A loophole in FDA regulations allows pharmaceutical marketers to urge men to talk to their doctors if they have certain "possible signs" of testosterone deficiency. "Virtually everybody asks about this now because the direct-to-consumer marketing is so aggressive," says Dr. Michael O'Leary, a urologist at Harvard-affiliated Brigham and Women's Hospital. "Tons of men who would never have asked me about it before started to do so when they saw ads that say 'Do you feel tired?'"
One study looking at alcohol consumption found that increasing alcohol consumption led to a higher level of free & total testosterone compared to a non-drinking control group (20). Drinking did however lower SHBG testosterone levels, though this type of testosterone is bound to a protein meaning our bodies cannot use it to build muscle or increase our mood.
Vitamin D deficiency is a growing epidemic in the US, and is profoundly affecting men’s health. The cholesterol-derived steroid hormone vitamin D is crucial for men’s health. It plays a role in the development of the sperm cell nucleus, and helps maintain semen quality and sperm count. Vitamin D can also increase your testosterone level, helping improve your libido. Have your vitamin D levels tested using a 25(OH)D or a 25-hydroxyvitamin D test. The optimal level of vitamin D is around 50 to 70 ng/ml for adults. There are three effective sources of vitamin D:
Sprinting has been shown numerous times that it has positive effects on testosterone levels. One 2011 study (ref 84) looked at weightlifters who performed 4x35m sprints twice a week. In contrast to the control group (who continued lifting but did not sprint), it was found that “After the 4-week training program, total testosterone and the total testosterone/cortisol ratio increased significantly in the (sprinters) EXP group”.
Currently available testosterone preparations in common use include intramuscular injections, subcutaneous pellets, buccal tablets, transdermal gels and patches (see Table 2). Oral testosterone is not widely used. Unmodified testosterone taken orally is largely subject to first-pass metabolism by the liver. Oral doses 100 fold greater than physiological testosterone production can be given to achieve adequate serum levels. Methyl testosterone esters have been associated with hepatotoxicity. There has been some use of testosterone undecanoate, which is an esterified derivative of testosterone that is absorbed via the lymphatic system and bypasses the liver. Unfortunately, it produces unpredictable testosterone levels and increases testosterone levels for only a short period after each oral dose (Schurmeyer et al 1983).
There are the testosterone deficiency signs, such as loss of sexual desire, erectile dysfunction, impaired fertility, chronic fatigue, etc. But it’s not always possible to understand which medical condition caused the decrease in testosterone levels. For example, if you always feel exhausted and have no sexual desire, it may provide evidence of depression.
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.
Zinc is involved in virtually every aspect of male reproduction, including testosterone metabolism. Several studies support the use of zinc for treating low sperm counts, especially when accompanied by low testosterone levels. In these studies, zinc has shown an ability to raise both sperm counts and testosterone levels. Many men may be suffering from low testosterone simply because of a zinc deficiency. Taking 30–45 mg of zinc per day is recommended; balance with 2–3 mg of copper for best results.
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).
It is now well-established that elderly men with type 2 diabetes mellitus have reduced levels of testosterone (Barrett-Connor 1992; Betancourt-Albrecht and Cunningham 2003). It is known, however, that obese men and diabetic men have reduced levels of SHBG (Barrett-Connor 1990) which could account for the lower total testosterone levels found in diabetic men. Dhindsa et al (2004) studied 103 male patients who had type 2 diabetes mellitus using free testosterone (done by equilibrium dialysis) or calculated free testosterone which takes SHBG levels into account. Of the 103 patients, 57 had free testosterone by equilibrium dialysis and of these, 14 (25%) had a free T below 0.174 nmol/L and were considered hypogonadal. Using a total testosterone of 10.4 nmol/L (300ng/dl) as the lower limit of normal 45 patients (43%) were in the hypogonadal range. They also found that LH and FSH concentrations were significantly lower in the hypogonadal group. The authors thus concluded that hypogonadotropic hypogonadism was a common finding in type 2 diabetes irrespective of glycemic control, duration of disease or the presence of complications of diabetes or obesity.
Under Federal Regulation, the Federal Trade Commission requires that disclosures on any relationship which provide any compensation at any time. From time to time, this website requires revenue to provide free services to all users. Some links on this website contain affiliate or referral links that compensates us for buying a product or service after being referral to from our website due to any mention or recommendation. For that we are compensated with a commission.
