Ok. So this product is meant to be taken continuously and without side-effects. But my question is, will there be replenishment from this product in aiding the body's natural ability to produce testosterone? In other words, will there ever be a time when I can say well I don't have to take this any more as my body is producing testosterone again on it's own and my muscle mass has been enhanced?
The illegal testosterone supplements give immediate results and can be obtained without a prescription. However, it is strongly recommended to avoid these boosters as they contain an anabolic steroid, which is harmful to the body. The legal kinds of them are the best testosterone supplements and are considered as safe and efficient for muscle growth and to increase sex drive, but they are also not completely devoid of adverse effects. There are many side effects associated with the use of these testosterone therapy. The natural testosterone boosters are the safest and highly recommended testosterone supplements.
While I do have a pretty manly mustache, I’m not a doctor or a medical expert. I’m a guy with a law degree he’s never used who blogs about manliness. What I’m about to share shouldn’t be taken as a substitute for qualified medical expertise. It’s simply my experience and views on the subject. Before you make any changes in lifestyle or diet, talk to your doctor or healthcare provider. Be smart.
Testosterone makes a contribution to nitric oxide formation. Nitric oxide, released from penile nerves stimulates guanylate cyclase which catalyzes the transformation of guanosine-5-triphosphate into 3′,5′-cyclic, guanosine monophosphate (cyclic GMP). Gyclic GMP causes vasodilatation and hence erection formation (Morelli et al 2005). The breakdown of cyclic GMP to GMP is mediated by the enzyme, phosphodiesterase type-5, the inhibitors of which (eg, sildenafil citrate) enhance erection formation and maintanence (Carson and Lue 2005).
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.
Afrisham, R., Sadejh-Nejadi, S., SoliemaniFar, O., Kooti, W., Ashtary-Larky, D., Alamiri, F., … Khaneh-Keshi, A. (2016, November 24). Salivary testosterone levels under psychological stress and its relationship with rumination and five personality traits in medical students. Psychiatry Investigations, 13(6), 637–643. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5128352/
Since then there have been many publications documenting suppressed testosterone and gonadotropins (Daniell 2006) in men using opioid medications whether these agents were administrated orally (Daniell 2002) or intrathecally (Finch et al 2000). Not only do opioids act centrally by suppressing GnRH, they also act directly on the testes inhibiting the release of testosterone by Leydig cells during stimulation with human chorionic gonadotropin (Purohit et al 1978). Although the large majority of men (and women) receiving opioids do develop hypogonadism, about 15 percent also develop central hypocorticism and 15 percent develop growth hormone deficiency (Abs et al 2000).
The prevalence of biochemical testosterone deficiency increases with age. This is partly due to decreasing testosterone levels associated with illness or debility but there is also convincing epidemiological data to show that serum free and total testosterone levels also fall with normal aging (Harman et al 2001; Feldman et al 2002). The symptoms of aging include tiredness, lack of energy, reduced strength, frailty, loss of libido, decreased sexual performance depression and mood change. Men with hypogonadism experience similar symptoms. This raises the question of whether some symptoms of aging could be due to relative androgen deficiency. On the other hand, similarities between normal aging and the symptoms of mild androgen deficiency make the clinical diagnosis of hypogonadism in aging men more challenging.

If you're a man who's experiencing symptoms such as decreased sex drive, erectile dysfunction, depressed mood, and difficulties with concentration and memory, and you think low testosterone may be to blame, you can have your levels tested. Since testosterone levels fluctuate throughout the day, you'll probably need more than a blood test to get a true picture of your levels.

