In 1927, the University of Chicago's Professor of Physiologic Chemistry, Fred C. Koch, established easy access to a large source of bovine testicles — the Chicago stockyards — and recruited students willing to endure the tedious work of extracting their isolates. In that year, Koch and his student, Lemuel McGee, derived 20 mg of a substance from a supply of 40 pounds of bovine testicles that, when administered to castrated roosters, pigs and rats, remasculinized them.[179] The group of Ernst Laqueur at the University of Amsterdam purified testosterone from bovine testicles in a similar manner in 1934, but isolation of the hormone from animal tissues in amounts permitting serious study in humans was not feasible until three European pharmaceutical giants—Schering (Berlin, Germany), Organon (Oss, Netherlands) and Ciba (Basel, Switzerland)—began full-scale steroid research and development programs in the 1930s.

That said, a group of researchers at the National University of Malaysia did a systemic literature review of longjack, looking for clinical research that demonstrated a relationship between the shrub and testosterone levels. Of 150 articles, only 11 met their inclusion criteria — involving humans and scientifically rigorous. However, of those 11 studies, seven “revealed remarkable association” between using longjack and improving male sexual health, while the remaining four “failed to demonstrate sufficient effects.” The team concluded that longjack looks “promising” when it comes to raising low testosterone, and that there is convincing evidence that it works.

If your need is greater though, there are other legal options to consider. DHEA is a precursor steroid hormone that is only available on prescription in the UK, but if taken under close supervision it can have dramatic effects. It must be taken under supervision though because too high a dose can cause mood changes and aggression — roid rage, in other words — as well as all the other unwanted by-products of too much testosterone.

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.
In the hepatic 17-ketosteroid pathway of testosterone metabolism, testosterone is converted in the liver by 5α-reductase and 5β-reductase into 5α-DHT and the inactive 5β-DHT, respectively.[1][151] Then, 5α-DHT and 5β-DHT are converted by 3α-HSD into 3α-androstanediol and 3α-etiocholanediol, respectively.[1][151] Subsequently, 3α-androstanediol and 3α-etiocholanediol are converted by 17β-HSD into androsterone and etiocholanolone, which is followed by their conjugation and excretion.[1][151] 3β-Androstanediol and 3β-etiocholanediol can also be formed in this pathway when 5α-DHT and 5β-DHT are acted upon by 3β-HSD instead of 3α-HSD, respectively, and they can then be transformed into epiandrosterone and epietiocholanolone, respectively.[153][154] A small portion of approximately 3% of testosterone is reversibly converted in the liver into androstenedione by 17β-HSD.[152]
The normal development of the prostate gland is dependent on the action of testosterone via the androgen receptor, and abnormal biosynthesis of the hormone or inactivating mutations of the androgen receptor are associated with a rudimentary prostate gland. Testosterone also requires conversion to dihydrotestosterone in the prostate gland for full activity. In view of this link between testosterone and prostate development, it is important to consider the impact that testosterone replacement may have on the prevalence and morbidity associated with benign prostatic hypertrophy (BPH) and prostate cancer, which are the common conditions related to pathological growth of the prostate gland.
Ghlissi, Z., Atheymen, R., Boujbiha, M. A., Sahnoun, Z., Makni Ayedi, F., Zeghal, K., ... Hakim, A. (2013, December). Antioxidant and androgenic effects of dietary ginger on reproductive function of male diabetic rats [Abstract]. International Journal of Food Sciences and Nutrition, 64 (8), 974–978. Retrieved from
Dr. Charles "Pat" Davis, MD, PhD, is a board certified Emergency Medicine doctor who currently practices as a consultant and staff member for hospitals. He has a PhD in Microbiology (UT at Austin), and the MD (Univ. Texas Medical Branch, Galveston). He is a Clinical Professor (retired) in the Division of Emergency Medicine, UT Health Science Center at San Antonio, and has been the Chief of Emergency Medicine at UT Medical Branch and at UTHSCSA with over 250 publications.
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.
Sleep apnea is another frequently listed contraindication to testosterone treatment. There have been a few reports of the development, or worsening, of sleep apnea during testosterone therapy (Matsumoto et al 1985) but sleep apnea is actually associated with lower serum testosterone levels (Luboshitzky et al 2002). The reduction in fat mass during treatment with testosterone could potentially be beneficial for sleep apnea, so many specialists will still consider patients for treatment with appropriate monitoring. It is wise to take a clinical history for sleep apnea during testosterone treatment in all men and perform sleep studies in those who develop symptoms.
Many clinical studies have looked at the effect of testosterone treatment on body composition in hypogonadal men or men with borderline low testosterone levels. Some of these studies specifically examine these changes in older men (Tenover 1992; Morley et al 1993; Urban et al 1995; Sih et al 1997; Snyder et al 1999; Kenny et al 2001; Ferrando et al 2002; Steidle et al 2003; Page et al 2005). The data from studies, on patients from all age groups, are consistent in showing an increase in fat free mass and decrease in fat mass or visceral adiposity with testosterone treatment. A recent meta-analysis of 16 randomized controlled trials of testosterone treatment effects on body composition confirms this pattern (Isidori et al 2005). There have been less consistent results with regard to the effects of testosterone treatment of muscle strength. Some studies have shown an increase in muscle strength (Ferrando et al 2002; Page et al 2005) with testosterone whilst others have not (Snyder et al 1999). Within the same trial some muscle group strengths may improve whilst others do not (Ly et al 2001). It is likely that the differences are partly due to the methodological variations in assessing strength, but it also possible that testosterone has different effects on the various muscle groups. The meta-analysis found trends toward significant improvements in dominant knee and hand grip strength only (Isidori et al 2005).

