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What is Testosterone
Testosterone and Testosterone Supplements

Testosterone and Testosterone Supplements

What is testosterone? 
What is Testosterone? Testosterone is a steroid hormone from the androgen group and is found in mammals, reptiles, birds, and other vertebrates. Almost everything has testosterone. In mammals, testosterone is secreted primarily in the testicles of males and the ovaries of females, although small amounts are also secreted by the adrenal glands. It is the principal male sex hormone and an anabolic steroid.
In men, testosterone plays a key role in the development of male reproductive tissues such as the testis and prostate as well as promoting secondary sexual characteristics such as increased muscle, bone mass, and the growth of body hair. In addition, testosterone is essential for health and well-being as well as the prevention of osteoporosis
On average, in adult males, levels of testosterone are about 7–8 times as great as in adult females, but, as the metabolic consumption of testosterone in males is greater, the daily production is about 20 times greater in men. Females are also more sensitive to the hormone. Testosterone is observed in most vertebrates. Fish make a slightly different form called 11-ketotestosterone. Its counterpart in insects is ecdysone. These ubiquitous steroids suggest that sex hormones have an ancient evolutionary history. 
In general, androgens promote protein synthesis and growth of those tissues with androgen receptors. Testosterone effects can be classified as virilizing and anabolic, though the distinction is somewhat artificial, as many of the effects can be considered both.
  1. Anabolic effects include growth of muscle mass and strength, increased bone density and strength, and stimulation of linear growth and bone maturation. Anabolism is the set of metabolic pathways that construct molecules from smaller units. These reactions require energy. One way of categorizing metabolic processes, whether at the cellular, organ or organism level is as "anabolic" or as "catabolic", which is the opposite. Anabolism is powered by catabolism, where large molecules are broken down into smaller parts and then used up in respiration. Many anabolic processes are powered by the hydrolysis of adenosine triphosphate (ATP). 
Anabolic processes tend toward "building up" organs and tissues. These processes produce growth and differentiation of cells and increase in body size, a process that involves synthesis of complex molecules. Examples of anabolic processes include the growth and mineralization of bone and increases in muscle mass. 
Endocrinologists have traditionally classified hormones as anabolic or catabolic, depending on which part of metabolism they stimulate. The classic anabolic hormones are the anabolic steroids, which stimulate protein synthesis and muscle growth, and insulin. The balance between anabolism and catabolism is also regulated by circadian rhythms, with processes such as glucose metabolism fluctuating to match an animal's normal periods of activity throughout the day. 
  1. Androgenic effects include maturation of the sex organs, particularly the penis and the formation of the scrotum in the fetus, and after birth (usually at puberty) a deepening of the voice, growth of the beard and axillary hair. Many of these fall into the category of male secondary sex characteristics
Androgen, also called androgenic hormone or testoid, is the broad term for any natural or synthetic compound, usually a steroid hormone, that stimulates or controls the development and maintenance of male characteristics in vertebrates by binding to androgen receptors. This includes the activity of the accessory male sex organs and development of male secondary sex characteristics. Androgens were first discovered in 1936. Androgens are also the original anabolic steroids and the precursor of all estrogens. The primary and most well-known androgen is testosterone. Dihydrotestosterone (DHT) and androstenedione are less known generally, but are of equal importance in male development. DHT in the embryo life causes differentiation of penis, scrotum and prostate. Later in life DHT contributes to male balding, prostate growth and sebaceous gland activity.
What testosterone effects? 
Testosterone effects can also be classified by the age of usual occurrence. For postnatal effects in both males and females, these are mostly dependent on the levels and duration of circulating free testosterone.
What is testosterone in adults?
Adult testosterone effects are more clearly demonstrable in males than in females, but are likely important to both sexes. Some of these effects may decline as testosterone levels decrease in the later decades of adult life.
What is Testosterone and sexual arousal?
Testosterone and sexual arousal. It has been found that 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). 
Testosterone levels follow a nyctohemeral rhythm that peaks early each day, regardless of sexual activity. 
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. 
An increase in testosterone levels has also been found to occur in both men and women who have masturbation-induced orgasms. 
What is Male sexual arousal?
Male sexual arousal. Higher levels of testosterone were associated with periods of sexual activity within subjects, but between subjects testosterone levels were higher for less sexually active individuals. Men who have sexual encounters with unfamiliar or multiple partners experience large increases of testosterone the morning after. 
Men who watch a sexually explicit movie have an average increase of 35% in testosterone, peaking at 60–90 minutes after the end of the film, but no increase is seen in men who watch sexually neutral films. Men who watch sexually explicit films also report increased optimism and decreased exhaustion. Previous research has found a link between relaxation following sexual arousal and testosterone levels. 
A 2002 study found that testosterone increased in heterosexual men after having had a brief conversation with a woman, and stayed the same after a conversation with a man. The increase in testosterone levels was associated with the degree that the women thought the men were trying to impress them. 
Men's levels of testosterone, a hormone known to affect men's mating behaviour, changes depending on whether they are exposed to an ovulating or nonovulating woman's body odour. Men who are exposed to scents of ovulating women maintained a stable testosterone level that was higher than the testosterone level of men exposed to nonovulation cues. Testosterone levels and sexual arousal in men are heavily aware of hormone cycles in females. This may be linked to the ovulatory shift hypothesis, where males are adapted to respond to the ovulation cycles of females by sensing when they are most fertile and whereby females look for preferred male mates when they are the most fertile; both actions may be driven by hormones.
In a 1991 study, males were exposed to either visual or auditory erotic stimuli and asked to complete a cognitive task, where the number of errors on the task indicated how distracted the participant was by the stimuli. It concluded that men with lower thresholds for sexual arousal have a greater likelihood to attend to sexual information and that testosterone may have an impact by enhancing their attention to the relevant stimuli. 
Sperm competition theory: Testosterone levels are shown to increase as a response to previously neutral stimuli when conditioned to become sexual in male rats. This reaction engages penile reflexes (such as erection and ejaculation) that aid in sperm competition when more than one male is present in mating encounters, allowing for more production of successful sperm and a higher chance of reproduction.
Female sexual arousal
Androgens may modulate the physiology of vaginal tissue and contribute to female genital sexual arousal. Women's level of testosterone is higher when measured pre-intercourse vs pre-cuddling, as well as post-intercourse vs post-cuddling. There is a time lag effect when testosterone is administered, on genital arousal in women. In addition, a continuous increase in vaginal sexual arousal may result in higher genital sensations and sexual appetitive behaviors. 
When females have a higher baseline level of testosterone, they have higher increases in sexual arousal levels but smaller increases in testosterone, indicating a ceiling effect on testosterone levels in females. Sexual thoughts also change the level of testosterone but not level of cortisol in the female body, and hormonal contraceptives may have an impact on the variation in testosterone response to sexual thoughts. 
Testosterone may prove to be an effective treatment in female sexual arousal disorders. Currently there is no FDA approved androgen preparation for the treatment of androgen insufficiency, however it has been used off-label to treat low libido and sexual dysfunction in older women. Testosterone may be a treatment for postmenopausal women as long as they are effectively estrogenized. 
Several hormones affect sexual arousal, including testosterone, cortisol, and estradiol. However, the specific roles of these hormones are not clear.  Testosterone is the most commonly studied hormone involved with sexuality. It plays a key role in sexual arousal in males, with strong effects on central arousal mechanisms. The connection between testosterone and sexual arousal is more complex in females. Research has found testosterone levels increase as a result of sexual cognitions in females that do not use hormonal contraception. Also, women who participate in polyandrous relationships have higher levels of testosterone. However, it is unclear whether higher levels of testosterone cause increased arousal and in turn multiple partners or whether sexual activity with multiple partners cause the increase in testosterone. Inconsistent study results point to the idea that while testosterone may play a role in the sexuality of some women, its effects can be obscured by the co-existence of psychological or affective factors in others.
As testosterone affects the entire body (often by enlarging; males have bigger hearts, lungs, liver, etc.), the brain is also affected by this "sexual" differentiation; the enzyme aromatase converts testosterone into estradiol that is responsible for masculinization of the brain in male mice. In humans, masculinization of the fetal brain appears, by observation of gender preference in patients with congenital diseases of androgen formation or androgen receptor function, to be associated with functional androgen receptors. 
There are some differences between a male and female brain (possibly the result of different testosterone levels), one of them being size: the male human brain is, on average, larger. In a Danish study from 2003, men were found to have a total myelinated fiber length of 176,000 km at the age of 20, whereas in women the total length was 149,000 km (approx. 15% less). 
A study conducted in 1996 found no immediate short term effects on mood or behavior from the administration of supraphysiologic doses of testosterone for 10 weeks on 43 healthy men. Another study found a correlation between testosterone and risk tolerance in career choice among women. 
