Posts Tagged ‘Testosterone’


// October 29th, 2010 // 2 Comments » // Hormones

A man’s prostate gland siphons testosterone from his bloodstream. Then an enzyme within the prostate gland converts the trapped testosterone to DHT. It is this DHT made by and retained within the prostate that is one of the factors responsible for prostate gland growth. As far as we know, the prostate gland does not pluck DHT from a man’s bloodstream. Further, when blood DHT levels rise, testosterone levels decline, making less testosterone available for the prostate gland to ensnare. With less testosterone to trap, DHT levels within the prostate gland decline; and prostate growth can be held in check. How do we know this?

Older men given testosterone usually have a slight but significant increase in their prostate specific antigen (PSA) levels. But when similarly aged men are given large doses of DHT, their PSA levels do not change. There are probably two reasons for this. When men receive testosterone supplements, their blood testosterone levels increase, making more testosterone available for the prostate to trap and convert to DHT. But when men receive large doses of DHT, their testosterone levels actually decline. There is not as much bloodstream testosterone for the prostate gland to trap, so less is available for conversion to DHT within the prostate gland.

There is a second and more subtle sequence of events that explains why testosterone, but not DHT, stimulates the prostate to generate more PSA. A female hormone, estradiol, is one of the natural by-products of testosterone metabolism. It turns out that estradiol is yet another stimulus to prostate gland growth. Dihydrotestosterone cannot be further metabolized to estradiol or any other prostate-stimulating estrogen. Thus, giving a man more testosterone will raise blood testosterone, estradiol, and dihydrotestosterone levels. The increases in blood testosterone and blood estradiol provide the prostate with two potent hormonal stimuli to prostate growth. Testosterone does this by being trapped by the prostate gland, and after being transformed to DHT, it can increase the growth of the prostate gland. Estradiol then is free to exert a direct stimulatory impact on other prostate cells.

DHT, on the other hand, does not enter the prostate gland and cannot be transformed into another male hormone or estradiol and therefore deprives the prostate of both testosterone and estradiol, nullifying the growth-promoting impact of these two hormones. As a consequence, neither PSA levels nor prostate size increase during DHT treatment.

The ability of DHT to maintain a male hormone presence while simultaneously lowering estradiol levels is what makes DHT an ideal hormone to treat young boys who develop breast enlargement (gynecomastia). DHT has not yet been approved for this use in this country, but in France, where DHT is approved, teenage boys with gynecomastia have benefited from DHT treatment. Published reports indicate that boys’ breast size returns to normal with DHT treatment.


// October 29th, 2010 // No Comments » // Impotence

A below-normal serum testosterone level (hypogonadism) is the most common hormone abnormality found in men with acquired immunodeficiency syndrome (AIDS). In some cases, this is the result of viruses or other microorganisms invading and disabling the testicle’s testosterone-producing capability. More often, the hypogonadism results from subnormal pituitary signals to the testicle, a condition referred to as secondary hypogonadism. Dr. Adrian Dobs of Johns Hopkins University Medical School was one of the first to note that men with AIDS experience many of the symptoms of hypogonadism. In one of her earlier studies in men with AIDS, she noted that 28 of 42 (67 percent) complained of decreased libido, and 14 Of 42 (33 percent) said they were impotent. In addition to the common symptoms immediately attributed to their hypogonadism, men infected with the AIDS virus often experience unexplained decline in weight and loss of muscle mass. This condition is referred to as the AIDS wasting syndrome (AWS) and, in addition to all the other problems AIDS patients have to cope with, AWS is a major cause of morbidity and premature death. We know that in men with spontaneous hypogonadism, loss of weight and muscle mass is common and that for these hypogonadal men, testosterone treatment helps restore weight and strength. Could testosterone treatment work as well in men with AWS?

Preliminary data from Drs. Judith and Richard Rabkin of the College of Physicians and Surgeons, Columbia University, suggest that providing supplemental testosterone or a testosterone analogue, like mesterolone, to men with AIDS who have low serum testosterone levels is beneficial, producing clear improvements in sexual interest, arousal, and overall sense of wellbeing. Some have even speculated that supplemental testosterone may also have a positive mood-elevating impact similar to that seen with traditional antidepressant therapy.

Men with AIDS were treated with a conventional dose of 100 mg of testosterone per week for eight weeks. They had a significant gain in weight and noted enhanced sexual interest and more energy, suggesting that this form of androgen supplementation is effective in alleviating many of the problems that men with AIDS find so troubling.

