Remember that each person is unique, and each body responds differently to treatment. TT may help erectile function, low sex drive, bone marrow density, anemia, lean body mass, and/or symptoms of depression. However, there is no strong evidence that TT will help memory recall, measures of diabetes, energy, tiredness, lipid profiles, or quality of life.
A 46 XY fetus is destined to become a male because the Y chromosome carries testicular determining gene which initiates transformation of the undifferentiated gonad into testes (Töhönen 2003). The testes subsequently produce both Mullerian Inhibiting Factor (to induce degeneration of the Mullerian system, the internal female ductal apparatus) and testosterone (to stimulate growth and development of the Wolffian system – epididymus, vas deferens, seminal vesicle and, after conversion to dihydrotestosterone (DHT) by the enzyme 5-α-reducase, the prostate gland). DHT is also the primary androgen to cause androgenization of the external genitalia.
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.
The University of Connecticut recently published findings stating that those who supplemented with whey protein produced less cortisol, a stress hormone, than those who did not supplement. Cortisol lowers production of sex hormones and is also responsible for belly fat formation. Ricotta is an excellent source of natural whey protein and amino acids, both of which are essential to muscle growth and avoiding the spare tire.
Early infancy androgen effects are the least understood. In the first weeks of life for male infants, testosterone levels rise. The levels remain in a pubertal range for a few months, but usually reach the barely detectable levels of childhood by 4–7 months of age. The function of this rise in humans is unknown. It has been theorized that brain masculinization is occurring since no significant changes have been identified in other parts of the body. The male brain is masculinized by the aromatization of testosterone into estrogen, which crosses the blood–brain barrier and enters the male brain, whereas female fetuses have α-fetoprotein, which binds the estrogen so that female brains are not affected.
The rise in testosterone levels during competition predicted aggression in males but not in females. Subjects who interacted with hand guns and an experimental game showed rise in testosterone and aggression. Natural selection might have evolved males to be more sensitive to competitive and status challenge situations and that the interacting roles of testosterone are the essential ingredient for aggressive behaviour in these situations. Testosterone produces aggression by activating subcortical areas in the brain, which may also be inhibited or suppressed by social norms or familial situations while still manifesting in diverse intensities and ways through thoughts, anger, verbal aggression, competition, dominance and physical violence. Testosterone mediates attraction to cruel and violent cues in men by promoting extended viewing of violent stimuli. Testosterone specific structural brain characteristic can predict aggressive behaviour in individuals.
Prolactin is suppressed by dopamine activity. Since supplementing L-DOPA suppresses prolactin (by increasing dopamine activity), supplementing L-DOPA would increase testosterone if prolactin was abnormally high. The average, healthy male does not have elevated prolactin (unless he’s on steroids), so supplementing with L-DOPA will not increase your testosterone levels.
Testosterone is a sex hormone that plays important roles in the body. In men, it’s thought to regulate sex drive (libido), bone mass, fat distribution, muscle mass and strength, and the production of red blood cells and sperm. A small amount of circulating testosterone is converted to estradiol, a form of estrogen. As men age, they often make less testosterone, and so they produce less estradiol as well. Thus, changes often attributed to testosterone deficiency might be partly or entirely due to the accompanying decline in estradiol.
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.
Great article with a lot of useful information. I completely agree with your top three picks. I have done a ton of research as well. Currently I am taking Testogen for over two months and it has worked for me. It has double my low T and I am 61 years old. I do feel better and have more energy. Even have morning wood sometimes and haven’t for a long time.
However, an important peculiarity of testosterone boosting products is their inability to cause addiction. Also, as opposed to steroids, the natural supplements don’t disturb the bodily functions. It means that these products don’t destroy the men’s hormone balance and don’t suppress the natural testosterone synthesis. Instead, the high-quality boosters successfully and safely eliminate the hormone imbalance issues in the men’s body.
The sexual hormone can encourage fair behavior. For the study, subjects took part in a behavioral experiment where the distribution of a real amount of money was decided. The rules allowed both fair and unfair offers. The negotiating partner could subsequently accept or decline the offer. The fairer the offer, the less probable a refusal by the negotiating partner. If no agreement was reached, neither party earned anything. Test subjects with an artificially enhanced testosterone level generally made better, fairer offers than those who received placebos, thus reducing the risk of a rejection of their offer to a minimum. Two later studies have empirically confirmed these results. However men with high testosterone were significantly 27% less generous in an ultimatum game. The Annual NY Academy of Sciences has also found anabolic steroid use which increase testosterone to be higher in teenagers, and this was associated with increased violence. Studies have also found administered testosterone to increase verbal aggression and anger in some participants.
Testosterone insufficiency has been associated with HIV infection in men (Dobs et al 1988). Early reports suggested that testosterone therapy may have an ameliorating effect on both depression and decreased energy in HIV infected men, even if testosterone levels were not reduced (Rabkin et al 1999; Grinspoon et al 2000; Rabkin et al 2000). Both depression and fatigue, however, are common features of HIV-positive men and may be associated with factors other than reduced levels of testosterone. The disease itself may induce depression and fatigue may be a consequence of the disease, per se, or of some of the medications used to control HIV.
We’ll be honest. Testosterone boosters don’t really boost. The best testosterone booster is like taking a multivitamin with extra herbs that might slightly and temporarily increase your testosterone levels. Like all supplements, finding the right testosterone booster means wading into a sea of ingredients, all promising to help. Of 133 testosterone boosters, we found only one with the right ingredients to help raise your testosterone levels: Beast Sports Nutrition - Super Test ($45.88 for 180 capsules, or $2.04 per day).
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).
