Archive for the ‘Testosterone’ Category

The University of Manchester is investigating whether increasing the testosterone levels of frail elderly men could improve their strength, energy and mobility.

This is the first study in the world to examine how testosterone treatment may impact this age-group, led by Professor Fred Wu of the Department of Endocrinology at Manchester Royal Infirmary.

Professor Wu said: “Levels of the male hormone testosterone fall by about 1% a year in men over 40, leading to decreases in muscle size and strength, increased body fat and thinner bones. The changes are also associated with decreased sexual interest, fatigue, mobility problems, depression, increased risk of falling and a general sense of weakness.

“Tests on younger and healthy older men suggest that testosterone replacement could help reverse these symptoms in the frail and elderly.”

Professor Wu’s team is expecting to publish the results in two years’ time, and hopes that if the treatment is proven to be effective it may be adopted as standard practice by the NHS.

As well as increasing strength, mobility and quality of life for elderly men, the move could significantly reduce the accident-rate and care requirements of this group and ultimately reduce demands on the NHS and social services.

Men aged 65+ who have lost weight, are easily tired, slow in walking and feel generally weak for no specific reason are being recruited for the study. Only those volunteers found to have low testosterone levels can be included in the trial.

The protocol for participants requires five visits to the Wellcome Trust Clinical Research Facility on Grafton Street at Manchester Royal Infirmary over the 12 month period. They will receive either testosterone or a dummy placebo in the form of a gel self-applied daily to the skin, for the first six months of the trial. Their muscle strength, mobility, bone-strength, muscle and fat content and general quality of life will then be assessed by the research team after both six and 12 months.

The research is being undertaken in partnership with Central Manchester and Manchester Children’s University Hospitals NHS Trust. Participants are free to withdraw from the study at any time, and all information will be collected in the strictest confidence.

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Article adapted by MD Sports from original press release.
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Contact: Jo Nightingale or Rachael McGraw
University of Manchester

NOTES FOR EDITORS

The University of Manchester (www.manchester.ac.uk) was formed by the merger of The Victoria University of Manchester and UMIST in October 2004, and with 36,000 students is the largest higher education institution in the country. Its Faculty of Medical & Human Sciences (www.mhs.manchester.ac.uk) is one of the largest faculties of clinical and health sciences in Europe, with a research income of over £37 million.

The School of Medicine (www.medicine.manchester.ac.uk) is the largest of the Faculty’s five Schools, with 1300 staff, almost 2000 undergraduates and a £32M research income. The School encompasses five teaching hospitals, and is closely linked to a range of general hospitals and community practices across the North West of England.

By studying the genes of a German child born with unusually well developed muscles, an international research team has discovered the first evidence that the gene whose loss makes “mighty mice” also controls muscle growth in people.

Writing in the June 24 issue of the New England Journal of Medicine, German neurologist Markus Schuelke, M.D., and the team show that the child’s extra-large muscles are due to an inherited mutation that effectively silences the myostatin gene, proving that its protein normally keeps muscle development in check in people.

People with muscle-wasting conditions such as muscular dystrophy, and others just wanting to “bulk up,” have eagerly followed work on myostatin, hoping for a way to counteract the protein’s effects in order to build or rebuild muscle mass. But while research with mice has continued to reveal myostatin’s role and the effects of interfering with it, no one knew whether any of the results would be relevant to humans.

“This is the first evidence that myostatin regulates muscle mass in people as it does in other animals,” says Se-Jin Lee, M.D., Ph.D., professor of molecular biology and genetics in the Institute for Basic Biomedical Sciences at Johns Hopkins and co-author on the study. “That gives us a great deal of hope that agents already known to block myostatin activity in mice may be able to increase muscle mass in humans, too.”

Lee and his team discovered in 1997 that knocking out the myostatin gene led to mice that were twice as muscular as their normal siblings, lending them the moniker “mighty mice.” Later, others showed that naturally bulky cattle, such as Belgian Blues, got their extra muscles from lack of myostatin, too.

An unusual opportunity to examine myostatin’s role in humans arose when Schuelke examined a newborn baby boy, almost five years ago, and was struck by the visible muscles on the infant’s upper legs and upper arms. When ultrasound proved that the muscles were roughly twice as large as other infants’, but otherwise normal, Schuelke realized that a naturally occurring mutation in the child’s myostatin gene might be the cause.

