"Some say it's just a part of aging, but that's a misconception," says Jason Hedges, MD, PhD, a urologist at Oregon Health and Science University in Portland. A gradual decline in testosterone can't explain a near-total lack of interest in sex, for example. And for Hedges' patients who are in their 20s, 30s, and early 40s and having erectile problems, other health problems may be a bigger issue than aging.
An international consensus document was recently published and provides guidance on the diagnosis, treatment and monitoring of late-onset hypogonadism (LOH) in men. The diagnosis of LOH requires biochemical and clinical components. Controversy in defining the clinical syndrome continues due to the high prevalence of hypogonadal symptoms in the aging male population and the non-specific nature of these symptoms. Further controversy surrounds setting a lower limit of normal testosterone, the limitations of the commonly available total testosterone result in assessing some patients and the unavailability of reliable measures of bioavailable or free testosterone for general clinical use. As with any clinical intervention testosterone treatment should be judged on a balance of risk versus benefit. The traditional benefits of testosterone on sexual function, mood, strength and quality of life remain the primary goals of treatment but possible beneficial effects on other parameters such as bone density, obesity, insulin resistance and angina are emerging and will be reviewed. Potential concerns regarding the effects of testosterone on prostate disease, aggression and polycythaemia will also be addressed. The options available for treatment have increased in recent years with the availability of a number of testosterone preparations which can reliably produce physiological serum concentrations.
The sex hormone testosterone is far more than just the stuff of the alpha male's swagger. Though it plays a more significant role in the life of the biological male, it is actually present in both sexes to some degree. Despite popular perceptions that testosterone primarily controls aggression and sex drive—although it does play a role in both of those things—research has shown that individual levels of testosterone are also correlated with our language skills and cognitive abilities. Testosterone occurs in the body naturally, but can be administered as a medication, too: its most common uses are in the treatment of hypogonadism and breast cancer, as well as in hormone therapy for transgender men.
Puberty occurs when there is an “awakening” of the hypothalamic-pituitary axis. The hypothalamus increases its secretion of gonadotropin releasing hormone (GnRH) which in turn stimulates the release of luteinizing hormone (LH) and follicle stimulating hormone (FSH). This leads to a significant increase in the production of testicular testosterone and the induction of the well-known secondary sex characteristics associated with puberty: growth spurt, increased libido, increased erectile function, acne, increased body hair, increased muscle mass, deepening of the voice, spermatogenesis, gynecomastia (usually transient).
Up Regulation – Many herbs available in natural test boosters function as testosterone up regulators or promoters. These function by use of specific natural compounds inside the herb, which once inside the body can naturally signal your DNA to express greater testosterone production. There is a variety of herbs that do this, and by signaling different ‘zones’ in your DNA. In addition, some many work better than others for different people due to variation in the genetic code between different people.
Sweet potatoes, white potatoes, russets, red potatoes, purple potatoes, etc. If it’s a potato, you should be eating it. Potatoes are excellent no-gluten source of testosterone boosting carbohydrates, and also very dense in nutrients. Stock pile your pantry full of them, and make potatoes your main carbohydrate source. Heck, if you can find potato chips that haven’t been laden with polyunsaturated fats, go for those too.
Dr. Anawalt called the diagnosis and treatment of low testosterone a careful balancing act. "You don't want to leave the impression that no one is at risk for low testosterone," he said. He explained that physicians need to be aware that men coming in with low libido, sexual function, osteoporosis, or new breast sensitivity might well have low testosterone. Besides measuring testosterone— usually two or even three times—confirmatory tests will also measure other hormones that regulate testosterone and sperm production in the testicle. "If they don't have that evidence," said Dr. Anawalt, "we will tell a man we don't think you're suffering from the effects of low testosterone."
