Dr. Anthony's Notes: I like Tribulus. It is a VERY common herb in almost all testosterone boosting products – again though, it may be more of a libido enhancer than anything. From my personal experience, it's effective when stacked with the other libido enhancing supplements in this guide. How To Take Tribulus: Take 200-400mg once per day of a 45-60% saponin extract product.
Dr. Anthony’s Notes: I use Maca often in cycles throughout the year. I typically buy the raw Maca powder, which has a VERY “dirt-like” earthy taste. Beware if you are a bit squeamish on tastes! How To Take Maca: 1500-3000mg of Maca powder is a typical dosage take daily alongside food. From personal experience, I've found that it’s best to buy the Maca powder as a standalone supplement and throw it into a blended protein shake to mask the taste.
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]

Testosterone treatment is unequivocally needed in classical hypogonadism for reasons discussed in subsequent subsections. In classical hypogonadism, testosterone production is usually clearly below the lower limit of normal and patients are highly symptomatic; the various symptoms are easily related to the deficiencies in various bodily systems where testosterone action is important. Symptoms of testosterone deficiency are listed in Table 2. A few prominent causes of classical hypogonadism are listed in Table 3.
What are the health benefits of kale? Kale is a leafy green vegetable featured in a variety of meals. With more nutritional value than spinach, kale may help to improve blood glucose, lower the risk of cancer, reduce blood pressure, and prevent asthma. Here, learn about the benefits and risks of consuming kale. We also feature tasty serving suggestions. Read now
Michael T. Murray, ND, is widely regarded as one of the leading authorities on natural medicine. He is the author of many books, including the classic Encyclopedia of Nutritional Supplements. His latest book is What the Drug Companies Won’t Tell You and Your Doctor Doesn’t Know. Visit him online at doctormurray.com.   Article Courtesy of Better Nutrition  

If in a 46 XY individual testosterone is either not produced in adequate concentrations as in gonadal dysgenesis (MacLaughlin and Donahue 2004), or in the absence of the enzyme 17 alpha-hydroxylase so that testosterone is not produced (Ergun-Longmire et al 2006), or testosterone androgen receptors are absent as in the androgen insensitivity syndrome (Hughes and Deeb 2006), phenotypic females will result.


Here’s a scary thought: You may be less of a man than your father was—at least hormonally. A study in the Journal of Clinical Endocrinology and Metabolism found that, on average, testosterone levels were higher in men of the same age in the ’80s than they were in the 2000s (due, researchers speculate, to higher rates of obesity and the wider use of medication these days).  
Testosterone is a steroid sex hormone found in both men and women. In men, testosterone is produced primarily by the Leydig (interstitial) cells of the testes when stimulated by luteinizing hormone (LH). It functions to stimulate spermatogenesis, promote physical and functional maturation of spermatozoa, maintain accessory organs of the male reproductive tract, support development of secondary sexual characteristics, stimulate growth and metabolism throughout the body and influence brain development by stimulating sexual behaviors and sexual drive. In women, testosterone is produced by the ovaries (25%), adrenals (25%) and via peripheral conversion from androstenedione (50%). Testerone in women functions to maintain libido and general wellbeing. Testosterone exerts a negative feedback mechanism on pituitary release of LH and follicle-stimulating hormone (FSH). Testosterone may be further converted to dihydrotestosterone or estradiol depending on the tissue.
The University of Connecticut recently published findings stating that those who supplemented with whey protein produced less cortisol, a stress hormone, than those who did not supplement. Cortisol lowers production of sex hormones and is also responsible for belly fat formation. Ricotta is an excellent source of natural whey protein and amino acids, both of which are essential to muscle growth and avoiding the spare tire.
Afrisham, R., Sadejh-Nejadi, S., SoliemaniFar, O., Kooti, W., Ashtary-Larky, D., Alamiri, F., … Khaneh-Keshi, A. (2016, November 24). Salivary testosterone levels under psychological stress and its relationship with rumination and five personality traits in medical students. Psychiatry Investigations, 13(6), 637–643. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5128352/
If you’re a frequent reader here in AM, you already know that increased dietary fat intake is directly correlated with increased testosterone production. And not only that, but the types of fat that increase T seem to be saturated fats (SFAs) and monounsaturated fats (MUFAs), while polyunsaturated (PUFAs) actually tend to lower testosterone (more here).
Studies have demonstrated reduced testosterone levels in men with heart failure as well as other endocrine changes (Tappler and Katz 1979; Kontoleon et al 2003). Treatment of cardiac failure with chronic mechanical circulatory support normalizes many of these changes, including testosterone levels (Noirhomme et al 1999). More recently, two double-blind randomized controlled trials of testosterone treatment for men with low or low-normal serum testosterone levels and heart failure have shown improvements in exercise capacity and symptoms (Pugh et al 2004; Malkin et al 2006). The mechanism of these benefits is currently unclear, although a study of the acute effects of buccal testosterone given to men with chronic cardiac failure under invasive monitoring showed that testosterone increased cardiac index and reduced systemic vascular resistance (Pugh et al 2003). Testosterone may prove useful in the management of cardiac failure but further research is needed.
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.
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.
There are studies that show Soy consumption in humans leads to lower sperm count, but unfortunately they did not look at testosterone levels in the study (40). This (41) particular study compared the estrogen production of men drinking soy protein to those drinking whey. After two weeks they found the estradiol levels were equal, however soy drinkers had LOWER Testosterone levels and HIGHER cortisol levels (both bad).
Zinc deficiency also negatively affects testosterone levels, according a 2014 article in the Journal of Plant Biochemistry and Physiology. The authors of this review note that zinc supplementation can increase circulating testosterone in some populations. In fact, daily supplementation with typical doses may double testosterone within a few months.