Recently, a panel with cooperation from international andrology and urology societies, published specific recommendations with regard to the diagnosis of Late-onset Hypogonadism (Nieschlag et al 2005). These are summarized in the following text. It is advised that at least two serum testosterone measurements, taken before 11 am on different mornings, are necessary to confirm the diagnosis. The second sample should also include measurement of gonadotrophin and prolactin levels, which may indicate the need for further investigations for pituitary disease. Patients with serum total testosterone consistently below 8 nmol/l invariably demonstrate the clinical syndrome of hypogonadism and are likely to benefit from treatment. Patients with serum total testosterone in the range 8–12 nmol/l often have symptoms attributable to hypogonadism and it may be decided to offer either a clinical trial of testosterone treatment or to make further efforts to define serum bioavailable or free testosterone and then reconsider treatment. Patients with serum total testosterone persistently above 12 nmol/l do not have hypogonadism and symptoms are likely to be due to other disease states or ageing per se so testosterone treatment is not indicated.

If you still feel the need to supplement, keep in mind that supplemental magnesium is more likely than dietary magnesium to cause adverse effects, which is why the FDA fixed at 350 mg the Tolerable Upper Intake Level for magnesium supplementation in adults. Also, you may want to avoid magnesium oxide: it has poor bioavailability (rats absorbed only 15% in one study,[43] and humans only 4% in another[44]) and can cause intestinal discomfort and diarrhea.

Testosterone is included in the World Health Organization's list of essential medicines, which are the most important medications needed in a basic health system.[107] It is available as a generic medication.[10] The price depends on the form of testosterone used.[108] It can be administered as a cream or transdermal patch that is applied to the skin, by injection into a muscle, as a tablet that is placed in the cheek, or by ingestion.[10]
Instead of turning to some drug that can only ameliorate symptoms and cause additional complications, I recommend using a natural saw palmetto supplement. Dr. Moerck says that there are about 100 clinical studies on the benefits of saw palmetto, one of them being a contributed to decreased prostate cancer risk. When choosing a saw palmetto supplement, you should be wary of the brand, as there are those that use an inactive form of the plant.

