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No one will argue with the well-established fact that the dramatic lows of testosterone as seen in castration or other significant primary testicular disturbances such as those induced by chemotherapy, radiation therapy, congenital problems, or as seen in secondary testicular insufficiency (eg, large compressive pituitary or hypothalamic tumors) produce dramatic signs and symptoms of testosterone deficiency that require testosterone replacement therapy. Less clear, or at least more controversial, is the necessity of treating the gentler reduction of testosterone seen in the aging process.

Cardiovascular disease, and its underlying pathological process atherosclerosis, is an important cause of morbidity and mortality in the developed and developing world. Coronary heart disease in particular is the commonest cause of death worldwide (AHA 2002; MacKay and Mensah 2004). As well as increasing with age, this disease is more common in the male versus female population internationally, which has led to interest in the potential role of sex hormones in modulating risk of development of atherosclerosis. Concerns about the potential adverse effects of testosterone treatment on cardiovascular disease have previously contributed to caution in prescribing testosterone to those who have, or who are at risk of, cardiovascular disease. Contrary to fears of the potential adverse effects of testosterone on cardiovascular disease, there are over forty epidemiological studies which have examined the relationship of testosterone levels to the presence or development of coronary heart disease, and none have shown a positive correlation. Many of these studies have found the presence of coronary heart disease to be associated with low testosterone levels (Reviews: Jones, Jones et al 2003; Jones et al 2005).
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).
When many people think of someone with a high level of testosterone, they may picture a man loaded with strength, sexual prowess, and machismo. But while high-T has been correlated with all those things, it’s also been correlated with aggression, sexual misconduct, and violence. One of testosterone’s most common uses—as a performance-enhancing steroid—illustrates both sides of the hormone. Injecting steroids can be a quick way for athletes to dramatically improve performance, but the side effects can also be extreme, and can include excessive body hair growth, sexual dysfunction, and the hard-to-corral anger known as “roid rage.”
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In contrast to steroids, testosterone boosters have a fully different mechanism of action. They are the products which contain the natural ingredients only. These ingredients act by stimulating the man’s body to synthesize own testosterone. So, testosterone levels grow naturally without negative health effects associated with the intake of steroids.

Attention, memory, and spatial ability are key cognitive functions affected by testosterone in humans. Preliminary evidence suggests that low testosterone levels may be a risk factor for cognitive decline and possibly for dementia of the Alzheimer's type,[100][101][102][103] a key argument in life extension medicine for the use of testosterone in anti-aging therapies. Much of the literature, however, suggests a curvilinear or even quadratic relationship between spatial performance and circulating testosterone,[104] where both hypo- and hypersecretion (deficient- and excessive-secretion) of circulating androgens have negative effects on cognition.
If you do take DAA I recommend cycling it (i.e. 5 days on, 2 off, over 4 weeks then 4 weeks off). And taking it with an aromatase inhibitor (which ensures the aspartic acid doesn’t get converted to estrogen). Especially as more studies are coming out showing the increase in testosterone is limited to a week or two before it drops back to normal levels.
The group's 2010 clinical practice guidelines make it clear that "the threshold testosterone level below which symptoms of androgen deficiency and adverse health outcomes occur and testosterone administration improves outcomes in the general population is not known." They also clearly advise against screening men in the general population to avoid "labeling and medicalization of otherwise healthy men for whom testing, treatment, and monitoring would represent a burden with unclear benefit."
Other side effects include increased risk of heart problems in older men with poor mobility, according to a 2009 study at Boston Medical Center. A 2017 study published in JAMA found that treatments increase coronary artery plaque volume. Additionally, the Food and Drug Administration (FDA) requires manufactures to include a notice on the labeling that states taking testosterone treatments can lead to possible increased risk of heart attacks and strokes. The FDA recommends that patients using testosterone should seek medical attention right away if they have these symptoms:
Longitudinal studies in male aging studies have shown that serum testosterone levels decline with age (Harman et al 2001; Feldman et al 2002). Total testosterone levels fall at an average of 1.6% per year whilst free and bioavailable levels fall by 2%–3% per year. The reduction in free and bioavailable testosterone levels is larger because aging is also associated with increases in SHBG levels (Feldman et al 2002). Cross-sectional data supports these trends but has usually shown smaller reductions in testosterone levels with aging (Feldman et al 2002). This is likely to reflect strict entry criteria to cross-sectional studies so that young healthy men are compared to older healthy men. During the course of longitudinal studies some men may develop pathologies which accentuate decreases in testosterone levels.
Few examples: In this 2014 study, a bunch of researchers tested multiple different diets with added Lactobacillus Reuteri on male rodents. In every single case, the addition of L.Reuterii to the feed increased testosterone levels, increased luteinizing hormone levels, increased testicular size & weight, prevented age-related testicular shrinkage, improved semen parameters, and even increased markers of social domination.