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).
What you really need to worry about is the level of triglycerides in your blood. High triglycerides are a big warning sign for potential cardiovascular problems and disease. Again, to keep your triglycerides low while on a high cholesterol diet, take in a lot of veggies, limit your carb intake (especially sugars), supplement with omega 3 fish oil (more fat to make your cholesterol better – ironic right?), and exercise regularly.
There is no definite age to recommend when is appropriate to start using a Testosterone Booster. It depends on the age in which you initially hit puberty, and how long your body produces testosterone at its peak level. If you feel as though your Testosterone levels have started to decline, usually characterised through a decrease in strength, energy, libido and ability to build size, then these are usually good determinants that it may be time to commence using a Natural Testosterone booster. The Typical age range is between 21- 25, however this is highly variable depending on your own genetics, training and diet.
Unlike women, who experience a rapid drop in hormone levels at menopause, men experience a more gradual decrease of testosterone levels over time. The older the man, the more likely he is to experience below-normal testosterone levels. Men with testosterone levels below 300 ng/dL may experience some degree of low T symptoms. Your doctor can conduct a blood test and recommend treatment if needed. They can discuss the potential benefits and risks of testosterone medication, as well.
The reliable measurement of serum free testosterone requires equilibrium dialysis. This is not appropriate for clinical use as it is very time consuming and therefore expensive. The amount of bioavailable testosterone can be measured as a percentage of the total testosterone after precipitation of the SHBG bound fraction using ammonium sulphate. The bioavailable testosterone is then calculated from the total testosterone level. This method has an excellent correlation with free testosterone (Tremblay and Dube 1974) but is not widely available for clinical use. In most clinical situations the available tests are total testosterone and SHBG which are both easily and reliably measured. Total testosterone is appropriate for the diagnosis of overt male hypogonadism where testosterone levels are very low and also in excluding hypogonadism in patients with normal/high-normal testosterone levels. With increasing age, a greater number of men have total testosterone levels just below the normal range or in the low-normal range. In these patients total testosterone can be an unreliable indicator of hypogonadal status. There are a number of formulae that calculate an estimated bioavailable or free testosterone level using the SHBG and total testosterone levels. Some of these have been shown to correlate well with laboratory measures and there is evidence that they more reliably indicate hypogonadism than total testosterone in cases of borderline biochemical hypogonadism (Vermeulen et al 1971; Morris et al 2004). It is important that such tests are validated for use in patient populations relevant to the patient under consideration.
Epidemiological studies suggest that many significant clinical findings and important disease states are linked to low testosterone levels. These include osteoporosis (Campion and Maricic 2003), Alzheimer’s disease (Moffat et al 2004), frailty, obesity (Svartberg, von Muhlen, Sundsfjord et al 2004), diabetes (Barrett-Connor 1992), hypercholesterolemia (Haffner et al 1993; Van Pottelbergh et al 2003), hypertension (Phillips et al 1993), cardiac failure (Tappler and Katz 1979; Kontoleon et al 2003) and ischemic heart disease (Barrett-Connor and Khaw 1988). The extent to which testosterone deficiency is involved in the pathogenesis of these conditions, or to which testosterone supplementation could be useful in their treatment is an area of great interest with many unanswered questions.
There are valid concerns about the safety of long-term treatment with testosterone particularly with respect to the cardiovascular system and the potential for stimulating prostate cancer development. There are no convincing hard data, however, to support these concerns. If anything, the data strongly suggest that adequate testosterone availability is cardioprotective and coronary risk factors such as diabetes, obesity and the metabolic syndrome are associated with reduced testosterone levels. It is certainly appropriate to avoid giving testosterone to men with prostate or breast cancer but it is not appropriate to accuse testosterone of inducing the development of de novo prostate cancers since evidence for this accusation is lacking (Wang et al 2004; Feneley and Carruthers 2006).
Dobs and colleagues found that men with an increased body mass index had both reduced testosterone and reduced high density lipoprotein (HDL) levels. Treatment with testosterone increased the levels of HDL (Dobs et al 2001). Rising levels of HDL are not a consistent finding with TRT. More often, however, one finds reduced total cholesterol, low density lipoprotein (LDL) cholesterol and triglyceride levels with TRT (Zgliczynski et al 1996; Whitsel et al 2001).