A large number of trials have demonstrated a positive effect of testosterone treatment on bone mineral density (Katznelson et al 1996; Behre et al 1997; Leifke et al 1998; Snyder et al 2000; Zacharin et al 2003; Wang, Cunningham et al 2004; Aminorroaya et al 2005; Benito et al 2005) and bone architecture (Benito et al 2005). These effects are often more impressive in longer trials, which have shown that adequate replacement will lead to near normal bone density but that the full effects may take two years or more (Snyder et al 2000; Wang, Cunningham et al 2004; Aminorroaya et al 2005). Three randomized placebo-controlled trials of testosterone treatment in aging males have been conducted (Snyder et al 1999; Kenny et al 2001; Amory et al 2004). One of these studies concerned men with a mean age of 71 years with two serum testosterone levels less than 12.1nmol/l. After 36 months of intramuscular testosterone treatment or placebo, there were significant increases in vertebral and hip bone mineral density. In this study, there was also a significant decrease in the bone resorption marker urinary deoxypyridinoline with testosterone treatment (Amory et al 2004). The second study contained men with low bioavailable testosterone levels and an average age of 76 years. Testosterone treatment in the form of transdermal patches was given for 1 year. During this trial there was a significant preservation of hip bone mineral density with testosterone treatment but testosterone had no effect on bone mineral density at other sites including the vertebrae. There were no significant alterations in bone turnover markers during testosterone treatment (Kenny et al 2001). The remaining study contained men of average age 73 years. Men were eligible for the study if their serum total testosterone levels were less than 16.5 nmol/L, meaning that the study contained men who would usually be considered eugonadal. The beneficial effects of testosterone on bone density were confined to the men who had lower serum testosterone levels at baseline and were seen only in the vertebrae. There were no significant changes in bone turnover markers. Testosterone in the trial was given via scrotal patches for a 36 month duration (Snyder et al 1999). A recent meta-analysis of the effects on bone density of testosterone treatment in men included data from these studies and two other randomized controlled trials. The findings were that testosterone produces a significant increase of 2.7% in the bone mineral density at the lumber spine but no overall change at the hip (Isidori et al 2005). These results from randomized controlled trials in aging men show much smaller benefits of testosterone treatment on bone density than have been seen in other trials. This could be due to the trials including patients who are not hypogonadal and being too short to allow for the maximal effects of testosterone. The meta-analysis also assessed the data concerning changes of bone formation and resorption markers during testosterone treatment. There was a significant decrease in bone resorption markers but no change in markers of bone formation suggesting that reduction of bone resorption may be the primary mode of action of testosterone in improving bone density (Isidori et al 2005).
In non-human primates, it may be that testosterone in puberty stimulates sexual arousal, which allows the primate to increasingly seek out sexual experiences with females and thus creates a sexual preference for females.[39] Some research has also indicated that if testosterone is eliminated in an adult male human or other adult male primate's system, its sexual motivation decreases, but there is no corresponding decrease in ability to engage in sexual activity (mounting, ejaculating, etc.).[39]
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.
In non-human primates, it may be that testosterone in puberty stimulates sexual arousal, which allows the primate to increasingly seek out sexual experiences with females and thus creates a sexual preference for females.[39] Some research has also indicated that if testosterone is eliminated in an adult male human or other adult male primate's system, its sexual motivation decreases, but there is no corresponding decrease in ability to engage in sexual activity (mounting, ejaculating, etc.).[39]
Type 2 diabetes is an important condition in terms of morbidity and mortality, and the prevalence is increasing in the developed and developing world. The prevalence also increases with age. Insulin resistance is a primary pathological feature of type 2 diabetes and predates the onset of diabetes by many years, during which time raised serum insulin levels compensate and maintain normoglycemia. Insulin resistance and/or impaired glucose tolerance are also part of the metabolic syndrome which also comprises an abnormal serum lipid profile, central obesity and hypertension. The metabolic syndrome can be considered to be a pre-diabetic condition and is itself linked to cardiovascular mortality. Table 1 shows the three commonly used definitions of the metabolic syndrome as per WHO, NCEPIII and IDF respectively (WHO 1999; NCEPIII 2001; Zimmet et al 2005).

