Many endocrinologists are sounding the alarm about the damaging effects that come with exposure to common household chemicals. Called “endocrine disruptors,” these chemicals interfere with our body’s hormone system and cause problems like weight gain and learning disabilities. One type of endocrine disruptor is particularly bad news for our testosterone levels.
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
That there is an association between depression and testosterone concentration seems possible because of the observation that depression may be associated with reduced testosterone concentrations, hypogonadal men may have their symptoms of depression relieved by TRT and that testosterone itself may have anti-depressant properties (Pope et al 2003). The evidence, however, is inconsistent. Seidman and colleagues (2002), for example, found that there was no relationship between testosterone and depression but there was an association of testosterone with dysthymia. McIntyre and colleagues (2006), on the other hand, found that middle-aged men with depression did have a reduction in bio-available testosterone.

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.


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Some of the effects of testosterone treatment are well recognised and it seems clear that testosterone treatment for aging hypogonadal men can be expected to increase lean body mass, decrease visceral fat mass, increase bone mineral density and decrease total cholesterol. Beneficial effects have been seen in many trials on other parameters such as glycemic control in diabetes, erectile dysfunction, cardiovascular risk factors, angina, mood and cognition. These potentially important effects require confirmation in larger clinical trials. Indeed, it is apparent that longer duration randomized controlled trials of testosterone treatment in large numbers of men are needed to confirm the effects of testosterone on many aspects of aging male health including cardiovascular health, psychiatric health, prostate cancer and functional capacity. In the absence of such studies, it is necessary to balance risk and benefit on the best available data. At the present time the data supports the treatment of hypogonadal men with testosterone to normalize testosterone levels and improve symptoms. Most men with hypogonadism do not have a contraindication to treatment, but it is important to monitor for adverse consequences including prostate complications and polycythemia.
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).

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
There is a negative correlation of testosterone levels with plasminogen activator inhibitor-1 (PAI-1) (Glueck et al 1993; Phillips 1993), which is a major prothrombotic factor and known to be associated with progression of atherosclerosis, as well as other prothrombotic factors fibrinogen, α2-antiplasmin and factor VII (Bonithon-Kopp et al 1988; Glueck et al 1993; Phillips 1993; De Pergola et al 1997). There is a positive correlation with tissue plasminogen activator (tPA) which is one of the major fibrinolytic agents (Glueck et al 1993). Interventional trials have shown a neutral effect of physiological testosterone replacement on the major clotting factors (Smith et al 2005) but supraphysiological androgen administration can produce a temporary mild pro-coagulant effect (Anderson et al 1995).
Do low levels of testosterone produce symptoms in middle-aged men? Absolutely. In fact, the classic symptoms were first recognized more than 70 years ago when two American physicians, Carl Heller, MD, and Gordon Myers, MD, showed the effectiveness of testosterone treatment for symptoms of fatigue, depression, irritability, low sex drive, erectile dysfunction, night sweats, and hot flashes in men. Over the years, subsequent studies have found that some—but not all—men with low, age-adjusted testosterone levels exhibit symptoms consistent with andropause. All experience improvement with testosterone therapy.
The biggest change I made to my diet was increasing my fat and cholesterol intake. There’s a reason why old school strong men would drink raw eggs — studies have suggested that higher fat and cholesterol consumption results in increased levels of total T; men eating low-fat diets typically have decreased testosterone levels. The emphasis on increasing fat and cholesterol consumption meant I got to eat like Ron Swanson for three months — bacon and eggs and steak was pretty much the staple of my diet.
In many of the studies we found, those who saw the most improvement in health, testosterone, or muscle gain were those with existing nutrient or vitamin deficiencies. This means that some gains may be due more to dietary changes and generally restoring nutrient and vitamin levels than any one magic ingredient, but also that making sure your diet includes healthy amounts of nutrients should be your first step.
Does zinc provide testosterone benefits? The answer is, yes. It is an essential mineral which is used in many processes within the body and has a similar role like vitamin D. Men who have a deficiency of zinc may suffer from low testosterone levels but taking zinc supplements can help them to improve the testosterone levels. Zinc deficiency is an essential factor in infertility because it also reduces the sperm count, but with supplements, the sperm count increases along with improvement in testosterone levels. It also helps to recover from high-intensity interval training because that also cause the decline in testosterone levels.

Directions — SUGGESTED USE: As a dietary supplement take 3 capsules daily, preferably with a meal, or as directed by a healthcare professional. — Take two capsules with a meal twice a day. On days that you are not training, take two capsules in the morning and two capsules at night. On days that you train, take two capsules about an hour before workouts and take two capsules in the morning or at night depending on when you train.
Before the ready availability of non-injectible testosterone preparations, and because of their ease of administration by the oral route, 17-alkylated steroids were popular surrogate agents for testosterone. These substances, however, were capable of inducing several risk factors for coronary artery disease (Kopera 1993; Hall and Hall 2005) and as a consequence, particularly after the revelations of extensive 17-alkylated anabolic steroid abuse by athletes, testosterone, became unjustly incriminated. The evidence, however, tends to suggest just the opposite; testosterone may even be cardioprotective. Dunajska and colleagues have demonstrated that when compared to controls, men with coronary artery disease tend to have: lower total testosterone levels and free androgen indices, more abdominal fat, higher blood sugar and insulin levels (Dunajska et al 2004).
THIS TOOL DOES NOT PROVIDE MEDICAL ADVICE. It is intended for general informational purposes only and does not address individual circumstances. It is not a substitute for professional medical advice, diagnosis or treatment and should not be relied on to make decisions about your health. Never ignore professional medical advice in seeking treatment because of something you have read on the WebMD Site. If you think you may have a medical emergency, immediately call your doctor or dial 911.

