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 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.
More can be learned from a large, randomized, placebo-controlled trial of finasteride treatment in 18,800 men aged 55 or more. Finasteride is a 5α-reductase inhibitor which acts to prevent the metabolism of testosterone to dihydrotestosterone (DHT) – the most active androgen in the prostate. The trial showed a greater overall incidence of prostate cancer in the control group, but men treated with finasteride were more likely to have high grade tumors (Thompson et al 2003), suggesting that reduced androgen exposure of the prostate may delay the presentation of prostate cancer and/or promote advanced disease in some other way.

Stick to protocols that stress large degrees of muscle mass and are moderate- to high-intensity. Additionally, more seasoned gym-goers may want to incorporate forced repetitions periodically into their programs, as testosterone increases have been observed with this type of training.14 Incorporating other post-failure training techniques such as dropsets or partials may similarly be associated with higher T production.
One study looking at alcohol consumption found that increasing alcohol consumption led to a higher level of free & total testosterone compared to a non-drinking control group (20). Drinking did however lower SHBG testosterone levels, though this type of testosterone is bound to a protein meaning our bodies cannot use it to build muscle or increase our mood.
Binge drinking on the other hand does impact Testosterone levels – especially on a short term basis. Two studies (22 & 23) show that large acute quantities of alcohol consumption in a short period led to decreases in Testosterone levels by a whooping 20-23% after 24hours! Note however this is drinking to extreme excess! Likewise, chronic alcohol abuse is known to reduce testosterone more notably (as seen in alcoholics).
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.
There is also a crazy case study about a Thai-male who reportedly got his DHT levels all the way to 158% above medical reference ranges after supplementing with Butea Superba (he visited the doctor and complained of too high libido), after some examination and questioning, the doctors thought it might be the supplement causing this sudden increase in androgenic hormones and they instructed him to seize the consumption. Within a week his blood serum 5-a DHT had fallen back to normal.
Important future developments will include selective androgen receptor modulators (SARMs). These drugs will be able to produce isolated effects of testosterone at androgen receptors. They are likely to become useful clinical drugs, but their initial worth may lie in facilitating research into the relative importance of testosterone’s action at the androgen receptor compared to at other sites or after conversion to other hormones. Testosterone will remain the treatment of choice for late onset hypogonadism for some time to come.
We know stress generates too much cortisol and shuts down sexual hormones since our bodies go into a "fight or flight" mode. Supplements that nourish our adrenals are key to correcting those imbalances. A few recommendations that I have include adrenal adaptogens such as maca, ashwagandha, Siberian ginseng, and rhodiola. Adaptogens are a great way to restore adrenal glands, balance hormones, and detoxify. Supplementing with 25 to 50 mg of DHEA, and a high-quality multivitamin with bioavailable B vitamins and high dose vitamin C can also be helpful. It's important to eat a diet high in quality omega-3s like salmon, oysters, and sardines. I suggest 2,000 to 6,000 mg per day of carnitine to improve energy production and mitochondrial function.
