Carbs play a big part in determining your Testosterone levels. Let's start with what to avoid. First, research shows that a large serving of sugar (75g of glucose), decreased Testosterone levels by as much as 25%! (25 & 26). I know this is a pretty extreme dosage, but you may want to avoid massive servings of sugar! Also, men who have Metabolic syndrome have lower Testosterone levels (27). Metabolic syndrome is often brought about by chronic high blood sugar which leads to insulin resistance.
Studies have demonstrated reduced testosterone levels in men with heart failure as well as other endocrine changes (Tappler and Katz 1979; Kontoleon et al 2003). Treatment of cardiac failure with chronic mechanical circulatory support normalizes many of these changes, including testosterone levels (Noirhomme et al 1999). More recently, two double-blind randomized controlled trials of testosterone treatment for men with low or low-normal serum testosterone levels and heart failure have shown improvements in exercise capacity and symptoms (Pugh et al 2004; Malkin et al 2006). The mechanism of these benefits is currently unclear, although a study of the acute effects of buccal testosterone given to men with chronic cardiac failure under invasive monitoring showed that testosterone increased cardiac index and reduced systemic vascular resistance (Pugh et al 2003). Testosterone may prove useful in the management of cardiac failure but further research is needed.
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).
In many of the studies we found, those who saw the most improvement in health, testosterone, or muscle gain were those with existing nutrient or vitamin deficiencies. This means that some gains may be due more to dietary changes and generally restoring nutrient and vitamin levels than any one magic ingredient, but also that making sure your diet includes healthy amounts of nutrients should be your first step.
Testosterone boosters are used by many athletes worldwide to achieve a significant muscle mass increase within a short period of time. 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. 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. 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. 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.
Alternately known as prasarini or Chinese fever vine, Paederia foetida is an herb that is commonly used in Ayurvedic traditions. While its traditional uses originally centered around intestinal health, especially as a treatment for diarrhea and dysentery, Paederia foetida has been shown to improve male vitality and vigor by increasing serum testosterone levels.
b) You can also use supplements to increase testosterone levels in your body. Zinc supplements are important to boost T-levels. Generally, the best source of this nutrient is from foods such as fish, meats, beans, raw milk, yogurt, raw cheese, etc. However, if you are a vegetarian, obtaining sufficient dietary zinc from natural foods alone can be difficult. This is where supplements come in, ensuring that you get the right amount of zinc required to give your testosterone levels a good boost.
There's the rub, so to speak. Recalling the cautionary lessons learned about sex steroid hormone therapy in postmenopausal women from theWomen's Health Initiative, Dr. Brad Anawalt wrote in the Journal of Clinical Endocrinology and Metabolism, "We are threatened with a reprise of promiscuous prescription of sex steroid hormone therapy in aging men, obese men, diabetic men, and other groups of men with a high prevalence of low serum androgen levels. We are threatened with a mad 'T' party."
In addition to conjugation and the 17-ketosteroid pathway, testosterone can also be hydroxylated and oxidized in the liver by cytochrome P450 enzymes, including CYP3A4, CYP3A5, CYP2C9, CYP2C19, and CYP2D6. 6β-Hydroxylation and to a lesser extent 16β-hydroxylation are the major transformations. The 6β-hydroxylation of testosterone is catalyzed mainly by CYP3A4 and to a lesser extent CYP3A5 and is responsible for 75 to 80% of cytochrome P450-mediated testosterone metabolism. In addition to 6β- and 16β-hydroxytestosterone, 1β-, 2α/β-, 11β-, and 15β-hydroxytestosterone are also formed as minor metabolites. Certain cytochrome P450 enzymes such as CYP2C9 and CYP2C19 can also oxidize testosterone at the C17 position to form androstenedione.
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Like other steroid hormones, testosterone is derived from cholesterol (see figure). The first step in the biosynthesis involves the oxidative cleavage of the side-chain of cholesterol by cholesterol side-chain cleavage enzyme (P450scc, CYP11A1), a mitochondrial cytochrome P450 oxidase with the loss of six carbon atoms to give pregnenolone. In the next step, two additional carbon atoms are removed by the CYP17A1 (17α-hydroxylase/17,20-lyase) enzyme in the endoplasmic reticulum to yield a variety of C19 steroids. In addition, the 3β-hydroxyl group is oxidized by 3β-hydroxysteroid dehydrogenase to produce androstenedione. In the final and rate limiting step, the C17 keto group androstenedione is reduced by 17β-hydroxysteroid dehydrogenase to yield testosterone.
"Bring back the younger inner you," says the Low T Center. According to its website, its president, Mr. (notably not "Dr.") Mike Sisk, "created these centers out of a need." They promise their testosterone injections "do not just help boost a low sex drive but can also boost energy, decrease body fat, irritability, and depression." They go so far as to claim that "research finds testosterone replacement can solve long-term health issues like Alzheimer's and heart disease."
