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?
A: Androderm comes in the form of a transdermal patch and is used for testosterone replacement therapy in patients who have insufficient levels of testosterone. Testosterone is a hormone produced in the body that plays a key role in many physiological processes in men. In some men, however, the body does not produce enough of the hormone, resulting in a variety of symptoms including decreased libido, erectile dysfunction, muscle loss, anemia and depression, among others. Androderm helps treat these symptoms and raise low testosterone levels by delivering therapeutic amounts of the hormone, which are absorbed through the skin. According to the prescribing information for Androderm, depression was a reported side effect of the medication. Other common side effects of Androderm include itching and redness at the application site, prostate abnormalities, headache, and burning or hardening of the skin at the application site. Less common side effects of Androderm include reduced libido (sex drive), fatigue, high blood pressure, anxiety, confusion, increased appetite, and body pain. For more specific information, consult with your doctor for guidance based on your health status and current medications, particularly before taking any action. Your physician can determine if your dosage of the medication needs to be adjusted or if an alternative medication should be considered. Lori Poulin, PharmD
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).
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.
The mechanism of age related decreases in serum testosterone levels has also been the subject of investigation. Metabolic clearance declines with age but this effect is less pronounced than a reduction in testosterone production, so the overall effect is to reduce serum testosterone levels. Gonadotrophin levels rise during aging (Feldman et al 2002) and testicular secretory responses to recombinant human chorionic gonadotrophin (hCG) are reduced (Mulligan et al 1999, 2001). This implies that the reduced production may be caused by primary testicular failure but in fact these changes are not adequate to fully explain the fall in testosterone levels. There are changes in the lutenising hormone (LH) production which consist of decreased LH pulse frequency and amplitude, (Veldhuis et al 1992; Pincus et al 1997) although pituitary production of LH in response to pharmacological stimulation with exogenous GnRH analogues is preserved (Mulligan et al 1999). It therefore seems likely that there are changes in endogenous production of GnRH which underlie the changes in LH secretion and have a role in the age related decline in testosterone. Thus the decreases in testosterone levels with aging seem to reflect changes at all levels of the hypothalamic-pituitary-testicular axis. With advancing age there is also a reduction in androgen receptor concentration in some target tissues and this may contribute to the clinical syndrome of LOH (Ono et al 1988; Gallon et al 1989).
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.
This project is supported by the Canadian Institutes of Health Research (award #111062), Alberta Innovates - Health Solutions, and by The Metabolomics Innovation Centre (TMIC), a nationally-funded research and core facility that supports a wide range of cutting-edge metabolomic studies. TMIC is funded by Genome Alberta, Genome British Columbia, and Genome Canada, a not-for-profit organization that is leading Canada's national genomics strategy with funding from the federal government. Maintenance, support, and commercial licensing is provided by OMx Personal Health Analytics, Inc. Designed by Educe Design & Innovation Inc.
Steven Doerr, MD, is a U.S. board-certified Emergency Medicine Physician. Dr. Doerr received his undergraduate degree in Spanish from the University of Colorado at Boulder. He graduated with his Medical Degree from the University Of Colorado Health Sciences Center in Denver, Colorado in 1998 and completed his residency training in Emergency Medicine from Denver Health Medical Center in Denver, Colorado in 2002, where he also served as Chief Resident.
A notable study out of Wayne State University in Indiana found that older men who had a mild zinc deficiency significantly increased their testosterone from 8.3 to 16.0 nmol/L—a 93 percent increase—following six months of zinc supplementation. Researchers of the study concluded that zinc may play an important role in modulating serum testosterone levels in normal healthy men.6
Why bother with such common micronutrients? Because it's not uncommon for athletes to suffer from zinc and magnesium deficiencies, partly due to inadequate replenishing of levels after intense bouts of exercise. Deficiencies in these key minerals can lead to a poor anabolic hormone profile, impaired immune function, and increased cortisol, ultimately leading to decreases in strength and performance.[6]
Such sort of injuries varies in severity and extent of damage markedly from one person to the other and withdrawal of the drug/supplement coupled with proper medical attention suffice in terms of alleviating the symptoms.[8,12] This was observed in the present case. However, the liver injury observed here may not be confidently linked to product consumption as the subject later reported that the following recovery he consumed two more courses of the booster with no side effects. Tests performed following hospital discharge, and repeated use of the product showed AST and ALT to be slightly high, whereas the rest of the blood parameters tested appeared to be normal. The AST/ALT ratio is considered to be a very important parameter for the evaluation of liver diseases, such as non-alcoholic fatty liver disease,[13] though it is rarely considered alone. Overall, the evidence was inconclusive in the present work in terms of linking the use of a testosterone booster with liver injury. However, even though a single case report cannot establish causality with statistical power.[13] Further research on the usage of a commercial testosterone booster within large populations for a long period is necessary to investigate whether the symptoms shown in the present case were significantly present in other athletes consuming the same commercial product or not. To guarantee an optimal outcome with no severe side effects, further research is warranted to confirm the present findings and determine whether the effects observed in this case report would be statistically significant in larger samples.

