I started doing prostate biopsies before putting men on testosterone therapy because the fear had always been that a hidden cancer might grow due to increased testosterone. It was also believed that low testosterone was protective. Well, we found prostate cancer in one of the first men with low testosterone we biopsied, even though his PSA level and digital rectal exam (DRE) were normal. As we did more of these, we found more and more cases, about one out of seven, despite normal DRE and normal PSA. When we had data for 77 men and the cancer rate was about the same, 14%, the Journal of the American Medical Association published our findings. At the time, that rate of prostate cancer in men with normal PSA was several times higher than anything published previously, and it approximated the risk of men who had an elevated PSA or an abnormal DRE. That was in 1996.
Epidemiological evidence supports a link between testosterone and glucose metabolism. Studies in non-diabetic men have found an inverse correlation of total or free testosterone with glucose and insulin levels (Simon et al 1992; Haffner et al 1994) and studies show lower testosterone levels in patients with the metabolic syndrome (Laaksonen et al 2003; Muller et al 2005; Kupelian et al 2006) or diabetes (Barrett-Connor 1992; Andersson et al 1994; Rhoden et al 2005). A study of patients with type 2 diabetes using measurement of serum free testosterone by the gold standard method of equilibrium dialysis, found a 33% prevalence of biochemical hypogonadism (Dhindsa et al 2004). The Barnsley study demonstrated a high prevalence of clinical and biochemical hypogonadism with 19% having total testosterone levels below 8 nmol/l and a further 25% between 8–12 nmol/l (Kapoor, Aldred et al 2007). There are also a number longitudinal studies linking low serum testosterone levels to the future development of the metabolic syndrome (Laaksonen et al 2004) or type 2 diabetes (Haffner et al 1996; Tibblin et al 1996; Stellato et al 2000; Oh et al 2002; Laaksonen et al 2004), indicating a possible role of hypogonadism in the pathogenesis of type 2 diabetes in men. Alternatively, it has been postulated that obesity may be the common link between low testosterone levels and insulin resistance, diabetes and cardiovascular disease (Phillips et al 2003; Kapoor et al 2005). With regard to this hypothesis, study findings vary as to whether the association of testosterone with diabetes occurs independently of obesity (Haffner et al 1996; Laaksonen et al 2003; Rhoden et al 2005).
More specifically, saw palmetto is frequently used to suppress prostate growth and combat abnormal urine flow that results from an enlarged prostate. The reason it is believed that saw palmetto can combat prostate hyperplasia is based on some research indicating it may block an enzyme (5-alpha-reductase) that converts testosterone into dihydrotestosterone (DHT).
An international consensus document was recently published and provides guidance on the diagnosis, treatment and monitoring of late-onset hypogonadism (LOH) in men. The diagnosis of LOH requires biochemical and clinical components. Controversy in defining the clinical syndrome continues due to the high prevalence of hypogonadal symptoms in the aging male population and the non-specific nature of these symptoms. Further controversy surrounds setting a lower limit of normal testosterone, the limitations of the commonly available total testosterone result in assessing some patients and the unavailability of reliable measures of bioavailable or free testosterone for general clinical use. As with any clinical intervention testosterone treatment should be judged on a balance of risk versus benefit. The traditional benefits of testosterone on sexual function, mood, strength and quality of life remain the primary goals of treatment but possible beneficial effects on other parameters such as bone density, obesity, insulin resistance and angina are emerging and will be reviewed. Potential concerns regarding the effects of testosterone on prostate disease, aggression and polycythaemia will also be addressed. The options available for treatment have increased in recent years with the availability of a number of testosterone preparations which can reliably produce physiological serum concentrations.
Zinc: Another potent ingredient to add to any testosterone booster is zinc. This study shows how zinc is able to prevent a decline in testosterone levels during intense and hard workouts performed by wrestlers. Researchers found that the group who was administered with a placebo had a reduction in testosterone, as opposed to the group who were supplemented with zinc. The placebo group had a notable drop in their testosterone count during this process. Zinc has also been shown to increase the number of free testosterone and lower SHBG.