The literature suggests that attention, memory, and spatial ability are key cognitive functions affected by testosterone in humans. Preliminary evidence suggests that low testosterone levels may be a risk factor for cognitive decline and possibly for dementia of the Alzheimer's type, a key argument in life extension medicine for the use of testosterone in anti-aging therapies. Much of the literature, however, suggests a curvilinear or even quadratic relationship between spatial performance and circulating testosterone, where both hypo- and hypersecretion (deficient- and excessive-secretion) of circulating androgens have negative effects on cognition.
Medical uses
What is testosterone replacement therapy (TRT)?
The original and primary use of testosterone is for the treatment of males with too little or no natural endogenous testosterone production—males with hypogonadism. Appropriate use for this purpose is legitimate hormone replacement therapy (testosterone replacement therapy [TRT]), which maintains serum testosterone levels in the normal range.
Testosterone has also been given for many other conditions and purposes besides replacement. Examples include reducing infertility, correcting lack of libido or erectile dysfunction, correcting osteoporosis, encouraging penile enlargement, encouraging height growth, encouraging bone marrow stimulation and reversing the effects of anemia, and even appetite stimulation. By the late 1940s, testosterone was being touted as an anti-aging wonder drug. Decline of testosterone production with age has led to interest in androgen replacement therapy
To take advantage of its virilizing effects, testosterone is often administered to transsexual men as part of the hormone replacement therapy, with a "target level" of the normal male testosterone level. Likewise, transsexual women are sometimes prescribed anti-androgens to decrease the level of testosterone in the body and allow for the effects of estrogen to develop.
Testosterone patches are effective at treating low libido in post-menopausal women. Low libido may also occur as a symptom or outcome of hormonal contraceptive use. Women may also use testosterone therapies to treat or prevent loss of bone density and muscle mass and to treat certain kinds of depression and low energy state. Women on testosterone therapies may experience an increase in body weight without an increase in body fat due to changes in bone and muscle density. The undesired effects of testosterone therapy in women are typically controlled with symptomatic treatments, such as hair removal and topical acne therapy. There is a theoretical risk that testosterone therapy increases the risk of breast or gynaecological cancers, and further research is needed to define any such risks more clearly. 
Appropriate testosterone therapy may improve the management of type 2 diabetes. Low testosterone has been associated with the development of Alzheimer's disease. A small trial in 2005 showed mixed results in using testosterone to combat the effects of aging. 
Large-scale trials to assess the effectiveness and long-term safety of testosterone are still lacking. 
Hormone replacement therapy
Testosterone levels decline gradually with age in human beings. The clinical significance of this decrease is debated (see andropause). There is disagreement about when to treat aging men with testosterone replacement therapy. The American Society of Andrology's position is that "testosterone replacement therapy in aging men is indicated when both clinical symptoms and signs suggestive of androgen deficiency and decreased testosterone levels are present." The American Association of Clinical Endocrinologists says "Hypogonadism is defined as a free testosterone level that is below the lower limit of normal for young adult control subjects. Previously, age-related decreases in free testosterone were once accepted as normal. Currently, they are not considered normal. Patients with borderline testosterone levels warrant a clinical trial of testosterone." 
There is not total agreement on the threshold of testosterone value below which a man would be considered hypogonadal. (Currently, there are no standards as to when to treat women.) Testosterone can be measured as "free" (that is, bioavailable and unbound) or, more commonly, "total" (including the percentage that is chemically bound and unavailable). In the United States, male total testosterone levels below 300 ng/dL from a morning serum sample are generally considered low. Identification of inadequate testosterone in an aging male by symptoms alone can be difficult.
Adverse effects of testosterone supplementation include minor side-effects such as acne and oily skin, and more significant complications such as increased hematocrit, which can require venipuncture in order to treat, exacerbation of sleep apnea and acceleration of pre-existing prostate cancer growth in individuals having undergone androgen deprivation. Another adverse effect may be significant hair loss and/or thinning of the hair. This may be prevented with 5-alpha reductase inhibitors ordinarily used for the treatment of benign prostatic hyperplasia such as finasteride or dutasteride. Exogenous testosterone also causes suppression of spermatogenesis and can lead to infertility. 
Further information: Hypogonadism
Testosterone insufficiency (also termed hypotestosteronism or hypotestosteronemia) is an abnormally low testosterone production. It may occur because of testicular dysfunction (primary hypogonadism) or hypothalamic-pituitary dysfunction (secondary hypogonadism) and may be congenital or acquired. An acquired form of hypotestosteronism is the decline in testosterone levels that occurs by aging, sometimes called "andropause" in men, as a comparison to the decline in estrogen that comes with menopause in women. In Western countries, average testosterone levels are receding in men of all ages. Several theories, from increases in obesity, to exposure to endocrine disruptors have been proposed as an explanation for this reduction. 
Testosterone can be used by an athlete in order to improve performance, but it is considered to be a form of doping in most sports. There are several application methods for testosterone, including intramuscular injections, transdermal gels and patches, and implantable pellets. Supplement of the hormone results in lower metabolic production via the Farquharson phenomenon, creating long-term dependence for improved performance level. 
Anabolic steroids (including testosterone) have also been taken to enhance muscle development, strength, or endurance. They do so directly by increasing the muscles' protein synthesis. As a result, muscle fibers become larger and repair faster than the average person's. After a series of scandals and publicity in the 1980s (such as Ben Johnson's improved performance at the 1988 Summer Olympics), prohibitions of anabolic steroid use were renewed or strengthened by many sports organizations. Testosterone and other anabolic steroids were designated a "controlled substance" by the United States Congress in 1990, with the Anabolic Steroid Control Act. The use is seen as being a seriously problematic issue in modern sport, particularly given the lengths to which athletes and professional laboratories go to in trying to conceal such abuse from sports regulators. Steroid abuse once again came into the spotlight recently as a result of the Chris Benoit double murder-suicide in 2007, however, there has been no evidence indicating steroid use as a contributing factor. 
Detection of abuse
A number of methods for detecting testosterone use by athletes have been employed, most based on a urine test. These include the testosterone/epitestosterone ratio (normally less than 6), the testosterone/luteinizing hormone ratio and the carbon-13 / carbon-12 ratio (pharmaceutical testosterone contains less carbon-13 than endogenous testosterone). In some testing programs, an individual's own historical results may serve as a reference interval for interpretation of a suspicious finding. Another approach being investigated is the detection of the administered form of testosterone, usually an ester, in hair. 
Mechanism of action
The effects of testosterone in humans and other vertebrates occur by way of two main mechanisms: by activation of the androgen receptor (directly or as DHT), and by conversion to estradiol and activation of certain estrogen receptors
Free testosterone (T) is transported into the cytoplasm of target tissue cells, where it can bind to the androgen receptor, or can be reduced to 5α-dihydrotestosterone (DHT) by the cytoplasmic enzyme 5-alpha reductase. DHT binds to the same androgen receptor even more strongly than testosterone, so that its androgenic potency is about 5 times that of T. The T-receptor or DHT-receptor complex undergoes a structural change that allows it to move into the cell nucleus and bind directly to specific nucleotide sequences of the chromosomal DNA. The areas of binding are called hormone response elements (HREs), and influence transcriptional activity of certain genes, producing the androgen effects.
Androgen receptors occur in many different vertebrate body system tissues, and both males and females respond similarly to similar levels. Greatly differing amounts of testosterone prenatally, at puberty, and throughout life account for a share of biological differences between males and females.
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). 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. 
What are the best pills for testosterone?
What is the best testosterone Gel or Cream?
How to increase testosterone? How do I increase my testosterone naturally?
If you're looking for ways to increase testosterone, then we don't need to tell you about the benefits. Maybe you've tried a testosterone pill and know how you feel when levels are high - more energy, increased focus, improved mood, and a wicked sex drive. Unfortunately, most men begin to notice low testosterone as they grow older, sometimes even in their twenties! Low testosterone is associated with worse moods, lower sex drive, and less ambition. Testosterone has so many benefits it would be ignorant to ignore it. Especially if fitness is a priority, a top concern should be to increase testosterone.
Unfortunately, many men think that the only ways to increase testosterone are through steroids or testosterone replacement therapy that have harmful effects. However, by simply making some small changes in their diet, lifestyle, and vitamin supplementation, men can optimize their testosterone levels.
Here are some ways to naturally increase your testosterone without using steroids or using harmful testosterone replacement therapy.
  1. Take fish oil regularly. Not only does it increase testosterone, but it cuts your chances of a heart attack in half, improves the condition of your skin and hair, promotes fat loss, improves recovery time after exercise, and aids your joints. 