For this reason I recommend doing your own research on this supplement before taking it. 5g of ground up dried powder is what was used in the studies. I recommend taking 1-2 capsules of the concentrated form from Paradise Herbs. Alternatively, the Aggressive Strength Test Booster also has MP in its formula so you may prefer to use that blend instead. 


“This study establishes testosterone levels at which various physiological functions start to become impaired, which may help provide a rationale for determining which men should be treated with testosterone supplements,” Finkelstein says. “But the biggest surprise was that some of the symptoms routinely attributed to testosterone deficiency are actually partially or almost exclusively caused by the decline in estrogens that is an inseparable result of lower testosterone levels.”
In 1927, the University of Chicago's Professor of Physiologic Chemistry, Fred C. Koch, established easy access to a large source of bovine testicles — the Chicago stockyards — and recruited students willing to endure the tedious work of extracting their isolates. In that year, Koch and his student, Lemuel McGee, derived 20 mg of a substance from a supply of 40 pounds of bovine testicles that, when administered to castrated roosters, pigs and rats, remasculinized them.[179] The group of Ernst Laqueur at the University of Amsterdam purified testosterone from bovine testicles in a similar manner in 1934, but isolation of the hormone from animal tissues in amounts permitting serious study in humans was not feasible until three European pharmaceutical giants—Schering (Berlin, Germany), Organon (Oss, Netherlands) and Ciba (Basel, Switzerland)—began full-scale steroid research and development programs in the 1930s.
Studies conducted in rats have indicated that their degree of sexual arousal is sensitive to reductions in testosterone. When testosterone-deprived rats were given medium levels of testosterone, their sexual behaviors (copulation, partner preference, etc.) resumed, but not when given low amounts of the same hormone. Therefore, these mammals may provide a model for studying clinical populations among humans suffering from sexual arousal deficits such as hypoactive sexual desire disorder.[37]
Few of the most often asked questions I get are: what do I eat to maintain high testosterone levels, and if I have a specific list of recommended foods that increase testosterone naturally. While there are many food related posts scattered around this blog, I’ve never really made an all-around post about what I would put into a high T pantry. Until now.
A: Testosterone production declines naturally with age. Low testosterone, or testosterone deficiency (TD), may result from disease or damage to the hypothalamus, pituitary gland, or testicles that inhibits hormone secretion and testosterone production. Treatment involves hormone replacement therapy. The method of delivery is determined by age and duration of deficiency. Oral testosterone, Testred (methyltestosterone), is associated with liver toxicity and liver tumors and so is prescribed sparingly. Transdermal delivery with a testosterone patch is becoming the most common method of treatment for testosterone deficiency in adults. A patch is worn, either on the scrotum or elsewhere on the body, and testosterone is released through the skin at controlled intervals. Patches are typically worn for 12 or 24 hours and can be worn during exercise, bathing, and strenuous activity. Two transdermal patches that are available are Androderm (nonscrotal) and Testoderm (scrotal). The Androderm patch is applied to the abdomen, lower back, thigh, or upper arm and should be applied at the same time every evening between 8 p.m. and midnight. If the patch falls off before noon, replace it with a fresh patch until it is time to reapply a new patch that evening. If the patch falls off after noon, do not replace it until you reapply a new patch that evening. The most common side effects associated with transdermal patch therapy include itching, discomfort, and irritation at the site of application. Some men may experience fluid retention, acne, and temporary abnormal breast development (gynecosmastia). AndroGel and Testim are transdermal gels that are applied once daily to the clean dry skin of the upper arms or abdomen. When used properly, these gels deliver testosterone for 24 hours. The gel must be allowed to dry on the skin before dressing and must be applied at least 6 hours before showering or swimming. Gels cannot be applied to the genitals. AndroGel is available in a metered-dose pump, which allows physicians to adjust the dosage of the medication. Side effects of transdermal gels include adverse reactions at the site of application, acne, headache, and hair loss (alopecia). For more specific information on treatments for low testosterone, consult with your doctor or pharmacist for guidance based on current health condition. Kimberly Hotz, PharmD
More can be learned from a large, randomized, placebo-controlled trial of finasteride treatment in 18,800 men aged 55 or more. Finasteride is a 5α-reductase inhibitor which acts to prevent the metabolism of testosterone to dihydrotestosterone (DHT) – the most active androgen in the prostate. The trial showed a greater overall incidence of prostate cancer in the control group, but men treated with finasteride were more likely to have high grade tumors (Thompson et al 2003), suggesting that reduced androgen exposure of the prostate may delay the presentation of prostate cancer and/or promote advanced disease in some other way.

