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There have been case reports of development of prostate cancer in patients during treatment with testosterone, including one case series of twenty patients (Gaylis et al 2005). It is not known whether this reflects an increase in incidence, as prostate cancer is very common and because the monitoring for cancer in patients treated with testosterone is greater. Randomized controlled trials of testosterone treatment have found a low incidence of prostate cancer and they do not provide evidence of a link between testosterone treatment and the development of prostate cancer (Rhoden and Morgentaler 2004). More large scale clinical trials of longer durations of testosterone replacement are required to confirm that testosterone treatment does not cause prostate cancer. Overall, it is not known whether testosterone treatment of aging males with hypogonadism increases the risk of prostate cancer, but monitoring for the condition is clearly vital. This should take the form of PSA blood test and rectal examination every three months for the first year of treatment and yearly thereafter (Nieschlag et al 2005). Age adjusted PSA reference ranges should be used to identify men who require further assessment. The concept of PSA velocity is also important and refers to the rate of increase in PSA per year. Patients with abnormal rectal examination suggestive of prostate cancer, PSA above the age specific reference range or a PSA velocity greater than 0.75 ng/ml/yr should be referred to a urologist for consideration of prostate biopsy.


Hypogonadism (as well as age-related low testosterone) is diagnosed with blood tests that measure the level of testosterone in the body. The Endocrine Society recommends testing for suspected low T with a total testosterone test. It may be performed in the morning when testosterone levels tend to be highest in young men, although this isn't necessarily the case in older men. The test may be repeated on another day if the results show a low T level. (5)

The aim of treatment for hypogonadism is to normalize serum testosterone levels and abolish symptoms or pathological states that are due to low testosterone levels. The exact target testosterone level is a matter of debate, but current recommendations advocate levels in the mid-lower normal adult range (Nieschlag et al 2005). Truly physiological testosterone replacement would require replication of the diurnal rhythm of serum testosterone levels, but there is no current evidence that this is beneficial (Nieschlag et al 2005).
The natural production of DHEA is also age-dependent. Prior to puberty, the body produces very little DHEA. Production of this prohormone peaks during your late 20’s or early 30’s. With age, DHEA production begins to decline. The adrenal glands also manufacture the stress hormone cortisol, which is in direct competition with DHEA for production because they use the same hormonal substrate known as pregnenolone. Chronic stress basically causes excessive cortisol levels and impairs DHEA production, which is why stress is another factor for low testosterone levels.
Vitamin D is a fat-soluble vitamin and is obtained from sunlight. In the active form, it acts as a steroid hormone in the body. These days many people suffer from vitamin D deficiency because lacking exposure to sunlight, but taking vitamin D supplements to improve the weakness. Low vitamin D levels also lower the testosterone levels, but with intake of vitamin D, the testosterone levels boost. In typical cases, vitamin D doesn’t show the significant result in testosterone levels but people who are vitamin D deficient shows an increase in testosterone levels.

Two of the immediate metabolites of testosterone, 5α-DHT and estradiol, are biologically important and can be formed both in the liver and in extrahepatic tissues.[151] Approximately 5 to 7% of testosterone is converted by 5α-reductase into 5α-DHT, with circulating levels of 5α-DHT about 10% of those of testosterone, and approximately 0.3% of testosterone is converted into estradiol by aromatase.[2][151][157][158] 5α-Reductase is highly expressed in the male reproductive organs (including the prostate gland, seminal vesicles, and epididymides),[159] skin, hair follicles, and brain[160] and aromatase is highly expressed in adipose tissue, bone, and the brain.[161][162] As much as 90% of testosterone is converted into 5α-DHT in so-called androgenic tissues with high 5α-reductase expression,[152] and due to the several-fold greater potency of 5α-DHT as an AR agonist relative to testosterone,[163] it has been estimated that the effects of testosterone are potentiated 2- to 3-fold in such tissues.[164]
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.