Sequencing the myostatin gene from the boy and his mother, who had been a professional athlete, revealed a single change in the building blocks of the gene’s DNA. Surprisingly, the change was not in the gene regions that correspond to the resulting protein, but in the intervening regions that are used only to create protein-making instructions, thus changing the gene’s protein-building message.

“The mutation caused the gene’s message, the messenger RNA, to be wrong,” says Hopkins

neurologist Kathryn Wagner, M.D., Ph.D., who tested the genetic mutation’s effect in laboratory studies. “If the message had been used to make a protein, it would be much shorter than it should be. But we think the process doesn’t even get that far; instead the cells just destroy the message.”

Co-authors from Wyeth Research, Cambridge, Mass., analyzed samples of the child’s blood for evidence of the myostatin protein and found none. “Both copies of the child’s myostatin gene have this mutation, so little if any of the myostatin protein is made,” says Schuelke. “As a result, he has about twice the muscle mass of other children.”

Completely lacking myostatin, the boy is stronger than other children his age, and fortunately has no signs of problems with his heart so far, Schuelke says. But he adds that it’s impossible to know whether the lack of myostatin in that crucial muscle might lead to problems as the boy gets older.

While other family members — the boy’s mother and her brother, father and grandfather — were also reported to have been usually strong, only the mother’s DNA was available for analysis along with her son’s. Schuelke discovered that only one copy of the mother’s myostatin gene had the mutation found in both copies of her son’s myostatin gene. (We have two copies of each gene; one inherited from the mother and one inherited from the father.)

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Article adapted by MD Sports Weblog from original press release.
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 Contact: Joanna Downer
Johns Hopkins Medical Institutions

 

The Johns Hopkins researchers were funded by the National Institutes of Health and the Muscular Dystrophy Association. The German researchers were funded by the parents’ self-help group (Helft dem muskelkranken Kind).

Authors on the paper are Schuekle, Christoph Hubner, Thomas Riebel and Wolfgang Komen of Charite, University Medical Center Berlin, Germany; Wagner and Lee of Johns Hopkins; Leslie Stolz and James Tobin of Wyeth Research, Cambridge, Ma.; and Thomas Braun of Martin-Luther-University, Halle-Wittenberg, Germany.

*Under a licensing agreement between MetaMorphix Inc. and The Johns Hopkins University, Lee is entitled to a share of royalty received by the University on sales of products described in this article. Lee also is entitled to a share of sublicensing income from arrangements between MetaMorphix and American Home Products (Wyeth Ayerst Laboratories) and Cape Aquaculture Technologies. Lee and the University own MetaMorphix Inc. stock, which is subject to certain restrictions under University policy. Lee owns Cape Aquaculture Technologies stock, which is subject to certain restrictions under University policy. Lee has served as a paid consultant to MetaMorphix Inc. The terms of these arrangements are being managed by The Johns Hopkins University in accordance with its conflict of interest policies.

Steroid use by a Major League Baseball slugger may produce only modest increases in muscle mass and bat and ball speed but still boost home run production by 50 percent or more, according to a new study by Tufts University physicist Roger Tobin.

Tobin, a specialist in condensed matter physics with a long-time interest in the physics of baseball, will publish his paper “On the potential of a chemical Bonds: Possible effects of steroids on home run production in baseball” in an upcoming issue of the American Journal of Physics.

As Tobin’s paper notes, Babe Ruth’s record of 60 home runs in a single season stood for 34 years until Roger Maris hit 61 homers in 1961. For the next 35 years, no player hit more than 52 home runs in one season. But between 1998 and 2006, players hit more than 60 home runs in a season six times. Barry Bonds hit 73 home runs in 2001 — topping Maris’ mark by an astonishing 20 percent.

According to Tobin, the explosion in home runs coincides with the dawn of the “steroid era” in sports in the mid-1990s, and that surge quickly dropped to historic levels in 2003, when Major League Baseball instituted steroid testing.

While the increase in home runs has been clouded by suspected use of performance-enhancing steroids, many have wondered why home-running hitting would be particularly vulnerable to performance enhancement. They have also asked if it is even physically and physiologically plausible that steroids could produce effects of the magnitude observed. The answer to both questions, says Tobin, is “yes.”