“I can't tell you how good the product is! I'm in the best shape of my life. I used to take blood pressure medication and I don't even take that anymore. It's changed every aspect of my life. I was a 40 waist and I'm down to a 36. I'm 54 years old, and people tell me I look better than I ever have, and I look like I'm in my early 40s! And I'm telling you it's the Andro. This product is so much better than even the advertisements! From taking Andro400 I immediately notice a burst of energy . . . and my skin color, my sexual advancements, my energy, plus the weight loss, the toning of the body, and the increase strength and endurance . . . it's like night and day where I was then and where I am now, and Andro400 has made the difference. And my wife also takes it, 1 pill every other day, and she has experienced an amazing transformation in her body alone, with her hair, her complexion, and as well as in the gym. It's an outstanding product. My customers, my friends, my family, everybody is noticing the difference!”
Before the ready availability of non-injectible testosterone preparations, and because of their ease of administration by the oral route, 17-alkylated steroids were popular surrogate agents for testosterone. These substances, however, were capable of inducing several risk factors for coronary artery disease (Kopera 1993; Hall and Hall 2005) and as a consequence, particularly after the revelations of extensive 17-alkylated anabolic steroid abuse by athletes, testosterone, became unjustly incriminated. The evidence, however, tends to suggest just the opposite; testosterone may even be cardioprotective. Dunajska and colleagues have demonstrated that when compared to controls, men with coronary artery disease tend to have: lower total testosterone levels and free androgen indices, more abdominal fat, higher blood sugar and insulin levels (Dunajska et al 2004).
I highly recommend using a great essential amino acid mix post-exercise in order to boost testosterone.  These essential amino acids and especially the concentrated branched chain amino acids leucine, isoleucine and valine stimulate muscle protein synthesis.  Getting these amino acids in the post-workout window dramatically boosts testosterone production (14).  I like using our Amino Strong and will often recommend a scoop pre-workout and post-workout for the best muscle building, testosterone boosting benefits.
Examine.com is intended to be used for educational and information purposes only. Examine.com and its Editors do not advocate nutritional supplementation over proper medical advice or treatment and this sentiment will never be expressed through pages hosted under Examine.com. If using any pharmaceuticals or drugs given to you by a doctor or received with a prescription, you must consult with the doctor in question or an equally qualified Health Care Professional prior to using any nutritional supplementation. If undergoing medical therapies, then consult with your respective Therapist or Health Care Professional about possible interactions between your Treatment, any Pharmaceuticals or Drugs being given, and possible nutritional supplements or practices hosted on Examine.com.
Like most supplements, Beast Sports contains several ingredients with little research about their long-term effects. WebMD describes Suma powder, Rhodiola Rosea, Cissus quadrangularis, Tribulus extract, and ashwagandha extract as possibly safe when taken for a short period of time (usually around 6-10 weeks). However, their long-term safety remains unknown. It also has a few ingredients, like cyanotis vaga root, safed musli, and polygonum cispidatum root extract for which there is a lack of data on even short term safety.
During the month before my experiment, I was definitely sleep deprived. Some nights I was only getting 4 to 5 hours. Testosterone killer! During my experiment I tried to get 8 to 9 hours of sleep at night as consistently as possible. I had to go to bed earlier, but I was only cutting into time that I would have been using to mindlessly surf the net anyway.
Erectile dysfunction is a common finding in the aging male. A prevalence of over 70% was found in men older than 70 in a recent cross-sectional study (Ponholzer et al 2005). Treatment with phosphodiesterase-5 (PDE-5) inhibitors is proven to be effective for the majority of men but some do not respond (Shabsigh and Anastasiadis 2003). The condition is multi-factorial, with contributions from emotional, vascular, neurological and pharmacological factors. The concept of erectile dysfunction as a vascular disease is particularly interesting in view of the evidence presented above, linking testosterone to atherosclerosis and describing its action as a vasodilator.