Testosterone is a steroid sex hormone found in both men and women. In men, testosterone is produced primarily by the Leydig (interstitial) cells of the testes when stimulated by luteinizing hormone (LH). It functions to stimulate spermatogenesis, promote physical and functional maturation of spermatozoa, maintain accessory organs of the male reproductive tract, support development of secondary sexual characteristics, stimulate growth and metabolism throughout the body and influence brain development by stimulating sexual behaviors and sexual drive. In women, testosterone is produced by the ovaries (25%), adrenals (25%) and via peripheral conversion from androstenedione (50%). Testerone in women functions to maintain libido and general wellbeing. Testosterone exerts a negative feedback mechanism on pituitary release of LH and follicle-stimulating hormone (FSH). Testosterone may be further converted to dihydrotestosterone or estradiol depending on the tissue.
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).
6)  Take Cold Showers:  Cold showers have been known to stimulate and boost testosterone production and improve metabolism, detoxification and brain function.  Start your shower with warm/hot water and turn it to cold for the last 30-60 seconds while pumping your muscles and creating a big shiver as your muscles contract.  That will help to boost internal heat and boost testosterone production.  This article will help you.
As we age, the body undergoes multiple degenerative changes at multiple sites and in multiple systems. The changes of aging are inevitable and inexorable and represent the march toward ultimate death. We are mortal beings whose destiny it is to die. As we come to learn about the processes of life we can better prepare ourselves for the finality of death and on the way perhaps retard the degenerative process, or repair it (for however long we may enjoy this repair), or substitute chemical compounds that our bodies once produced in abundance, an abundance which fades with the advance of age.

In this study, an ethical approval No. 20171008 was obtained from Ethical Committee of Qassim province, Ministry of Health, Saudi Arabia. At the beginning, a written informed consent was taken from a 30-year-old man for participation in this study. The patient came to the King Saud Hospital, Unaizah, Qassim, Saudi Arabia, with abdominal pain. He looked pale and hazy, hence, immediately admitted. A battery of lab tests was ordered by the attending physician. Moreover, abdominal ultrasound imaging was performed. The results of the tests showed high levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST), indicating liver injury. Other serum parameters, such as total proteins, albumin, and iron, in addition to the levels of kidney and heart enzymes were all found to be in the normal range. A complete blood count showed normal levels of red blood cells, white blood cells, and platelets. The ultrasound images of the man’s abdomen were all found to be normal as well [Figure 2]. The patient, a sportsman, described that he was taking a testosterone commercial booster product called the Universal Nutrition Animal Stak for the purpose of enhancing his testosterone profile to achieve a better performance and body composition. The attending physician decided to admit the man for 1 week. Some medications were prescribed, and the patient was discharged later after having fully recovered.
Overall there is evidence that testosterone treatment increases lean body mass and reduces obesity, particularly visceral obesity, in a variety of populations including aging men. With regard to muscle changes, some studies demonstrate improvements in maximal strength but the results are inconsistent and it has not been demonstrated that these changes lead to clinically important improvements in mobility, endurance or quality of life. Studies are needed to clarify this. Changes in abdominal obesity are particularly important as visceral fat is now recognised as predisposing the metabolic syndrome, diabetes and cardiovascular disease.

Now that we know chronic insulin spikes lead to lower Testosterone production, I hope I haven’t sent you running into the low carb camp! There are a few studies out there showing that long term low carb or ketogenic dieting leads to higher cortisol levels (especially with subjects who are training), and decreased testosterone levels (28 & 29). I have used low carb diets in the past with successful results (winning a national bodybuilding title), however the key is to use cyclical carb re-feeds. If you’re going to go on a low carb diet for whatever reason, be sure to work in a large carb reefed once a week.
4. Foods rich in vitamin A. Vitamin A is more commonly known for its association with eyesight improvement, but it is also a vitamin supplements the production of testosterone. The June 2004 issue of the Clinical Endocrinology journal published research conducted by Israel’s Kaplan Medical Center. This study involved Israeli boys that had delays in puberty. These boys were given Vitamin A supplements and foods rich in Vitamin A over the course of 6 months, and most of them showed an improvement with their testosterone levels. If you want to boost the level of testosterone in your body, food types that are rich in Vitamin A are carrots, sweet potatoes, squash, cantaloupe and eggs.
