^ Jump up to: a b Travison TG, Vesper HW, Orwoll E, Wu F, Kaufman JM, Wang Y, Lapauw B, Fiers T, Matsumoto AM, Bhasin S (April 2017). "Harmonized Reference Ranges for Circulating Testosterone Levels in Men of Four Cohort Studies in the United States and Europe". The Journal of Clinical Endocrinology and Metabolism. 102 (4): 1161–1173. doi:10.1210/jc.2016-2935. PMC 5460736. PMID 28324103.
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).
The final two studies looked directly at soy vs testosterone levels. The first looked at introducing consumption of soya flour on testosterone levels. They found that those who ate the Soy flour lowered their T levels during the study (43). And the second study looked at the consumption of soy protein isolates (powder) in healthy men. They found that testosterone levels decreased upon consumption of soy powder (45).
Prostate hyperplasia (BPH), or simply an enlarged prostate, is a serious problem among men, especially those over age 60. As I’ve pointed out, high testosterone levels are not a precursor to an enlarged prostate or cancer; rather, excessive DHT and estrogen levels formed as metabolites of testosterone are. Conventional medicine uses two classes of drugs to treat BPH, each having a number of serious side effects. These are:
When we face stress, our adrenal glands secrete cortisol to prepare our bodies and minds to handle the stressful situation — the primal fight-or-flight response. In small dosages, cortisol is fine and even useful, but elevated cortisol levels for prolonged periods can do some serious damage to our bodies and minds. One area that seems to take a hit when cortisol is high is our testosterone levels. Several studies have shown a link between cortisol and testosterone. When cortisol levels are high, testosterone levels are low; and when testosterone levels are high, cortisol levels are low.
There is a polymorphic CAG repeat sequence in the androgen receptor gene, which codes for a variable number of glutamine amino acids in the part of the receptor affecting gene transcription. A receptor with a short CAG sequence produces greater activity when androgens attach, and men with shorter CAG polymorphisms exhibit androgenic traits, such as preserved bone density (Zitzmann et al 2001) and prostate growth during testosterone treatment (Zitzmann et al 2003). Indirect evidence of the importance of androgens in the development of prostate cancer is provided by case control study findings of a shorter, more active CAG repeat sequence in the androgen receptor gene of patients with prostate cancer compared with controls (Hsing et al 2000, 2002).
The testosterone booster pills are effective from 4 to 8 hours. To maintain testosterone levels high during the whole day, you need a multiple daily dosing regimen. 2-times daily dosing still not always can improve hormone production to the greatest extent. 3-4-times daily dosing is the best solution to make your body normalize testosterone synthesis and prevent it from decreasing before you take another pill. Don’t forget that the regularity of daily supplement intake is crucial if you really aspire to give a boost to hormone production.
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Here’s one proof: in a number of British rivers, 50 percent of male fish were found to produce eggs in their testes. According to EurekAlert,3 EDCs have been entering rivers and other waterways through sewage systems for years, altering the biology of male fish. It was also found that fish species affected by EDCs had 76 percent reduction in their reproductive function.
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.
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).
Watch out for ingredients that interfere with blood clotting If you are taking any kind of blood medication, take aspirin or ibuprofen, or have any kind of blood-related condition, you’ll want to consult your doctor before taking any of these supplements. Fenugreek, Forskolin, and Acetyl-L-carnitine are just a few of the ingredients that can make these situations worse and increase your chances of bruising and bleeding.
Decreased testosterone production in men with rheumatoid arthritis is a common finding (Stafford et al 2000), and it is now generally recognized that androgens have the capacity to suppress both the hormonal and cellular immune response and so act as one of the body’s natural anti-inflammatory agents (Cutolo et al 2002). This known anti-inflammatory action of testosterone has led to studying the effect of testosterone therapy in men with rheumatoid disease. Although not all studies have reported positive effects of testosterone treatment (Hall et al 1996), some studies do demonstrate an improvement in both clinical and chemical markers of the immune response (Cutolo et al 1991; Cutolo 2000). This observation would go along with more recent evidence that testosterone or its metabolites protects immunity by preserving the number of regulatory T cells and the activation of CD8+ T cells (Page et al 2006).
