The changes in average serum testosterone levels with aging mean that the proportion of men fulfilling a biochemically defined diagnosis of hypogonadism increases with aging. Twenty percent of men aged over 60 have total testosterone levels below the normal range and the figure rises to 50% in those aged over 80. The figures concerning free testosterone are even higher as would be expected in view of the concurrent decrease in SHBG levels (Harman et al 2001).
6. Foods rich in vitamin D. If you’ve been thinking of increasing your testosterone levels, you better stock up on those mushrooms, salmon and milk. Clinical Endocrinology’s August 2010 issue published a study that was conducted by Austria’s Medical University Graz. According to the researchers, mushroom, salmon and dairy products are examples of food that are rich in Vitamin D. These researchers also found a relationship between Vitamin D and testosterone. Their study has shown that individuals with high levels of Vitamin D also had high testosterone levels. The obvious inverse relationship was true as well.  Click here for a convincing study on HUMAN BEINGS to back this up.
A related issue is the potential use of testosterone as a coronary vasodilator and anti-anginal agent. Testosterone has been shown to act as a vasodilator of coronary arteries at physiological concentrations during angiography (Webb, McNeill et al 1999). Furthermore men given a testosterone injection prior to exercise testing showed improved performance, as assessed by ST changes compared to placebo (Rosano et al 1999; Webb, Adamson et al 1999). Administration of one to three months of testosterone treatment has also been shown to improve symptoms of angina and exercise test performance (Wu and Weng 1993; English et al 2000; Malkin, Pugh, Morris et al 2004). Longer term studies are underway. It is thought that testosterone improves angina due its vasodilatory action, which occurs independently of the androgen receptor, via blockade of L-type calcium channels at the cell membrane of the vascular smooth muscle in an action similar to the dihydropyridine calcium-channel blockers such as nifedipine (Hall et al 2006).
Kostic TS, Stojkov NJ, Bjelic MM, Mihajlovic AI, Janjic MM, Andric SA: Pharmacological doses of testosterone upregulated androgen receptor and 3-Beta-hydroxysteroid dehydrogenase/delta-5-delta-4 isomerase and impaired leydig cells steroidogenesis in adult rats. Toxicol Sci. 2011 Jun;121(2):397-407. doi: 10.1093/toxsci/kfr063. Epub 2011 Apr 6. [PubMed:21427060]
February 22, 2018 - Since our last review, the manufacturers of two of our top picks have gone out of business, and some new testosterone boosters have entered the arena. We’ve updated this review to evaluate the current field of testosterone supplements, as well as beef up analysis on what kind of results you can expect from t-boosters. Our only current top pick, Beast Sports Nutrition, is a new player in the industry that contains all four of the ingredients with studies showing a positive effect on testosterone.

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Testosterone was first used as a clinical drug as early as 1937, but with little understanding of its mechanisms. The hormone is now widely prescribed to men whose bodies naturally produce low levels. But the levels at which testosterone deficiency become medically relevant still aren’t well understood. Normal testosterone production varies widely in men, so it’s difficult to know what levels have medical significance. The hormone’s mechanisms of action are also unclear.
This supplement contains herbal remedies to enhance the male hormone and increase a man's sexual desire. Ingredients found in the product include horney goat weed, milk thistle, tribulis terristris, wild yam, saw palmetto and maca. The manufacturer of the supplement claims that it is endorsed by a doctor for male enhancement. Recommended dosage is one capsule taken before engaging in sexual activity. Women should not take a testosterone supplement unless otherwise advised by a physician.
Dr. Anthony’s Notes: DHEA is a powerful supplement for testosterone, energy, and overall well-being in our older Fit Fathers. A small dose of 25-50mg/day is enough to exert noticeable benefits. This supplement is over-the-counter. Verdict: this is one of the testosterone supplements that work. How To Take DHEA: Take 25-50mg once per day with food. Special Medical Note: DHEA is a MILD CYP3A4 inhibitor (a liver enzyme that processes MANY very common medications). This is the same isoenzyme that Grapefruit inhibits – albeit DHEA inhibits to a much weaker degree. If you’ve ever heard “don’t eat grapefruit with your Lipitor (cholesterol medication)”… this is the reason why. When we inhibit the CYP3A4 enzyme, more of the medications you're taking circulates (it’s not metabolized as fast). Check with your doctor for medication interactions before using DHEA.

The real danger comes when you eat a diet high in sugars and carbohydrates (90% of Americans). The sugar binds to LDL (So-called bad cholesterol – PS: It’s not even cholesterol, it’s a protein) and renders it inert. When inert, the LDL cannot pull good cholesterol (HDL) into your cells. This is bad. So what you need to do in conduction with your high fat diet is take in a lot of cruciferous vegetables, limit your carb intake, don’t touch toxic sugars. And exercise regularly.