The first of the natural testosterone boosters is intermittent fasting. One of the biggest intermittent fasting benefits? It’s been shown to increase testosterone by nearly 200 percent or even up to 400 percent. (4) In addition, a study by the University of Virginia Medical School noted that growth hormone levels increased 2,000 percent over the baseline in men who ate no calories for 24 hours, and growth hormone levels are correlated with testosterone. (5)
Trials of testosterone treatment in men with type 2 diabetes have also taken place. A recent randomized controlled crossover trial assessed the effects of intramuscular testosterone replacement to achieve levels within the physiological range, compared with placebo injections in 24 men with diabetes, hypogonadism and a mean age of 64 years (Kapoor et al 2006). Ten of these men were insulin treated. Testosterone treatment led to a significant reduction in glycated hemoglobin (HbA1C) and fasting glucose compared to placebo. Testosterone also produced a significant reduction in insulin resistance, measured by the homeostatic model assessment (HOMA), in the fourteen non-insulin treated patients. It is not possible to measure insulin resistance in patients treated with insulin but five out of ten of these patients had a reduction of insulin dose during the study. Other significant changes during testosterone treatment in this trial were reduced total cholesterol, waist circumference and waist-hip ratio. Similarly, a placebo-controlled but non-blinded trial in 24 men with visceral obesity, diabetes, hypogonadism and mean age 57 years found that three months of oral testosterone treatment led to significant reductions in HbA1C, fasting glucose, post-prandial glucose, weight, fat mass and waist-hip ratio (Boyanov et al 2003). In contrast, an uncontrolled study of 150 mg intramuscular testosterone given to 10 patients, average age 64 years, with diabetes and hypogonadism found no significant change in diabetes control, fasting glucose or insulin levels (Corrales et al 2004). Another uncontrolled study showed no beneficial effect of testosterone treatment on insulin resistance, measured by HOMA and ‘minimal model’ of area under acute insulin response curves, in 11 patients with type 2 diabetes aged between 33 and 73 years (Lee et al 2005). Body mass index was within the normal range in this population and there was no change in waist-hip ratio or weight during testosterone treatment. Baseline testosterone levels were in the low-normal range and patients received a relatively small dose of 100 mg intramuscular testosterone every three weeks. A good increase in testosterone levels during the trial is described but it is not stated at which time during the three week cycle the testosterone levels were tested, so the lack of response could reflect an insufficient overall testosterone dose in the trial period.
In males, the testosterone test can help find the reason for sexual problems, like reduced sex drive or erectile dysfunction. If you’re having a hard time getting your partner pregnant, the test can tell if your blood testosterone level is low. It can also screen for problems with the hypothalamus or pituitary gland. This controls how much testosterone your body makes.
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]
The definition of the metabolic syndrome continues to be a work in progress. Within the last decade a number of definitions have emerged each with its own set of criteria although there is considerable overlap among them. The most recent definition seems to enjoy considerable consensus. It requires central adiposity (>94 cm waist circumference) plus two of, increased triglycerides, decreased HDL cholesterol, hypertension, insulin resistance as evidenced by impaired glucose tolerance, or frank diabetes (Alberti 2005). Almost immediately on the heels of this consensus, came a number of specific chemical markers which have been proposed to complement the basic definition of the metabolic syndrome (Eckel et al 2005).
The most common "out of balance" testosterone levels are found to be on the low side of normal; this occurs because a male's highest testosterone level usually peaks at about age 20, and then it decreases slowly with age. It has been suggested that a 1% decrease in testosterone level per year is not unusual for middle-aged (30 to 50 years old) and older males. While this decrease may not be noticeable in some men, others may experience significant changes starting in their middle-aged years or more commonly at age 60 and above. This drop in testosterone levels is sometimes termed hypogonadism, "male menopause" or andropause.
Overall, few patients have a compelling contraindication to testosterone treatment. The majority of men with late onset hypogonadism can be safely treated with testosterone but all will require monitoring of prostate parameters HDL cholesterol, hematocrit and psychological state. It is also wise to monitor symptoms of sleep apnea. Other specific concerns may be raised by the mode of delivery such as local side effects from transdermal testosterone.
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,6 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).
