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 data has associated low testosterone levels with atherogenic lipid parameters, including lower HDL cholesterol (Lichtenstein et al 1987; Haffner et al 1993; Van Pottelbergh et al 2003) and higher total cholesterol (Haffner et al 1993; Van Pottelbergh et al 2003), LDL cholesterol (Haffner et al 1993) and triglyceride levels (Lichtenstein et al 1987; Haffner et al 1993). Furthermore, these relationships are independent of other factors such as age, obesity and glucose levels (Haffner et al 1993; Van Pottelbergh et al 2003). Interventional trails of testosterone replacement have shown that treatment causes a decrease in total cholesterol. A recent meta-analysis of 17 randomized controlled trials confirmed this and found that the magnitude of changes was larger in trials of patients with lower baseline testosterone levels (Isidori et al 2005). The same meta-analysis found no significant overall change in LDL or HDL cholesterol levels but in trials with baseline testosterone levels greater than 10 nmol/l, there was a small reduction in HDL cholesterol with testosterone treatment.
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).
Elevated testosterone levels have been demonstrated to increase the growth of body muscles and contribute to better activation of the nervous system, resulting in more power and strength, a better mood, enhanced libido, and many other benefits.[3] Previous researches done on the anabolic role of testosterone and its impact on muscular strength in training-induced adaptations has provided rather conflicting findings, and a positive correlation between testosterone-mediated responses and both functional performance and body composition was found.[4,5] There are a number of naturally occurring substances that can boost testosterone levels in the body. Foods containing such substances are known as testosterone-foods; and they tend to be rich in vitamins, antioxidants, and minerals like zinc, which plays a key role in testosterone production.[2,6-8]
It doesn’t get more natural than getting a good night’s sleep. Research published in the Journal of the American Medical Association showed that lack of sleep can greatly reduce a healthy young man’s testosterone levels. That effect is clear after only one week of reduced sleep. Testosterone levels were particularly low between 2 and 10 p.m. on sleep-restricted days. Study participants also reported a decreased sense of wellbeing as their blood testosterone levels dropped.
I was reading in the university health news daily website that a study performed by researchers at the University of Texas M.D. Anderson Cancer Center found that men with prostate cancer who ate 3 tablespoons of milled or ground flax seeds each day had decreased prostate cancer cell proliferation compared to similar men who did not eat flax seeds. According to the American Cancer Society, men who supplement their diets with flax seed have lower PSA levels and slower growth of benign as well as cancerous prostate cells.
TT may help you but it may have adverse (harmful) results. (See discussion of these side effects below.) The Federal Drug Administration (FDA) has said that testosterone drug labels should state that there is a risk for heart disease and stroke for some men using testosterone products. All men should be checked for heart disease and stroke before, and periodically while on, TT. The AUA however, on careful review of evidence-based peer review literature, has stated that there is no strong evidence that TT either increases or decreases the risk of cardiovascular events.
At the present time, it is suggested that androgen replacement should take the form of natural testosterone. Some of the effects of testosterone are mediated after conversion to estrogen or dihydrotestosterone by the enzymes aromatase and 5a-reductase enzymes respectively. Other effects occur independently of the traditional action of testosterone via the classical androgen receptor- for example, its action as a vasodilator via a cell membrane action as described previously. It is therefore important that the androgen used to treat hypogonadism is amenable to the action of these metabolizing enzymes and can also mediate the non-androgen receptor actions of testosterone. Use of natural testosterone ensures this and reduces the chance of non-testosterone mediated adverse effects. There are now a number of testosterone preparations which can meet these recommendations and the main factor in deciding between them is patient choice.
Reordering. My husband has been very tired (lazy), but unable to sleep, and quickly started gaining a belly. I give him his vitamins so he never knows what he is taking. Only 3 days after taking this, he played an entire soccer game and commented on how much more energy he had and how he just feels better all around. I then told him what he was taking. He has continued taking and he is like his old self again. His energy has not only come back on the soccer field, but in other areas, as well.

Late onset hypogonadism reflects a particular pathophysiology and it may not be appropriate to extrapolate results from studies concerning the effects of testosterone in treating hypogonadism of other etiology to aging males. For this reason, the age of men treated in clinical trials is certainly relevant. Other important factors include patient comorbidities and the preparation and route of testosterone replacement used in the study, which can affect the production of estrogen and dihydrotestosterone, testosterone’s active metabolites

