's levels of testosterone, a hormone known to affect men's mating behaviour, changes depending on whether they are exposed to an ovulating or nonovulating woman's body odour. Men who are exposed to scents of ovulating women maintained a stable testosterone level that was higher than the testosterone level of men exposed to nonovulation cues. Testosterone levels and sexual arousal in men are heavily aware of hormone cycles in females.[46] This may be linked to the ovulatory shift hypothesis,[47] where males are adapted to respond to the ovulation cycles of females by sensing when they are most fertile and whereby females look for preferred male mates when they are the most fertile; both actions may be driven by hormones.
Estrogen is important in men, but too high of a level has all sorts of negative consequences – ranging from heart attacks to prostate cancer (32 & 33). The balance between testosterone and estrogen (or estradiol) is critical for a man. If the ratio is out and estrogen starts to dominate you run into all sorts of issues – such as breast cell growth, prostate enlargement and of course lower testosterone.
Japanese Knotweed (a.k.a Hu Zhang or Polygonum cuspidatum) is highlighted by WebMD as needing more evidence to rate its effectiveness in a number of different areas: like treating constipation and liver or heart disease. They also warn that it can interact poorly with medications that are changed and broken down by the liver, and those that slow blood clotting (anticoagulants and antiplatelets).

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:

One study looking at alcohol consumption found that increasing alcohol consumption led to a higher level of free & total testosterone compared to a non-drinking control group (20). Drinking did however lower SHBG testosterone levels, though this type of testosterone is bound to a protein meaning our bodies cannot use it to build muscle or increase our mood.

Testosterone [Figure 1] is the main male sex hormone. It is responsible for male sexuality and is the main hormone-producing the features associated with masculinity such as substantial muscle mass, facial hair, libido, and sperm production.[1] Besides, the hormone has other vital functions as the basic chemical composition of testosterone is steroidal; and steroids are known to have significant physiological, as well as psychological, effects in male individuals, especially adults.[1] Testosterone production is reduced gradually in men starting from the age of 30.[2] Hence, testosterone blood concentrations slowly diminish as age progresses. As a result, men may experience a number of physiological and psychological events, such as a lack of sex-drive, erectile dysfunction, acute depression, fatigue, low energy levels, and insomnia.[3]
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).
Fatherhood decreases testosterone levels in men, suggesting that the emotions and behavior tied to decreased testosterone promote paternal care. In humans and other species that utilize allomaternal care, paternal investment in offspring is beneficial to said offspring's survival because it allows the parental dyad to raise multiple children simultaneously. This increases the reproductive fitness of the parents, because their offspring are more likely to survive and reproduce. Paternal care increases offspring survival due to increased access to higher quality food and reduced physical and immunological threats.[60] This is particularly beneficial for humans since offspring are dependent on parents for extended periods of time and mothers have relatively short inter-birth intervals.[61] While extent of paternal care varies between cultures, higher investment in direct child care has been seen to be correlated with lower average testosterone levels as well as temporary fluctuations.[62] For instance, fluctuation in testosterone levels when a child is in distress has been found to be indicative of fathering styles. If a father's testosterone levels decrease in response to hearing their baby cry, it is an indication of empathizing with the baby. This is associated with increased nurturing behavior and better outcomes for the infant.[63]
Why niacinamide could positively impact 5-a reduced androgens? It’s complex, but simply put, its a crucial part of this compound called NADPH (Nicotinamide adenine dinucleotide phosphate). And NADPH is a co-factor in many anabolic/androgenic reactions of the body, including both testosterone and dihydrotestosterone production (NADPH is needed for the production of 5-ar enzyme).
Great article with a lot of useful information. I completely agree with your top three picks. I have done a ton of research as well. Currently I am taking Testogen for over two months and it has worked for me. It has double my low T and I am 61 years old. I do feel better and have more energy. Even have morning wood sometimes and haven’t for a long time.
Hoffman, J., Ratamess, N., Kang, J., Magine, G., Faigenbaum, A. & Stout, J. (2006, August). Effect of creatine and beta-alanine supplementation on performance and endocrine responses in strength/power athletes [Abstract]. International Journal of Sport Nutrition and Exercise Metabolism, 16(4), 430–46. Retrieved from https://www.ncbi.nlm.nih.gov/pubmed/17136944
It is important to note that you can certainly boost testosterone naturally without supplementation. Supplements are expensive now a days and a lot of people do not like taking tons of pills. Plus, a lot of these vitamins and minerals are only needed if deficient, so I recommend getting routine blood work done to see where you are short. I can almost guarantee you will come out vitamin D deficient, so while you don’t have to take these, they will certainly help.
It goes without saying that a healthy diet, quality sleep, productive lifestyle, and regular exercises can contribute to the overall increase of testosterone. However, it is also true that these activities are very often not enough for guys who have the problems with naturally low testosterone levels. This situation also includes people who want to boost their existing testosterone levels.
The natural production of DHEA is also age-dependent. Prior to puberty, the body produces very little DHEA. Production of this prohormone peaks during your late 20’s or early 30’s. With age, DHEA production begins to decline. The adrenal glands also manufacture the stress hormone cortisol, which is in direct competition with DHEA for production because they use the same hormonal substrate known as pregnenolone. Chronic stress basically causes excessive cortisol levels and impairs DHEA production, which is why stress is another factor for low testosterone levels.
Testing is the only way you can validate a low-T diagnosis and measure treatment progress. I always say, "Test, don’t guess!" Your doctor may "suspect" you have hormone imbalances by your symptoms, but you should ask that they do testing to confirm unhealthy levels. Testing also ensures your doctor rules out other issues that may simply have similar symptoms. With your test results in hand, your physician can best determine what the optimal levels are for you and determine the best course of treatment.