One of the most important nutrients that can help boost testosterone levels is vitamin D3. In 2011, the results of a study published in the journal Hormone and Metabolic Research announced that vitamin D supplementation boosts testosterone naturally in overweight men by up to 30 percent. (12) This is pretty exciting because research has shown that vitamin D3 is also linked to helping to prevent and treat cancer! (13)
Regardless of the method of testosterone treatment chosen, patients will require regular monitoring during the first year of treatment in order to monitor clinical response to testosterone, testosterone levels and adverse effects, including prostate cancer (see Table 2). It is recommended that patients should be reviewed at least every three months during this time. Once treatment has been established, less frequent review is appropriate but the care of the patient should be the responsibility of an appropriately trained specialist with sufficient experience of managing patients treated with testosterone.
A related issue is the potential use of testosterone as a coronary vasodilator and anti-anginal agent. Testosterone has been shown to act as a vasodilator of coronary arteries at physiological concentrations during angiography (Webb, McNeill et al 1999). Furthermore men given a testosterone injection prior to exercise testing showed improved performance, as assessed by ST changes compared to placebo (Rosano et al 1999; Webb, Adamson et al 1999). Administration of one to three months of testosterone treatment has also been shown to improve symptoms of angina and exercise test performance (Wu and Weng 1993; English et al 2000; Malkin, Pugh, Morris et al 2004). Longer term studies are underway. It is thought that testosterone improves angina due its vasodilatory action, which occurs independently of the androgen receptor, via blockade of L-type calcium channels at the cell membrane of the vascular smooth muscle in an action similar to the dihydropyridine calcium-channel blockers such as nifedipine (Hall et al 2006).
^ Jump up to: a b Sapienza P, Zingales L, Maestripieri D (September 2009). "Gender differences in financial risk aversion and career choices are affected by testosterone". Proceedings of the National Academy of Sciences of the United States of America. 106 (36): 15268–73. Bibcode:2009PNAS..10615268S. doi:10.1073/pnas.0907352106. PMC 2741240. PMID 19706398.

The aim of treatment for hypogonadism is to normalize serum testosterone levels and abolish symptoms or pathological states that are due to low testosterone levels. The exact target testosterone level is a matter of debate, but current recommendations advocate levels in the mid-lower normal adult range (Nieschlag et al 2005). Truly physiological testosterone replacement would require replication of the diurnal rhythm of serum testosterone levels, but there is no current evidence that this is beneficial (Nieschlag et al 2005).
Vitamin D supplementation may potentially boost testosterone levels, but further research is needed to determine if it really has an effect on the testosterone levels of young people and athletes. The truth is likely similar to zinc and magnesium — being in a deficient state causes your testosterone levels to drop below baseline, and supplementing it just takes you right back to baseline (but not any higher).
Cross-sectional studies conducted at the time of diagnosis of BPH have failed to show consistent differences in testosterone levels between patients and controls. A prospective study also failed to demonstrate a correlation between testosterone and the development of BPH (Gann et al 1995). Clinical trials have shown that testosterone treatment of hypogonadal men does cause growth of the prostate, but only to the size seen in normal men, and also causes a small increase in prostate specific antigen (PSA) within the normal range (Rhoden and Morgentaler 2005). Despite growth of the prostate a number of studies have failed to detect any adverse effects on symptoms of urinary obstruction or physiological measurements such as flow rates and residual volumes (Snyder et al 1999; Kenny et al 2000, 2001). Despite the lack of evidence linking symptoms of BPH to testosterone treatment, it remains important to monitor for any new or deteriorating problems when commencing patients on testosterone treatment, as the small growth of prostate tissue may adversely affect a certain subset of individuals.
Testosterone has several positive effects on sexual function, but its most significant effect is on libido, sexual interest and arousal. Boys going through puberty develop an enhanced interest in sex (thoughts, fantasies, masturbation, intercourse) as a consequence of rising levels of testosterone. Hypogonadal men usually have a significant improvement in libido when TRT is initiated (Wang et al 2000; Morley and Perry 2003).
Saw palmetto: Uses, dosage, and side effects Saw palmetto is an extract from the berries of a type of palm tree. The berries have traditionally been used to ease urinary and reproductive problems. The extract is now used in herbal remedies to stabilize testosterone. Learn about its use, its effectiveness, the science behind the claims, and any side effects. Read now
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