  2. Eat eggs, nuts, olive oil, and garlic. These three things are easy to implement in your diet. Nuts and garlic are also a very good way to increase testosterone, as they contain healthy fats that are required for its production. Garlic contains a compound called allicin, which is great for testosterone. 
  1. Supplements with Zinc, Fenugreek Extract, Vitamin D, Eucommia Ulmoides Bark Extract, Calcium D Glucarate, Diindolymethane (DIM), Urtica Dioica Extract, Apigenin, MCP (Modified Citrus Pectin)*, Cordyceps* (Grown Wild In Tibet), Milk Thistle Extract*, Rhodiola Rosea Extract, Brown Rice Extract.   
Zinc is absolutely necessary to maintain and increase testosterone, and unfortunately many of us are deficient. Zinc also inhibits something called the aromatase enzyme, which converts testosterone to estrogen. All in all, zinc is a very powerful element. It's even better to take ZMA, which is zinc combined with magnesium. You can find ZMA at most health food stores.
Vitamin D, a steroid hormone, is essential for the healthy development of the nucleus of the sperm cell, and helps maintain semen quality and sperm count. Vitamin D also increases levels of testosterone, which may boost libido. In one study, overweight men who were given vitamin D supplements had a significant increase in testosterone levels after one year. Vitamin D deficiency is currently at epidemic proportions in the United States and many other regions around the world, largely because people do not spend enough time in the sun to facilitate this important process of vitamin D production.
So the first step to ensuring you are receiving all the benefits of vitamin D is to find out what your levels are using a 25(OH)D test, also called 25-hydroxyvitamin D.
To get your levels into the healthy range, sun exposure is the BEST way to optimize your vitamin D levels; exposing a large amount of your skin until it turns the lightest shade of pink, as near to solar noon as possible, is typically necessary to achieve adequate vitamin D production. If sun exposure is not an option, a safe tanning bed (with electronic ballasts rather than magnetic ballasts, to avoid unnecessary exposure to EMF fields) can be used.
  1. Broccoli and green vegetables. Broccoli is important to our testosterone levels because it, like zinc, inhibits the conversion of testosterone to estrogen. What use is it to increase testosterone if our bodies are just going to turn it into its opposite!
  1. Get in shape. Your muscle to fat ratio has a significant effect on your testosterone levels. Basically, you want more muscle and less fat. By following these tips, you will notice an increase in testosterone naturally, but when you add in regular exercise, it will have quite an impact.
1.   Lose Weight
If you're overweight, shedding the excess pounds may increase your testosterone levels, according to research presented at the Endocrine Society's 2012 meeting. Overweight men are more likely to have low testosterone levels to begin with, so this is an important trick to increase your body's testosterone production when you need it most.
If you are serious about losing weight, you have got to strictly limit the amount of processed sugar in your diet, as evidence is mounting that excess sugar, and fructose in particular, is the primary driving factor in the obesity epidemic. So cutting soda from your diet is essential, as is limiting fructose found in processed foods, fruit juice, excessive fruit and so-called "healthy" sweeteners like agave.
Ideally you should keep your total fructose consumption below 25 grams per day and this includes fruits. This is especially true if you have insulin resistance and are overweight, have high blood pressure, diabetes or high cholesterol.
In addition to eliminating or severely limiting fructose, it will be vital to eliminate all grains and milk (even raw) in your diet. Milk has a sugar called lactose, which has been shown to increase insulin resistance so it will be wise to avoid it if you are seeking to lose weight. 
Refined carbohydrates like breakfast cereals, bagels, waffles, pretzels, and most other processed foods also quickly break down to sugar, increase your insulin levels, and cause insulin resistance, which is the number one underlying factor of nearly every chronic disease and condition known to man, including weight gain.
As you cut these dietary troublemakers from your meals, you need to replace them with healthy substitutes like vegetables and healthy fats (including natural saturated fats!). Your body prefers the carbohydrates in micronutrient-dense vegetables rather than grains and sugars because it slows the conversion to simple sugars like glucose, and decreases your insulin level. When you cut grains and sugar from your meals, you typically will need to radically increase the amount of vegetables you eat, as well as make sure you are also consuming protein and healthy fats regularly.
I've detailed a step-by-step guide to this type of healthy eating program in my comprehensive nutrition plan, and I urge you to consult this guide if you are trying to lose weight.
The foods you choose to eat will be the driving force behind successfully achieving your weight loss goals -- high-intensity, short-burst-type exercises, such as my Peak Fitness Program, two to three times per week, combined with a comprehensive fitness plan, is important too, and has an additional benefit as well (see below)!
2.   High-Intensity Exercise like Peak Fitness (Especially Combined with Intermittent Fasting)
Both intermittent fasting and short intense exercise have been shown to boost testosterone. Short intense exercise has a proven positive effect on increasing testosterone levels and preventing its decline. That's unlike aerobics or prolonged moderate exercise, which have shown to have negative or no effect on testosterone levels.
Intermittent fasting boosts testosterone by increasing the expression of satiety hormones including insulin, leptin, adiponectin, glucagon-like peptide-1 (GLP-1), colecystokinin (CKK) and melanocortins, all of which are known to potentiate healthy testosterone actions, increase libido and prevent age-related testosterone decline. 
Having a whey protein meal after exercise can further enhance the satiety/testosterone-boosting impact (hunger hormones cause the opposite effect on your testosterone and libido). Here's a summary of what a typical high-intensity Peak Fitness routine might look like:
  • Warm up for three minutes 
  • Exercise as hard and fast as you can for 30 seconds. You should feel like you couldn't possibly go on another few seconds 
  • Recover at a slow to moderate pace for 90 seconds 
  • Repeat the high intensity exercise and recovery 7 more times 
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.
Keep in mind that you can use virtually any type of equipment you want for this – an elliptical machine, a treadmill, swimming, even sprinting outdoors (although you will need to do this very carefully to avoid injury) -- as long as you're pushing yourself as hard as you can for 30 seconds. But do be sure to stretch properly and start slowly to avoid injury. Start with two or three repetitions and work your way up, don't expect to do all eight repetitions the first time you try this, especially if you are out of shape.
You can find more information about this in an article previously written on intermittent fasting.
3.   Consume Plenty of Zinc
The mineral zinc is important for testosterone production, and supplementing your diet for as little as six weeks has been shown to cause a marked improvement in testosterone among men with low levels. Likewise, research has shown that restricting dietary sources of zinc leads to a significant decrease in testosterone, while zinc supplementation increases it-- and even protects men from exercised-induced reductions in testosterone levels.
It's estimated that up to 45 percent of adults over the age of 60 may have lower than recommended zinc intakes; even when dietary supplements were added in, an estimated 20-25 percent of older adults still had inadequate zinc intakes, according to a National Health and Nutrition Examination Survey.
Your diet is the best source of zinc; along with protein-rich foods like meats and fish, other good dietary sources of zinc include raw milk, raw cheese, beans, and yogurt or kefir made from raw milk. It can be difficult to obtain enough dietary zinc if you're a vegetarian, and also for meat-eaters as well, largely because of conventional farming methods that rely heavily on chemical fertilizers and pesticides. These chemicals deplete the soil of nutrients ... nutrients like zinc that must be absorbed by plants in order to be passed on to you.
In many cases, you may further deplete the nutrients in your food by the way you prepare it. For most food, cooking it will drastically reduce its levels of nutrients like zinc … particularly over-cooking, which many people do.
If you decide to use a zinc supplement, stick to a dosage of less than 40 mg a day, as this is the recommended adult upper limit. Taking too much zinc can interfere with your body's ability to absorb other minerals, especially copper, and may cause nausea as a side effect.
4.   Strength Training
In addition to Peak Fitness, strength training is also known to boost testosterone levels, provided you are doing so intensely enough. When strength training to boost testosterone, you'll want to increase the weight and lower your number of reps, and then focus on exercises that work a large number of muscles, such as dead lifts or squats. 
You can "turbo-charge" your weight training by going slower. By slowing down your movement, you're actually turning it into a high-intensity exercise. Super slow movement allows your muscle, at the microscopic level, to access the maximum number of cross-bridges between the protein filaments that produce movement in the muscle. 
6.   Reduce Stress
When you're under a lot of stress, your body releases high levels of the stress hormone cortisol. This hormone actually blocks the effects of testosterone,  presumably because, from a biological standpoint, testosterone-associated behaviors (mating, competing, aggression) may have lowered your chances of survival in an emergency (hence, the "fight or flight" response is dominant, courtesy of cortisol).
In the modern world, chronic stress, and subsequently elevated levels of cortisol, could mean that testosterone's effects are blocked in the long term, which is what you want to avoid. 
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.