Epidemiological studies suggest that many significant clinical findings and important disease states are linked to low testosterone levels. These include osteoporosis (Campion and Maricic 2003), Alzheimer’s disease (Moffat et al 2004), frailty, obesity (Svartberg, von Muhlen, Sundsfjord et al 2004), diabetes (Barrett-Connor 1992), hypercholesterolemia (Haffner et al 1993; Van Pottelbergh et al 2003), hypertension (Phillips et al 1993), cardiac failure (Tappler and Katz 1979; Kontoleon et al 2003) and ischemic heart disease (Barrett-Connor and Khaw 1988). The extent to which testosterone deficiency is involved in the pathogenesis of these conditions, or to which testosterone supplementation could be useful in their treatment is an area of great interest with many unanswered questions.

It's important to understand that your body requires saturated fats from animal and vegetable sources (such as meat, dairy, certain oils, and tropical plants like coconut) for optimal functioning, and if you neglect this important food group in favor of sugar, grains and other starchy carbs, your health and weight are almost guaranteed to suffer. Examples of healthy fats you can eat more of to give your testosterone levels a boost include:


6., 7. JK, Udani, George AA, Musthapa M, Pakdaman MN, and Abas A. "Effects of a Proprietary Freeze-Dried Water Extract of Eurycoma Longifolia (Physta) and Polygonum minus on Sexual Performance and Well-Being in Men: A Randomized, Double-Blind, Placebo-Controlled Study." National Center for Biotechnology Information. U.S. National Library of Medicine, 12 Jan. 2014.
It goes without saying that what you eat significantly influences your hormone balance and body composition. This is nothing new. There are countless athletes and bodybuilders who are paying a close attention to what they eat for a reason. For example, if you consume a lot of so-called junk food, then you inevitably end up with a poor nutritional profile. In plain English, you can forget about a six-pack and the high testosterone.
Bisphenol-A also known under the name of BPA is a chemical compound which is very widespread for manufacturing a wide spectrum of plastic items and aluminum cans. Many studies have already proven the fact that even the smallest amount of BPA is very harmful to the human health. This compound causes hormonal imbalance and even may lead to prostate cancer.
Copyright © 2019 Leaf Group Ltd. Use of this web site constitutes acceptance of the LIVESTRONG.COM Terms of Use , Privacy Policy and Copyright Policy . The material appearing on LIVESTRONG.COM is for educational use only. It should not be used as a substitute for professional medical advice, diagnosis or treatment. LIVESTRONG is a registered trademark of the LIVESTRONG Foundation. The LIVESTRONG Foundation and LIVESTRONG.COM do not endorse any of the products or services that are advertised on the web site. Moreover, we do not select every advertiser or advertisement that appears on the web site-many of the advertisements are served by third party advertising companies.
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).
Dobs and colleagues found that men with an increased body mass index had both reduced testosterone and reduced high density lipoprotein (HDL) levels. Treatment with testosterone increased the levels of HDL (Dobs et al 2001). Rising levels of HDL are not a consistent finding with TRT. More often, however, one finds reduced total cholesterol, low density lipoprotein (LDL) cholesterol and triglyceride levels with TRT (Zgliczynski et al 1996; Whitsel et al 2001).