The reasons for considering such therapy become evident from the many associations, indicated above, that reduced testosterone has with a variety of both physiological functions (bone metabolism, muscle mass, cognitive function, libido, erectile function) and pathophysiological states (metabolic syndrome, diabetes mellitus, obesity, insulin resistance, autoimmune disease). Although a definitive long-term, large scale placebo-controlled double-blind study of testosterone therapy in the aging male has not yet been carried out, multiple shorter-term trials have suggested improvement by testosterone with a resultant enhancement of muscle mass, bone density, libido, erectile function, mood, motivation and general sense of well-being.
"By expanding the boundaries of this disease to common symptoms in aging males, such as fatigue and reduced libido, drug companies seek to increase their markets and boost their sales," wrote Barbara Mintzes, an assistant professor at the University of British Columbia School of Public Health, and Agnes Vitry, a senior research fellow at the University of South Australia, in a 2012 article in the Medical Journal of Australia .
That said, keep in mind that using leucine as a free form amino acid can be highly counterproductive as when free form amino acids are artificially administrated, they rapidly enter your circulation while disrupting insulin function, and impairing your body's glycemic control. Food-based leucine is really the ideal form that can benefit your muscles without side effects.

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).
Research is always highlighting the dangers of long-term stress, which can elevate levels of the hormone cortisol. Unnatural elevations in cortisol can quickly reduce testosterone. These hormones work in a seesaw-like manner: as one goes up, the other comes down. Stress and high cortisol can also increase food intake, weight gain and the storage of harmful body fat around your organs. In turn, these changes may negatively impact your testosterone levels. For both optimal health and hormone levels, you should try to reduce repetitive stressful situations in your life. Focus on a diet based on whole foods, regular exercise, good sleep, laughter and a balanced lifestyle, all of which can reduce stress and improve your health and testosterone levels.

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?


Other side effects include increased risk of heart problems in older men with poor mobility, according to a 2009 study at Boston Medical Center. A 2017 study published in JAMA found that treatments increase coronary artery plaque volume. Additionally, the Food and Drug Administration (FDA) requires manufactures to include a notice on the labeling that states taking testosterone treatments can lead to possible increased risk of heart attacks and strokes. The FDA recommends that patients using testosterone should seek medical attention right away if they have these symptoms:
Growth of spermatogenic tissue in testicles, male fertility, penis or clitoris enlargement, increased libido and frequency of erection or clitoral engorgement occurs. Growth of jaw, brow, chin, and nose and remodeling of facial bone contours, in conjunction with human growth hormone occurs.[21] Completion of bone maturation and termination of growth. This occurs indirectly via estradiol metabolites and hence more gradually in men than women. Increased muscle strength and mass, shoulders become broader and rib cage expands, deepening of voice, growth of the Adam's apple. Enlargement of sebaceous glands. This might cause acne, subcutaneous fat in face decreases. Pubic hair extends to thighs and up toward umbilicus, development of facial hair (sideburns, beard, moustache), loss of scalp hair (androgenetic alopecia), increase in chest hair, periareolar hair, perianal hair, leg hair, armpit hair.

Everyone knows that carbohydrates are extremely important for testosterone production, but instead of reaching for grains during your next meal, stack your plate high with potatoes. Research reveals that grains have inflammatory properties, but the testosterone-friendly starches in potatoes will have the bodybuilder in your life smiling at dinnertime!
The effects of testosterone in humans and other vertebrates occur by way of multiple mechanisms: by activation of the androgen receptor (directly or as DHT), and by conversion to estradiol and activation of certain estrogen receptors.[109][110] Androgens such as testosterone have also been found to bind to and activate membrane androgen receptors.[111][112][113]
Did you know that a meat-free diet can lower your T-levels by 14%? When your body lacks protein, it boosts the production of other hormones that deactivate testosterone. However, on the other hand, it has been found that a diet that is excessively rich in saturated fats found in meats like beef and lamb can also lower T-levels. Venison is the middle ground and is also excellent for muscle growth.
Overall there is evidence that testosterone treatment increases lean body mass and reduces obesity, particularly visceral obesity, in a variety of populations including aging men. With regard to muscle changes, some studies demonstrate improvements in maximal strength but the results are inconsistent and it has not been demonstrated that these changes lead to clinically important improvements in mobility, endurance or quality of life. Studies are needed to clarify this. Changes in abdominal obesity are particularly important as visceral fat is now recognised as predisposing the metabolic syndrome, diabetes and cardiovascular disease.
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.
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
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:
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).

Men on long-term testosterone appear to have a higher risk of cardiovascular problems, like heart attacks, strokes, and deaths from heart disease. For example, in 2010, researchers halted the Testosterone in Older Men study when early results showed that men on hormone treatments had noticeably more heart problems. "In older men, theoretical cardiac side effects become a little more immediate," Dr. Pallais says.
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