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.

Likewise, there are also natural ways to pep up your testosterone through diet, exercise and other lifestyle changes. So if you’re the wrong side of 30 and not feeling as strong in the gym anymore, or if you’re gaining weight where there wasn’t weight before, or if you can't find the energy to finish the day, let alone pleasure your partner, then keep reading — our expert advice may restore you to the peak of masculinity.
Scientists in Italy found that subjects who consumed roughly 3 grams of D-AA for 12 days observed a 42 percent increase in testosterone levels.[12] The researchers also noted that the D-AA group still had 22 percent more testosterone than the placebo group three days after they stopped supplementing. Conversely, a more recent article published in Nutrition Research found no increase in testosterone levels in resistance-trained males after supplementing with 3 grams of D-AA for 28 days.[13]

Estrogen is important in men, but too high of a level has all sorts of negative consequences – ranging from heart attacks to prostate cancer (32 & 33). The balance between testosterone and estrogen (or estradiol) is critical for a man. If the ratio is out and estrogen starts to dominate you run into all sorts of issues – such as breast cell growth, prostate enlargement and of course lower testosterone.

Cross-sectional studies have found a positive association between serum testosterone and some measures of cognitive ability in men (Barrett-Connor, Goodman-Gruen et al 1999; Yaffe et al 2002). Longitudinal studies have found that free testosterone levels correlate positively with future cognitive abilities and reduced rate of cognitive decline (Moffat et al 2002) and that, compared with controls, testosterone levels are reduced in men with Alzheimer’s disease at least 10 years prior to diagnosis (Moffat et al 2004). Studies of the effects of induced androgen deficiency in patients with prostate cancer have shown that profoundly lowering testosterone leads to worsening cognitive functions (Almeida et al 2004; Salminen et al 2004) and increased levels of serum amyloid (Gandy et al 2001; Almeida et al 2004), which is central to the pathogenesis of Alzheimer’s disease (Parihar and Hemnani 2004). Furthermore, testosterone reduces amyloid-induced hippocampal neurotoxity in vitro (Pike 2001) as well as exhibiting other neuroprotective effects (Pouliot et al 1996). The epidemiological and experimental data propose a potential role of testosterone in protecting cognitive function and preventing Alzheimer’s disease.

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).
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   Article Courtesy of Better Nutrition  
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.
The testicles produce an enzyme called 11ßHSD-1 which protects your testosterone molecules from the effects cortisol.  During times of prolonged stress and chronically elevated cortisol, there simply is too much cortisol for 11ßHSD-1 to handle.  This results in testosterone molecules being destroyed inside the gonads before they even enter the bloodstream (8, 9).
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.
When testosterone and endorphins in ejaculated semen meet the cervical wall after sexual intercourse, females receive a spike in testosterone, endorphin, and oxytocin levels, and males after orgasm during copulation experience an increase in endorphins and a marked increase in oxytocin levels. This adds to the hospitable physiological environment in the female internal reproductive tract for conceiving, and later for nurturing the conceptus in the pre-embryonic stages, and stimulates feelings of love, desire, and paternal care in the male (this is the only time male oxytocin levels rival a female's).[citation needed]
Low testosterone levels may contribute to decreased sex drive, erectile dysfunction, fragile bones, and other health issues. Having low testosterone levels may also indicate an underlying medical condition. See your doctor if you suspect you have low testosterone. A simple blood test is all it takes to check if your testosterone falls within the normal range.