The hormone also plays a role in sex drive, sperm production, fat distribution, red cell production, and maintenance of muscle strength and mass, according to the Mayo Clinic. For these reasons, testosterone is associated with overall health and well-being in men. One 2008 study published in the journal Frontiers of Hormone Research even linked testosterone to the prevention of osteoporosis in men.
Tailor the above recommendations to your personal needs and lifestyle. If you’re a vegetarian drop the bacon and steak, but keep the whey protein and eggs. If you have an injury that prevents you from heavy weightlifting, move as much as you can in the way that you can. There are no studies out there which can tell you exactly what will happen if you do X and Y, but not Z. And I certainly can’t tell you either. Don’t be afraid of self-education – that’s how I learned all this – and embrace the idea of conducting your own experiment and being your own test subject. Incorporate as many of the recommendations above as you’re comfortable with, consult your doctor, and track your results.
Use natural grooming products. Most grooming products these days contain parabens, another type of xenoestrogen. And by most, I mean more than 75% of all products. To reduce my exposure as much as possible, I became a hippy during my experiment and started using all natural, paraben-free grooming products. You can find most of these items at most health food stores:
Another effect that can limit treatment is polycythemia, which occurs due to various stimulatory effects of testosterone on erythropoiesis (Zitzmann and Nieschlag 2004). Polycythemia is known to produce increased rates of cerebral ischemia and there have been reports of stroke during testosterone induced polycythaemia (Krauss et al 1991). It is necessary to monitor hematocrit during testosterone treatment, and hematocrit greater than 50% should prompt either a reduction of dose if testosterone levels are high or high-normal, or cessation of treatment if levels are low-normal. On the other hand, late onset hypogonadism frequently results in anemia which will then normalize during physiological testosterone replacement.
Formulated to counter the natural decline in production of testosterone as men age, Testogenix has been scientifically engineered to significantly boost the body’s production of free testosterone Testogenix users report improved stamina, energy levels, overall muscle gains, and sexual performance. There is simply no better way to send your testosterone levels through the roof! Testogenix is GUARANTEED to deliver lasting results! Click To Read More...
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.
As already indicated previously, testosterone levels, particularly bioavailable testosterone, fall with advancing age. This decline in testosterone availability may start to occur early in the forth decade but it usually becomes clinically manifest in the 50s and 60s. Although there is continuing debate about the best way to diagnose hypogonadism in the aging male, there appears to be a general consensus that symptomatic men with reduced levels of testosterone should be given a trial of testosterone therapy if there is no contraindication to do so (Bain et al 2007).
Free testosterone (T) is transported into the cytoplasm of target tissue cells, where it can bind to the androgen receptor, or can be reduced to 5α-dihydrotestosterone (DHT) by the cytoplasmic enzyme 5α-reductase. DHT binds to the same androgen receptor even more strongly than testosterone, so that its androgenic potency is about 5 times that of T.[114] The T-receptor or DHT-receptor complex undergoes a structural change that allows it to move into the cell nucleus and bind directly to specific nucleotide sequences of the chromosomal DNA. The areas of binding are called hormone response elements (HREs), and influence transcriptional activity of certain genes, producing the androgen effects.
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).
Ensure that you get adequate restful sleep each night. Sleeping less than the recommended 6 to 8 hours per night increases stress hormones, which lowers testosterone production. Additionally, learn to manage stress levels in healthy ways to naturally increase testosterone. Hormone replacement therapy may be required for some men with low testosterone levels. Consult your physician about treatment options.
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.
Free testosterone (T) is transported into the cytoplasm of target tissue cells, where it can bind to the androgen receptor, or can be reduced to 5α-dihydrotestosterone (DHT) by the cytoplasmic enzyme 5α-reductase. DHT binds to the same androgen receptor even more strongly than testosterone, so that its androgenic potency is about 5 times that of T.[114] The T-receptor or DHT-receptor complex undergoes a structural change that allows it to move into the cell nucleus and bind directly to specific nucleotide sequences of the chromosomal DNA. The areas of binding are called hormone response elements (HREs), and influence transcriptional activity of certain genes, producing the androgen effects.
Hypogonadism is a disease in which the body is unable to produce normal amounts of testosterone due to a problem with the testicles or with the pituitary gland that controls the testicles. Testosterone replacement therapy can improve the signs and symptoms of low testosterone in these men. Doctors may prescribe testosterone as injections, pellets, patches or gels.
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