When you create a visual image of how you'd like to feel, your subconscious will understand and begin to help you by making the needed biochemical and neurological changes.
7.   Limit or Eliminate Sugar from Your Diet
Testosterone levels decrease after you eat sugar, which is likely because the sugar leads to a high insulin level, another factor leading to low testosterone.
Based on USDA estimates, the average American consumes 12 teaspoons of sugar a day, which equates to about TWO TONS of sugar during a lifetime.
Why we eat this much sugar is not difficult to understand -- it tastes good, and it gives us pleasure by triggering an innate process in your brain via dopamine and opioid signals.
What it is doing to us on both a physical and emotional level is another story entirely, and most people stand to reap major improvements in their health by cutting back on, or eliminating, sugar altogether from their diets. Remember foods that contain added sugar and fructose, as well as grains like bread and pasta, should all be limited.
If you're struggling with sugar addiction and having trouble dealing with cravings, I highly recommend trying an energy psychology technique called Turbo Tapping, which has helped many "soda addicts" kick their sweet habit, and it should work for any type of sweet craving you may have.
8.   Eat Healthy Fats
By healthy, this means not only mon- and polyunsaturated fats, like that found in avocadoes and nuts, but also saturated, as these are essential for building testosterone. Research shows that a diet with less than 40 percent of energy as fat (and that mainly from animal sources, i.e. saturated) lead to a decrease in testosterone levels.
My personal diet is about 60-70 percent healthy fat, and other experts agree that the ideal diet includes somewhere between 50-70 percent fat. 
It's important to understand that your body requires saturated fats from animal and vegetable sources (such as meat, dairy, certain oils, and tropical plants like coconut) for optimal functioning, and if you neglect this important food group in favor of sugar, grains and other starchy carbs, your health and weight are almost guaranteed to suffer. Examples of healthy fats you can eat more of to give your testosterone levels a boost include:
Boost Your Intake of Branch Chain Amino Acids (BCAA) from Foods Like Whey Protein
Research suggests that BCAAs result in higher testosterone levels, particularly when taken along with resistance training.  While BCAAs are available in supplement form, you'll find the highest concentrations of BCAAs like leucine in dairy products – especially quality cheeses and whey protein.
Even when getting leucine from your natural food supply, it's often wasted or used as a building block instead of an anabolic agent. So to create the correct anabolic environment, you need to boost leucine consumption way beyond mere maintenance levels.
That said, keep in mind that using leucine as a free form amino acid can be highly counterproductive as when free form amino acids are artificially administrated, they rapidly enter your circulation while disrupting insulin function, and impairing your body's glycemic control. Food-based leucine is really the ideal form that can benefit your muscles without side effects. 
  1. Cox RM, John-Alder HB (December 2005). "Testosterone has opposite effects on male growth in lizards (Sceloporus spp.) with opposite patterns of sexual size dimorphism". J. Exp. Biol. 208 (Pt 24): 4679–87. doi:10.1242/jeb.01948. PMID 16326949.
  2. Reed WL, Clark ME, Parker PG, Raouf SA, Arguedas N, Monk DS, Snajdr E, Nolan V, Ketterson ED (May 2006). "Physiological effects on demography: a long-term experimental study of testosterone's effects on fitness". Am. Nat. 167 (5): 667–83. doi:10.1086/503054. PMID 16671011. Lay summaryScienceDaily.
    1. Mooradian AD, Morley JE, Korenman SG (February 1987). "Biological actions of androgens". Endocr. Rev. 8 (1): 1–28. doi:10.1210/edrv-8-1-1. PMID 3549275.
  3. Bassil N, Alkaade S, Morley JE (June 2009). "The benefits and risks of testosterone replacement therapy: a review". Ther Clin Risk Manag 5 (3): 427–48. PMC 2701485. PMID 19707253.
  4. Tuck SP, Francis RM (2009). "Testosterone, bone and osteoporosis". Front Horm Res. Frontiers of Hormone Research 37: 123–32. doi:10.1159/000176049. ISBN 978-3-8055-8622-1. PMID 19011293.
  5. Torjesen PA, Sandnes L (March 2004). "Serum testosterone in women as measured by an automated immunoassay and a RIA". Clin. Chem. 50 (3): 678; author reply 678–9. doi:10.1373/clinchem.2003.027565. PMID 14981046.
  6. Southren AL, Gordon GG, Tochimoto S, Pinzon G, Lane DR, Stypulkowski W (May 1967). "Mean plasma concentration, metabolic clearance and basal plasma production rates of testosterone in normal young men and women using a constant infusion procedure: effect of time of day and plasma concentration on the metabolic clearance rate of testosterone". J. Clin. Endocrinol. Metab. 27 (5): 686–94. doi:10.1210/jcem-27-5-686. PMID 6025472.
  7. Southren AL, Tochimoto S, Carmody NC, Isurugi K (November 1965). "Plasma production rates of testosterone in normal adult men and women and in patients with the syndrome of feminizing testes". J. Clin. Endocrinol. Metab. 25 (11): 1441–50. doi:10.1210/jcem-25-11-1441. PMID 5843701.
  8. Dabbs M, Dabbs JM (2000). Heroes, rogues, and lovers: testosterone and behavior. New York: McGraw-Hill. ISBN 0-07-135739-4.
  9. Nelson, Randy F. (2005). An introduction to behavioral endocrinology. Sunderland, Mass: Sinauer Associates. p. 143. ISBN 0-87893-617-3.
  10. De Loof A (October 2006). "Ecdysteroids: the overlooked sex steroids of insects? Males: the black box". Insect Science 13 (5): 325–338. doi:10.1111/j.1744-7917.2006.00101.x.
  11. Mechoulam R, Brueggemeier RW, Denlinger DL (September 1984). "Estrogens in insects". Journal Cellular and Molecular Life Sciences 40 (9): 942–944. doi:10.1007/BF01946450.
    1. Swaab DF, Garcia-Falgueras A (2009). "Sexual differentiation of the human brain in relation to gender identity and sexual orientation". Funct. Neurol. 24 (1): 17–28. PMID 19403051.
  12. Browne KR (2002). Biology at work: rethinking sexual equality. New Brunswick, N.J: Rutgers University Press. p. 112. ISBN 0-8135-3053-9.
  13. Forest MG, Cathiard AM, Bertrand JA (July 1973). "Evidence of testicular activity in early infancy". J. Clin. Endocrinol. Metab. 37 (1): 148–51. doi:10.1210/jcem-37-1-148. PMID 4715291.
  14. Corbier P, Edwards DA, Roffi J (1992). "The neonatal testosterone surge: a comparative study". Arch Int Physiol Biochim Biophys 100 (2): 127–31. doi:10.3109/13813459209035274. PMID 1379488.
  15. Dakin CL, Wilson CA, Kalló I, Coen CW, Davies DC (May 2008). "Neonatal stimulation of 5-HT(2) receptors reduces androgen receptor expression in the rat anteroventral periventricular nucleus and sexually dimorphic preoptic area". Eur. J. Neurosci. 27 (9): 2473–80. doi:10.1111/j.1460-9568.2008.06216.x. PMID 18445234.
  16. Kalat JW (2009). "Reproductive behaviors". Biological psychology. Belmont, Calif: Wadsworth, Cengage Learning. p. 321. ISBN 0-495-60300-7.
    1. Bhasin S, Storer TW, Berman N, Callegari C, Clevenger B, Phillips J, Bunnell TJ, Tricker R, Shirazi A, Casaburi R (July 1996). "The effects of supraphysiologic doses of testosterone on muscle size and strength in normal men". N. Engl. J. Med. 335 (1): 1–7. doi:10.1056/NEJM199607043350101. PMID 8637535.
  17. Mehta PH, Jones AC, Josephs RA (June 2008). "The social endocrinology of dominance: basal testosterone predicts cortisol changes and behavior following victory and defeat". J Pers Soc Psychol 94 (6): 1078–93. doi:10.1037/0022-3514.94.6.1078. PMID 18505319.
  18. Ajayi AA, Halushka PV (May 2005). "Castration reduces platelet thromboxane A2 receptor density and aggregability". QJM 98 (5): 349–56. doi:10.1093/qjmed/hci054. PMID 15820970.
  19. Ajayi AA, Mathur R, Halushka PV (June 1995). "Testosterone increases human platelet thromboxane A2 receptor density and aggregation responses". Circulation 91 (11): 2742–7. doi:10.1161/01.CIR.91.11.2742. PMID 7758179.
  20. Van Anders SM, Watson NV (2006). "Menstrual cycle irregularities are associated with testosterone levels in healthy premenopausal women". Am. J. Hum. Biol. 18 (6): 841–4. doi:10.1002/ajhb.20555. PMID 17039468.