The bones and the brain are two important tissues in humans where the primary effect of testosterone is by way of aromatization to estradiol. In the bones, estradiol accelerates ossification of cartilage into bone, leading to closure of the epiphyses and conclusion of growth. In the central nervous system, testosterone is aromatized to estradiol. Estradiol rather than testosterone serves as the most important feedback signal to the hypothalamus (especially affecting LH secretion).[115] In many mammals, prenatal or perinatal "masculinization" of the sexually dimorphic areas of the brain by estradiol derived from testosterone programs later male sexual behavior.[116]


To find the best testosterone booster, we collected every supplement available on BodyBuilding.com, and cross-checked our list against the top results on best of lists like MensFitness, BroScience, and BodyNutrition. We only looked at pills since some of the ingredients in testosterone boosters have a reputation for tasting bad, and powders just prolong the experience. There are a lot — 133 of them to be precise — and they all claim to boost testosterone levels. Testosterone (for men) is “thought to regulate sex drive (libido), bone mass, fat distribution, muscle mass and strength, and the production of red blood cells and sperm.” If a supplement can increase your natural testosterone levels, the rest should follow. As we mentioned above, it’s not that simple, and at best, you’ll experience only a short-lived boost.
Osteoporosis refers to pathological loss of bone density and strength. It is an important condition due to its prevalence and association with bone fractures; most commonly of the hip, vertebra and forearm. Men are relatively protected from the development of osteoporosis by a higher peak bone mass compared with women (Campion and Maricic 2003). Furthermore, women lose bone at an accelerated rate immediately following the menopause. Nevertheless, men start to lose bone mass during early adult life and experience an increase in the rate of bone loss with age (Scopacasa et al 2002). Women of a given age have a higher prevalence of osteoporosis in comparison to men but the prevalence increases with age in both sexes. As a result, men have a lower incidence of osteoporotic fractures than women of a given age but the gap between the sexes narrows with advancing age (Chang et al 2004) and there is evidence that hip fractures in men are associated with greater mortality than in women (Campion and Maricic 2003).
The Organon group in the Netherlands were the first to isolate the hormone, identified in a May 1935 paper "On Crystalline Male Hormone from Testicles (Testosterone)".[180] They named the hormone testosterone, from the stems of testicle and sterol, and the suffix of ketone. The structure was worked out by Schering's Adolf Butenandt, at the Chemisches Institut of Technical University in Gdańsk.[181][182]
A number of epidemiological studies have found that bone mineral density in the aging male population is positively associated with endogenous androgen levels (Murphy et al 1993; Ongphiphadhanakul et al 1995; Rucker et al 2004). Testosterone levels in young men have been shown to correlate with bone size, indicating a role in determination of peak bone mass and protection from future osteoporosis (Lorentzon et al 2005). Male hypogonadism has been shown to be a risk factor for hip fracture (Jackson et al 1992) and a recent study showed a high prevalence of hypogonadism in a group of male patients with average age 75 years presenting with minimal trauma fractures compared to stroke victims who acted as controls (Leifke et al 2005). Estrogen is a well known determinant of bone density in women and some investigators have found serum estrogen to be a strong determinant of male bone density (Khosla et al 1998; Khosla et al 2001). Serum estrogen was also found to correlate better than testosterone with peak bone mass (Khosla et al 2001) but this is in contradiction of a more recent study showing a negative correlation of estrogen with peak bone size (Lorentzon et al 2005). Men with aromatase deficiency (Carani et al 1997) or defunctioning estrogen receptor mutations (Smith et al 1994) have been found to have abnormally low bone density despite normal or high testosterone levels which further emphasizes the important influence of estrogen on male bone density.