Everyone knows that carbohydrates are extremely important for testosterone production, but instead of reaching for grains during your next meal, stack your plate high with potatoes. Research reveals that grains have inflammatory properties, but the testosterone-friendly starches in potatoes will have the bodybuilder in your life smiling at dinnertime!
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).
Binge drinking on the other hand does impact Testosterone levels – especially on a short term basis. Two studies (22 & 23) show that large acute quantities of alcohol consumption in a short period led to decreases in Testosterone levels by a whooping 20-23% after 24hours! Note however this is drinking to extreme excess! Likewise, chronic alcohol abuse is known to reduce testosterone more notably (as seen in alcoholics).
A number of epidemiological studies have found that bone mineral density in the aging male population is positively associated with endogenous androgen levels (Murphy et al 1993; Ongphiphadhanakul et al 1995; Rucker et al 2004). Testosterone levels in young men have been shown to correlate with bone size, indicating a role in determination of peak bone mass and protection from future osteoporosis (Lorentzon et al 2005). Male hypogonadism has been shown to be a risk factor for hip fracture (Jackson et al 1992) and a recent study showed a high prevalence of hypogonadism in a group of male patients with average age 75 years presenting with minimal trauma fractures compared to stroke victims who acted as controls (Leifke et al 2005). Estrogen is a well known determinant of bone density in women and some investigators have found serum estrogen to be a strong determinant of male bone density (Khosla et al 1998; Khosla et al 2001). Serum estrogen was also found to correlate better than testosterone with peak bone mass (Khosla et al 2001) but this is in contradiction of a more recent study showing a negative correlation of estrogen with peak bone size (Lorentzon et al 2005). Men with aromatase deficiency (Carani et al 1997) or defunctioning estrogen receptor mutations (Smith et al 1994) have been found to have abnormally low bone density despite normal or high testosterone levels which further emphasizes the important influence of estrogen on male bone density.
The finding of hypogonadism in diabetic men is not just a scientific curiosity, it may have practical management implications. Kapoor and colleagues (2006) undertook a placebo-controlled double blind study to determine the effect of testosterone therapy on insulin resistance and glycemic control in hypogonadal men with type 2 diabetes. They found that men treated with testosterone had reductions in glycated hemoglobin insulin resistance, fasting blood sugar, waist circumference, waist/hip ratio and total cholesterol.
Male hypogonadism is a clinical syndrome caused by a lack of androgens or their action. Causes of hypogonadism may reflect abnormalities of the hypothalamus, pituitary, testes or target tissues. Increases in the amount of testosterone converted to estrogen under the action of the enzyme aromatase may also contribute to hypogonadism. Most aspects of the clinical syndrome are unrelated to the location of the cause. A greater factor in the production of a clinical syndrome is the age of onset. The development of hypogonadism with aging is known as late-onset hypogonadism and is characterised by loss of vitality, fatigue, loss of libido, erectile dysfunction, somnolence, depression and poor concentration. Hypogonadal ageing men also gain fat mass and lose bone mass, muscle mass and strength.
Testosterone is a steroid from the androstane class containing a keto and hydroxyl groups at the three and seventeen positions respectively. It is biosynthesized in several steps from cholesterol and is converted in the liver to inactive metabolites. It exerts its action through binding to and activation of the androgen receptor. In humans and most other vertebrates, testosterone is secreted primarily by the testicles of males and, to a lesser extent, the ovaries of females. On average, in adult males, levels of testosterone are about 7 to 8 times as great as in adult females. As the metabolism of testosterone in males is more pronounced, the daily production is about 20 times greater in men. Females are also more sensitive to the hormone.
In a recent study of male workers, men with low testosterone levels had an increased chance of severe erectile dysfunction (Kratzik et al 2005), although such a link had not been found previously (Rhoden et al 2002). Certainly erectile dysfunction is considered part of the clinical syndrome of hypogonadism, and questions regarding erectile dysfunction form part of the clinical assessment of patients with hypogonadism (Morley et al 2000; Moore et al 2004).
Cardiovascular disease, and its underlying pathological process atherosclerosis, is an important cause of morbidity and mortality in the developed and developing world. Coronary heart disease in particular is the commonest cause of death worldwide (AHA 2002; MacKay and Mensah 2004). As well as increasing with age, this disease is more common in the male versus female population internationally, which has led to interest in the potential role of sex hormones in modulating risk of development of atherosclerosis. Concerns about the potential adverse effects of testosterone treatment on cardiovascular disease have previously contributed to caution in prescribing testosterone to those who have, or who are at risk of, cardiovascular disease. Contrary to fears of the potential adverse effects of testosterone on cardiovascular disease, there are over forty epidemiological studies which have examined the relationship of testosterone levels to the presence or development of coronary heart disease, and none have shown a positive correlation. Many of these studies have found the presence of coronary heart disease to be associated with low testosterone levels (Reviews: Jones, Jones et al 2003; Jones et al 2005).
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.
Instead of turning to some drug that can only ameliorate symptoms and cause additional complications, I recommend using a natural saw palmetto supplement. Dr. Moerck says that there are about 100 clinical studies on the benefits of saw palmetto, one of them being a contributed to decreased prostate cancer risk. When choosing a saw palmetto supplement, you should be wary of the brand, as there are those that use an inactive form of the plant.
The regulation of testosterone production is tightly controlled to maintain normal levels in blood, although levels are usually highest in the morning and fall after that. The hypothalamus and the pituitary gland are important in controlling the amount of testosterone produced by the testes. In response to gonadotrophin-releasing hormone from the hypothalamus, the pituitary gland produces luteinising hormone which travels in the bloodstream to the gonads and stimulates the production and release of testosterone.