It may be unlikely to completely eliminate products with EDCs, but there are a number of practical strategies that you can try to limit your exposure to these gender-bending substances. The first step would be to stop using Teflon cookware, as EDCs can leach out from contaminated cookware. Replace them with ceramic ones. Stop eating out of cans, as the sealant used for the can liner is almost always made from powerful endocrine-disrupting petrochemicals known as bisphenols, e.g. Bisphenol A,
High intensity exercise is crucial to boost testosterone (13).  Exercises should be explosive in nature and maximize the resistant overload on the muscles.  Large muscle group compound lifts such as squats, deadlifts & burpees are some of the best testosterone boosting exercises.  The training session should be short (5-30 mins) and have very little rest periods between sets.
The best test boosters promote increased testosterone through natural signaling that your body recognizes. This is possible due to the many complex pathways that all lead to the production of testosterone. With these many pathways come many options for reaching your goals, allowing you to choose the best method for your age and body type. Here are the primary mechanisms that result in natural testosterone production:
We’ll be honest. Testosterone boosters don’t really boost. The best testosterone booster is like taking a multivitamin with extra herbs that might slightly and temporarily increase your testosterone levels. Like all supplements, finding the right testosterone booster means wading into a sea of ingredients, all promising to help. Of 133 testosterone boosters, we found only one with the right ingredients to help raise your testosterone levels: Beast Sports Nutrition - Super Test ($45.88 for 180 capsules, or $2.04 per day).
Before assessing the evidence of testosterone’s action in the aging male it is important to note certain methodological considerations which are common to the interpretation of any clinical trial of testosterone replacement. Many interventional trials of the effects of testosterone on human health and disease have been conducted. There is considerable heterogenicity in terms of study design and these differences have a potential to significantly affect the results seen in various studies. Gonadal status at baseline and the testosterone level produced by testosterone treatment in the study are of particular importance because the effects of altering testosterone from subphysiological to physiological levels may be different from those of altering physiological levels to supraphysiological. Another important factor is the length of treatment. Randomised controlled trials of testosterone have ranged from one to thirty-six months in duration (Isidori et al 2005) although some uncontrolled studies have lasted up to 42 months. Many effects of testosterone are thought to fully develop in the first few months of treatment but effects on bone, for example, have been shown to continue over two years or more (Snyder et al 2000; Wang, Cunningham et al 2004).
Sexual arousal - boosting testosterone can improve sexual arousal, even if you have normal testosterone levels. Higher levels of testosterone can make it easier for you to get aroused and can boost your sex drive generally. While this doesn’t affect the physical action of your erections, if you are not getting hard because you’re not aroused then boosting testosterone could help.
Most studies support a link between adult criminality and testosterone, although the relationship is modest if examined separately for each sex. Nearly all studies of juvenile delinquency and testosterone are not significant. Most studies have also found testosterone to be associated with behaviors or personality traits linked with criminality such as antisocial behavior and alcoholism. Many studies have also been done on the relationship between more general aggressive behavior/feelings and testosterone. About half the studies have found a relationship and about half no relationship.[66]

Consider testosterone replacement therapy if nothing else helps. Sometimes low testosterone can keep you from living your life the way you want. Additionally, it may cause health concerns for younger males, like delayed puberty or decreased bone density. If natural remedies aren’t working for you, your doctor can offer you the following options:[22]
Before taking any supplements, at either end of the spectrum, you need to check whether it’s low testosterone that is actually causing the problem. Taking something that you don’t need could potentially cause irreversible issues. For that reason, steroid hormones like DHEA should never be prescribed without having blood tests first. Roked also recommends regular blood monitoring to make sure you’re taking the correct dosage.

Garlic contains a compound that reduces the levels of cortisol, a type of stress hormone. This compound is known as allicin. Testosterone and cortisol vie for the same sites within muscle cells. When you get rid of the cortisol, you make sure that the testosterone can get working and keep yourself stress-free too. Experts claim that uncooked garlic is the best in this case as it is the most potent, so add it to your diet starting today.

