We should probably start with the elephant in the room: do these supplements increase testosterone? The answer is probably yes. There are some ingredients that help convince your body to produce more testosterone, but there’s a catch. Testosterone boosters aren’t actually great at boosting; that is, at pushing your testosterone levels above your healthy, normal balance. Boosters typically act more like restorers — helping bring low testosterone levels back to that healthy equilibrium rather than boosting you above normal testosterone levels. Just like how if you have anemia, taking a vitamin B12 supplement can help restore your energy and reduce fatigue, but if your B12 levels are good, a supplement won’t give you super energy levels to stay awake for three days — your body will likely just process (read: pee) out the extra.
Mínguez-Alarcón, L., Chavarro, J. E., Mendiola, J., Roca, M., Tanrikut, C., Vioque, J., ... Torres-Cantero, A. M. (2017, March–April). Fatty acid intake in relation to reproductive hormones and testicular volume among young healthy men [Abstract]. Asian Journal of Andrology, 19(2), 184–190. Retrieved from https://www.ncbi.nlm.nih.gov/pubmed/27834316
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).

A large number of trials have demonstrated a positive effect of testosterone treatment on bone mineral density (Katznelson et al 1996; Behre et al 1997; Leifke et al 1998; Snyder et al 2000; Zacharin et al 2003; Wang, Cunningham et al 2004; Aminorroaya et al 2005; Benito et al 2005) and bone architecture (Benito et al 2005). These effects are often more impressive in longer trials, which have shown that adequate replacement will lead to near normal bone density but that the full effects may take two years or more (Snyder et al 2000; Wang, Cunningham et al 2004; Aminorroaya et al 2005). Three randomized placebo-controlled trials of testosterone treatment in aging males have been conducted (Snyder et al 1999; Kenny et al 2001; Amory et al 2004). One of these studies concerned men with a mean age of 71 years with two serum testosterone levels less than 12.1nmol/l. After 36 months of intramuscular testosterone treatment or placebo, there were significant increases in vertebral and hip bone mineral density. In this study, there was also a significant decrease in the bone resorption marker urinary deoxypyridinoline with testosterone treatment (Amory et al 2004). The second study contained men with low bioavailable testosterone levels and an average age of 76 years. Testosterone treatment in the form of transdermal patches was given for 1 year. During this trial there was a significant preservation of hip bone mineral density with testosterone treatment but testosterone had no effect on bone mineral density at other sites including the vertebrae. There were no significant alterations in bone turnover markers during testosterone treatment (Kenny et al 2001). The remaining study contained men of average age 73 years. Men were eligible for the study if their serum total testosterone levels were less than 16.5 nmol/L, meaning that the study contained men who would usually be considered eugonadal. The beneficial effects of testosterone on bone density were confined to the men who had lower serum testosterone levels at baseline and were seen only in the vertebrae. There were no significant changes in bone turnover markers. Testosterone in the trial was given via scrotal patches for a 36 month duration (Snyder et al 1999). A recent meta-analysis of the effects on bone density of testosterone treatment in men included data from these studies and two other randomized controlled trials. The findings were that testosterone produces a significant increase of 2.7% in the bone mineral density at the lumber spine but no overall change at the hip (Isidori et al 2005). These results from randomized controlled trials in aging men show much smaller benefits of testosterone treatment on bone density than have been seen in other trials. This could be due to the trials including patients who are not hypogonadal and being too short to allow for the maximal effects of testosterone. The meta-analysis also assessed the data concerning changes of bone formation and resorption markers during testosterone treatment. There was a significant decrease in bone resorption markers but no change in markers of bone formation suggesting that reduction of bone resorption may be the primary mode of action of testosterone in improving bone density (Isidori et al 2005).