Scientists in Italy found that subjects who consumed roughly 3 grams of D-AA for 12 days observed a 42 percent increase in testosterone levels. The researchers also noted that the D-AA group still had 22 percent more testosterone than the placebo group three days after they stopped supplementing. Conversely, a more recent article published in Nutrition Research found no increase in testosterone levels in resistance-trained males after supplementing with 3 grams of D-AA for 28 days.
Fenugreek is often found in Indian, Turkish, and Persian cuisine. Multiple studies have found it to improve testosterone levels, and in particular, sexual performance. Scientists at Babu Banarasi Das University and King George’s Medical University in India have found that fenugreek improved testosterone levels. Testosterone levels increased for 90% of the volunteers, sperm morphology (the size and shape of sperm) improved for 14.6%, and more than 50% of volunteers experienced improvements in mental alertness, mood, and libido.
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Sleep apnea is another frequently listed contraindication to testosterone treatment. There have been a few reports of the development, or worsening, of sleep apnea during testosterone therapy (Matsumoto et al 1985) but sleep apnea is actually associated with lower serum testosterone levels (Luboshitzky et al 2002). The reduction in fat mass during treatment with testosterone could potentially be beneficial for sleep apnea, so many specialists will still consider patients for treatment with appropriate monitoring. It is wise to take a clinical history for sleep apnea during testosterone treatment in all men and perform sleep studies in those who develop symptoms.
One of the few testosterone boosters on the market to feature Eurycoma Longifolia, a patented ingredient that was developed at Massachusetts Institute of Technology (MIT) for the treatment of sexual dysfunction and male fertility, Tongkat Ali supports increased sex drive through multiple pathways, including boosting one’s free testosterone levels. Great as a standalone testosterone booster and a staple in many people’s post cycle after an anabolic cycle.
If you do take DAA I recommend cycling it (i.e. 5 days on, 2 off, over 4 weeks then 4 weeks off). And taking it with an aromatase inhibitor (which ensures the aspartic acid doesn’t get converted to estrogen). Especially as more studies are coming out showing the increase in testosterone is limited to a week or two before it drops back to normal levels.
My preference is to start men on testosterone, for a couple of reasons. First, if a man has successful return of his own erections, it’s like a home run for him. He doesn’t have to take a pill in anticipation of having sex. He can have sex whenever he wants. Second, the benefits of testosterone-replacement therapy often go way beyond erectile dysfunction. That may be what brought the patient into the office originally, but then he comes back saying how much better he feels in general, how much more energetic and motivated he is, how his drives on the golf course seem to be going farther, and how his mood is better.
I have been on testosterone injections for about six months now. My urologist has me taking 50mg a week. I noticed that when I take the injection my normal resting heart rate is about 61 beats a minute, on the day of the injection it goes up to about 84 BPM. I also notice a tightness in my chest/esophagus area for about 24-48 hours and than it subsides. I have also noticed it appears to make my eyes water on the day of the injection. I have gotten off the injections because that is the obvious thing to do, but the dillema is than my personal life with the wife suffers. I am in great shape and work out all the time. Is there anything you can recommended I do to mitigate the increased blood pressure and increased heart beat? My last blood test showed normal except my estrogen was right at the recommended max but still with in limits. Any advice would be appreciated.
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Inaccurate or misinterpreted test results can either falsely diagnose or miss a case of testosterone deficiency. Your testosterone level should be measured between 7 am and 10 am, when it's at its peak. Confirm a low reading with a second test on a different day. It may require multiple measurements and careful interpretation to establish bioavailable testosterone, or the amount of the hormone that is able to have effects on the body. Consider getting a second opinion from an endocrinologist.
Herbalists have used _Trifolium pratense_, red clover, to treat menopausal symptoms like hot flashes. The mechanisms underlying these effects remain unknown. Testosterone decreases hot flashes in some postmenopausal women, so red clover may work in this way. A 2015 paper in the Avicenna Journal of Phytomedicine reviewed the literature testing this idea.