As more men with AIDS were subjected to detailed hormonal studies, it became apparent that not all, even those who were suffering from AWS, had below-normal testosterone levels. In June 1996, Dr. Richard Horton of the University of Southern California Medical School found that some men with AWS have normal testosterone levels but are unable to efficiently convert testosterone to a second male hormone, dihydrotestosterone (DHT). He speculated that it was the subnormal DHT levels that were most likely responsible for their inability to gain weight in AWS.


// October 29th, 2010 // 1 Comment » // Hormones

Recognizing that testosterone is the major male hormone and estrogens the hormones of femininity does not mean that gender alone determines exclusive rights to either hormone. Men have small amounts of an estrogen, specifically estradiol, in their bloodstream, and in parallel fashion, women’s adrenal glands and ovaries routinely produce small amounts of testosterone. The exact role of the sex hormones of the opposite sex in people has been something of a mystery, but there is increasing evidence that a man’s estrogens play a role in stimulating prostate gland growth and that testosterone’s presence in a women may be a key factor in maintaining her libido.

Our knowledge of the factors that stimulate or suppress male sexual function, though imperfect, is nonetheless substantially more advanced than our understanding of the hormonal determinants of female sexuality. In adolescent boys, timing of androgen (testosterone) secretion and sexual interest coincide, whereas in young women, androgen secretion and orgasmic capacity are not closely linked. Male hormone production is evident in young girls as early as age ten, when the first wisps of pubic hair appear in response to the increased secretion of the adrenal androgen dehydroepiandrosterone sulfate (DHEA-S), but orgasms are not evident until later. Further, a woman’s androgen levels, both adrenal DHEA and ovarian testosterone, remain fairly constant after the late teens or early twenties, whereas her capacity for orgasms increases steadily.

The best prognosticator of a woman’s sexual activity is her free testosterone level, but this hormone does not appear to influence female sexual behavior as much as cues from peer group women. Adolescent girls tend to be sexually active when their friends are.

Certain androgens such as androstenedione and free testosterone increase just prior to ovulation. This androgen burst coincides with increased sexual activity in all mammals except for the human female, who tends to have an increase in her sexual activity at the conclusion of her menstrual period when her androgens are at their lowest levels.

The pivotal role of testosterone in female libido has not been appreciated until recently and only in those women have had their ovaries surgically removed during a total abdominal hysterectomy. It was at this time that women noted a profound diminution in their sex drive. Initially, popular psychologists ascribed this diminution in libido to despondency over the loss of their uterus and inability to bear children. But women who had a simple hysterectomy with their ovaries left intact did not experience the same sexual fate as their sisters who had both their ovaries and uterus removed. There was something about their remaining ovarian tissue that allowed these women to maintain their libido. Now it appears that that something was testosterone.

Much of our current scientific knowledge about the role of testosterone in female sexuality comes from the extensive studies in Australia and Canada. Only recently has testosterone supplementation for postmenopausal women become popular in this country, and that has been largely due to the efforts of Dr. Susan Rako, a Boston psychiatrist who writes that she became interested in testosterone on her own in 1988 when “her hormones crashed” around the time of her menopause. Traditional HRT to correct her estrogen deficiency, it seems, was not sufficient to correct her “loss of sexual and vital energy.” With testosterone supplementation, she felt better and was energized and revitalized.

Eager to share her experience with others, she published a book entitled The Hormone of Desire: The Truth About Sexuality, Menopause, and Testosterone, extolling the benefits and downplaying the adverse effects of bolstering testosterone levels in postmenopausal women.

The very first reports of testosterone supplementation had indeed focused on postmenopausal women who, like Dr. Rako, complained of a loss of sexual desire while receiving conventional estrogen and progesterone hormone replacement therapy (HRT).

Studies in Australia and Canada relied on a visual analog scale, asking women “On a scale of 0-100 with 100 being entirely normal, how would you rate your sex drive?” before and during treatment. Women scored themselves low at 20 before and 85 after 6 weeks of estrogen plus testosterone, but were unchanged after estrogen alone.

In Canada, Dr. Barbara Sherwin evaluated not just libido but overall sense of well-being, energy, and appetite in postmenopausal women with no ovaries. She found that compared to placebo or estrogen alone, women who received a combination of estrogen and testosterone, this time by intramuscular injection and not by pellet implantation, had a significant improvement in their well-being, energy level, and appetite. This improvement carries a cost, for all of the testosterone-treated women grew hair on their faces and had a worsening of their cholesterol profile, making them theoretically more susceptible to atherosclerosis. Mindful of the need for safer testosterone delivery systems to activate libido without fostering facial hair growth, new testosterone cremes and lotions are being formulated.