There is increasing interest in the group of patients who fail to respond to treatment with PDE-5 inhibitors and have low serum testosterone levels. Evidence from placebo-controlled trials in this group of men shows that testosterone treatment added to PDE-5 inhibitors improves erectile function compared to PDE-5 inhibitors alone (Aversa et al 2003; Shabsigh et al 2004).
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.
Some of the effects of testosterone treatment are well recognised and it seems clear that testosterone treatment for aging hypogonadal men can be expected to increase lean body mass, decrease visceral fat mass, increase bone mineral density and decrease total cholesterol. Beneficial effects have been seen in many trials on other parameters such as glycemic control in diabetes, erectile dysfunction, cardiovascular risk factors, angina, mood and cognition. These potentially important effects require confirmation in larger clinical trials. Indeed, it is apparent that longer duration randomized controlled trials of testosterone treatment in large numbers of men are needed to confirm the effects of testosterone on many aspects of aging male health including cardiovascular health, psychiatric health, prostate cancer and functional capacity. In the absence of such studies, it is necessary to balance risk and benefit on the best available data. At the present time the data supports the treatment of hypogonadal men with testosterone to normalize testosterone levels and improve symptoms. Most men with hypogonadism do not have a contraindication to treatment, but it is important to monitor for adverse consequences including prostate complications and polycythemia.
Cross-sectional studies have not shown raised testosterone levels at the time of diagnosis of prostate cancer, and in fact, low testosterone at the time of diagnosis has been linked with more locally aggressive and malignant tumors (Massengill et al 2003; Imamoto et al 2005; Isom-Batz et al 2005). This may reflect loss of hormone related control of the tumor or the effect of a more aggressive tumor in decreasing testosterone levels. One study found that 14% of hypogonadal men, with normal digital rectal examination and PSA levels, had histological prostate cancer on biopsy. It is possible that low androgen levels masked the usual evidence of prostate cancer in this population (Morgentaler et al 1996). Most longitudinal studies have not shown a correlation between testosterone levels and the future development of prostate cancer (Carter et al 1995; Heikkila et al 1999; Stattin et al 2004) but a recent study did find a positive association (Parsons et al 2005). Interpretation of such data requires care, as the presentation of prostate cancer could be altered or delayed in patients with lower testosterone levels.
It seems like today it’s a badge of honor to train every day until exhaustion. The ethos is to push yourself harder and harder every day. If that’s your philosophy towards exercise, you might be sabotaging your testosterone levels (as well as your 20 Mile March). Studies have shown that overtraining can reduce testosterone levels significantly. Yes, it’s important to exercise hard, but it’s even more important to give your body rest so it can recuperate from the damage you inflicted upon it.
It is hard to know how many men among us have TD, although data suggest that overall about 2.1% (about 2 men in every 100) may have TD. As few as 1% of younger men may have TD, while as many as 50% of men over 80 years old may have TD. People who study the condition often use different cut-off points for the numbers, so you may hear different numbers being stated.
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.
Some of the effects of testosterone treatment are well recognised and it seems clear that testosterone treatment for aging hypogonadal men can be expected to increase lean body mass, decrease visceral fat mass, increase bone mineral density and decrease total cholesterol. Beneficial effects have been seen in many trials on other parameters such as glycemic control in diabetes, erectile dysfunction, cardiovascular risk factors, angina, mood and cognition. These potentially important effects require confirmation in larger clinical trials. Indeed, it is apparent that longer duration randomized controlled trials of testosterone treatment in large numbers of men are needed to confirm the effects of testosterone on many aspects of aging male health including cardiovascular health, psychiatric health, prostate cancer and functional capacity. In the absence of such studies, it is necessary to balance risk and benefit on the best available data. At the present time the data supports the treatment of hypogonadal men with testosterone to normalize testosterone levels and improve symptoms. Most men with hypogonadism do not have a contraindication to treatment, but it is important to monitor for adverse consequences including prostate complications and polycythemia.
The sex hormone testosterone is far more than just the stuff of the alpha male's swagger. Though it plays a more significant role in the life of the biological male, it is actually present in both sexes to some degree. Despite popular perceptions that testosterone primarily controls aggression and sex drive—although it does play a role in both of those things—research has shown that individual levels of testosterone are also correlated with our language skills and cognitive abilities. Testosterone occurs in the body naturally, but can be administered as a medication, too: its most common uses are in the treatment of hypogonadism and breast cancer, as well as in hormone therapy for transgender men.
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).
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.

During the month before my experiment, I was definitely sleep deprived. Some nights I was only getting 4 to 5 hours. Testosterone killer! During my experiment I tried to get 8 to 9 hours of sleep at night as consistently as possible. I had to go to bed earlier, but I was only cutting into time that I would have been using to mindlessly surf the net anyway.
Testosterone is significantly correlated with aggression and competitive behaviour and is directly facilitated by the latter. There are two theories on the role of testosterone in aggression and competition.[77] The first one is the challenge hypothesis which states that testosterone would increase during puberty thus facilitating reproductive and competitive behaviour which would include aggression.[77] Thus it is the challenge of competition among males of the species that facilitates aggression and violence.[77] Studies conducted have found direct correlation between testosterone and dominance especially among the most violent criminals in prison who had the highest testosterone levels.[77] The same research also found fathers (those outside competitive environments) had the lowest testosterone levels compared to other males.[77]
The biggest change I made to my diet was increasing my fat and cholesterol intake. There’s a reason why old school strong men would drink raw eggs — studies have suggested that higher fat and cholesterol consumption results in increased levels of total T; men eating low-fat diets typically have decreased testosterone levels. The emphasis on increasing fat and cholesterol consumption meant I got to eat like Ron Swanson for three months — bacon and eggs and steak was pretty much the staple of my diet.