Epidemiological data has associated low testosterone levels with atherogenic lipid parameters, including lower HDL cholesterol (Lichtenstein et al 1987; Haffner et al 1993; Van Pottelbergh et al 2003) and higher total cholesterol (Haffner et al 1993; Van Pottelbergh et al 2003), LDL cholesterol (Haffner et al 1993) and triglyceride levels (Lichtenstein et al 1987; Haffner et al 1993). Furthermore, these relationships are independent of other factors such as age, obesity and glucose levels (Haffner et al 1993; Van Pottelbergh et al 2003). Interventional trails of testosterone replacement have shown that treatment causes a decrease in total cholesterol. A recent meta-analysis of 17 randomized controlled trials confirmed this and found that the magnitude of changes was larger in trials of patients with lower baseline testosterone levels (Isidori et al 2005). The same meta-analysis found no significant overall change in LDL or HDL cholesterol levels but in trials with baseline testosterone levels greater than 10 nmol/l, there was a small reduction in HDL cholesterol with testosterone treatment.
Researchers found that the simple act ‘expressing power through open, expansive postures’ (i.e. standing up straight and proud) can increase Testosterone and decrease cortisol (58), along with improving feelings of power and tolerance for risk. Easy! Your mother was right – don’t slouch. This could be a handy trick before making a speech or going on a date!
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).
Dr. Darryn Willoughby, a professor of health, human performance and recreation and the director of the Exercise and Biochemical Nutrition Laboratory at Baylor University, told us that even in studies where there was an increase in testosterone, it was only around 15–20 percent. “In men with clinically normal testosterone levels, this modest increase will most likely not be anabolic enough to improve exercise performance,” he says. So if you have normal testosterone levels, and are simply trying to get an extra edge in gaining muscle, losing weight, or some extra time in the bedroom — you might see some results from taking a testosterone booster. But really, these will be most useful for men with low testosterone trying to get back to a healthy testosterone range.

When females have a higher baseline level of testosterone, they have higher increases in sexual arousal levels but smaller increases in testosterone, indicating a ceiling effect on testosterone levels in females. Sexual thoughts also change the level of testosterone but not level of cortisol in the female body, and hormonal contraceptives may affect the variation in testosterone response to sexual thoughts.[51]


Insulin causes lower Testosterone levels, so go easy on the carbs and eat more protein right? Well you need to be careful with protein consumption – Excess protein without fat can also cause insulin spikes. So go easy on that chicken breast with a side of egg white omelets washed down with a protein shake. From an insulin point of view you may as well drink a can of soda with some aminos acid! So what should you do? Eat more fat.
There is an increased incidence of hypogonadism in men with rheumatoid arthritis. Tengstrand et al (2002) studied hormonal levels in 104 men with rheumatoid arthritis and 99 age-matched healthy men. They divided their subjects into 3 age groups: 30–49, 40–59, 60–69. Mean non-sex hormone binding globulin-bound testosterone (bioavailable testosterone) was lower in men with rheumatoid arthritis for each of the three groups. LH was also found to be lower in the patients with rheumatoid arthritis suggesting a hypothalamic-pituitary cause of the reduced bioavailable testosterone. Of the 104 men with rheumatoid arthritis, 33 had hypogonadism compared to 7 of the 99 healthy controls.
Caffeine. Use caffeine moderately. Too much of the jittery juice increases cortisol, which decreases testosterone. Moreover, consuming caffeine late in the day hurts sleep, which lowers testosterone production. But one recent study indicates that caffeine consumed before working out may boost testosterone levels and help you exercise more efficiently. During my experiment I popped a piece of caffeinated gum five minutes before my workouts. Each piece had 100 mg of caffeine, about the same amount in a cup of coffee. That was usually it for my caffeine intake that day.
Androgens may modulate the physiology of vaginal tissue and contribute to female genital sexual arousal.[48] Women's level of testosterone is higher when measured pre-intercourse vs pre-cuddling, as well as post-intercourse vs post-cuddling.[49] There is a time lag effect when testosterone is administered, on genital arousal in women. In addition, a continuous increase in vaginal sexual arousal may result in higher genital sensations and sexual appetitive behaviors.[50]
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.
Xenoestrogen is a chemical that imitates estrogen in the human body. When men are exposed to too much of this estrogen-imitating chemical, T levels drop significantly. The problem is xenoestrogen is freaking everywhere — plastics, shampoos, gasoline, cows, toothpaste. You name it and chances are there are xenoestrogen in it. The ubiquitous nature of this chemical in our modern world is one reason some endocrinologists believe that testosterone levels are lower in men today than in decades past. It’s also a reason doctors say the number of boys born with hypospadias — a birth defect in which the opening of the urethra is on the underside of the penis and not at the tip — has doubled.  Note to expecting parents: make sure mom stays away from xenoestrogens during the pregnancy.
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).

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).
Present in much greater levels in men than women, testosterone initiates the development of the male internal and external reproductive organs during foetal development and is essential for the production of sperm in adult life. This hormone also signals the body to make new blood cells, ensures that muscles and bones stay strong during and after puberty and enhances libido both in men and women. Testosterone is linked to many of the changes seen in boys during puberty (including an increase in height, body and pubic hair growth, enlargement of the penis, testes and prostate gland, and changes in sexual and aggressive behaviour). It also regulates the secretion of luteinising hormone and follicle stimulating hormone. To effect these changes, testosterone is often converted into another androgen called dihydrotestosterone. 
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