Such sort of injuries varies in severity and extent of damage markedly from one person to the other and withdrawal of the drug/supplement coupled with proper medical attention suffice in terms of alleviating the symptoms.[8,12] This was observed in the present case. However, the liver injury observed here may not be confidently linked to product consumption as the subject later reported that the following recovery he consumed two more courses of the booster with no side effects. Tests performed following hospital discharge, and repeated use of the product showed AST and ALT to be slightly high, whereas the rest of the blood parameters tested appeared to be normal. The AST/ALT ratio is considered to be a very important parameter for the evaluation of liver diseases, such as non-alcoholic fatty liver disease,[13] though it is rarely considered alone. Overall, the evidence was inconclusive in the present work in terms of linking the use of a testosterone booster with liver injury. However, even though a single case report cannot establish causality with statistical power.[13] Further research on the usage of a commercial testosterone booster within large populations for a long period is necessary to investigate whether the symptoms shown in the present case were significantly present in other athletes consuming the same commercial product or not. To guarantee an optimal outcome with no severe side effects, further research is warranted to confirm the present findings and determine whether the effects observed in this case report would be statistically significant in larger samples.
Changes in body composition are seen with aging. In general terms, aging males are prone to loss of muscle mass and a gain in fat mass, especially in the form of visceral or central fat. An epidemiological study of community dwelling men aged between 24 and 85 years has confirmed that total and free testosterone levels are inversely correlated with waist circumference and that testosterone levels are specifically related to this measure of central obesity rather than general obesity (Svartberg, von Muhlen, Sundsfjord et al 2004). Prospective studies show that testosterone levels predict future development of central obesity (Khaw and Barrett-Connor 1992; Tsai et al 2000). Reductions in free testosterone also correlate with age related declines in fat free mass (muscle mass) and muscle strength (Baumgartner et al 1999; Roy et al 2002). Studies in hypogonadal men confirm an increase in fat mass and decrease in fat free mass versus comparable eugonadal men (Katznelson et al 1998). Taken together, the epidemiological data suggest that a hypogonadal state promotes loss of muscle mass and a gain in fat mass, particularly visceral fat and therefore mimics the changes of ‘normal’ aging.
Pregnant or nursing women who are exposed to EDCs can transfer these chemicals to their child. Exposure to EDCs during pregnancy affects the development of male fetuses. Fewer boys have been born in the United States and Japan in the last three decades. The more women are exposed to these hormone-disrupting substances, the greater the chance that their sons will have smaller genitals and incomplete testicular descent, leading to poor reproductive health in the long term. EDCs are also a threat to male fertility, as they contribute to testicular cancer and lower sperm count. All of these birth defects and abnormalities, collectively referred to as Testicular Dysgenesis Syndrome (TDS), are linked to the impaired production of testosterone.5
The regulation of testosterone production is tightly controlled to maintain normal levels in blood, although levels are usually highest in the morning and fall after that. The hypothalamus and the pituitary gland are important in controlling the amount of testosterone produced by the testes. In response to gonadotrophin-releasing hormone from the hypothalamus, the pituitary gland produces luteinising hormone which travels in the bloodstream to the gonads and stimulates the production and release of testosterone.
×