Osteoporosis refers to pathological loss of bone density and strength. It is an important condition due to its prevalence and association with bone fractures; most commonly of the hip, vertebra and forearm. Men are relatively protected from the development of osteoporosis by a higher peak bone mass compared with women (Campion and Maricic 2003). Furthermore, women lose bone at an accelerated rate immediately following the menopause. Nevertheless, men start to lose bone mass during early adult life and experience an increase in the rate of bone loss with age (Scopacasa et al 2002). Women of a given age have a higher prevalence of osteoporosis in comparison to men but the prevalence increases with age in both sexes. As a result, men have a lower incidence of osteoporotic fractures than women of a given age but the gap between the sexes narrows with advancing age (Chang et al 2004) and there is evidence that hip fractures in men are associated with greater mortality than in women (Campion and Maricic 2003).

Individuals with metabolic syndrome are at increased risk for developing coronary artery disease and diabetes mellitus. Predicting who might develop the metabolic syndrome would allow preventive measures to be taken in addition to weight control and other lifestyle modifications such as cessation of smoking and increased exercise. It is known that with decreasing testosterone availability in aging males there is an increase in fat mass and decrease in lean body mass (van den Beld et al 2000), there are disorders of insulin and glucose metabolism (Haffner et al 1996) and dyslipidemia (Tsai et al 2004). Kupelian and colleagues (2006) in analyzing data from the Massachusetts Male Aging Study demonstrated that men with low levels of testosterone, sex hormone-binding globulin, or clinical androgen deficiency, especially men with a BMI of greater than 25, were at increased risk of developing the metabolic syndrome and hence, diabetes mellitus and/or coronary artery disease.
In general, the normal range in males is about 270 to 1070 ng/dL with an average level of 679 ng/dL. A normal male testosterone level peaks at about age 20, and then it slowly declines. Testosterone levels above or below the normal range are considered by many to be out of balance. Moreover, some researchers suggest that the healthiest men have testosterone levels between 400 - 600 ng/dL.

Both testosterone and 5α-DHT are metabolized mainly in the liver.[1][151] Approximately 50% of testosterone is metabolized via conjugation into testosterone glucuronide and to a lesser extent testosterone sulfate by glucuronosyltransferases and sulfotransferases, respectively.[1] An additional 40% of testosterone is metabolized in equal proportions into the 17-ketosteroids androsterone and etiocholanolone via the combined actions of 5α- and 5β-reductases, 3α-hydroxysteroid dehydrogenase, and 17β-HSD, in that order.[1][151][152] Androsterone and etiocholanolone are then glucuronidated and to a lesser extent sulfated similarly to testosterone.[1][151] The conjugates of testosterone and its hepatic metabolites are released from the liver into circulation and excreted in the urine and bile.[1][151][152] Only a small fraction (2%) of testosterone is excreted unchanged in the urine.[151]
During the second trimester, androgen level is associated with sex formation.[13] 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.[14]
If you want to naturally boost testosterone and HGH then combining weight training with HIIT workouts (high intensity interval training). Go to the gym at least three days a week, ideally at least three days a week, and lift heavy weights. Lifting heavy weights 6–12 reps with larger muscle groups like your quadriceps, hamstrings, back, shoulders and chest will help your body pack on the maximum amount of muscle. Specifically, lifting at least 30 minutes up to as long as an hour or so can be very, very beneficial boost low testosterone levels.

Pellets. Your doctor will place the testosterone pellets under the skin of your upper hip or buttocks. Your doctor will give a shot of local anesthesia to numb your skin, then make a small cut and place the pellets inside the fatty tissues underneath your skin. This medication dissolves slowly and is released over about 3-6 months, depending on the number of pellets. 


The testicles produce an enzyme called 11ßHSD-1 which protects your testosterone molecules from the effects cortisol.  During times of prolonged stress and chronically elevated cortisol, there simply is too much cortisol for 11ßHSD-1 to handle.  This results in testosterone molecules being destroyed inside the gonads before they even enter the bloodstream (8, 9).