“I see people who've been doing things in the gym and they've never been told that it can shut off your own production and it can also irreversibly lower your sperm count,” says Roked. “These are all quite serious issues that even though they may be rare if it happened to you it would cause a big impact on your life, so I'd say it's always best to do things with a specialist, but also for anyone it's not a great idea to take things that aren't needed."
That testosterone decreases with age has been clearly established by many studies over many years in several different populations of men (Harman et al 2001; Feldman et al 2002; Araujo et al 2004; Kaufman and Vermeulen 2005). Of even greater significance is the steeper fall of the most biologically active fraction of total testosterone, non-sex hormone binding globulin (SHBG)- bound testosterone, or bioavailable testosterone (bio-T). The classical, but not the only approach to measuring bio-T, is to precipitate out SHBG (and hence the testosterone which is strongly bound to it as well) and measure the remainder as total testosterone (Tremblay 2003). Vermeulen et al (1999) have devised a less tedious and less expensive method of measuring a surrogate for bio-T, namely calculated bio-T, inserting total T, albumin, SHBG and a constant into a mathematical formulation. There is a strong correlation between actual bio-T and calculated bio-T (Emadi-Konjin et al 2003).

Robert Clark aka "The Troglodyte" is a 39 year old father of 3, Author, Fitness Trainer, Nutritional Researcher, Obstacle Course Racer, Avid Trail Runner and CrossFit Warrior. He is dedicated to helping others achieve their fitness goals. His extensive work in the field of natural testosterone elevation, inspired the creation of Alpha Wolf Nutrition where he serves as the Lead Product Researcher.

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!

Visit your doctor if you’re experiencing symptoms for the first time. Low testosterone levels cause similar symptoms to other conditions, so it’s best to get a diagnosis from a doctor. During your appointment, talk to your doctor about any medications you are taking, as well as any recent life changes, as there may be an easy-to-treat underlying cause for your low hormones.[19] Here are the most common symptoms of low testosterone:[20]
Among the changes which occur with aging are those that affect several aspects of the endocrine system which reduces its secretions to varying degrees in different individuals. These reductions in secretions are identified by a poor but widely recognized appellation, the “pauses”: menopause (decreased ovarian function), adrenopause (decreased adrenal function, especially with regard to dehydroepiandrosterone secretion), somatopause (decreased growth hormone production), andropause (decreased hypothalamic-pituitary testicular function with diminished testosterone availability and impaired spermatogenesis) (Lamberts 1997).

Carbs play a big part in determining your Testosterone levels. Let's start with what to avoid. First, research shows that a large serving of sugar (75g of glucose), decreased Testosterone levels by as much as 25%! (25 & 26). I know this is a pretty extreme dosage, but you may want to avoid massive servings of sugar! Also, men who have Metabolic syndrome have lower Testosterone levels (27). Metabolic syndrome is often brought about by chronic high blood sugar which leads to insulin resistance.

“Poor lifestyle can mimic the symptoms of low testosterone and can actually cause low testosterone as well,” says Hodzovic. “The main culprits include lack of sleep, excessive stress, too little or too much exercise and too little or too much body fat. Getting healthy and active and eating a balanced nutritious diet along with enough sleep are the most important things to do.
^ David KG, Dingemanse E, Freud JL (May 1935). "Über krystallinisches mannliches Hormon aus Hoden (Testosteron) wirksamer als aus harn oder aus Cholesterin bereitetes Androsteron" [On crystalline male hormone from testicles (testosterone) effective as from urine or from cholesterol]. Hoppe-Seyler's Z Physiol Chem (in German). 233 (5–6): 281–83. doi:10.1515/bchm2.1935.233.5-6.281.

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.
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.
“Poor lifestyle can mimic the symptoms of low testosterone and can actually cause low testosterone as well,” says Hodzovic. “The main culprits include lack of sleep, excessive stress, too little or too much exercise and too little or too much body fat. Getting healthy and active and eating a balanced nutritious diet along with enough sleep are the most important things to do.
There are three categories of healthy fat. Number one is healthy saturated fat. The truth about saturated fat is it’s actually good for you if it’s the proper kind. Healthy saturated fat is found in coconut oil and raw, fermented dairy products like goat milk kefir, yogurt, or raw goat or sheep milk cheese. However, avoid conventional dairy because it will actually damper your testosterone.
There are positive correlations between positive orgasm experience in women and testosterone levels where relaxation was a key perception of the experience. There is no correlation between testosterone and men's perceptions of their orgasm experience, and also no correlation between higher testosterone levels and greater sexual assertiveness in either sex.[34]

Experts have also found that fertile men have a lot of D-aspartic acid. D-aspartic acid is a complex amino acid linked with virility not found commonly. Oysters not only hold a good dose of D-aspartic acid but also has N-methyl-D-aspartate. N-methyl-D-aspartate sparks the production of sex hormones. Eating daily oysters has shown to be raising testosterone levels a lot in as little as six weeks.
Testosterone is an important enzyme that is most often associated with the process of puberty. However, both men and women have testosterone, and it is responsible for more than just transforming boys into men. Testosterone is also involved in maintaining bone density and regulating the levels of your red blood cells. Testosterone has also been shown to have a positive effect on muscle protein synthesis, essentially meaning that more testosterone can result in bigger muscles.