For example, the study published in Obesity Research tells that the scientists measured testosterone levels in two groups of middle-aged men with obesity. One group underwent a 16-week weight loss program, while the second group did nothing. Each participant of the first group lost 20 kg on the average. And these participants experienced a significant increase in testosterone levels. So, the fight against overweight is very important for those who want to overcome testosterone deficiency. But starvation is strictly forbidden because this is a stressful situation which leads to the sharp decline in T levels.
A: According to the package insert, there are several longer-term side effects that have occurred with testosterone therapy. Testosterone can stimulate the growth of cancerous tissue. Prostate cancer or enlargement of the prostate can develop during prolonged therapy with testosterone, and these conditions are more likely to occur in elderly men. In patients receiving testosterone therapy, tests for prostate cancer should be performed as is current practice. Androgen therapy, such as testosterone, can cause a loss of blood sugar control in patients with diabetes. Close monitoring of blood glucose is recommended. Male patients can experience feminization during prolonged therapy with testosterone. The side effects of feminization include breast soreness and enlargement. These side effects are generally reversible when treatment is stopped. Hair loss resembling male pattern baldness has also occurred. Sexual side effects including decreased ejaculatory volume and low sperm counts have occurred in patients receiving long-term therapy or excessive doses. For more information, please consult with your health care provider and visit //www.everydayhealth.com/drugs/testosterone. Michelle McDermott, PharmD

The finding of hypogonadism in diabetic men is not just a scientific curiosity, it may have practical management implications. Kapoor and colleagues (2006) undertook a placebo-controlled double blind study to determine the effect of testosterone therapy on insulin resistance and glycemic control in hypogonadal men with type 2 diabetes. They found that men treated with testosterone had reductions in glycated hemoglobin insulin resistance, fasting blood sugar, waist circumference, waist/hip ratio and total cholesterol.
Great article with a lot of useful information. I completely agree with your top three picks. I have done a ton of research as well. Currently I am taking Testogen for over two months and it has worked for me. It has double my low T and I am 61 years old. I do feel better and have more energy. Even have morning wood sometimes and haven’t for a long time.
A 2010 study published in the journal Hormones and Behavior first suggested this when researchers evaluated the “dual-hormone hypothesis” clinically. (11) They discovered that when cortisol is elevated, testosterone responds by elevating as well but soon after bottoms out at a much lower level than before cortisol kicked in! That means you want to find ways to relieve stress to keep your testosterone levels up.
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).
If testosterone deficiency occurs during fetal development, then male characteristics may not completely develop. If testosterone deficiency occurs during puberty, a boy’s growth may slow and no growth spurt will be seen. The child may have reduced development of pubic hair, growth of the penis and testes, and deepening of the voice. Around the time of puberty, boys with too little testosterone may also have less than normal strength and endurance, and their arms and legs may continue to grow out of proportion with the rest of their body.
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