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.
No one will argue with the well-established fact that the dramatic lows of testosterone as seen in castration or other significant primary testicular disturbances such as those induced by chemotherapy, radiation therapy, congenital problems, or as seen in secondary testicular insufficiency (eg, large compressive pituitary or hypothalamic tumors) produce dramatic signs and symptoms of testosterone deficiency that require testosterone replacement therapy. Less clear, or at least more controversial, is the necessity of treating the gentler reduction of testosterone seen in the aging process.
The chemical synthesis of testosterone from cholesterol was achieved in August that year by Butenandt and Hanisch. Only a week later, the Ciba group in Zurich, Leopold Ruzicka (1887–1976) and A. Wettstein, published their synthesis of testosterone. These independent partial syntheses of testosterone from a cholesterol base earned both Butenandt and Ruzicka the joint 1939 Nobel Prize in Chemistry. Testosterone was identified as 17β-hydroxyandrost-4-en-3-one (C19H28O2), a solid polycyclic alcohol with a hydroxyl group at the 17th carbon atom. This also made it obvious that additional modifications on the synthesized testosterone could be made, i.e., esterification and alkylation.
Researchers at Ball State University found that “strength training can induce growth hormone and testosterone release.” (6) Another study from the University of Nebraska Medical Center researched the acute effects of weight lifting on serum testosterone levels. (7) The results concluded that even moderate weight lifting and light weightlifting increased serum testosterone levels in participants.
Testosterone is used as a medication for the treatment of males with too little or no natural testosterone production, certain forms of breast cancer, and gender dysphoria in transgender men. This is known as hormone replacement therapy (HRT) or testosterone replacement therapy (TRT), which maintains serum testosterone levels in the normal range. Decline of testosterone production with age has led to interest in androgen replacement therapy. It is unclear if the use of testosterone for low levels due to aging is beneficial or harmful.
As you can see, the entire workout is only 20 minutes. Twenty minutes! That really is a beautiful thing. And within those 20 minutes, 75 percent of that time is warming up, recovering or cooling down. You're really only working out intensely for four minutes. It's hard to believe if you have never done this that you can actually get that much benefit from four minutes of exercise. That's all it is.
It may be unlikely to completely eliminate products with EDCs, but there are a number of practical strategies that you can try to limit your exposure to these gender-bending substances. The first step would be to stop using Teflon cookware, as EDCs can leach out from contaminated cookware. Replace them with ceramic ones. Stop eating out of cans, as the sealant used for the can liner is almost always made from powerful endocrine-disrupting petrochemicals known as bisphenols, e.g. Bisphenol A,
With the decline of ovarian function in menopause, not only do estrogen levels decline, but so does testosterone availability, since the ovaries contribute, either by direct secretion or through precursor production, about 50 percent of circulating testosterone. The other 50 percent is supplied by the adrenal glands. Many post-menopausal or oophorectomized women are symptomatic as a consequence of reduced testosterone, the leading symptom being loss of libido (Sherwin and Gelfand 1987; Simon et al 2005). There is an increasing trend toward testosterone supplementation in these women. Such supplementation may also lead, not only to increased libido, but to increased bone mineral density and an improvement in general overall sense of well-being including energy, strength, motivation and mood (Davis et al 1995; Davis et al 2000).
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.
The partial synthesis in the 1930s of abundant, potent testosterone esters permitted the characterization of the hormone's effects, so that Kochakian and Murlin (1936) were able to show that testosterone raised nitrogen retention (a mechanism central to anabolism) in the dog, after which Allan Kenyon's group was able to demonstrate both anabolic and androgenic effects of testosterone propionate in eunuchoidal men, boys, and women. The period of the early 1930s to the 1950s has been called "The Golden Age of Steroid Chemistry", and work during this period progressed quickly. Research in this golden age proved that this newly synthesized compound—testosterone—or rather family of compounds (for many derivatives were developed from 1940 to 1960), was a potent multiplier of muscle, strength, and well-being.
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.
Aromatase inhibitors can boost testosterone on their own, but they can also complement other testosterone boosters. If you take a supplement that increases testosterone without inhibiting the aromatase enzyme (through hypothalamic stimulation, for instance), you may find yourself with more estradiol than you need, a situation that taking an aromatase inhibitor may remedy.