In accordance with sperm competition theory, testosterone levels are shown to increase as a response to previously neutral stimuli when conditioned to become sexual in male rats.[40] This reaction engages penile reflexes (such as erection and ejaculation) that aid in sperm competition when more than one male is present in mating encounters, allowing for more production of successful sperm and a higher chance of reproduction.
That said, magnesium is one of a few ingredients demonstrated to impact testosterone levels. Researchers at Italy’s University of Palermo found that magnesium improved participants’ anabolic hormone status — including their testosterone levels. In a follow-up study, they confirm that even adjusting for age differences in their participant group, “magnesium was positively associated with total testosterone.” They propose that magnesium supplementation might help improve muscle performance in aging men — a group particularly vulnerable to declining/low testosterone levels. Outside of Italy, researchers at Turkey’s Selçuk University found that magnesium supplementation increased testosterone levels for both athletes and more sedentary men alike.
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.
Testosterone may prove to be an effective treatment in female sexual arousal disorders,[52] and is available as a dermal patch. There is no FDA approved androgen preparation for the treatment of androgen insufficiency; however, it has been used off-label to treat low libido and sexual dysfunction in older women. Testosterone may be a treatment for postmenopausal women as long as they are effectively estrogenized.[52]
Zinc is involved in virtually every aspect of male reproduction, including testosterone metabolism. Several studies support the use of zinc for treating low sperm counts, especially when accompanied by low testosterone levels. In these studies, zinc has shown an ability to raise both sperm counts and testosterone levels. Many men may be suffering from low testosterone simply because of a zinc deficiency. Taking 30–45 mg of zinc per day is recommended; balance with 2–3 mg of copper for best results.
Zinc is little more of a nice-to-have ingredient than a must-have. It’s on our radar as an ingredient that possibly boosts testosterone levels, and while we couldn’t find enough supporting evidence that taking zinc would increase natural testosterone, low zinc levels have been connected to infertility. A low zinc level is also possibly a sign of hypogonadism. The closest support we found is in a study which found that people recovered from nutritional deficiency-related problems more quickly if they took a zinc supplement than those who did not. Zinc is available in many foods, such as oysters, fortified breakfast cereals, and red meat.

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).


Dr. Anthony’s Notes: Vitamin D has about 100 other beneficial body functions outside of it's impact on testosterone. Make sure you take the active Vitamin D3 (not D2 – from plant sources!) It’s also advisable to get 20 minutes of sunshine daily (weather permitting) – without sunscreen. Verdict: this is one of the natural testosterone supplements that work. Best Food Sources of Vitamin D3: Wild Alaskan Salmon (#1), Sardines, Eggs How To Take Vitamin D3: Using 3000-5000IU of Vitamin D3 per day is a good safe, research supported dose. Your physician can also test your blood for D3 levels for more precise monitoring.
Elevated testosterone levels have been demonstrated to increase the growth of body muscles and contribute to better activation of the nervous system, resulting in more power and strength, a better mood, enhanced libido, and many other benefits.[3] Previous researches done on the anabolic role of testosterone and its impact on muscular strength in training-induced adaptations has provided rather conflicting findings, and a positive correlation between testosterone-mediated responses and both functional performance and body composition was found.[4,5] There are a number of naturally occurring substances that can boost testosterone levels in the body. Foods containing such substances are known as testosterone-foods; and they tend to be rich in vitamins, antioxidants, and minerals like zinc, which plays a key role in testosterone production.[2,6-8]
A study published in the Journal of Steroid Biochemistry studied the effects of diet on serum sex hormones in healthy men. Results showed that when men decreased their healthy fat intake, serum concentrations of androstenedione, testosterone and free testosterone also decreased. (8) This indicates you can add low testosterone to the list of low-fat diet risks.
^ Butenandt A, Hanisch G (1935). "Uber die Umwandlung des Dehydroandrosterons in Androstenol-(17)-one-(3) (Testosterone); um Weg zur Darstellung des Testosterons auf Cholesterin (Vorlauf Mitteilung). [The conversion of dehydroandrosterone into androstenol-(17)-one-3 (testosterone); a method for the production of testosterone from cholesterol (preliminary communication)]". Chemische Berichte (in German). 68 (9): 1859–62. doi:10.1002/cber.19350680937.
Transdermal preparations of testosterone utilize the fact that the skin readily absorbs steroid hormones. Initial transdermal preparations took the form of scrotal patches with testosterone loaded on to a membranous patch. Absorption from the scrotal skin was particularly good and physiological levels of testosterone with diurnal variation were reliably attained. The scrotal patches are now rarely used because they require regular shaving or clipping of scrotal hair and because they produce rather high levels of dihydrotestosterone compared to testosterone (Behre et al 1999). Subsequently, non-scrotal patches were developed but the absorptive capacity of non-scrotal skin is much lower, so these patches contain additional chemicals which enhance absorption. The non-scrotal skin patches produce physiological testosterone levels without supraphysiological dihydrotestosterone levels. Unfortunately, the patches produce a high rate of local skin reactions often leading to discontinuation (Parker and Armitage 1999). In the last few years, transdermal testosterone gel preparations have become available. These require daily application by patients and produce steady state physiological testosterone levels within a few days in most patients (Swerdloff et al 2000; Steidle et al 2003). The advantages compared with testosterone patches include invisibility, reduced skin irritation and the ability to adjust dosage, but concerns about transfer to women and children on close skin contact necessitate showering after application or coverage with clothes.
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).

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


Inaccurate or misinterpreted test results can either falsely diagnose or miss a case of testosterone deficiency. Your testosterone level should be measured between 7 am and 10 am, when it's at its peak. Confirm a low reading with a second test on a different day. It may require multiple measurements and careful interpretation to establish bioavailable testosterone, or the amount of the hormone that is able to have effects on the body. Consider getting a second opinion from an endocrinologist.
×