^ David KG, Dingemanse E, Freud JL (May 1935). "Über krystallinisches mannliches Hormon aus Hoden (Testosteron) wirksamer als aus harn oder aus Cholesterin bereitetes Androsteron" [On crystalline male hormone from testicles (testosterone) effective as from urine or from cholesterol]. Hoppe-Seyler's Z Physiol Chem (in German). 233 (5–6): 281–83. doi:10.1515/bchm2.1935.233.5-6.281.
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.
These results have been echoed in clinical trials. A meta-analysis of 24 RCTs looked at weight loss caused by diet or bariatric surgery:[22] In the diet studies, the average 9.8% weight loss was linked to a testosterone increase of 2.9 nmol/L (84 ng/dL). In the bariatric-surgery studies, the average 32% weight loss was linked to a testosterone increase of 8.7 nmol/L (251 ng/dL).
Another recent development is the production of adhesive tablets which are applied twice daily to the buccal mucosa on the gum above the incisor teeth. The tablets gradually release testosterone into the systemic venous circulation and steady state physiological concentrations are achieved in most patients within two days (Ross et al 2004). Some patients do not like the feeling of the tablet in the mouth or find that there is an abnormal taste in the mouth, but local adverse effects are usually mild and transient (Wang, Swerdloff et al 2004).

Consume vegetable carbohydrates and healthy fats. Your body requires the carbohydrates from fresh vegetables rather than grains and sugars. In addition to mono- or polyunsaturated fats found in avocados and raw nuts, saturated fats are also essential to building your testosterone production. According to research, there was a decrease in testosterone stores in people who consumed a diet low in animal-based fat.11 Aside from avocados and raw nuts, ideal sources of healthy fat that can boost your testosterone levels include:
A blood test is the only way to diagnose a low testosterone level or a reduction in the bioavailability of testosterone. Some men have a lower than normal testosterone level without signs or symptoms. For most men, no treatment is needed. But for some others, very low testosterone levels lead to a condition in which bones become weak and brittle (osteoporosis). For others, low testosterone might cause changes in sexual function, sleep patterns, emotions and the body.
All the active substances available in TestoGen are fully natural. And their efficacy and safety is science-backed. So, if you don’t have individual sensitivity to the supplement ingredients and purchase the product directly from the manufacturer instead of purchasing from unknown suppliers, the likelihood of side effects during the supplementation is minimal. And the customer feedback proves this.

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.


Ten healthy men aged around 24 years old spent 1 week sleeping for 8 hours per night at home, they then spent the next 11 nights in a lab. They slept for 10 hours per night for 3 nights, followed by 8 nights of restricted sleep, when they slept for only 5 hours. Doctors checked their blood every 15 to 30 minutes during the last night that they slept 10 hours, as well as on the sleep-restricted session.


Other Potential risks that can be caused by use of testosterone supplements are: People who take good testosterone supplements or any other kind of testosterone boosters can also experience many other side effects, including stomachache, problems with urination, dizziness, mood changes, intermittent breathing during sleep, changes in testicles, appetite loss, inflammation of gums, weight gain, nausea, painful erection, and protracted erection.
The hypogonadal-obesity-adipocytokine cycle hypothesis. Adipose tissue contains the enzyme aromatase which metabolises testosterone to oestrogen. This results in reduced testosterone levels, which increase the action of lipoprotein lipase and increase fat mass, thus increasing aromatisation of testosterone and completing the cycle. Visceral fat also promotes lower testosterone levels by reducing pituitary LH pulse amplitude via leptin and/or other factors. In vitro studies have shown that leptin also inhibits testosterone production directly at the testes. Visceral adiposity could also provide the link between testosterone and insulin resistance (Jones 2007).
Male hypogonadism becomes more common with increasing age and is currently an under-treated condition. The diagnosis of hypogonadism in the aging male requires a combination of symptoms and low serum testosterone levels. The currently available testosterone preparations can produce consistent physiological testosterone levels and provide for patient preference.

This doesn’t mean Super Test is perfect — we take a closer look at some of its ingredients below — but it beats out the competition. Every other supplement we looked at either didn’t have all four ingredients, overdosed us on vitamins or minerals (a good way to develop kidney and liver problems), contained ingredients that would harm us, or some combination thereof.


Your first step should be to see your doctor. If you think you have low testosterone, we cannot stress enough that you should proceed with caution and talk to a medical professional — taking a booster can definitely do more harm than good. Low testosterone can be a symptom of more serious problems, like a pituitary disorder or a side-effect of medication, and a booster can mask the root cause. A doctor will be able to evaluate your testosterone levels with a simple blood test, and if you both decide a booster is the way to go, give the ingredients of any supplement a once-over to make sure that they’re not at risk of making your personal health situation worse.


"Some say it's just a part of aging, but that's a misconception," says Jason Hedges, MD, PhD, a urologist at Oregon Health and Science University in Portland. A gradual decline in testosterone can't explain a near-total lack of interest in sex, for example. And for Hedges' patients who are in their 20s, 30s, and early 40s and having erectile problems, other health problems may be a bigger issue than aging.
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