Both men and women with Alzheimer’s Disease were found to have an increased concentration of SHBG and decreased free androgen index when compared with controls (Paoletti et al 2004). In a prospective study of 574 men whose baseline age span was 32–87 years and who were followed for a mean of 19.1 years (range, 4–37), the risk of developing Alzheimers’ Disease decreased 26 percent for each 10 unit increase in free testosterone index. The authors concluded that testosterone may be important for the prevention and treatment of AD (Moffat et al 2004).
In a recent study of male workers, men with low testosterone levels had an increased chance of severe erectile dysfunction (Kratzik et al 2005), although such a link had not been found previously (Rhoden et al 2002). Certainly erectile dysfunction is considered part of the clinical syndrome of hypogonadism, and questions regarding erectile dysfunction form part of the clinical assessment of patients with hypogonadism (Morley et al 2000; Moore et al 2004).
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. 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.
These "disease-awareness" campaigns—ostensibly a public service intended to educate those potentially at risk about a condition they may not even have heard of but "could" have—are subtle, even insidious. They may not mention a specific product, but a bit of sleuthing reveals that their sponsors are usually pharmaceutical companies that "just happen" to manufacture products used to treat the real (or at least alleged) condition.
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
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.
Testosterone is a steroid from the androstane class containing a keto and hydroxyl groups at the three and seventeen positions respectively. It is biosynthesized in several steps from cholesterol and is converted in the liver to inactive metabolites. It exerts its action through binding to and activation of the androgen receptor. In humans and most other vertebrates, testosterone is secreted primarily by the testicles of males and, to a lesser extent, the ovaries of females. On average, in adult males, levels of testosterone are about 7 to 8 times as great as in adult females. As the metabolism of testosterone in males is more pronounced, the daily production is about 20 times greater in men. Females are also more sensitive to the hormone.
Brassaiopsis glomerulata is a tree indigenous to Vietnam. While the plant has traditionally been used to remedy back pain and rheumatism, studies show that Brassaiopsis also contains a few compounds that inhibit aromatase. As mentioned above, aromatase is an enzyme that can turn androgens, particularly testosterone, into estrogen. Too much aromatase can significantly reduce testosterone levels while increasing estrogen, causing an imbalance in your body’s chemistry. By inhibiting aromatase, the compounds in Brassaiopsis can effectively boost testosterone levels and prevent them from turning into estrogen.
As you cut these dietary troublemakers from your meals, you need to replace them with healthy substitutes like vegetables and healthy fats (including natural saturated fats!). Your body prefers the carbohydrates in micronutrient-dense vegetables rather than grains and sugars because it slows the conversion to simple sugars like glucose, and decreases your insulin level. When you cut grains and sugar from your meals, you typically will need to radically increase the amount of vegetables you eat, as well as make sure you are also consuming protein and healthy fats regularly.
Robert Clark aka "The Troglodyte" is a 39 year old father of 3, Author, Fitness Trainer, Nutritional Researcher, Obstacle Course Racer, Avid Trail Runner and CrossFit Warrior. He is dedicated to helping others achieve their fitness goals. His extensive work in the field of natural testosterone elevation, inspired the creation of Alpha Wolf Nutrition where he serves as the Lead Product Researcher.
Take 1 teaspoon. Incredibly dense in nutrients and feed by bees to the larvae who grows on to be the queen bee. I found one human study where a 4g daily serving led to an small increase in testosterone in older men (ref 78). There are also numerous animal studies (ref 79) showing positive effects. Personally I source NZ manuka royal jelly from Manuka Health.
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“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.”
Travison, T. G., Vesper, H. W., Orwoll, E, Wu, F., Kaufman, J. M., Wang, Y., …Bhasin, S. (2017, April1). Harmonized reference ranges for circulating testosterone levels in men of four cohort studies in the United States and Europe. The Journal of Clinical Endocrinology & Metabolism, 102(4), 1161–1173. Retrieved from https://academic.oup.com/jcem/article/102/4/1161/2884621
Richard J. Wassersug, PhD, an adjunct professor of urology at the University of British Columbia, described his personal experience with androgen deprivation therapy (ADT). "If you are on ADT," he said, "and you see those Low T ads, what are you supposed to make of it? This produces a cognitive dissonance." He called the ads "hurtful" for suggesting that low testosterone makes a man less of a man.
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.
Zinc is little more of a nice-to-have ingredient than a must-have. It’s on our radar as an ingredient that possibly boosts testosterone levels, and while we couldn’t find enough supporting evidence that taking zinc would increase natural testosterone, low zinc levels have been connected to infertility. A low zinc level is also possibly a sign of hypogonadism. The closest support we found is in a study which found that people recovered from nutritional deficiency-related problems more quickly if they took a zinc supplement than those who did not. Zinc is available in many foods, such as oysters, fortified breakfast cereals, and red meat.