  21. Morgentaler A, Schulman C (2009). "Testosterone and prostate safety". Front Horm Res. Frontiers of Hormone Research 37: 197–203. doi:10.1159/000176054. ISBN 978-3-8055-8622-1. PMID 19011298.
  22. Rhoden, E.L., M.A. Averbeck, and P.E. Teloken (2008). "Androgen replacement in men undergoing treatment for prostate cancer". J Sex Med 5 (9): 2202–8. doi:10.1111/j.1743-6109.2008.00925.x. PMID 18638000.
  23. Morgentaler, A. and A.M. Traish (2009). "Shifting the paradigm of testosterone and prostate cancer: the saturation model and the limits of androgen-dependent growth". Eur Urol 55 (2): 310–20. doi:10.1016/j.eururo.2008.09.024. PMID 18838208.
  24. Haddad RM, Kennedy CC, Caples SM, Tracz MJ, Boloña ER, Sideras K, Uraga MV, Erwin PJ, Montori VM (January 2007). "Testosterone and cardiovascular risk in men: a systematic review and meta-analysis of randomized placebo-controlled trials". Mayo Clin. Proc. 82 (1): 29–39. doi:10.4065/82.1.29. PMID 17285783.
  25. Jones TH, Saad F (April 2009). "The effects of testosterone on risk factors for, and the mediators of, the atherosclerotic process". Atherosclerosis 207 (2): 318–27. doi:10.1016/j.atherosclerosis.2009.04.016. PMID 19464009.
  26. Stanworth RD, Jones TH (2008). "Testosterone for the aging male; current evidence and recommended practice". Clin Interv Aging 3 (1): 25–44. PMC 2544367. PMID 18488876.
  27. Mehta PH, Josephs RA (December 2006). "Testosterone change after losing predicts the decision to compete again". Horm Behav 50 (5): 684–92. doi:10.1016/j.yhbeh.2006.07.001. PMID 16928375.
  28. Booth A, Johnson DR, Granger DA (February 1999). "Testosterone and men's health". J Behav Med 22 (1): 1–19. doi:10.1023/A:1018705001117. PMID 10196726. Lay summaryCNN.
    1. Marazziti D, Canale D (August 2004). "Hormonal changes when falling in love". Psychoneuroendocrinology 29 (7): 931–6. doi:10.1016/j.psyneuen.2003.08.006. PMID 15177709.
  29. Berg SJ, Wynne-Edwards KE (2001). "Changes in testosterone, cortisol, and estradiol levels in men becoming fathers". Mayo Clinic Proceedings 76 (1): 582–592. doi:10.4065/76.6.582.
    1. van Anders SM, Watson NV (July 2006). "Relationship status and testosterone in North American heterosexual and non-heterosexual men and women: cross-sectional and longitudinal data". Psychoneuroendocrinology 31 (6): 715–23. doi:10.1016/j.psyneuen.2006.01.008. PMID 16621328.
    2. Booth A, Dabbs JM (1993). "Testosterone and Men's Marriages". Social Forces 72 (2): 463–477. doi:10.1093/sf/72.2.463.
  30. Mazur A, Michalek J (1998). "Marriage, Divorce, and Male Testosterone". Social Forces 77 (1): 315–330. doi:10.1093/sf/77.1.315.
  31. Gray PB, Chapman JF, Burnham TC, McIntyre MH, Lipson SF, Ellison PT (2004). "Human male pair bonding and testosterone". Human Nature 15 (2): 119–131. doi:10.1007/s12110-004-1016-6.
  32. Gray PB, Campbell BC, Marlowe FW, Lipson SF, Ellison PT (October 2004). "Social variables predict between-subject but not day-to-day variation in the testosterone of US men". Psychoneuroendocrinology 29 (9): 1153–62. doi:10.1016/j.psyneuen.2004.01.008. PMID 15219639.
  33. van Anders SM, Watson NV (February 2007). "Testosterone levels in women and men who are single, in long-distance relationships, or same-city relationships". Horm Behav 51 (2): 286–91. doi:10.1016/j.yhbeh.2006.11.005. PMID 17196592.
  34. Fox CA, Ismail AA, Love DN, Kirkham KE, Loraine JA (January 1972). "Studies on the relationship between plasma testosterone levels and human sexual activity". J. Endocrinol. 52 (1): 51–8. doi:10.1677/joe.0.0520051. PMID 5061159.
  35. van Anders SM, Dunn EJ (August 2009). "Are gonadal steroids linked with orgasm perceptions and sexual assertiveness in women and men?". Horm Behav 56 (2): 206–13. doi:10.1016/j.yhbeh.2009.04.007. PMID 19409392.
  36. Exton MS, Bindert A, Krüger T, Scheller F, Hartmann U, Schedlowski M (1999). "Cardiovascular and endocrine alterations after masturbation-induced orgasm in women". Psychosom Med 61 (3): 280–9. PMID 10367606.
  37. Purvis K, Landgren BM, Cekan Z, Diczfalusy E (September 1976). "Endocrine effects of masturbation in men". J. Endocrinol. 70 (3): 439–44. doi:10.1677/joe.0.0700439. PMID 135817.
  38. Harding SM, Velotta JP (May 2011). "Comparing the relative amount of testosterone required to restore sexual arousal, motivation, and performance in male rats". Horm Behav 59 (5): 666–73. doi:10.1016/j.yhbeh.2010.09.009. PMID 20920505.
  39. James PJ, Nyby JG, Saviolakis GA (September 2006). "Sexually stimulated testosterone release in male mice (Mus musculus): roles of genotype and sexual arousal". Horm Behav 50 (3): 424–31. doi:10.1016/j.yhbeh.2006.05.004. PMID 16828762.
    1. Wallen K (September 2001). "Sex and context: hormones and primate sexual motivation". Horm Behav 40 (2): 339–57. doi:10.1006/hbeh.2001.1696. PMID 11534996.
  40. Kraemer HC, Becker HB, Brodie HK, Doering CH, Moos RH, Hamburg DA (March 1976). "Orgasmic frequency and plasma testosterone levels in normal human males". Arch Sex Behav 5 (2): 125–32. doi:10.1007/BF01541869. PMID 1275688.
  41. Hirschenhauser K, Frigerio D, Grammer K, Magnusson MS (September 2002). "Monthly patterns of testosterone and behavior in prospective fathers". Horm Behav 42 (2): 172–81. doi:10.1006/hbeh.2002.1815. PMID 12367570.
  42. Pirke KM, Kockott G, Dittmar F (November 1974). "Psychosexual stimulation and plasma testosterone in man". Arch Sex Behav 3 (6): 577–84. doi:10.1007/BF01541140. PMID 4429441.
  43. Hellhammer DH, Hubert W, Schürmeyer T (1985). "Changes in saliva testosterone after psychological stimulation in men". Psychoneuroendocrinology 10 (1): 77–81. doi:10.1016/0306-4530(85)90041-1. PMID 4001279.
  44. Rowland DL, Heiman JR, Gladue BA, Hatch JP, Doering CH, Weiler SJ (1987). "Endocrine, psychological and genital response to sexual arousal in men". Psychoneuroendocrinology 12 (2): 149–58. doi:10.1016/0306-4530(87)90045-X. PMID 3602262.
  45. Roney JR, Mahler SV, Maestripieri D (2003). "Behavioral and hormonal responses of men to brief interactions with women". Evolution and Human Behavior 24 (6): 365–375. doi:10.1016/S1090-5138(03)00053-9.
  46. Miller SL, Maner JK (February 2010). "Scent of a woman: men's testosterone responses to olfactory ovulation cues". Psychol Sci 21 (2): 276–83. doi:10.1177/0956797609357733. PMID 20424057.
  47. Gangestead SW, Thornhill R, Garver-Apgar CE (2005). "Adaptations to Ovulation: Implications for Sexual and Social Behavior". Current Directions in Psychological Science 14 (6): 312–316. doi:10.1111/j.0963-7214.2005.00388.x.
  48. Alexander GM, Sherwin BB (September 1991). "The association between testosterone, sexual arousal, and selective attention for erotic stimuli in men". Horm Behav 25 (3): 367–81. doi:10.1016/0018-506X(91)90008-6. PMID 1937428.
  49. Hart BL (December 1983). "Role of testosterone secretion and penile reflexes in sexual behavior and sperm competition in male rats: a theoretical contribution". Physiol. Behav. 31 (6): 823–7. doi:10.1016/0031-9384(83)90279-2. PMID 6665072.
  50. Traish AM, Kim N, Min K, Munarriz R, Goldstein I (April 2002). "Role of androgens in female genital sexual arousal: receptor expression, structure, and function". Fertil. Steril. 77 Suppl 4: S11–8. PMID 12007897.