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.
There are three ways to increase testosterone activity naturally with simple lifestyle choices. The first is to increase total testosterone production. Second is to increase the amount of free and active testosterone that can stimulate testosterone receptors. The third is to unblock testosterone receptors, opening them up for testosterone stimulation.
Type 2 diabetes is an important condition in terms of morbidity and mortality, and the prevalence is increasing in the developed and developing world. The prevalence also increases with age. Insulin resistance is a primary pathological feature of type 2 diabetes and predates the onset of diabetes by many years, during which time raised serum insulin levels compensate and maintain normoglycemia. Insulin resistance and/or impaired glucose tolerance are also part of the metabolic syndrome which also comprises an abnormal serum lipid profile, central obesity and hypertension. The metabolic syndrome can be considered to be a pre-diabetic condition and is itself linked to cardiovascular mortality. Table 1 shows the three commonly used definitions of the metabolic syndrome as per WHO, NCEPIII and IDF respectively (WHO 1999; NCEPIII 2001; Zimmet et al 2005).
Testosterone makes you angry. This is probably the most common myth about T. The reality is that there’s no concrete evidence that high testosterone levels cause anger and violent outbursts. In fact, the opposite might be true; low testosterone, not high T, is what causes anger and irritability in men. As discussed above, having low T levels has been linked to depression in men and it just so happens that two of the primary symptoms of depression in men are increased angry outbursts and irritability. So if you’re chronically angry, you might be depressed, and you might be depressed because you have low T. As I mentioned above, I became less moody and irritable during my experiment, which I attribute to the boost in my testosterone levels.
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.
Another benefit of the increased muscle mass was that I got stronger. My bench press, squat, and deadlift all enjoyed significant gains during my experiment. It’s great to be able to bench press 225 pounds again for 5 sets of 5 like I used to in high school, and I’m on track to beat my maxes on the bench and squat that my 18-year-old self set over 12 years ago.
During the second trimester, androgen level is associated with sex formation. This period affects the femininization or masculinization of the fetus and can be a better predictor of feminine or masculine behaviours such as sex typed behaviour than an adult's own levels. A mother's testosterone level during pregnancy is correlated with her daughter's sex-typical behavior as an adult, and the correlation is even stronger than with the daughter's own adult testosterone level.
Studies have demonstrated reduced testosterone levels in men with heart failure as well as other endocrine changes (Tappler and Katz 1979; Kontoleon et al 2003). Treatment of cardiac failure with chronic mechanical circulatory support normalizes many of these changes, including testosterone levels (Noirhomme et al 1999). More recently, two double-blind randomized controlled trials of testosterone treatment for men with low or low-normal serum testosterone levels and heart failure have shown improvements in exercise capacity and symptoms (Pugh et al 2004; Malkin et al 2006). The mechanism of these benefits is currently unclear, although a study of the acute effects of buccal testosterone given to men with chronic cardiac failure under invasive monitoring showed that testosterone increased cardiac index and reduced systemic vascular resistance (Pugh et al 2003). Testosterone may prove useful in the management of cardiac failure but further research is needed.
Falling in love decreases men's testosterone levels while increasing women's testosterone levels. There has been speculation that these changes in testosterone result in the temporary reduction of differences in behavior between the sexes. However, it is suggested that after the "honeymoon phase" ends—about four years into a relationship—this change in testosterone levels is no longer apparent. Men who produce less testosterone are more likely to be in a relationship or married, and men who produce more testosterone are more likely to divorce; however, causality cannot be determined in this correlation. Marriage or commitment could cause a decrease in testosterone levels. Single men who have not had relationship experience have lower testosterone levels than single men with experience. It is suggested that these single men with prior experience are in a more competitive state than their non-experienced counterparts. Married men who engage in bond-maintenance activities such as spending the day with their spouse/and or child have no different testosterone levels compared to times when they do not engage in such activities. Collectively, these results suggest that the presence of competitive activities rather than bond-maintenance activities are more relevant to changes in testosterone levels.