Capitalizing on the recent enthusiasm for providing supplemental testosterone to enhance libido in postmenopausal women, some have started to cautiously explore the potential benefit of a combined estrogen and testosterone pill. Reasoning that unsightly facial hair and disordered lipid profiles are dose related, the manufacturers of Estratest, the most common estrogen and testosterone combination pill, have now come out with Estratest-LD, the LD signifying that the pill contains a lower dose of testosterone than the parent compound. However, the testosterone in both pills is methyltestosterone, one of the 17-alkylated testosterone products known to have significant side effects. We do not yet know the benefits of long-term androgen therapy in women, but we do know of some of the reported risks of this treatment. Most of the currently available testosterone in pills may carry a burden of liver toxicity. (See earlier comments on AAS.)

Doctors are still uneasy about issuing a blanket recommendation for testosterone pills for all postmenopausal women with diminished libido. As additional data emerge from placebo-controlled studies, we should be able to learn whether androgen supplementation is not only effective but also a safe treatment for postmenopausal women with low sexual desire and inhibited sexual arousal.

However, a limited trial of testosterone may be precisely what Linda needs. She may do just as well with either testosterone pills or patches to resurrect her lost libido. For example, to circumvent the liver toxicity of testosterone pills, testosterone patches have been used with some success.
The testosterone patches differ in some respects from those used by men both in dose and use. Men have to change their patches daily, but women seem to be able to go three to four days before changing patches. The use of testosterone patches in women is quite new. We will have a better sense of the value of testosterone patches in postmenopausal women when results of additional research studies are made available.


// October 29th, 2010 // No Comments » // Steroids

The carefully crafted and meticulously executed Bhasin study cited above used a single consistent very high dose of testosterone. Its conclusions will most likely satisfy both scientists and athletes. But those who endorse and promote “off-label” AAS use view most scientific studies with disdain because these reports failed to replicate the complex sequencing of steroid administration preferred by those who rely on AAS to gain a competitive edge. Athletes tend not to take medication in the strictly controlled amounts required for credible research studies. Rather, they cycle AAS use to maximize benefit and decrease the risk of detection in urine assays. A practice known as “stacking,” the ritual sequencing of more than one steroid, is common. Athletes believe that by using more than one AAS they will be able to activate more and different types of androgen activity (androgen receptors). There is no scientific proof that this practice actually works, for there is only one androgen receptor and it is already filled to maximum capacity by the doses of AAS routinely used by athletes. Some also believe that optimum benefit cannot be achieved with any single AAS schedule. To avoid a “plateau,” they scramble the order of AAS administration, often beginning their cycle with low doses, then building with sequentially higher doses before tapering down just prior to competition, constructing in essence an AAS “pyramid.”

Androgens are known to be potent stimuli to prostate growth. Anxiety over the impact of unfettered, relentless androgen stimulation on prostate size has been a cause of considerable anxiety among physicians but has apparently not been one for athletes preoccupied with long-term consequences of “off-label” AAS use. Rather, it is the expectation of short-term gain, not long-term consequences, that is of paramount concern to the current crop of AAS aficionados. They tend to equate prostate problems with the remote destination of advanced age, which is not a primary concern of young competitive athletes.

AAS users believe they are clever enough to manipulate drug treatment to fend off the short-term adverse effects of AAS use and are cocky enough to believe they will have the same good fortune in sidestepping the more pernicious long-term consequences of continued androgen bombardment of their bodies. Still, several of the short-term problems — acne, fluid retention, balding, and breast enlargement — caused by high-dose AAS use do require attention. To cope with these bothersome problems, athletes have once again dipped into the pharmacy to concoct “the array.”


// October 29th, 2010 // No Comments » // Hormones

Although men and women who compete in sports routinely depend on testosterone to increase muscle bulk, tone, and function, doctors have had a hard time accepting what for athletes is a matter of faith. This is because those who do use supplemental male hormones also train vigorously. It has been impossible to sort out how much improvement in a man or woman’s athletic performance is due to obsessive and diligent training and how much to testosterone.