Dobs and colleagues found that men with an increased body mass index had both reduced testosterone and reduced high density lipoprotein (HDL) levels. Treatment with testosterone increased the levels of HDL (Dobs et al 2001). Rising levels of HDL are not a consistent finding with TRT. More often, however, one finds reduced total cholesterol, low density lipoprotein (LDL) cholesterol and triglyceride levels with TRT (Zgliczynski et al 1996; Whitsel et al 2001).
In the hepatic 17-ketosteroid pathway of testosterone metabolism, testosterone is converted in the liver by 5α-reductase and 5β-reductase into 5α-DHT and the inactive 5β-DHT, respectively. Then, 5α-DHT and 5β-DHT are converted by 3α-HSD into 3α-androstanediol and 3α-etiocholanediol, respectively. Subsequently, 3α-androstanediol and 3α-etiocholanediol are converted by 17β-HSD into androsterone and etiocholanolone, which is followed by their conjugation and excretion. 3β-Androstanediol and 3β-etiocholanediol can also be formed in this pathway when 5α-DHT and 5β-DHT are acted upon by 3β-HSD instead of 3α-HSD, respectively, and they can then be transformed into epiandrosterone and epietiocholanolone, respectively. A small portion of approximately 3% of testosterone is reversibly converted in the liver into androstenedione by 17β-HSD.
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.
The bones and the brain are two important tissues in humans where the primary effect of testosterone is by way of aromatization to estradiol. In the bones, estradiol accelerates ossification of cartilage into bone, leading to closure of the epiphyses and conclusion of growth. In the central nervous system, testosterone is aromatized to estradiol. Estradiol rather than testosterone serves as the most important feedback signal to the hypothalamus (especially affecting LH secretion). In many mammals, prenatal or perinatal "masculinization" of the sexually dimorphic areas of the brain by estradiol derived from testosterone programs later male sexual behavior.
In accordance with sperm competition theory, testosterone levels are shown to increase as a response to previously neutral stimuli when conditioned to become sexual in male rats. This reaction engages penile reflexes (such as erection and ejaculation) that aid in sperm competition when more than one male is present in mating encounters, allowing for more production of successful sperm and a higher chance of reproduction.
A: There are no over-the-counter products approved by the U.S. Food and Drug Administration (FDA) to increase testosterone levels. There are several prescription medication options available. Please consult with your health care provider in regards to your testosterone levels and to determine which treatment option best meets your individual needs. For more specific information, consult with your doctor or pharmacist for guidance based on your health status and current medications, particularly before taking any action. Kristen Dore, PharmD
Testosterone is a stimulant of hematopoiesis in the bone marrow and consequently, increases the hematocrit (Shahidi 1973). Men with unexplained anemia should have their testosterone measured and if reduced, these men should be treated with testosterone. Because of the erythropoietin stimulating effect of testosterone, one of the parameters to be monitored during testosterone treatment is hematocrit since a small percent of testosterone-treated men develop polycythemia.
What are the health benefits of kale? Kale is a leafy green vegetable featured in a variety of meals. With more nutritional value than spinach, kale may help to improve blood glucose, lower the risk of cancer, reduce blood pressure, and prevent asthma. Here, learn about the benefits and risks of consuming kale. We also feature tasty serving suggestions. Read now
Longjack, also known as Tongkat ali and pasak bumi, is a shrub hailing from Southeast Asia purporting to improve libido. It’s gaining traction in the scientific community for potentially increasing testosterone levels, and researchers at South Africa’s University of the Western Cape found that longjack improved testosterone levels and muscular strength in physically active seniors (a population with typically low testosterone).
A loophole in FDA regulations allows pharmaceutical marketers to urge men to talk to their doctors if they have certain "possible signs" of testosterone deficiency. "Virtually everybody asks about this now because the direct-to-consumer marketing is so aggressive," says Dr. Michael O'Leary, a urologist at Harvard-affiliated Brigham and Women's Hospital. "Tons of men who would never have asked me about it before started to do so when they saw ads that say 'Do you feel tired?'"