Testosterone is the main hormone associated with muscle mass, strength gains, and libido. But that's far from the only thing it does in the body. As Chris Lockwood, Ph.D., explains in the article "All About Testosterone," it impacts everything from mood and memory to bone health—but yes, to be clear, it also makes muscles bigger and stronger, and helps increase endurance and athletic performance.
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:
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!
Does the diminution that age brings with it in both total and bioavailable T have any clinical significance? This question leads us to the theme of this paper, “The Many Faces of Testosterone”. If testosterone were simply a “sex hormone” involved only with sexual desire and arousal we might tend to dismiss testosterone treatment in the aging man as merely a “life-style” therapy without any substantive basis for broad physiological necessity. The fact is, however, that the sexual attributes of testosterone are the least of its physiological necessities and that testosterone has a broad spectrum of demonstrated physiological functions as well as a wide variety of physiological and pathophysiological associations about which we are just learning.
The most common "out of balance" testosterone levels are found to be on the low side of normal; this occurs because a male's highest testosterone level usually peaks at about age 20, and then it decreases slowly with age. It has been suggested that a 1% decrease in testosterone level per year is not unusual for middle-aged (30 to 50 years old) and older males. While this decrease may not be noticeable in some men, others may experience significant changes starting in their middle-aged years or more commonly at age 60 and above. This drop in testosterone levels is sometimes termed hypogonadism, "male menopause" or andropause.
Another effect that can limit treatment is polycythemia, which occurs due to various stimulatory effects of testosterone on erythropoiesis (Zitzmann and Nieschlag 2004). Polycythemia is known to produce increased rates of cerebral ischemia and there have been reports of stroke during testosterone induced polycythaemia (Krauss et al 1991). It is necessary to monitor hematocrit during testosterone treatment, and hematocrit greater than 50% should prompt either a reduction of dose if testosterone levels are high or high-normal, or cessation of treatment if levels are low-normal. On the other hand, late onset hypogonadism frequently results in anemia which will then normalize during physiological testosterone replacement.
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.
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
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).
Vitamin C (unnecessary). I don’t know where I first heard about vitamin C’s supposed T-boosting benefits, but it’s one of those things you see all over the internet when you Google “how to increase testosterone.” Without trying to find the research that backs up that claim, I took a vitamin C supplement during my experiment. I later found some research that suggests that vitamin C does increase testosterone levels in diabetic mice, but because I wasn’t diabetic (nor a mouse), I’m not sure how much the vitamin C helped. I’ve actually stopped taking vitamin C supplements. I’m likely getting more than enough with my diet. Unless you have diabetes, you probably won’t see much benefit from this supplement. Don’t waste your money.
Keep in mind that you can use virtually any type of equipment you want for this – an elliptical machine, a treadmill, swimming, even sprinting outdoors (although you will need to do this very carefully to avoid injury) -- as long as you're pushing yourself as hard as you can for 30 seconds. But do be sure to stretch properly and start slowly to avoid injury. Start with two or three repetitions and work your way up, don't expect to do all eight repetitions the first time you try this, especially if you are out of shape.

According to the Mayo Clinic, testosterone therapy can help treat hypogonadism. This condition occurs when the body can’t produce enough testosterone on its own. However, it’s unclear whether supplements can help. A study published in found no scientific reason to prescribe testosterone to men over 65 years of age with normal or low to normal testosterone levels.
There are valid concerns about the safety of long-term treatment with testosterone particularly with respect to the cardiovascular system and the potential for stimulating prostate cancer development. There are no convincing hard data, however, to support these concerns. If anything, the data strongly suggest that adequate testosterone availability is cardioprotective and coronary risk factors such as diabetes, obesity and the metabolic syndrome are associated with reduced testosterone levels. It is certainly appropriate to avoid giving testosterone to men with prostate or breast cancer but it is not appropriate to accuse testosterone of inducing the development of de novo prostate cancers since evidence for this accusation is lacking (Wang et al 2004; Feneley and Carruthers 2006).

The converse is also true; there is an increased incidence of rheumatic/autoimmune disease in men with hypogonadism. Jimenez-Balderas et al (2001) carried out neuroendocrine, genetic and rheumatologic investigations in hypogonadal men. Of the 13 hypogonadal patients, 8 (61%) had rheumatic autoimmune disease (ankylosing spondylitis, systemic lupus erythemetosus, rheumatoid arthritis, dermatomyositis). There is a low frequency of those diseases (0.83%) in the general population.
A notable study out of Wayne State University in Indiana found that older men who had a mild zinc deficiency significantly increased their testosterone from 8.3 to 16.0 nmol/L—a 93 percent increase—following six months of zinc supplementation. Researchers of the study concluded that zinc may play an important role in modulating serum testosterone levels in normal healthy men.6
Falling in love decreases men's testosterone levels while increasing women's testosterone levels. There has been speculation that these changes in testosterone result in the temporary reduction of differences in behavior between the sexes.[53] However, it is suggested that after the "honeymoon phase" ends—about four years into a relationship—this change in testosterone levels is no longer apparent.[53] Men who produce less testosterone are more likely to be in a relationship[54] or married,[55] and men who produce more testosterone are more likely to divorce;[55] however, causality cannot be determined in this correlation. Marriage or commitment could cause a decrease in testosterone levels.[56] Single men who have not had relationship experience have lower testosterone levels than single men with experience. It is suggested that these single men with prior experience are in a more competitive state than their non-experienced counterparts.[57] Married men who engage in bond-maintenance activities such as spending the day with their spouse/and or child have no different testosterone levels compared to times when they do not engage in such activities. Collectively, these results suggest that the presence of competitive activities rather than bond-maintenance activities are more relevant to changes in testosterone levels.[58]
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