We should probably start with the elephant in the room: do these supplements increase testosterone? The answer is probably yes. There are some ingredients that help convince your body to produce more testosterone, but there’s a catch. Testosterone boosters aren’t actually great at boosting; that is, at pushing your testosterone levels above your healthy, normal balance. Boosters typically act more like restorers — helping bring low testosterone levels back to that healthy equilibrium rather than boosting you above normal testosterone levels. Just like how if you have anemia, taking a vitamin B12 supplement can help restore your energy and reduce fatigue, but if your B12 levels are good, a supplement won’t give you super energy levels to stay awake for three days — your body will likely just process (read: pee) out the extra.
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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.
One long-term study observed that those who slept only four hours per night had borderline deficient levels. Other long-term studies support this. One study calculated that for every additional hour of sleep you get, testosterone levels rise 15% higher, on average. Although some people seem to do fine with less sleep, research suggests around 7–10 hours of sleep per night is best for long-term health and your testosterone.
The prevalence of biochemical testosterone deficiency increases with age. This is partly due to decreasing testosterone levels associated with illness or debility but there is also convincing epidemiological data to show that serum free and total testosterone levels also fall with normal aging (Harman et al 2001; Feldman et al 2002). The symptoms of aging include tiredness, lack of energy, reduced strength, frailty, loss of libido, decreased sexual performance depression and mood change. Men with hypogonadism experience similar symptoms. This raises the question of whether some symptoms of aging could be due to relative androgen deficiency. On the other hand, similarities between normal aging and the symptoms of mild androgen deficiency make the clinical diagnosis of hypogonadism in aging men more challenging.
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
Infertility in men and women Infertility or a couple being unable to conceive a child can cause significant stress and unhappiness. There are numerous reasons for both male and female infertility but many ways in which medical assistance can overcome problems that people may face. Everything concerning infertility is discussed and explained here. Read now
DHEA (dehydroepiandrosterone) extract - this is a chemical that used in your body which a ‘hormone precursor’. This means it’s the chemical used by the body to create hormones like oestrogen or testosterone. When taken as supplement it is believed to boost testosterone levels, but DHEA has not been shown to increase testosterone in men. DHEA comes in two form:
We all remember the time during our teens where our body underwent majority of its changes that led us into adulthood. As far as testosterone levels go, this period of time is where the production of this hormone peaked. Testosterone levels during these teenage years remain high and consistent, and therefore it is not advisable to use a testosterone boosting supplement during this time. This is because, Natural Testosterone Boosters work by encouraging your body to increase it;s natural levels back to their maximum capacity. If your body is already producing it’s maximum amount of Testosterone, these products will be ineffective for you. You should be prioritising quality, intense training sessions with adequate nutrition, rich in protein and carbohydrates to elicit growth and repair.
The production of the stress hormone cortisol blocks the production and effects of testosterone. From a biological perspective, cortisol increases your “fight or flight” response, thereby lowering testosterone-associated functions such as mating, competing, and aggression. Chronic stress can take a toll on testosterone production, as well as your overall health. Therefore, stress management is equally important to a healthy diet and regular exercise. Tools you can use to stay stress-free include prayer, meditation, laughter, and yoga. Relaxation skills, such as deep breathing and visualization, can also promote your emotional health.
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.
With the decline of ovarian function in menopause, not only do estrogen levels decline, but so does testosterone availability, since the ovaries contribute, either by direct secretion or through precursor production, about 50 percent of circulating testosterone. The other 50 percent is supplied by the adrenal glands. Many post-menopausal or oophorectomized women are symptomatic as a consequence of reduced testosterone, the leading symptom being loss of libido (Sherwin and Gelfand 1987; Simon et al 2005). There is an increasing trend toward testosterone supplementation in these women. Such supplementation may also lead, not only to increased libido, but to increased bone mineral density and an improvement in general overall sense of well-being including energy, strength, motivation and mood (Davis et al 1995; Davis et al 2000).

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).


Opioid substances are in common use both licit and illicit. Opiates are potent analgesics but they are also highly addictive. They are frequently prescribed for both acute and chronic pain and when used chronically, often induce opiate dependence in the user. Pain clinics regularly use narcotic agents in many of their patients. Methadone, in particular, is regularly prescribed to opiate addicts who have entered a program aimed at reducing narcotic dosage and ultimately weaning the patient off it altogether. Most men who are on chronic high doses of an opiate become hypogonadal. This was first recognized in the 1970’s when heroin addicts were found to have suppressed levels of testosterone (Brambilla et al 1977). Also suppressed were LH and FSH pointing to a probable inhibition of GnRH release.
Men can experience a range of symptoms if testosterone decreases more than it should. Low testosterone, or low T, is diagnosed when levels fall below 300 nanograms per deciliter (ng/dL). A normal range is typically 300–1000 ng/dL, according to the U.S. Food and Drug Administration. A blood test called a serum testosterone test is used to determine your level of circulating testosterone.
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).

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.


Testosterone boosters are a class of herbal supplements aimed at naturally increasing your testosterone levels. Usually, they contain micronutrients that men are commonly deficient in, such as zinc, and which have been connected in research to healthy testosterone levels. They also may contain adaptogens, which are a class of supplement that are thought to help the body adapt to stress, or ingredients which have been connected to improved sleep. Sleep restriction has been shown to reduce testosterone in healthy young men, and as Chris Lockwood, Ph.D., notes, disturbed sleep is a common symptom of low T-levels.[1]
Regardless of the method of testosterone treatment chosen, patients will require regular monitoring during the first year of treatment in order to monitor clinical response to testosterone, testosterone levels and adverse effects, including prostate cancer (see Table 2). It is recommended that patients should be reviewed at least every three months during this time. Once treatment has been established, less frequent review is appropriate but the care of the patient should be the responsibility of an appropriately trained specialist with sufficient experience of managing patients treated with testosterone.
While it would be nice to buy a testosterone pill from the local supplement store and have your testosterone levels go up, such a magic pill does not exist. As you can see from the above rundown, while a few supplements may be somewhat effective if your T levels are already low, none will significantly raise your testosterone above a baseline level. Thus, the basics of keeping your T levels high remain pretty simple:
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
Testosterone belongs to a class of male hormones called androgens, which are sometimes called steroids or anabolic steroids. In men, testosterone is produced mainly in the testes, with a small amount made in the adrenal glands. The brain's hypothalamus and pituitary gland control testosterone production. The hypothalamus instructs the pituitary gland on how much testosterone to produce, and the pituitary gland passes the message on to the testes. These communications happen through chemicals and hormones in the bloodstream.
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.
As already indicated previously, testosterone levels, particularly bioavailable testosterone, fall with advancing age. This decline in testosterone availability may start to occur early in the forth decade but it usually becomes clinically manifest in the 50s and 60s. Although there is continuing debate about the best way to diagnose hypogonadism in the aging male, there appears to be a general consensus that symptomatic men with reduced levels of testosterone should be given a trial of testosterone therapy if there is no contraindication to do so (Bain et al 2007).
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Tribulus terrestris is an ingredient commonly presented as improving testosterone levels, but has not been found to be more effective than a placebo or possess any testosterone increasing properties. WebMD cautions that it interferes with Lithium and diabetes medications, and in general, not enough is known about tribulus terrestris to recommend a dosage for anyone.
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.
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