  51. van Anders SM, Hamilton LD, Schmidt N, Watson NV (April 2007). "Associations between testosterone secretion and sexual activity in women". Horm Behav 51 (4): 477–82. doi:10.1016/j.yhbeh.2007.01.003. PMID 17320881.
  52. Tuiten A, Van Honk J, Koppeschaar H, Bernaards C, Thijssen J, Verbaten R (February 2000). "Time course of effects of testosterone administration on sexual arousal in women". Arch. Gen. Psychiatry 57 (2): 149–53; discussion 155–6. doi:10.1001/archpsyc.57.2.149. PMID 10665617.
  53. Goldey KL, van Anders SM (May 2011). "Sexy thoughts: effects of sexual cognitions on testosterone, cortisol, and arousal in women". Horm Behav 59 (5): 754–64. doi:10.1016/j.yhbeh.2010.12.005. PMID 21185838.
    1. Bolour S, Braunstein G (2005). "Testosterone therapy in women: a review". Int. J. Impot. Res. 17 (5): 399–408. doi:10.1038/sj.ijir.3901334. PMID 15889125.
  54. Sapienza P, Zingales L, Maestripieri D (September 2009). "Gender differences in financial risk aversion and career choices are affected by testosterone". Proc. Natl. Acad. Sci. U.S.A. 106 (36): 15268–73. Bibcode:2009PNAS..10615268S. doi:10.1073/pnas.0907352106. PMC 2741240. PMID 19706398.
  55. Apicella CL, Dreber A, Campbell B, Gray PB, Hoffman M, Little AC (November 2008). "Testosterone and financial risk preferences". Evolution and Human Behavior 29 (6): 384–390. doi:10.1016/j.evolhumbehav.2008.07.001.
  56. Zak PJ, Kurzban R, Ahmadi S, Swerdloff RS, Park J, Efremidze L, Redwine K, Morgan K, Matzner W (2009). "Testosterone administration decreases generosity in the ultimatum game". In Aleman, André. PLoS ONE 4 (12): e8330. Bibcode:2009PLoSO...4.8330Z. doi:10.1371/journal.pone.0008330. PMC 2789942. PMID 20016825.
  57. Wilson JD (September 2001). "Androgens, androgen receptors, and male gender role behavior". Horm Behav 40 (2): 358–66. doi:10.1006/hbeh.2001.1684. PMID 11534997.
  58. Cosgrove KP, Mazure CM, Staley JK (October 2007). "Evolving knowledge of sex differences in brain structure, function, and chemistry". Biol. Psychiatry 62 (8): 847–55. doi:10.1016/j.biopsych.2007.03.001. PMC 2711771. PMID 17544382.
  59. Marner L, Nyengaard JR, Tang Y, Pakkenberg B (July 2003). "Marked loss of myelinated nerve fibers in the human brain with age". J. Comp. Neurol. 462 (2): 144–52. doi:10.1002/cne.10714. PMID 12794739.
  60. Paola Sapienzaa, Luigi Zingales and Dario Maestripieri (2009). "Gender differences in financial risk aversion and career choices are affected by testosterone". PNAS 106 (36): 15268–15273. Bibcode:2009PNAS..10615268S. doi:10.1073/pnas.0907352106. PMC 2741240. PMID 19706398.
  61. "Testosterone Affects Some Women's Career Choices". NPR. August 28, 2009.
  62. Hogervorst E, Bandelow S, Combrinck M, Smith AD (2004). "Low free testosterone is an independent risk factor for Alzheimer's disease". Exp. Gerontol. 39 (11–12): 1633–9. doi:10.1016/j.exger.2004.06.019. PMID 15582279.
  63. Moffat SD, Zonderman AB, Metter EJ, Kawas C, Blackman MR, Harman SM, Resnick SM (January 2004). "Free testosterone and risk for Alzheimer disease in older men". Neurology 62 (2): 188–93. doi:10.1212/WNL.62.2.188. PMID 14745052.
    1. Pike CJ, Rosario ER, Nguyen TV (April 2006). "Androgens, aging, and Alzheimer's disease". Endocrine 29 (2): 233–41. doi:10.1385/ENDO:29:2:233. PMID 16785599.
    2. Rosario ER, Chang L, Stanczyk FZ, Pike CJ (September 2004). "Age-related testosterone depletion and the development of Alzheimer disease". JAMA 292 (12): 1431–2. doi:10.1001/jama.292.12.1431-b. PMID 15383512.
  64. Moffat SD, Hampson E (April 1996). "A curvilinear relationship between testosterone and spatial cognition in humans: possible influence of hand preference". Psychoneuroendocrinology 21 (3): 323–37. doi:10.1016/0306-4530(95)00051-8. PMID 8817730.
  65. Wright J, Ellis L, Beaver K (2009). Handbook of crime correlates. San Diego: Academic Press. pp. 208–210. ISBN 0-12-373612-9.
  66. Soma KK, Scotti MA, Newman AE, Charlier TD, Demas GE (October 2008). "Novel mechanisms for neuroendocrine regulation of aggression". Front Neuroendocrinol 29 (4): 476–89. doi:10.1016/j.yfrne.2007.12.003. PMID 18280561.
  67. Soma KK, Sullivan KA, Tramontin AD, Saldanha CJ, Schlinger BA, Wingfield JC (2000). "Acute and chronic effects of an aromatase inhibitor on territorial aggression in breeding and nonbreeding male song sparrows". J. Comp. Physiol. A 186 (7–8): 759–69. doi:10.1007/s003590000129. PMID 11016791.
  68. Jakobsson et al. (2006). Large Differences in Testosterone Excretion in Korean and Swedish Men Are Strongly Associated with a UDP-Glucuronosyl Transferase 2B17 Polymorphism. The Journal of Clinical Endocrinology & Metabolism. 91 (2).
  69. Mazur, A. (2009). The age-testosterone relationship in black, white, and Mexican-American men, and reasons for ethnic differences. Aging Male, 12(2/3), 66-76. doi:10.1080/13685530903071802
  70. Ettinger, B. et al. (1997). Racial Differences in Bone Density between Young Adult Black and White Subjects Persist after Adjustment for Anthropometric, Lifestyle, and Biochemical Differences. The Journal of Clinical Endocrinology & Metabolism. 82, (2).
    1. de Kruif P (1945). The Male Hormone. New York: Harcourt, Brace.
  71. Myers JB, Meacham RB (2003). "Androgen Replacement Therapy in the Aging Male". Rev Urol 5 (4): 216–26. PMC 1508369. PMID 16985841.
  72. "Gender dysphoria - Treatment". NHS Page last reviewed: 21/05/2012. Retrieved 31 October 2013. 
    1. Davis SR, Moreau M, Kroll R, Bouchard C, Panay N, Gass M, Braunstein GD, Hirschberg AL, Rodenberg C, Pack S, Koch H, Moufarege A, Studd J (November 2008). "Testosterone for low libido in postmenopausal women not taking estrogen". N. Engl. J. Med. 359 (19): 2005–17. doi:10.1056/NEJMoa0707302. PMID 18987368.
  73. Traish AM, Saad F, Guay A (2009). "The dark side of testosterone deficiency: II. Type 2 diabetes and insulin resistance". J. Androl. 30 (1): 23–32. doi:10.2164/jandrol.108.005751. PMID 18772488.
  74. Emmelot-Vonk MH, Verhaar HJ, Nakhai Pour HR, Aleman A, Lock TM, Bosch JL, Grobbee DE, van der Schouw YT (January 2008). "Effect of testosterone supplementation on functional mobility, cognition, and other parameters in older men: a randomized controlled trial". JAMA 299 (1): 39–52. doi:10.1001/jama.2007.51. PMID 18167405.
  75. Cunningham GR (2008-06-25). "Testosterone treatment in aging men". Retrieved 2009-07-17.
  76. "Testosterone replacement therapy for male aging: ASA position statement". J. Androl. 27 (2): 133–4. 2006. PMID 16474019.
  77. Guay AT, Spark RF, Bansal S, Cunningham GR, Goodman NF, Nankin HR, Petak SM, Perez JB (2003). "American Association of Clinical Endocrinologists medical guidelines for clinical practice for the evaluation and treatment of male sexual dysfunction: a couple's problem—2003 update". Endocr Pract 9 (1): 77–95. doi:10.4158/EP.9.1.77. PMID 12917096.
  78. Holt EH, Zieve D (2008-03-18). "Testosterone". MedlinePlus Medical Encyclopedia. U.S. National Library of Medicine. Retrieved 2009-07-17.
  79. "Contraceptive efficacy of testosterone-induced azoospermia in normal men. World Health Organization Task Force on methods for the regulation of male fertility". Lancet 336 (8721): 955–9. October 1990. doi:10.1016/0140-6736(90)92416-F. PMID 1977002.