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.


The second theory is similar and is known as "evolutionary neuroandrogenic (ENA) theory of male aggression".[78][79] Testosterone and other androgens have evolved to masculinize a brain in order to be competitive even to the point of risking harm to the person and others. By doing so, individuals with masculinized brains as a result of pre-natal and adult life testosterone and androgens enhance their resource acquiring abilities in order to survive, attract and copulate with mates as much as possible.[78] The masculinization of the brain is not just mediated by testosterone levels at the adult stage, but also testosterone exposure in the womb as a fetus. Higher pre-natal testosterone indicated by a low digit ratio as well as adult testosterone levels increased risk of fouls or aggression among male players in a soccer game.[80] Studies have also found higher pre-natal testosterone or lower digit ratio to be correlated with higher aggression in males.[81][82][83][84][85]
Bhatia et al (2006) studied 70 male patients with type2 diabetes mellitus (age range 24–78 years). Thirty-seven subjects were found to have hypogonadism based on a calculated free testosterone level of less than 6.5 μg/dl. The hypogonadal group had a statistically significant lower hematocrit. Anemia was observed in 23% of the patients (16 out of 70). In 14 of 15 anemic patients calculated free testosterone was low.

This paper will aim to review the current evidence of clinical effects of testosterone treatment within an aging male population. As with any other clinical intervention a decision to treat patients with testosterone requires a balance of risk versus benefit. We shall try to facilitate this by examining the effects of testosterone on the various symptoms and organs involved.
The chemical synthesis of testosterone from cholesterol was achieved in August that year by Butenandt and Hanisch.[183] Only a week later, the Ciba group in Zurich, Leopold Ruzicka (1887–1976) and A. Wettstein, published their synthesis of testosterone.[184] These independent partial syntheses of testosterone from a cholesterol base earned both Butenandt and Ruzicka the joint 1939 Nobel Prize in Chemistry.[182][185] Testosterone was identified as 17β-hydroxyandrost-4-en-3-one (C19H28O2), a solid polycyclic alcohol with a hydroxyl group at the 17th carbon atom. This also made it obvious that additional modifications on the synthesized testosterone could be made, i.e., esterification and alkylation.
Testosterone boosters are supplementary substances that can be used for the purpose of increasing testosterone levels in the blood. This study aimed to evaluate the side effects and health risks of testosterone boosters among athletes. A sportsman came to the King Saud Hospital, Unaizah, Qassim, Saudi Arabia, suffering from abdominal pain. The attending doctor requested general laboratory tests. He admitted to having consumed two courses of a testosterone booster over a period of 42 days following the instructions of the manufacturer. In total, the athlete in question consumed several courses, twice before the abdominal pain started and twice after it subsided. The blood tests and reports suggested that the commercial product consumed might negatively affect several hepatic functions and resulted in slightly increased testosterone concentrations after the fourth course. In conclusion, administration of testosterone booster products, although obtained from trusted sources, may still present some health risks. Further studies with large sample size and for a long period need to be done to confirm the current findings.
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.
This being my initial use of product I do find an overall improvement in mind and body "maleness" related to focused goal and strength improvements. Has it turned me into a super stud..no, but at a recent 60th birthday, increased desire has added to performance and that is what I was looking for.I have reinstated diet and exercise that also has made physical and mental health achievements Will finish current bottle, and evaluate overall products worth once completed. Further evaluation pending...
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Some of these signs and symptoms can be caused by various underlying factors, including medication side effects, obstructive sleep apnea, thyroid problems, diabetes and depression. It's also possible that these conditions may be the cause of low testosterone levels, and treatment of these problems may cause testosterone levels to rise. A blood test is the only way to diagnose a low testosterone level.
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