Doctors’ experience with hypogonadal men — that is, men with lower than normal testosterone levels — has been instructive. When testosteronedeficient men are given just enough hormone to regularize their blood testosterone levels, they have an unequivocal 11-percent increase in lean body (muscle) mass. Further, individual muscle groups such as upper arm and thigh muscle mass expanded by 21 percent and 11 percent, respectively, with proper hormone treatment. This impressive augmentation of muscle bulk can occur after just ten weeks of testosterone therapy.
But these were not normal men, for below-normal testosterone levels had left them with below-normal muscle mass. The testosterone treatment merely brought them back to their predetermined baseline, and no further. For men who already have normal male hormone levels, the advantages of further testosterone supplementation are less clear.

Designing a study to answer a question as apparently straightforward as “Does testosterone use increase a man’s strength?” has proven to be a remarkably challenging task.

Much of our current thinking about anabolic steroids changed on July 4, 1996. On that date, Dr. Shalender Bhasin and his colleagues in California and Oregon reconciled the differences between skeptical physicians and steroid-conscious athletes.

In a carefully controlled study, Dr. Bhasin demonstrated for the first time that massive doses of androgens, in this case 600 mg of testosterone weekly (roughly fifteen times the normal man’s testosterone output of 42 mg per week), did increase weight, muscle mass, and strength.

The greatest gains in muscle mass and strength were observed in trained athletes who received testosterone and also participated in a supervised exercise program. Athletes in the testosterone plus exercise group who weighed 167 pounds at baseline weighed 180 pounds after ten weeks of high-dose testosterone. Their bench-press strength — 213 pounds before-was 261 pounds at week ten.

Trained athletes who exercised regularly but received placebo injections had no significant weight gain (188 at start, and 190 pounds at ten weeks). Their bench-press strength was 240 pounds before and 261 pounds after ten weeks of supervised training.

Thus, compared to placebo-treated men, testosterone-treated athletes gained thirteen more pounds (most of it muscle) and could lift more weight than they could at the outset. The eleven-pound weight gain and the ability to bench press twenty-seven more pounds than the placebo-treated men was significant, proving that massive doses of testosterone did increase weight, muscle mass, and muscle strength.

But what about the average man or the proverbial “couch potato” who does not have the time, energy, or inclination to commit himself to a lengthy and intensive program of physical conditioning? Will he also experience an increase in body weight and improved muscle strength after receiving enormous amounts of testosterone? The answer is “yes,” but to a significantly lesser degree.

For example, placebo-treated untrained men had no increase in body weight and could bench press the same amount of weight before and at week ten of the study. With testosterone, their weight increased from 181 to 189 pounds. Their bench-press prowess, 213 pounds at baseline, was up to 231 pounds after ten weeks of high-dose testosterone therapy, once again demonstrating the profound impact of very large doses of testosterone on both muscle mass and muscle strength. (See Table 13.2. )

To achieve these striking results, doctors had to give deep intramuscular injections of extraordinary doses of testosterone. Blood testosterone levels increased to values a man would never be able to achieve on his own. Those who volunteered to take part in this study had entirely normal serum testosterone values between 430 and 550 ng/dl. (The normal serum testosterone range is 300-1,000 ng/dl.) The amount of testosterone administered left men so awash in testosterone that one week after the last testosterone injection, serum testosterone levels were 3,244 ng/dl, or 300 percent higher than the highest serum testosterone level a man could hope to achieve naturally.

Because serum testosterone levels reached such extraordinary heights, far greater than would be possible under normal physiologic conditions, the dose of testosterone administered is said to be “supraphysiologic,” that is, more than the body is programmed to make or cope with. During ten weeks of supraphysiologic testosterone treatment, men noted some increased acne, but not much else in the way of adverse effects. Tests designed to test their level of aggression before and during the onslaught of testosterone did not uncover any heightened tendency toward aggressive or antisocial behavior. But this was only a short-term study. The adverse effects of large doses of testosterone are more readily apparent with long-term high-dose testosterone use.


// October 29th, 2010 // No Comments » // Hormones

Testosterone made in the testicles is released into a man’s bloodstream to transform cells scattered throughout the body. As an androgen (a male hormone), testosterone can only work on androgen receptors. Cells without androgen receptors would not be expected to, and do not, respond to testosterone. However, androgen receptors are widespread. So this male hormone can accelerate, slow down, or wreak havoc with a remarkably diverse array of individual and uniquely male physical responses.