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).

Studies conducted in rats have indicated that their degree of sexual arousal is sensitive to reductions in testosterone. When testosterone-deprived rats were given medium levels of testosterone, their sexual behaviors (copulation, partner preference, etc.) resumed, but not when given low amounts of the same hormone. Therefore, these mammals may provide a model for studying clinical populations among humans suffering from sexual arousal deficits such as hypoactive sexual desire disorder.[37]
Phthalates are found to cause poor testosterone synthesis by disrupting an enzyme required to create the male hormone. Women with high levels of DEHP and DBP (two types of phthalates) in their system during pregnancy were found to have sons that had feminine characteristics Phthalates are found in vinyl flooring, detergents, automotive plastics, soaps and shampoos, deodorants, perfumes, hair sprays, plastic bags and food packaging, among a long list of common products. Aside from phthalates, other chemicals that possess gender-bending traits are:
Any day that you don’t get 20 minutes of direct sunlight on your skin, you want to supplement with 5,000 IUs of vitamin D3. If you get your blood levels tested and you’re extremely low — below 50 IUs — you typically want to do 5,000 IUs twice a day for three months until you get those numbers up. You can do everything in the world, but if your vitamin D levels aren’t right, your testosterone levels will stay low.
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.
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.
Our culture sees meat and fat as the enemy, while carbs and sugars are treated like gold. High fructose corn syrup is in almost everything you buy, and this sugar is known to wreak absolute havoc on our endocrine systems. Food companies are well aware that this stuff is destroying you, but as long as people continue to indulge on it they will continue to produce it.
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.
There is a polymorphic CAG repeat sequence in the androgen receptor gene, which codes for a variable number of glutamine amino acids in the part of the receptor affecting gene transcription. A receptor with a short CAG sequence produces greater activity when androgens attach, and men with shorter CAG polymorphisms exhibit androgenic traits, such as preserved bone density (Zitzmann et al 2001) and prostate growth during testosterone treatment (Zitzmann et al 2003). Indirect evidence of the importance of androgens in the development of prostate cancer is provided by case control study findings of a shorter, more active CAG repeat sequence in the androgen receptor gene of patients with prostate cancer compared with controls (Hsing et al 2000, 2002).
So out of all the natural testosterone boosting supplements out there I only really recommend tongkat ali extract, d-aspartic acid, and ashwagandha. There are a many others out there, but none that meet the standard that these do. And most of the other ones are actually in Testofuel. But remember, use at your own discretion. Even natural supplements can have side effects, so talk to your doctor first, and start slow.
Thanks for all the time and energy you put into this . Very informative . Great read. As far as intermittent fasting ,it’s the best. Check out Kinobody on YouTube for great info. I just stopped T injections and was looking for a good Tongkat Ali . Is Herbolab better than SD200 from Pure Science Supplements . I know there is a lot of garbage out there,just want the best quality . Thanks again .
Epidemiological evidence supports a link between testosterone and glucose metabolism. Studies in non-diabetic men have found an inverse correlation of total or free testosterone with glucose and insulin levels (Simon et al 1992; Haffner et al 1994) and studies show lower testosterone levels in patients with the metabolic syndrome (Laaksonen et al 2003; Muller et al 2005; Kupelian et al 2006) or diabetes (Barrett-Connor 1992; Andersson et al 1994; Rhoden et al 2005). A study of patients with type 2 diabetes using measurement of serum free testosterone by the gold standard method of equilibrium dialysis, found a 33% prevalence of biochemical hypogonadism (Dhindsa et al 2004). The Barnsley study demonstrated a high prevalence of clinical and biochemical hypogonadism with 19% having total testosterone levels below 8 nmol/l and a further 25% between 8–12 nmol/l (Kapoor, Aldred et al 2007). There are also a number longitudinal studies linking low serum testosterone levels to the future development of the metabolic syndrome (Laaksonen et al 2004) or type 2 diabetes (Haffner et al 1996; Tibblin et al 1996; Stellato et al 2000; Oh et al 2002; Laaksonen et al 2004), indicating a possible role of hypogonadism in the pathogenesis of type 2 diabetes in men. Alternatively, it has been postulated that obesity may be the common link between low testosterone levels and insulin resistance, diabetes and cardiovascular disease (Phillips et al 2003; Kapoor et al 2005). With regard to this hypothesis, study findings vary as to whether the association of testosterone with diabetes occurs independently of obesity (Haffner et al 1996; Laaksonen et al 2003; Rhoden et al 2005).
A study out of the University of Mary Hardin-Baylor in Belton, Texas, examined the effects of fenugreek supplementation on strength and body composition in resistance-trained men. Researchers found that while both the placebo and fenugreek groups significantly increased their strength during the first four weeks, only the fenugreek group saw significant increases in strength after eight weeks of training and supplementation.[5]

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).

