Why bother with such common micronutrients? Because it's not uncommon for athletes to suffer from zinc and magnesium deficiencies, partly due to inadequate replenishing of levels after intense bouts of exercise. Deficiencies in these key minerals can lead to a poor anabolic hormone profile, impaired immune function, and increased cortisol, ultimately leading to decreases in strength and performance.[6]
If you remember Popeye the Sailor Man, then your childhood was probably awesome. You might remember that Popeye takes spinach and he becomes miraculously powerful within seconds. Although it's not an accurate depiction of spinach's abilities, it is safe to say that it shouldn't be avoided in a man's diet. Spinach may not be excessively rich in zinc yet it holds many other vitamins and minerals.

The hypogonadal-obesity-adipocytokine cycle hypothesis. Adipose tissue contains the enzyme aromatase which metabolises testosterone to oestrogen. This results in reduced testosterone levels, which increase the action of lipoprotein lipase and increase fat mass, thus increasing aromatisation of testosterone and completing the cycle. Visceral fat also promotes lower testosterone levels by reducing pituitary LH pulse amplitude via leptin and/or other factors. In vitro studies have shown that leptin also inhibits testosterone production directly at the testes. Visceral adiposity could also provide the link between testosterone and insulin resistance (Jones 2007).
When testosterone and endorphins in ejaculated semen meet the cervical wall after sexual intercourse, females receive a spike in testosterone, endorphin, and oxytocin levels, and males after orgasm during copulation experience an increase in endorphins and a marked increase in oxytocin levels. This adds to the hospitable physiological environment in the female internal reproductive tract for conceiving, and later for nurturing the conceptus in the pre-embryonic stages, and stimulates feelings of love, desire, and paternal care in the male (this is the only time male oxytocin levels rival a female's).[citation needed]
I recommend using a trans-mucosal DHEA cream. Applying it to the rectum or if you are a a woman, your vagina, will allow the mucous epithelial membranes that line your mucosa to perform effective absorption. These membranes regulate absorption and inhibit the production of unwanted metabolites of DHEA. I personally apply 50 milligrams of trans-rectal DHEA cream twice a day – this has improved my own testosterone levels significantly. However, please note that I do NOT recommend prolonged supplementation of hormones. Doing so can trick your body into halting its own DHEA production and may cause your adrenals to become seriously impaired down.
This causes your body to burn fat for the next 36 hours to replace your body’s vital energy stores. It addition to increasing your T-levels, it can help burn between 3–9 times more fat, lower your resting heart rate, lower blood pressure, keep your brain young by increasing circulation, and aids in detoxification by stimulating the lymphatic system.
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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.
If a man's testosterone looks below the normal range, there is a good chance he could end up on hormone supplements—often indefinitely. "There is a bit of a testosterone trap," Dr. Pallais says. "Men get started on testosterone replacement and they feel better, but then it's hard to come off of it. On treatment, the body stops making testosterone. Men can often feel a big difference when they stop therapy because their body's testosterone production has not yet recovered."
Smith and colleagues (2005) undertook a prospective study on the contribution of stress to coronary heart disease. Their study, which involved 2512 men aged 45 to 59 years, looked at a number of metabolic parameters. They found that an increased cortisol to testosterone ratio was associated with a high risk of coronary artery disease and that this risk was mediated by components of the insulin resistance syndrome. They reported that high cortisol and low testosterone levels are associated with a worsening of insulin resistance and that there is evidence to support the possibility of improving this pattern by treatment with testosterone.
Testosterone is more than a “male sex hormone”. It is an important contributor to the robust metabolic functioning of multiple bodily systems. The abuse of anabolic steroids by athletes over the years has been one of the major detractors from the investigation and treatment of clinical states that could be caused by or related to male hypogonadism. The unwarranted fear that testosterone therapy would induce prostate cancer has also deterred physicians form pursuing more aggressively the possibility of hypogonadism in symptomatic male patients. In addition to these two mythologies, many physicians believe that testosterone is bad for the male heart. The classical anabolic agents, 17-alkylated steroids, are, indeed, potentially harmful to the liver, to insulin action to lipid metabolism. These substances, however, are not testosterone, which has none of these adverse effects. The current evidence, in fact, strongly suggests that testosterone may be cardioprotective. There is virtually no evidence to implicate testosterone as a cause of prostate cancer. It may exacerbate an existing prostate cancer, although the evidence is flimsy, but it does not likely cause the cancer in the first place. Testosterone has stimulatory effects on bones, muscles, erythropoietin, libido, mood and cognition centres in the brain, penile erection. It is reduced in metabolic syndrome and diabetes and therapy with testosterone in these conditions may provide amelioration by lowering LDL cholesterol, blood sugar, glycated hemoglobin and insulin resistance. The best measure is bio-available testosterone which is the fraction of testosterone not bound to sex hormone binding globulin. Several forms of testosterone administration are available making compliance much less of an issue with testosterone replacement therapy.
In the hepatic 17-ketosteroid pathway of testosterone metabolism, testosterone is converted in the liver by 5α-reductase and 5β-reductase into 5α-DHT and the inactive 5β-DHT, respectively.[1][151] Then, 5α-DHT and 5β-DHT are converted by 3α-HSD into 3α-androstanediol and 3α-etiocholanediol, respectively.[1][151] Subsequently, 3α-androstanediol and 3α-etiocholanediol are converted by 17β-HSD into androsterone and etiocholanolone, which is followed by their conjugation and excretion.[1][151] 3β-Androstanediol and 3β-etiocholanediol can also be formed in this pathway when 5α-DHT and 5β-DHT are acted upon by 3β-HSD instead of 3α-HSD, respectively, and they can then be transformed into epiandrosterone and epietiocholanolone, respectively.[153][154] A small portion of approximately 3% of testosterone is reversibly converted in the liver into androstenedione by 17β-HSD.[152]
Testosterone is a hormone with multifaceted physiological functions and multiple associations with pathophysiological states. It is an important hormone in male reproductive and metabolic function from intrauterine life to old age. In severe or classical hypogonadal states there is little controversy about the need to administer testosterone by an intramuscular, oral or transdermal formulation. There is controversy about making the diagnosis in the less severe cases of hypogonadism associated with the aging male but the current evidence suggests that this is efficacious in appropriately selected men and that there is little if any risk in giving aging symptomatic hypogonadal men a 6 month trial of therapy to determine whether symptoms will improve.
If in a 46 XY individual testosterone is either not produced in adequate concentrations as in gonadal dysgenesis (MacLaughlin and Donahue 2004), or in the absence of the enzyme 17 alpha-hydroxylase so that testosterone is not produced (Ergun-Longmire et al 2006), or testosterone androgen receptors are absent as in the androgen insensitivity syndrome (Hughes and Deeb 2006), phenotypic females will result.
Dixon Troyer is the President of Operations at 3 Elements Lifestyle, LLC., a Fitness and Weight Loss company that specializes in YOU! With more than 15 years of gym and club experience, owning, operating and managing clubs of all sizes, Dixon lectures, delivers seminars and workshops on the practical skills required to successfully help you with your health and fitness goals. Dixon also helps you build the teamwork, management, and training necessary to open your own fitness center.