As one would expect, testosterone is vital for normal male sexual behavior. Testosterone has other functions — some advantageous, others less savory, and still others downright harmful. Listed below are some of the ways testosterone makes its presence known in different parts of the body. Testosterone interacts with androgen receptors on muscle to increase muscle mass and seeks out bone marrow androgen receptors to stimulate bone marrow to make more red blood cells. Other consequences of testosterone-androgen receptor interplay force the kidney to hold on to more sodium, stimulate the skin to develop acne, help build strong bones, increase body hair while simultaneously accelerating the loss of scalp hair, and thicken a man’s vocal cords, giving him a deep voice.

Testosterone’s power in bringing about all of these remarkable physical changes is well documented, but when most men think of testosterone, they tend to focus primarily on the muscle-building and sexuality-enhancing properties of this male hormone. Other, more subtle issues like the important role of testosterone in maintaining a woman’s sex drive and the invigorating


// October 29th, 2010 // No Comments » // Hormones, Impotence

All is not wine and roses; testosterone also has a dark side because it is a steroid. The word “steroid” refers to the peculiar chicken-wire structure of this hormone. Other vital hormones made in the adrenal glands and the ovaries also have a steroid configuration. These steroid hormones course innocently through our bloodstreams every moment of every day. Neither the ovary’s estrogens nor the adrenal gland’s cortisone shares testosterone’s nefarious legacy.
• When you read in the paper that an athlete has been disqualified from competition because he or she “tested positive for steroids,” testosterone or one of its close androgenic (male hormone) relatives is the steroid they are referring to.
• Rival industries, one devoted to promoting, the other to detecting, illegal male hormone use among athletes are now firmly in place.
• Androgen enthusiasts have amassed enough information to publish their own Anabolic Steroid Hormone Users Bible with surprisingly accurate descriptions of individual anabolic steroids and tips on how to cope with common problems linked with steroid use. This information is considered so valuable that it is printed in blue ink on thin paper so that it cannot be photocopied.
• The anabolic steroid watchdogs, on the other hand, have been busy devising methods to detect inappropriate and illegal use of male hormone supplements in athletes and bodybuilders. It is now possible to distinguish between a competitive athlete’s own naturally occurring male hormones and illegal male hormone supplements just by examining athletes’ urine samples to look for the telltale disruptions in the testosterone-epitestosterone ratios.
• To bedevil those intent on rooting out inappropriate anabolic steroid use, an equally ardent counterindustry has conjured up means to avoid detection by spiking the urine with a few drops of alcohol to foil test results.
• When lawyers seek to find extenuating circumstances to explain what motivated their client to commit some violent act, they frequently invoke “steroid rage” defense. They use this strategy to plead that the “accused should be excused” because at the time of the crime while in the grip of these mighty male hormones, he was powerless to control his aggression.
• In Europe, Israel, and California, men convicted of repeated sexual offenses for molesting children are offered the opportunity to avoid, or have a more lenient, prison sentence if they agree to a chemical castration to nullify the impact of testosterone as one means of discouraging further deviant sexual behavior.
• Does this mean that testosterone turns men into sexual deviants? No, but men who are inclined to a pattern of aberrant sexual behavior need testosterone to fuel their misdirected sexual urges. Take away their testosterone, and they stop preying on children.

What is it about testosterone that inspires so much passion? How much of what they say is true? We are just starting to get answers to these questions.


// October 29th, 2010 // No Comments » // Hormones, Impotence


Before Viagra, everybody was talking about testosterone.

Newsweek’s cover story on testosterone, coupled with a feature on another male hormone called DHEA, antedated that same weekly magazine’s different, but equally enthusiastic, cover story on Viagra. Both testosterone and DHEA were also featured in prominent stories in the Wall Street Journal, and on the CBS Evening News. Male hormones were then and still are one hot topic.

Testosterone, we are told, will give men of all ages massive muscles, invigorate aging men, spice up the sexual desire of menopausal women. Further, this special male hormone is said to work wonders to improve flagging muscle strength and is being touted as a panacea to resolve many of the problems currently plaguing both young and older men and women today. Could all this hype really be true, and if so, why aren’t more men taking testosterone supplements?

How to Enhance a Man’s Testosterone Output?

// October 29th, 2010 // No Comments » // Hormones

Three techniques, one old and two new, have been developed to allow men to increase the testosterone output of their testicles.