Home Runs Disproportionately Affected

“A change of only a few percent in the average speed of the batted ball, which can reasonably be expected from steroid use, is enough to increase home run production by at least 50 percent,” he says. This disproportionate effect arises because home runs are relatively rare events that occur on the “tail of the range distribution” of batted balls.

“In most any statistical distribution — of people’s heights, SAT scores, or how far baseballs are hit — there’s a large bump where most of the values fall, with the graph falling rapidly as you move away from that region in either direction toward the rarer values,” explains Tobin. “It’s a well-known statistical property of such distributions that a relatively small shift in the center point of the distribution can produce a much larger proportional change in the number of values well above or below the center. Because the distribution’s ‘tail’ is particularly sensitive to small changes in the peak and/or width, home run records can be more strongly affected by steroid use than other athletic accomplishments.”

Muscle Mass Boosts Bat and Ball Speed

Tobin reviewed previous studies of the effect of steroid use and concluded that muscle mass, the force exerted by those muscles and the kinetic energy of the bat could each be increased by about 10 percent through the use of steroids. According to his calculations, the speed of the bat as it strikes the pitched ball will be about 5 percent higher than without the use of steroids and the speed of the ball as it leaves the bat will be about 4 percent higher.

To determine the ultimate impact on home run production, Tobin then analyzed a variety of models for trajectory of the baseball, accounting for gravity, air resistance and lift force due to the ball’s spin. While there was considerable variation among the models, “the salient point,” he says, “is that a 4 percent increase in ball speed, which can reasonably be expected from steroid use, can increase home run production by anywhere from 50 percent to 100 percent.”

What About the Pitchers?

Tobin applied a similar, though less extensive, mechanical analysis to pitching and found that smaller impacts were possible. He calculated that a 10 percent increase in muscle mass should increase the speed of a thrown ball by about 5 percent, or four to five miles per hours for a pitcher with a 90 mile per hour fastball. That translates to a reduction in earned run average of about 0.5 runs per game.

“That is enough to have a meaningful effect on the success of a pitcher, but it is not nearly as dramatic as the effects on home run production,” says Tobin. “The unusual sensitivity of home run production to bat speed results in much more dramatic effects, and focuses attention disproportionately on the hitters.”

A Reasonable Suspicion

Tobin is quick to acknowledge that athletes in many sports today achieve at a higher level than athletes of the past, and that this trend is not evidence of cheating. He also points out that many other changes, including adjustments in ballpark dimensions, league expansions, entry of African-American athletes, and lowering of the pitcher’s mound, could affect major league batting — although he says that none of those changes coincide with the sudden burst of home run production in the mid-1990s.

“Physics cannot tell us whether a particular home run was steroid-assisted, or even whether an extraordinary individual performance indicates the use of illicit means,” says Tobin.

But analysis of the physics, combined with physiology, yields telling results. “These results certainly do not prove that recent performances are tainted, but they suggest that some suspicion is reasonable,” he concludes.

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Article adapted by MD Sports Weblog from original press release.
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Tufts University, located on three Massachusetts campuses in Boston, Medford/Somerville, and Grafton, and in Talloires, France, is recognized among the premier research universities in the United States. Tufts enjoys a global reputation for academic excellence and for the preparation of students as leaders in a wide range of professions. A growing number of teaching and research initiatives span all Tufts campuses, and collaboration among the faculty and students in the undergraduate, graduate and professional programs across the university’s schools is widely encouraged.

Source: Kim Thurler
Tufts University

Myostatin (MSTN) is a transforming growth factor-ß (TGF-ß) family member that plays a critical role in regulating skeletal muscle mass [1]. Mice engineered to carry a deletion of the Mstn gene have about a doubling of skeletal muscle mass throughout the body as a result of a combination of muscle fiber hyperplasia and hypertrophy [2]. Moreover, loss of myostatin activity resulting either from postnatal inactivation of the Mstn gene [3], [4] or following administration of various myostatin inhibitors to wild type adult mice [5][7] can also lead to significant muscle growth. Hence, myostatin appears to play as least two distinct roles, one to regulate the number of muscle fibers that are formed during development and a second to regulate growth of muscle fibers postnatally. The function of myostatin appears to have been conserved across species, as inactivating mutations in the myostatin gene have been demonstrated to cause increased muscling in cattle [8][11] , sheep [12], dogs [13] and humans [14]. As a result, there has been considerable effort directed at developing strategies to modulate myostatin activity in clinical settings where enhancing muscle growth may be beneficial. In this regard, loss of myostatin activity has been demonstrated to improve muscle mass and function in dystrophic mice [15][17] and to have beneficial effects on fat and glucose metabolism in mouse models of obesity and type II diabetes [18].