  80. Gould DC, Petty R (August 2000). "The male menopause: does it exist?: For: Some men need investigation and testosterone treatment". West. J. Med. 173 (2): 76–8. doi:10.1136/ewjm.173.2.76. PMC 1070997. PMID 10924412.
  81. Travison TG, Araujo AB, O'Donnell AB, Kupelian V, McKinlay JB (January 2007). "A population-level decline in serum testosterone levels in American men". J. Clin. Endocrinol. Metab. 92 (1): 196–202. doi:10.1210/jc.2006-1375. PMID 17062768.
  82. Dindyal S (2007). "The sperm count has been decreasing steadily for many years in Western industrialised countries: Is there an endocrine basis for this decrease?". The Internet Journal of Urology 2 (1): 1–21.
  83. Bhasin S (January 2007). "Secular decline in male reproductive function: Is manliness threatened?". J. Clin. Endocrinol. Metab. 92 (1): 44–5. doi:10.1210/jc.2006-2438. PMID 17209224.
  84. "Anabolic Steroid Control Act". United States Sentencing Commission. 1990.
  85. Strahm E, Emery C, Saugy M, Dvorak J, Saudan C (December 2009). "Detection of testosterone administration based on the carbon isotope ratio profiling of endogenous steroids: international reference populations of professional soccer players". Br J Sports Med 43 (13): 1041–4. doi:10.1136/bjsm.2009.058669. PMC 2784500. PMID 19549614.
  86. Kicman AT, Cowan DA (January 2009). "Subject-based profiling for the detection of testosterone administration in sport". Drug Test Anal 1 (1): 22–4. doi:10.1002/dta.14. PMID 20355155.
  87. Pozo OJ, Deventer K, Van Eenoo P, Rubens R, Delbeke FT (August 2009). "Quantification of testosterone undecanoate in human hair by liquid chromatography-tandem mass spectrometry". Biomed. Chromatogr. 23 (8): 873–80. doi:10.1002/bmc.1199. PMID 19353724.
  88. Baselt RC (2008). Disposition of Toxic Drugs & Chemicals in Man (8th ed.). Foster City, Calif: Biomedical Publications. pp. 1501–1504. ISBN 978-0-9626523-7-0.
  89. "Testosterone Pregnancy and Breastfeeding Warnings". Retrieved 1 February 2014.
    1. Fernández-Balsells, MM; Murad, MH; Lane, M; Lampropulos, JF; Albuquerque, F; Mullan, RJ; Agrwal, N; Elamin, MB; Gallegos-Orozco, JF; Wang, AT; Erwin, PJ; Bhasin, S; Montori, VM (June 2010). "Clinical review 1: Adverse effects of testosterone therapy in adult men: a systematic review and meta-analysis.". The Journal of Clinical Endocrinology and Metabolism 95 (6): 2560–75. doi:10.1210/jc.2009-2575. PMID 20525906
  90. Haddad, RM; Kennedy, CC; Caples, SM; Tracz, MJ; Boloña, ER; Sideras, K; Uraga, MV; Erwin, PJ; Montori, VM (January 2007). "Testosterone and cardiovascular risk in men: a systematic review and meta-analysis of randomized placebo-controlled trials.". Mayo Clinic proceedings. Mayo Clinic 82 (1): 29–39. doi:10.4065/82.1.29. PMID 17285783
  91. "Testosterone Products: Drug Safety Communication - FDA Investigating Risk of Cardiovascular Events". FDA. Jan 31,2014. Retrieved 3 February 2014. 
  92. Rhoden EL, Averbeck MA (November 2009). "Testosterone therapy and prostate carcinoma". Curr Urol Rep 10 (6): 453–9. doi:10.1007/s11934-009-0072-1. PMID 19863857.
  93. Gaylis FD, Lin DW, Ignatoff JM, Amling CL, Tutrone RF, Cosgrove DJ (August 2005). "Prostate cancer in men using testosterone supplementation". J. Urol. 174 (2): 534–8; discussion 538. doi:10.1097/01.ju.0000165166.36280.60. PMID 16006887.
    1. Calistro Alvarado L (2010). "Population differences in the testosterone levels of young men are associated with prostate cancer disparities in older men". Am. J. Hum. Biol. 22 (4): 449–55. doi:10.1002/ajhb.21016. PMID 20087895.
  94. Bostwick DG, Burke HB, Djakiew D, Euling S, Ho SM, Landolph J, Morrison H, Sonawane B, Shifflett T, Waters DJ, Timms B (November 2004). "Human prostate cancer risk factors". Cancer 101 (10 Suppl): 2371–490. doi:10.1002/cncr.20408. PMID 15495199. Lay summaryMercer University School of Medicine.
  96. Waterman MR, Keeney DS (1992). "Genes involved in androgen biosynthesis and the male phenotype". Horm. Res. 38 (5–6): 217–21. doi:10.1159/000182546. PMID 1307739.
  97. Zuber MX, Simpson ER, Waterman MR (December 1986). "Expression of bovine 17 alpha-hydroxylase cytochrome P-450 cDNA in nonsteroidogenic (COS 1) cells". Science 234 (4781): 1258–61. Bibcode:1986Sci...234.1258Z. doi:10.1126/science.3535074. PMID 3535074.
  98. Zouboulis CC, Degitz K (2004). "Androgen action on human skin – from basic research to clinical significance". Exp. Dermatol. 13 Suppl 4: 5–10. doi:10.1111/j.1600-0625.2004.00255.x. PMID 15507105.
  99. Brooks RV (November 1975). "Androgens". Clin Endocrinol Metab 4 (3): 503–20. doi:10.1016/S0300-595X(75)80045-4. PMID 58744.
  100. Payne AH, O'Shaughnessy P (1996). "Structure, function, and regulation of steroidogenic enzymes in the Leydig cell". In Payne AH, Hardy MP, Russell LD. Leydig Cell. Vienna [Il]: Cache River Press. pp. 260–285. ISBN 0-9627422-7-9.
  101. Swerdloff RS, Wang C, Bhasin S (April 1992). "Developments in the control of testicular function". Baillieres Clin. Endocrinol. Metab. 6 (2): 451–83. doi:10.1016/S0950-351X(05)80158-2. PMID 1377467.
  102. Håkonsen LB, Thulstrup AM, Aggerholm AS, Olsen J, Bonde JP, Andersen CY, Bungum M, Ernst EH, Hansen ML, Ernst EH, Ramlau-Hansen CH (2011). "Does weight loss improve semen quality and reproductive hormones? Results from a cohort of severely obese men". Reprod Health 8: 24. doi:10.1186/1742-4755-8-24. PMC 3177768. PMID 21849026.
  103. Pilz S, Frisch S, Koertke H, Kuhn J, Dreier J, Obermayer-Pietsch B, Wehr E, Zittermann A (March 2011). "Effect of vitamin D supplementation on testosterone levels in men". Horm. Metab. Res. 43 (3): 223–5. doi:10.1055/s-0030-1269854. PMID 21154195.
  104. Prasad AS, Mantzoros CS, Beck FW, Hess JW, Brewer GJ (May 1996). "Zinc status and serum testosterone levels of healthy adults". Nutrition 12 (5): 344–8. doi:10.1016/S0899-9007(96)80058-X. PMID 8875519.
  105. Koehler K, Parr MK, Geyer H, Mester J, Schänzer W (January 2009). "Serum testosterone and urinary excretion of steroid hormone metabolites after administration of a high-dose zinc supplement". Eur J Clin Nutr 63 (1): 65–70. doi:10.1038/sj.ejcn.1602899. PMID 17882141.
  106. Schultheiss OC, Campbell KL, McClelland DC (December 1999). "Implicit power motivation moderates men's testosterone responses to imagined and real dominance success". Horm Behav 36 (3): 234–41. doi:10.1006/hbeh.1999.1542. PMID 10603287.
  107. Liu PY, Pincus SM, Takahashi PY, Roebuck PD, Iranmanesh A, Keenan DM, Veldhuis JD (January 2006). "Aging attenuates both the regularity and joint synchrony of LH and testosterone secretion in normal men: analyses via a model of graded GnRH receptor blockade". Am. J. Physiol. Endocrinol. Metab. 290 (1): E34–E41. doi:10.1152/ajpendo.00227.2005. PMID 16339924.
  108. Andersen ML, Tufik S (October 2008). "The effects of testosterone on sleep and sleep-disordered breathing in men: its bidirectional interaction with erectile function". Sleep Med Rev 12 (5): 365–79. doi:10.1016/j.smrv.2007.12.003. PMID 18519168.
