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).
Testosterone boosters are used by many athletes worldwide to achieve a significant muscle mass increase within a short period of time.[1] However; one cannot be completely confident in terms of the quality and efficacy of such products because of several reasons, such as the possibility of bad storage conditions and originating from an unreliable source. Over the years, some consumers of testosterone boosters have complained of kidney and liver abnormalities that could be linked to their use of boosters.[10] Cases of erroneous product administration have occurred in the past as athletes may not follow the instructions on the label fully, which can lead to many side effects.[11] In the present case, a man was admitted to a hospital because of a severe abdominal pain. The pain was later found to be caused by liver injury. The diagnosis confirmed that the levels of the key hepatic enzymes were markedly elevated. The medical complications observed were found to have occurred following the consumption of two courses of a commercial testosterone booster. According to researchers based in the US, about 13% of the annual cases of acute liver failure are attributable to idiosyncratic drug- and/or supplement-induced liver injury.[12] Marked increase in the levels of ALT, AST, and gamma-glutamyl transferase was observed after consuming the first course of the commercial testosterone booster, and they started to decline after the 2nd and 3rd course. This abruptly increases the levels of liver enzymes after the first course may be attributed to the interruption effect of commercial testosterone booster on liver function as a result of the effects of its ingredients.
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).
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.
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.
Let’s do a quick review of what I shared in the introduction to this series. August of last year was a tough month for me, primarily because of a huge and grueling project we were in the midst of here on the site. I was stressed out and my sleeping, healthy eating habits, and workout regimen all suffered. At the end of the month I got my testosterone levels tested and found that my total T was 383 ng/dL and my free T was 7.2 pg/mL – close to the average for an 85-100-year-old man.
Dr. Anthony’s Notes: DHEA is a powerful supplement for testosterone, energy, and overall well-being in our older Fit Fathers. A small dose of 25-50mg/day is enough to exert noticeable benefits. This supplement is over-the-counter. Verdict: this is one of the testosterone supplements that work. How To Take DHEA: Take 25-50mg once per day with food. Special Medical Note: DHEA is a MILD CYP3A4 inhibitor (a liver enzyme that processes MANY very common medications). This is the same isoenzyme that Grapefruit inhibits – albeit DHEA inhibits to a much weaker degree. If you’ve ever heard “don’t eat grapefruit with your Lipitor (cholesterol medication)”… this is the reason why. When we inhibit the CYP3A4 enzyme, more of the medications you're taking circulates (it’s not metabolized as fast). Check with your doctor for medication interactions before using DHEA.
Testosterone is an important hormone for both men and women. Even though it’s often associated with a man’s libido, testosterone occurs in both sexes from birth. In females, it plays a part in sexual drive, energy, and physical strength. In males, it stimulates the beginning of sexual development and helps maintain a man’s health throughout his life.
Like most supplements, Beast Sports contains several ingredients with little research about their long-term effects. WebMD describes Suma powder, Rhodiola Rosea, Cissus quadrangularis, Tribulus extract, and ashwagandha extract as possibly safe when taken for a short period of time (usually around 6-10 weeks). However, their long-term safety remains unknown. It also has a few ingredients, like cyanotis vaga root, safed musli, and polygonum cispidatum root extract for which there is a lack of data on even short term safety.
Zinc is so important relating to hormone balance and many other functions (fertility, immunity, and insulin sensitivity to name just a few), as well as dopamine production—which helps support mood, drive, and interest. Many men, especially over the age of 60, have low zinc levels. A great start is to eat more foods containing zinc like oysters, fermented foods, and proteins (preferably grass-fed beef and wild-caught salmon). I often recommend 50 to 60 mg daily if taking as a supplement.
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.
Anabolic–androgenic steroids (AASs) are synthetic derivatives of testosterone that are commonly used among athletes aged 18–40 years, but many reports have demonstrated the presence of numerous toxic and hormonal effects as a result of long-term use of an AAS.[9] Testosterone-foods act as natural libido boosters. Due to the growing interest in herbal ingredients and other dietary supplements worldwide, the use of testosterone boosters is becoming more and more mainstream among athletes, but several side effects were documented. Hence, this study established to help in the assessment of the side effects and health risks which could occur among athletes consuming testosterone boosters.
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]

The natural production of DHEA is also age-dependent. Prior to puberty, the body produces very little DHEA. Production of this prohormone peaks during your late 20’s or early 30’s. With age, DHEA production begins to decline. The adrenal glands also manufacture the stress hormone cortisol, which is in direct competition with DHEA for production because they use the same hormonal substrate known as pregnenolone. Chronic stress basically causes excessive cortisol levels and impairs DHEA production, which is why stress is another factor for low testosterone levels.
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.

Testosterone is an androgenic sex hormone produced by the testicles (and in smaller amounts in women’s ovaries), and is often associated with “manhood.” Primarily, this hormone plays a great role in men’s sexual and reproductive function. It also contributes to their muscle mass, hair growth, maintaining bone density, red blood cell production, and emotional health.

So if you’re intent on maximizing your testosterone levels, and/or you have applied all of the above and you’re still not satisfied with your results (which would be surprising) then you could try the below. I will point out that some of these tips may not have the scientific evidence to back them up like the previous points, but I can assure you that either I have or do use them (and have positive results), or a client has used them with pleasing results, or finally it is such a new conception that there isn’t enough evidence to prove it one way or another.
“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.”
Drumstick vegetable or Moringa oleifera is known for being 'libido-booster' in India. Whenever a guy buys a bunch of drumsticks in the market, people usually stare at him with the face 'he's planning a party tonight!' Although many studies are needed to prove it, Moringa is a rich source of magnesium, calcium and vitamin c. Moringa can also be considered a decent source of anti-oxidants.
Saw palmetto: Uses, dosage, and side effects Saw palmetto is an extract from the berries of a type of palm tree. The berries have traditionally been used to ease urinary and reproductive problems. The extract is now used in herbal remedies to stabilize testosterone. Learn about its use, its effectiveness, the science behind the claims, and any side effects. Read now
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