The reliable measurement of serum free testosterone requires equilibrium dialysis. This is not appropriate for clinical use as it is very time consuming and therefore expensive. The amount of bioavailable testosterone can be measured as a percentage of the total testosterone after precipitation of the SHBG bound fraction using ammonium sulphate. The bioavailable testosterone is then calculated from the total testosterone level. This method has an excellent correlation with free testosterone (Tremblay and Dube 1974) but is not widely available for clinical use. In most clinical situations the available tests are total testosterone and SHBG which are both easily and reliably measured. Total testosterone is appropriate for the diagnosis of overt male hypogonadism where testosterone levels are very low and also in excluding hypogonadism in patients with normal/high-normal testosterone levels. With increasing age, a greater number of men have total testosterone levels just below the normal range or in the low-normal range. In these patients total testosterone can be an unreliable indicator of hypogonadal status. There are a number of formulae that calculate an estimated bioavailable or free testosterone level using the SHBG and total testosterone levels. Some of these have been shown to correlate well with laboratory measures and there is evidence that they more reliably indicate hypogonadism than total testosterone in cases of borderline biochemical hypogonadism (Vermeulen et al 1971; Morris et al 2004). It is important that such tests are validated for use in patient populations relevant to the patient under consideration.
‘Testosterone boosting’ products  - found online, or in health food or body-building shops, these products claim to boost testosterone levels if you buy them. The majority of these products will not have the effect you want and are not worth spending money on. Any of these products that do have a real effect may have a form of prescription medication in which is both dangerous and illegal.
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.

Testosterone boosters are used by many athletes worldwide to achieve a significant muscle mass increase within a short period of time.[1] However; one cannot be completely confident in terms of the quality and efficacy of such products because of several reasons, such as the possibility of bad storage conditions and originating from an unreliable source. Over the years, some consumers of testosterone boosters have complained of kidney and liver abnormalities that could be linked to their use of boosters.[10] Cases of erroneous product administration have occurred in the past as athletes may not follow the instructions on the label fully, which can lead to many side effects.[11] In the present case, a man was admitted to a hospital because of a severe abdominal pain. The pain was later found to be caused by liver injury. The diagnosis confirmed that the levels of the key hepatic enzymes were markedly elevated. The medical complications observed were found to have occurred following the consumption of two courses of a commercial testosterone booster. According to researchers based in the US, about 13% of the annual cases of acute liver failure are attributable to idiosyncratic drug- and/or supplement-induced liver injury.[12] Marked increase in the levels of ALT, AST, and gamma-glutamyl transferase was observed after consuming the first course of the commercial testosterone booster, and they started to decline after the 2nd and 3rd course. This abruptly increases the levels of liver enzymes after the first course may be attributed to the interruption effect of commercial testosterone booster on liver function as a result of the effects of its ingredients.

Examine.com is intended to be used for educational and information purposes only. Examine.com and its Editors do not advocate nutritional supplementation over proper medical advice or treatment and this sentiment will never be expressed through pages hosted under Examine.com. If using any pharmaceuticals or drugs given to you by a doctor or received with a prescription, you must consult with the doctor in question or an equally qualified Health Care Professional prior to using any nutritional supplementation. If undergoing medical therapies, then consult with your respective Therapist or Health Care Professional about possible interactions between your Treatment, any Pharmaceuticals or Drugs being given, and possible nutritional supplements or practices hosted on Examine.com.


Total levels of testosterone in the body are 264 to 916 ng/dL in men age 19 to 39 years,[165] while mean testosterone levels in adult men have been reported as 630 ng/dL.[166] Levels of testosterone in men decline with age.[165] In women, mean levels of total testosterone have been reported to be 32.6 ng/dL.[167][168] In women with hyperandrogenism, mean levels of total testosterone have been reported to be 62.1 ng/dL.[167][168]
There is an increased incidence of hypogonadism in men with rheumatoid arthritis. Tengstrand et al (2002) studied hormonal levels in 104 men with rheumatoid arthritis and 99 age-matched healthy men. They divided their subjects into 3 age groups: 30–49, 40–59, 60–69. Mean non-sex hormone binding globulin-bound testosterone (bioavailable testosterone) was lower in men with rheumatoid arthritis for each of the three groups. LH was also found to be lower in the patients with rheumatoid arthritis suggesting a hypothalamic-pituitary cause of the reduced bioavailable testosterone. Of the 104 men with rheumatoid arthritis, 33 had hypogonadism compared to 7 of the 99 healthy controls.
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.
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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