Currently available testosterone preparations in common use include intramuscular injections, subcutaneous pellets, buccal tablets, transdermal gels and patches (see Table 2). Oral testosterone is not widely used. Unmodified testosterone taken orally is largely subject to first-pass metabolism by the liver. Oral doses 100 fold greater than physiological testosterone production can be given to achieve adequate serum levels. Methyl testosterone esters have been associated with hepatotoxicity. There has been some use of testosterone undecanoate, which is an esterified derivative of testosterone that is absorbed via the lymphatic system and bypasses the liver. Unfortunately, it produces unpredictable testosterone levels and increases testosterone levels for only a short period after each oral dose (Schurmeyer et al 1983).
Such sort of injuries varies in severity and extent of damage markedly from one person to the other and withdrawal of the drug/supplement coupled with proper medical attention suffice in terms of alleviating the symptoms.[8,12] This was observed in the present case. However, the liver injury observed here may not be confidently linked to product consumption as the subject later reported that the following recovery he consumed two more courses of the booster with no side effects. Tests performed following hospital discharge, and repeated use of the product showed AST and ALT to be slightly high, whereas the rest of the blood parameters tested appeared to be normal. The AST/ALT ratio is considered to be a very important parameter for the evaluation of liver diseases, such as non-alcoholic fatty liver disease,[13] though it is rarely considered alone. Overall, the evidence was inconclusive in the present work in terms of linking the use of a testosterone booster with liver injury. However, even though a single case report cannot establish causality with statistical power.[13] Further research on the usage of a commercial testosterone booster within large populations for a long period is necessary to investigate whether the symptoms shown in the present case were significantly present in other athletes consuming the same commercial product or not. To guarantee an optimal outcome with no severe side effects, further research is warranted to confirm the present findings and determine whether the effects observed in this case report would be statistically significant in larger samples.
Zaima, N., Kinoshita, S., Hieda, N., Kugo, H., Narisawa, K., Yamamoto, A., ... Moriyama, T. (2016, September). Effect of dietary fish oil on mouse testosterone level and the distribution of eicosapentaenoic acid-containing phosphatidylcholine in testicular interstitium. Biochemistry and Biophysics Reports, 7, 259–265. Retrieved from

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).

Ashwagandha is sometimes included in testosterone supplements because of the hypothesis that it improves fertility. However, we couldn’t find sufficient evidence to support this claim (at best, one study found that ashwagandha might improve cardiorespiratory endurance). WebMD advocates caution when taking this herb, as it may interact with immunosuppressants, sedative medications, and thyroid hormone medications.
It seems that adequate testosterone levels are an important influence on sexual symptoms in the aging male and also influence the response of men to PDE-5 inhibitors, the first line treatment for erectile dysfunction in men. Many would now suggest screening for testosterone deficiency in all men presenting with erectile dysfunction (Gore and Rajfer 2004; Shabsigh 2005). This would seem appropriate because, in addition to benefits on sexual function, identification and treatment of hypogonadal men with testosterone could improve other symptoms of hypogonadism and protect against other conditions such as osteoporosis.

As you can see, the entire workout is only 20 minutes. Twenty minutes! That really is a beautiful thing. And within those 20 minutes, 75 percent of that time is warming up, recovering or cooling down. You're really only working out intensely for four minutes. It's hard to believe if you have never done this that you can actually get that much benefit from four minutes of exercise. That's all it is.
My favorite overall tool to manage stress is EFT (Emotional Freedom Technique), which is like acupuncture without the needles. It's a handy, free tool for unloading emotional baggage quickly and painlessly, and so easy that even children can learn it. Other common stress-reduction tools with a high success rate include prayer, meditation, laughter and yoga, for example. Learning relaxation skills, such as deep breathing and positive visualization, which is the "language" of the subconscious.

Saw palmetto: Uses, dosage, and side effects Saw palmetto is an extract from the berries of a type of palm tree. The berries have traditionally been used to ease urinary and reproductive problems. The extract is now used in herbal remedies to stabilize testosterone. Learn about its use, its effectiveness, the science behind the claims, and any side effects. Read now