“I'm 55 years old and hitting the ball further than I've ever hit, and I'm not getting tired going 18 holes! And when I play softball I'm hitting the ball further. I work for the DWP in LA and it's a very physically demanding job. Andro400 really helps because we work 16 hour days a lot. I was turning down a lot of overtime, but when I started taking Andro400, it got me through the day. I really notice a difference – even my wife did. It really works!”

A number of research groups have tried to further define the relationship of testosterone and body composition by artificial alteration of testosterone levels in eugonadal populations. Induction of a hypogonadal state in healthy men (Mauras et al 1998) or men with prostate cancer (Smith et al 2001) using a gonadotrophin-releasing-hormone (GnRH) analogue was shown to produce increases in fat mass and decreased fat free mass. Another experimental approach in healthy men featured suppression of endogenous testosterone production with a GnRH analogue, followed by treatment with different doses of weekly intramuscular testosterone esters for 20 weeks. Initially the experiments involved men aged 18–35 years (Bhasin et al 2001) but subsequently the study was repeated with a similar protocol in men aged 60–75 years (Bhasin et al 2005). The different doses given were shown to produce a range of serum concentrations from subphysiological to supraphysiological (Bhasin et al 2001). A given testosterone dose produced higher serum concentrations of testosterone in the older age group (Bhasin et al 2005). Subphysiological dosing of testosterone produced a gain in fat mass and loss of fat free mass during the study. There were sequential decreases in fat mass and increases in fat free mass with each increase of testosterone dose. These changes in body composition were seen in physiological and supraphysiological treatment doses. The trend was similar in younger versus older men but the gain of fat mass at the lowest testosterone dose was less prominent in older patients (Bhasin et al 2001; Bhasin et al 2005). With regard to muscle function, the investigators showed dose dependent increases in leg strength and power with testosterone treatment in young and older men but there was no improvement in fatigability (Storer et al 2003; Bhasin et al 2005).

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
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.

There is increasing interest in the group of patients who fail to respond to treatment with PDE-5 inhibitors and have low serum testosterone levels. Evidence from placebo-controlled trials in this group of men shows that testosterone treatment added to PDE-5 inhibitors improves erectile function compared to PDE-5 inhibitors alone (Aversa et al 2003; Shabsigh et al 2004).


Among the changes which occur with aging are those that affect several aspects of the endocrine system which reduces its secretions to varying degrees in different individuals. These reductions in secretions are identified by a poor but widely recognized appellation, the “pauses”: menopause (decreased ovarian function), adrenopause (decreased adrenal function, especially with regard to dehydroepiandrosterone secretion), somatopause (decreased growth hormone production), andropause (decreased hypothalamic-pituitary testicular function with diminished testosterone availability and impaired spermatogenesis) (Lamberts 1997).
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).
Consume enough zinc. Zinc is a mineral needed for many body functions including healthy immune function, bone strength and the production of testosterone. In fact, low levels of zinc are correlated to low levels of testosterone in men and teenage boys.[8] Mild zinc deficiency is now fairly common among Americans, so there's a good chance your teenage boy (particularly if he isn't a healthy eater) may be deficient. Ask your doctor for a blood test to get a better idea, but in the meantime, focus on serving and eating foods that are rich in zinc, such as meats, fish, low-fat milk, hard cheeses, beans and some nuts and seeds.
Testosterone is a hormone that is secreted in both men and women. It is responsible for sex drive, as well as protein processing for muscle mass development and strength. Testosterone declines with age, illness and poor nutrition in both genders, though this change may be more marked in men. Synthetic hormone replacement therapy can cause adverse side effects. A natural way to raise the body’s testosterone levels safely include supplementing the diet with specific nutrients and physical exercise.
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.
1) Eat a good diet daily consisting of 10 servings of fresh vegetables (recommend juicing, and go heavy on the carrots & broccoli), lots of cholesterol in the form of eggs, butter, bacon, avocados, good fat, and take in moderate levels of protein. Avoid all trans fat and limit sugars, carbohydrates and any grains. Lastly, snack on nuts throughout the day between meals to keep your metabolism going.
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.
Dr. Darryn Willoughby, a professor of health, human performance and recreation and the director of the Exercise and Biochemical Nutrition Laboratory at Baylor University, told us that even in studies where there was an increase in testosterone, it was only around 15–20 percent. “In men with clinically normal testosterone levels, this modest increase will most likely not be anabolic enough to improve exercise performance,” he says. So if you have normal testosterone levels, and are simply trying to get an extra edge in gaining muscle, losing weight, or some extra time in the bedroom — you might see some results from taking a testosterone booster. But really, these will be most useful for men with low testosterone trying to get back to a healthy testosterone range.
Fenugreek is often found in Indian, Turkish, and Persian cuisine. Multiple studies have found it to improve testosterone levels, and in particular, sexual performance. Scientists at Babu Banarasi Das University and King George’s Medical University in India have found that fenugreek improved testosterone levels. Testosterone levels increased for 90% of the volunteers, sperm morphology (the size and shape of sperm) improved for 14.6%, and more than 50% of volunteers experienced improvements in mental alertness, mood, and libido.

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.
Testosterone is a steroid from the androstane class containing a keto and hydroxyl groups at the three and seventeen positions respectively. It is biosynthesized in several steps from cholesterol and is converted in the liver to inactive metabolites.[5] It exerts its action through binding to and activation of the androgen receptor.[5] In humans and most other vertebrates, testosterone is secreted primarily by the testicles of males and, to a lesser extent, the ovaries of females. On average, in adult males, levels of testosterone are about 7 to 8 times as great as in adult females.[6] As the metabolism of testosterone in males is more pronounced, the daily production is about 20 times greater in men.[7][8] Females are also more sensitive to the hormone.[9]

Thus, alcohol metabolism destroys the essential coenzyme required for T synthesis. Alcohol also contributes to the release of special endorphins which inhibit hormone production. In addition, drinking too much alcohol leads to the elevation of estrogen levels in men because of the conversion of testosterone in estrogen. It means that T levels come down with a run.
Sharma, R., Oni, O. A., Gupta, K., Chen, G., Sharma, M., Dawn, B., … & Barua, R. S. (2015, August 6). Normalization of testosterone level is associated with reduced incidence of myocardial infarction. European Heart Journal, 36(40), 2706-2715. Retrieved from https://academic.oup.com/eurheartj/article/36/40/2706/2293361/Normalization-of-testosterone-level-is-associated
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