  109. Marin DP, Figueira AJ Junior, Pinto LG (2006). "One session of resistance training may increase serum testosterone and triiodetironine in young men". Medicine & Science in Sports & Exercise 38 (5): S285. doi:10.1249/00005768-200605001-01235.
  110. Hulmi JJ, Ahtiainen JP, Selänne H, Volek JS, Häkkinen K, Kovanen V, Mero AA (May 2008). "Androgen receptors and testosterone in men—effects of protein ingestion, resistance exercise and fiber type". J. Steroid Biochem. Mol. Biol. 110 (1–2): 130–7. doi:10.1016/j.jsbmb.2008.03.030. PMID 18455389.
  111. Josephs RA, Guinn JS, Harper ML, Askari F (November 2001). "Liquorice consumption and salivary testosterone concentrations". Lancet 358 (9293): 1613–4. doi:10.1016/S0140-6736(01)06664-8. PMID 11716893.
  112. Armanini D, Mattarello MJ, Fiore C, Bonanni G, Scaroni C, Sartorato P, Palermo M (2004). "Licorice reduces serum testosterone in healthy women". Steroids 69 (11–12): 763–6. doi:10.1016/j.steroids.2004.09.005. PMID 15579328.
  113. Akdoğan M, Tamer MN, Cüre E, Cüre MC, Köroğlu BK, Delibaş N (May 2007). "Effect of spearmint (Mentha spicata Labiatae) teas on androgen levels in women with hirsutism". Phytother Res 21 (5): 444–7. doi:10.1002/ptr.2074. PMID 17310494.
  114. Kumar V, Kural MR, Pereira BM, Roy P (December 2008). "Spearmint induced hypothalamic oxidative stress and testicular anti-androgenicity in male rats – altered levels of gene expression, enzymes and hormones". Food Chem. Toxicol. 46 (12): 3563–70. doi:10.1016/j.fct.2008.08.027. PMID 18804513.
  115. Grant P (February 2010). "Spearmint herbal tea has significant anti-androgen effects in polycystic ovarian syndrome. A randomized controlled trial". Phytother Res 24 (2): 186–8. doi:10.1002/ptr.2900. PMID 19585478.
  116. Carney DR, Cuddy AJ, Yap AJ (October 2010). "Power posing: brief nonverbal displays affect neuroendocrine levels and risk tolerance". Psychol Sci. 21 (10): 1363–1368. doi:10.1177/0956797610383437. PMID 20855902
  117. Randall VA (April 1994). "Role of 5 alpha-reductase in health and disease". Baillieres Clin. Endocrinol. Metab. 8 (2): 405–31. doi:10.1016/S0950-351X(05)80259-9. PMID 8092979.
  118. Meinhardt U, Mullis PE (August 2002). "The essential role of the aromatase/p450arom". Semin. Reprod. Med. 20 (3): 277–84. doi:10.1055/s-2002-35374. PMID 12428207.
  119. Trager L (1977). Steroidhormone: Biosynthese, Stoffwechsel, Wirkung (in German). Springer-Verlag. p. 349. ISBN 0-387-08012-0.
  120. Hiipakka RA, Liao S (October 1998). "Molecular mechanism of androgen action". Trends Endocrinol. Metab. 9 (8): 317–24. doi:10.1016/S1043-2760(98)00081-2. PMID 18406296.
  121. McPhaul MJ, Young M (September 2001). "Complexities of androgen action". J. Am. Acad. Dermatol. 45 (3 Suppl): S87–94. doi:10.1067/mjd.2001.117429. PMID 11511858.
  122. Breiner M, Romalo G, Schweikert HU (August 1986). "Inhibition of androgen receptor binding by natural and synthetic steroids in cultured human genital skin fibroblasts". Klin. Wochenschr. 64 (16): 732–7. doi:10.1007/BF01734339. PMID 3762019.
    1. Bratoeff E, Cabeza M, Ramirez E, Heuze Y, Flores E (2005). "Recent advances in the chemistry and pharmacological activity of new steroidal antiandrogens and 5 alpha-reductase inhibitors". Curr. Med. Chem. 12 (8): 927–43. doi:10.2174/0929867053507306. PMID 15853706.
  123. Engel JB, Schally AV (February 2007). "Drug Insight: clinical use of agonists and antagonists of luteinizing-hormone-releasing hormone". Nat Clin Pract Endocrinol Metab 3 (2): 157–67. doi:10.1038/ncpendmet0399. PMID 17237842.
  124. "Testosterone Information".
  125. "Striant Official FDA information, side effects and uses".
  126. "AndroGel Official FDA information, side effects and uses".
  127. "Testim (patches and gel) medical facts".
  128. "Testopel Pellets".
  129. Berthold AA (1849). "Transplantation der Hoden" [Transplantation of testis]. Arch. Anat. Physiol. Wissensch. (in German) 16: 42–6.
  130. Brown-Sequard CE (1889). "The effects produced on man by subcutaneous injections of liquid obtained from the testicles of animals". Lancet 2 (3438): 105. doi:10.1016/S0140-6736(00)64118-1.
  131. Gallagher TF, Koch FC (November 1929). "The testicular hormone". J. Biol. Chem. 84 (2): 495–500.
  132. David KG., Dingemanse E, Freud J. Laqueur E (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 Seylers Z Physiol Chem (in German) 233 (5–6): 281. doi:10.1515/bchm2.1935.233.5-6.281.
  133. Butenandt A, Hanisch G (1935). "Umwandlung des Dehydroandrosterons in Androstendiol und Testosterone; ein Weg zur Darstellung des Testosterons aus Cholestrin" [About Testosterone. Conversion of Dehydro-androsterons into androstendiol and testosterone; a way for the structure assignment of testosterone from cholestrol]. Hoppe Seylers Z Physiol Chem (in German) 237 (2): 89. doi:10.1515/bchm2.1935.237.1-3.89.
    1. Freeman ER, Bloom DA, McGuire EJ (February 2001). "A brief history of testosterone". J. Urol. 165 (2): 371–3. doi:10.1097/00005392-200102000-00004. PMID 11176375.
  134. Butenandt A, Hanisch G (1935). "Uber die Umwandlung des Dehydroandrosterons in Androstenol-(17)-one-(3) (Testosterone); um Weg zur Darstellung des Testosterons auf Cholesterin (Vorlauf Mitteilung). [The conversion of dehydroandrosterone into androstenol-(17)-one-3 (testosterone); a method for the production of testosterone from cholesterol (preliminary communication)]". Chemische Berichte (in German) 68: 1859–1862.
  135. Ruzicka L, Wettstein A (1935). "Uber die kristallinische Herstellung des Testikelhormons, Testosteron (Androsten-3-ol-17-ol) [The crystalline production of the testicle hormone, testosterone (Androsten-3-ol-17-ol)]". Helvetica Chimica Acta (in German) 18: 1264–1275. doi:10.1002/hlca.193501801176.
  136. Hoberman JM, Yesalis CE (February 1995). "The history of synthetic testosterone". Sci. Am. 272 (2): 76–81. doi:10.1038/scientificamerican0295-76. PMID 7817189.
  137. Kenyon AT, Knowlton K, Sandiford I, Koch FC, Lotwin,G (February 1940). "A comparative study of the metabolic effects of testosterone propionate in normal men and women and in eunuchoidism". Endocrinology 26 (1): 26–45. doi:10.1210/Endo-26-1-26.
  138. Schwarz S, Onken D, Schubert A (July 1999). "The steroid story of Jenapharm: from the late 1940s to the early 1970s". Steroids 64 (7): 439–45. doi:10.1016/S0039-128X(99)00003-3. PMID 10443899.
    1. Arch Androl. 1981 Aug;7(1):69-73. 
    2. Nutrition. 1996 May;12(5):344-8. 
    3. Neuro Endocrinol Lett. 2007 Oct;28(5):681-5. 
    4. National Institutes of Health, Office of Dietary Supplements, Zinc 
    5. Horm Metab Res. 2011 Mar;43(3):223-5. Epub 2010 Dec 10. 
    6. Horm Behav. 2010 Nov;58(5):898-906. Epub 2010 Sep 15. 
    7. Study presented at The Endocrine Society’s 91st Annual Meeting, June 13, 2009, Washington, D.C. 
    8. J Steroid Biochem. 1984 Jan;20(1):459-64. 

Information above is based on years of experience by professional colleagues, doctors, herbal healers, drug-free practiners, scientists and research conducted throughout the world, with extensive review of scientific literature and new clinical discoveries. Listed information is solely intended to be used for educational purposes only and is not intended as a basis for diagnosis, treatment, or to cure any disease. No medical claims, systemic administration claims are made, nor implied for the use of any of the information used above. These statements have not been evaluated by the US Food and Drug Administration (FDA). 


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