1. Human chorionic gonadotropin as an LH surrogate.
2. Pulsatile GnRH release via implantable pump.
3. Clomiphene.

Human Chorionic Gonadotropin is an LH surrogate. The testicles of men with secondary hypogonadism are inherently normal but lack the appropriate stimulus to make testosterone. If that stimulus can be provided, the testicles should be able to function once again.

Produced by women during pregnancy, human chorionic gonadotropin (hCG) acts directly on a man’s testicular Leydig cells to stimulate testosterone production. Synthetic hCG is available and when injected into the muscle of the shoulder or buttocks enters the bloodstream and acts just like LH to provoke a brisk increase in serum testosterone levels. Unfortunately, the effect of a single hCG injection is short-lived; twice-weekly injections are needed. This is more troublesome than a testosterone injection once a month. Today, hCG treatment is reserved for infertile men with low sperm counts.

HCG acts directly on the testicle, bypassing the hypothalamus and pituitary. The two new treatment methods increase testosterone production by activating a man’s hypothalamus or pituitary.

GnRH Pump Therapy. Dr. William Crowley of Massachusetts General Hospital has developed a small battery-powered pump that is loaded with the hypothalamic hormone GnRH. The patient wears the device on his hip. A thin tube extending from the pump ends in a needle that is placed under the skin of impotent men with GnRH deficiency (idiopathic hypogonadotropic hypogonadism). The pump is programmed to release pulses of GnRH to stimulate pulsatile release of both pituitary LH and FSH. Exposed to LH pulses, the testicle starts manufacturing testosterone, and potency is restored. Pulsatile FSH release is also activated so that sperm production increases gradually. This enables a group of men previously thought to be hopelessly impotent and infertile to have a normal sex life and become fathers.

Clomiphene. Clomiphene, a medication commonly used to treat infertile women, can also stimulate testosterone production in some men with secondary hypogonadism. Clomiphene is effective in men because it increases pulsatile pituitary LH stimulation of the testicle. Early pilot studies have been encouraging. One clomiphene tablet every other day can maintain normal testosterone levels. This avoids the peaks and valleys of blood testosterone values resulting from testosterone injections. We know this about clomiphene because several investigators, my own group included, have performed clinical investigations to determine how this medication activates and enhances testosterone secretion in men. Clomiphene therapy for men is still considered an experimental or investigational treatment. Clomiphene is currently an FDA-approved medication only for the treatment of infertility in women.

Problems with Testosterone Patch Therapy

// October 29th, 2010 // No Comments » // Hormones

To be effective in transferring testosterone from the patch into a man’s bloodstream, patches must remain in close proximity to the skin. The adhesive in the patch usually takes care of this, but the bond between the adhesive and skin breaks down when men sweat. None of the patches are effective when wet. Men who like to go to the gym to exercise learn this very quickly and will often remove their patch and store it on a shelf in their lockers just before starting their workout. Then they can work up a sweat during exercise or plunge into a pool or hot tub without compromising the effectiveness of their patch. When they have concluded their workout they can shower and towel off, and once dry, can safely reaffix the testosterone patch to maintain its effectiveness.

It is not just those men who exercise at the gym who must follow these guidelines. Men who sweat copiously while gardening or doing heavy labor or perspire during periods of increased stress must be aware that sweating will limit the effectiveness of their testosterone-impregnated patches and take similar precautions.

Skin Reactions with Testosterone Patches

The key element needed for the patches to work is a substance called a chemical “enhancer.” It is the enhancer that makes it possible for testosterone to get out of the patch, go through the skin, and enter the bloodstream. Differences in enhancer properties define both effectiveness and toxicity, with Testo-derm’s enhancer working only when applied to thin scrotal skin, whereas the enhancer in the Androderm and Testoderm TTS patches is significantly stronger, permitting diffusion of testosterone across all skin surfaces, but not without extracting a toll. Skin irritation, rashes, itching, and occasionally blisters and hives are among the reactions commonly associated with the use of the Androderm and Testoderm TTS patches. (Curiously, skin irritation is less common with the scrotal Testoderm patch.) Some men have no skin irritation at all with either the Androderm or Testoderm TTS body patch, whereas others do. Men who have fairer skin seem to be more likely to develop these skin reactions and rashes. Those who are susceptible to skin reactions can minimize or totally prevent the occurrence of the rash by pretreating the skin with a pea-sized dollop of a cortisone-like cream called triamcinolone. (I usually offer a prescription for triamcinolone cream whenever I write a prescription for either Androderm or Testoderm TTS patches.)