Myostatin is synthesized as a precursor protein that undergoes proteolytic processing to generate an N-terminal propeptide and a C-terminal dimer, which is the biologically active species. Following proteolytic processing, the propeptide remains bound to the C-terminal dimer and maintains it in an inactive, latent complex [6], [19], [20], which represents one of the major forms of myostatin that circulates in the blood [21], [22]. In addition to the propeptide, other binding proteins are capable of regulating myostatin activity in vitro, including follistatin [19], [21], FLRG [22], and Gasp-1 [23]. We previously showed that follistatin can also block myostatin activity in vivo; specifically, we showed that follistatin can ameliorate the cachexia induced by high level expression of myostatin in nude mice [21] and that transgenic mice expressing follistatin in muscle have dramatic increases in muscle mass [19]. Here, I show that overexpression of follistatin can also cause substantial muscle growth in mice lacking myostatin, demonstrating that other TGF-ß related ligands normally cooperate with myostatin to suppress muscle growth and that the capacity for enhancing muscle growth by targeting this signaling pathway is much larger than previously appreciated.

Results

Increased muscle mass in transgenic mice expressing FLRG

Previous studies have identified several proteins that are normally found in a complex with myostatin in the blood [22], [23]. One of these is the follistatin related protein, FLRG, which has been demonstrated to be capable of inhibiting myostatin activity in vitro. To determine whether FLRG can also inhibit myostatin activity in vivo, I generated a construct in which the FLRG coding sequence was placed downstream of a myosin light chain promoter/enhancer. From pronuclear injections of this construct, a total of four transgenic mouse lines (Z111A, Z111B, Z116A, and Z116B) were obtained containing independently segregating insertion sites. Each of these four transgenic lines was backcrossed at least 6 times to C57 BL/6 mice prior to analysis in order to control for genetic background effects. Northern analysis revealed that in three of these lines the transgene was expressed in skeletal muscles but not in any of the non-skeletal muscle tissues examined (Figure 1); in the fourth line, Z111B, the expression of the transgene was below the level of detection in these blots. As shown in Table 1, all four lines exhibited significant increases in muscle weights compared to wild type control mice. These increases were observed in all four muscles that were examined as well as in both sexes. Moreover, the rank order of magnitude of these increases correlated with the rank order of expression levels of the transgene; in the highest-expressing line, Z116A, muscle weights were increased by 57–81% in females and 87–116% in males compared to wild type mice. Hence, FLRG is capable of increasing muscle growth in a dose-dependent manner when expressed as a transgene in skeletal muscle.

The research was funded by grants from the NIH and the Muscular Dystrophy Association and by a gift from Merck Research Laboratories.

See http://www.jhu.edu/sejinlee/%20for%20more%20information for more information.
Citation: Lee S-J (2007) Quadrupling Muscle Mass in Mice by Targeting TGF-ß Signaling Pathways. PLoS ONE 2(8): e789. doi:10.1371/journal.pone.0000789

LINK TO THE PUBLISHED ARTICLE http://www.plosone.org/doi/pone.0000789

Source: Nick Zagorski
Johns Hopkins Medical Institutions

Use of growth hormone to boost athletic performance can lead to diabetes, reports a study published ahead of print in the British Journal of Sports Medicine.

The study reports the case of a 36 year old professional body-builder who required emergency care for chest pain.

He had lost 40 kg in 12 months, during which he had also experienced excessive urination, thirst, and appetite.

He admitted to using anabolic steroids for 15 years and artificial growth hormone for the past three. He had also taken insulin, a year after starting on the growth hormone.

This was done to counter the effects of high blood sugar, but he had stopped taking it after a couple of episodes of acute low blood sugar (hypoglycaemia) while at the gym.

Tests revealed that his liver was inflamed, his kidneys were enlarged and that he had very high blood sugar. He was also dehydrated, and diagnosed with diabetes.

He was given intravenous fluids and gradually increasing amounts of insulin over five days, after which he was discharged. His symptoms completely cleared up, and he was no longer diabetic.