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.


However, it is usually found in much smaller amounts. A standard amount is about 1,000 milligrams, but you will see that the top 5 all contain about 1,500 milligrams or more. (Monster T contains 3,500 milligrams per serving but is missing other ingredients.) Testogen contains the highest amount of D-aspartic acid that we have seen except for Monster T. 

Some boys even develop enlarged testicles and penis, armpit or pubic hair, as well as facial hair as early as age nine! Early puberty is not something to be taken lightly because it can significantly influence physical and psychological health, including an increased risk of hormone-related cancers. Precocious sexual development may also lead to emotional and behavioral issues, such as:


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.
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And remember, saturated fats work best (along with monounsaturated fats – olive oil, almonds, avocados etc.). In fact higher intakes of polyunsaturated fats (canola oil, sunflower oil, soybean oil, safflower oil, margarine etc.) are linked to LOWER testosterone levels (14 & 15). I explore the dangers of PUFA's in a lot more detail in this article - PUFA's: The Worst Thing For Your Health That You Eat Everyday.
Testosterone treatment is unequivocally needed in classical hypogonadism for reasons discussed in subsequent subsections. In classical hypogonadism, testosterone production is usually clearly below the lower limit of normal and patients are highly symptomatic; the various symptoms are easily related to the deficiencies in various bodily systems where testosterone action is important. Symptoms of testosterone deficiency are listed in Table 2. A few prominent causes of classical hypogonadism are listed in Table 3.
Sportsmen are permitted to use the boosters to trigger the mechanism of testosterone synthesis in the body. These products won a wide popularity among the sportsmen. The matter is that the supplements work by substantially enhancing sports performance, reviving strength, boosting endurance, coping with excessive stress levels, and decreasing time necessary for recovery after exhausting exercises.

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.
Using steroids eventually trains your body to realize that it doesn’t have to produce as much testosterone to reach its equilibrium, so to reach the same highs you’ll need to take more steroids, and when you stop taking them, your body will need to readjust — you’ll be living with low testosterone for a while (and you’ll need to see a doctor if your body doesn’t readjust on its own). Forcing your body to stay above your natural testosterone, even if you’re naturally low, can create this kind of dependency which ultimately decreases the amount of testosterone your body will produce on its own.

I know the experiment didn’t simply bring me back to my pre-August levels because of the fact that when I learned that the original test I took can sometimes overestimate your T levels, I took a more accurate test around four months after the start of the experiment (I’ve continued the lifestyle changes made during the experiment) and my total T had gone up again to 826.9 ng/dL.
Testosterone was first used as a clinical drug as early as 1937, but with little understanding of its mechanisms. The hormone is now widely prescribed to men whose bodies naturally produce low levels. But the levels at which testosterone deficiency become medically relevant still aren’t well understood. Normal testosterone production varies widely in men, so it’s difficult to know what levels have medical significance. The hormone’s mechanisms of action are also unclear.
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