Dr. Anthony’s Notes: Here's a funny little effect – fenugreek can make you sweet and your urine smell sweet like Maple Syrup. Hell, this could be a good thing for you! This supplement is commonly used for good reasons – it's quite effective for enhancing libido when stacked with the other herbs on this list. Medical Note: Fenugreek may interact with blood thinning medications (Warfarin, Coumadin, Xarleto). Check with your doctor before taking any of these supplements. How To Take Fenugreek: Take 400-600mg (capsule) with food; it's best to take a product standardized for fenuside.
Zaima, N., Kinoshita, S., Hieda, N., Kugo, H., Narisawa, K., Yamamoto, A., ... Moriyama, T. (2016, September). Effect of dietary fish oil on mouse testosterone level and the distribution of eicosapentaenoic acid-containing phosphatidylcholine in testicular interstitium. Biochemistry and Biophysics Reports, 7, 259–265. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5613343/

And remember, saturated fats work best (along with monounsaturated fats – olive oil, almonds, avocados etc.). In fact higher intakes of polyunsaturated fats (canola oil, sunflower oil, soybean oil, safflower oil, margarine etc.) are linked to LOWER testosterone levels (14 & 15). I explore the dangers of PUFA's in a lot more detail in this article - PUFA's: The Worst Thing For Your Health That You Eat Everyday.
Among my favorite stress management tools is the Emotional Freedom Technique (EFT), a method similar to acupuncture but without the use of needles. EFT is known to eliminate negative behavior and instill a positive mentality. Always bear in mind that your emotional health is strongly linked to your physical health, and you have to pay attention to your negative feelings as much as you do to the foods you eat.
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.
Epidemiological studies have also assessed links between serum testosterone and non-coronary atherosclerosis. A study of over 1000 people aged 55 years and over found an inverse correlation between serum total and bioavailable testosterone and the amount of aortic atherosclerosis in men, as assessed by radiological methods (Hak et al 2002). Increased intima-media thickness (IMT) is an early sign of atherosclerosis and has also been shown to predict cardiovascular mortality (Murakami et al 2005). Cross-sectional studies have found that testosterone levels are negatively correlated with carotid IMT in independently living men aged 74–93 years (van den Beld et al 2003), diabetic men (Fukui et al 2003) and young obese men (De Pergola et al 2003). A 4-year follow up study of the latter population showed that free testosterone was also inversely correlated with the rate of increase of IMT (Muller et al 2004).
Using steroids eventually trains your body to realize that it doesn’t have to produce as much testosterone to reach its equilibrium, so to reach the same highs you’ll need to take more steroids, and when you stop taking them, your body will need to readjust — you’ll be living with low testosterone for a while (and you’ll need to see a doctor if your body doesn’t readjust on its own). Forcing your body to stay above your natural testosterone, even if you’re naturally low, can create this kind of dependency which ultimately decreases the amount of testosterone your body will produce on its own.
A recent study compared total and bioavailable testosterone levels with inflammatory cytokines in men aged 65 and over. There was an inverse correlation with the pro-inflammatory soluble interleukin-6 receptor, but no association with interleukin-6 (IL-6), highly sensitive CRP (hsCRP), tumor necrosis factor-α (TNF-α) or interleukin-1β (IL-1β (Maggio et al 2006). Another trial found that young men with idiopathic hypogonadotrophic hypogonadism had higher levels of proinflammatory factors interleukin-2 (IL-2), interleukin-4 (IL-4), complement C3c and total immunoglobulin in comparison to controls (Yesilova et al 2000). Testosterone treatment in a group of hypogonadal men, mostly with known coronary artery disease, induced anti-inflammatory changes in the cytokine profile of reduced IL-1β and TNF-α and increased IL-10 (Malkin, Pugh, Jones et al 2004).
The aim of treatment for hypogonadism is to normalize serum testosterone levels and abolish symptoms or pathological states that are due to low testosterone levels. The exact target testosterone level is a matter of debate, but current recommendations advocate levels in the mid-lower normal adult range (Nieschlag et al 2005). Truly physiological testosterone replacement would require replication of the diurnal rhythm of serum testosterone levels, but there is no current evidence that this is beneficial (Nieschlag et al 2005).
The bones and the brain are two important tissues in humans where the primary effect of testosterone is by way of aromatization to estradiol. In the bones, estradiol accelerates ossification of cartilage into bone, leading to closure of the epiphyses and conclusion of growth. In the central nervous system, testosterone is aromatized to estradiol. Estradiol rather than testosterone serves as the most important feedback signal to the hypothalamus (especially affecting LH secretion).[115] In many mammals, prenatal or perinatal "masculinization" of the sexually dimorphic areas of the brain by estradiol derived from testosterone programs later male sexual behavior.[116]
The effect excess testosterone has on the body depends on both age and sex. It is unlikely that adult men will develop a disorder in which they produce too much testosterone and it is often difficult to spot that an adult male has too much testosterone. More obviously, young children with too much testosterone may enter a false growth spurt and show signs of early puberty and young girls may experience abnormal changes to their genitalia. In both males and females, too much testosterone can lead to precocious puberty and result in infertility. 
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