The use of growth hormone has steadily risen among amateur athletes and bodybuilders all round the world, say the authors, because it is easy to buy online and difficult to detect in screening tests—unlike anabolic steroids.

The authors believe that this is the first reported case of diabetes associated with the use of high dose growth hormone, and urge anyone taking high doses to regularly check their blood sugar levels.

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Article adapted by MD Only Sports Weblog from original press release.
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Contact: Emma Dickinson
BMJ Specialty Journals

We could not survive without hormones. They are among the most common and vital chemical messengers in the body. From head to toe, each moment of life, they signal cells to perform tasks that range from the ordinary to the extraordinary. Among their many roles, hormones help regulate body temperature, blood pressure, and blood sugar levels. In childhood, they help us “grow up.” In the teen years, they are the driving force behind puberty.

What Is A Hormone?

Hormones are powerful chemicals that help keep our bodies working normally. The term hormone is derived from the Greek word, hormo, which means to set in motion. And that’s precisely what hormones do in the body. They stimulate, regulate, and control the function of various tissues and organs. Made by specialized groups of cells within structures called glands, hormones are involved in almost every biological process including sexual reproduction, growth, metabolism, and immune function. These glands, including the pituitary, thyroid, adrenals, ovaries, and testes, release various hormones into the body as needed.

Levels of some hormones like parathyroid hormone, which helps regulate calcium levels in the blood and bone, actually increase as a normal part of aging and may be involved in bone loss leading to osteoporosis. But the levels of a number of other hormones, such as testosterone in men and estrogen in women, tend to decrease over time. In other cases, the body may fail to make enough of a hormone due to diseases and disorders that can develop at any age. When this occurs, hormone supplements—pills, shots, topical (rub-on) gels, and medicated skin patches—may be prescribed.

How Hormones Work

Most hormones exist in very low concentrations in the bloodstream. Each hormone molecule travels through the blood until it reaches a cell with a receptor that it matches. Then, the hormone molecule latches onto the receptor and sends a signal into the cell. These signals may instruct the cell to multiply, to make proteins or enzymes, or to perform other vital tasks. Some hormones can even stimulate a cell to release other hormones. However, no single hormone affects all cells in the same way. One hormone, for example, may stimulate a cell to perform one task, while the same hormone can have an entirely different influence over another cell. The response of some cells to hormonal stimulation also may change throughout life.

DHEA

Dehydroepiandrosterone or DHEA is made from cholesterol by the adrenal glands, which sit on top of each kidney. Production of this substance peaks in the mid-20s, and gradually declines with age in most people. What this drop means or how it affects the aging process, if at all, is unclear. In fact, scientists are somewhat mystified by DHEA and have not fully sorted out what it does in the body. However, researchers do know that the body converts DHEA into two hormones that are known to affect us in many ways: estrogen and testosterone.

Human Growth Hormone

Human growth hormone (hGH) is made by the pituitary gland, a pea-sized structure located at the base of the brain. It is important for normal development and maintenance of tissues and organs and is especially important for normal growth in children.

Studies have shown that injections of supplemental hGH are helpful to certain people. Sometimes children are unusually short because their bodies do not make enough  GH. When they receive injections of this hormone, their growth improves. Young adults who have no pituitary gland (because of surgery for a pituitary tumor, for example) cannot make the hormone and they become obese. When they are given hGH, they lose weight.

Like some other hormones, blood levels of hGH often decrease as people age.Although there is no conclusive evidence that hGH can prevent aging, some people spend a great deal of money on supplements. These supplements are claimed by some to increase muscle, decrease fat, and to boost an individual’s stamina and sense of well being. Shots—the only proven way of getting the body to make use of supplemental hGH—can cost more than $15,000 a year. They are available only by prescription and should be given by a doctor. Some dietary supplements, known as human growth hormone releasers, are marketed as a low-cost alternative to hGH shots. But claims that these over-the-counter products retard the aging process need to be examined. While some studies have shown that supplemental hGH does increase muscle mass, it seems to have less impact on muscle strength or function in older adults.

Testosterone

Ask an average man about testosterone, and he might tell you that this hormone helps transform a boy into a man. Or, he might tell that you that it has something to do with sex drive.   Or, if he has read news stories in recent years, he might mention male menopause, a condition thought to be caused by diminishing testosterone levels in aging men.

Testosterone is indeed a vital sex hormone that plays an important role in puberty. In men, testosterone not only regulates sex drive (libido), it also helps regulate bone mass, fat distribution, muscle mass and strength, and the production of red blood cells and sperm.But contrary to what some people believe, testosterone isn’t exclusively a male hormone.  

Women produce small amounts of it in their bodies as well. In men, testosterone is produced in the testes, the reproductive glands that also produce sperm. The amount of testosterone produced in the testes is regulated by the hypothalamus and the pituitary gland.

As men age, their testes often produce somewhat less testosterone than they did during adolescence and early adulthood, when productionof this hormone peaks. In fact, many of the changes that take place in older men often are incorrectly blamed on decreasing testosterone levels. Some men who have erectile difficulty (impotence), for instance, may be tempted to blame this problem on lowered testosterone. However, in many cases, erectile difficulties are due to circulatory problems, not low  testosterone. Still, some men may be helped by testosterone supplementation. For these few men who have extreme deficiencies, testosterone therapy in the form of patches, injections, or topical gels may offer substantial benefit.

Testosterone products may help a man with exceptionally low testosterone levels maintain strong muscles and bones, and increase sex drive. However, what effects testosterone replacement may have in healthy older men without these extreme deficiencies requires more research.The NIA is investigating the role of testosterone therapy in delaying or preventing frailty. Results from preliminary studies involving small groups of men have been inconclusive, and it remains unclear to what degree supplementation of this hormone can sharpen memory or help men maintain stout muscles, sturdy bones, and robust sexual activity.

Many other questions remain about the use of this hormone in late life. It is unclear, for example, whether men who are at the lower end of the normal range of testosterone production would benefit from supplementation.Some investigators are also concerned about the long-term harmful effects that supplemental testosterone might have on the aging body. While some epidemiologic studies suggest that higher levels of testosterone are not associated with the higher incidence of prostate cancer, it is not yet known if testosterone therapy increases the risk of such cancer, the second leading cause of cancer death among men.

The bottom line: Although some older men who have tried testosterone therapy report feeling more energetic or younger, testosterone supplementation remains a scientifically unproven method for preventing or relieving any physical and psychological changes that men with normal testosterone levels may experience as they get older. The NIA is expanding its research to gather more evidence on the risks and benefits of testosterone supplementation in aging men with low testosterone levels.

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Article adapted by MD Only Sports Weblog from original press release.
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Source:  National Institute on Aging

What is testosterone?

Testosterone is a vital sex hormone that plays an important role in puberty. But contrary to what some people believe, testosterone isn’t exclusively a male hormone. Women produce small amounts of it in their bodies as well. In men, testosterone is produced in the testes, the reproductive glands that also produce sperm. The amount of testosterone produced in the testes is regulated by the hypothalamus and the pituitary gland.

What is a hormone?

Hormones, such as testosterone, are powerful chemicals that help keep our bodies working normally. The term hormone is derived from the Greek word, hormo, which means to set in motion. And that’s precisely what hormones do. They stimulate, regulate, and control the function of various tissues and organs. Made by specialized groups of cells within structures called glands, hormones are involved in almost every biological process, including sexual reproduction, growth, metabolism, and immune function. These glands, including the pituitary, thyroid, adrenals, ovaries and testes, release various hormones into the body as needed. Do testosterone levels diminish with age? Does “male menopause occur?”

There is scant evidence that “male menopause,” a condition supposedly caused by diminishing testosterone levels in aging men, exists. As men age, their testes often produce somewhat less testosterone than they did during adolescence and early adulthood, when production of this hormone peaks. But it is important to keep in mind that the range of normal testosterone production is large. Many older men have testosterone levels within the normal range of healthy younger men. Others have levels well below this range. However, the likelihood that a man will ever experience a major shut down of hormone production, similar to a woman’s menopause, is remote.

In fact, many of the changes that take place in older men often are incorrectly blamed on decreasing testosterone levels. Some men who have erectile difficulty (impotence), for instance, may be tempted to blame this problem on lowered testosterone. However, in many cases, erectile difficulties are due to circulatory problems, not low testosterone.

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Article adapted by MD Only Sports Weblog from original press release.
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U.S. NATIONAL INSTITUTES OF HEALTH