Category: testosterone

The debate on the effect of anabolic substances on the structure of the heart reached another phase, since Finnish scientists studied twenty local bodybuilders who had just finished their cycles. Steroids don’t damage the heart, the researchers found. But the combination of steroids and growth hormone does.


Since the eighties scientists have been discussing whether steroids enlarge the heart, when several sports investigators learned steroid use was associated with enlargement of the left ventricular mass – the part of the heart that pumps oxygenated blood through the body. An overdeveloped left ventricle causes arrhythmia and, in severe cases, death. In 2001 Australian physicians found the hypertrophy in clean strength athletes and postulated that this condition was caused by weight training, not steroid use. They also found that the hypertrophy didn’t impair their subjects’ health.

The new Finnish study, published in the International Journal of Sports Medicine in the summer of 2003, doesn’t contradict the Australian study. Nevertheless, it provides insight into the relationship between anabolic substances and heart hypertrophy.


The Finnish ran an advertorial in a bodybuilding magazine on their project. Twenty bodybuilders, who had planned to do a cycle and bought their medication on the black market, responded. Before their cycle started the bodybuilders had their medication checked and analysed by the pharmacological department of the university. Not unnecessary, because up to fifty percent of the European black steroids may be counterfeited, according to the latest estimates.

Sixteen bodybuilders used steroids only. The weekly doses varied from a few hundred milligrams to more than thousand milligrams.

Four athletes stacked their steroids with growth hormone. All four used moderate dosages of two, three or four IU’s during four to six weeks. The growth hormone was injected once daily, mostly in the evening. In this group steroid doses were 1,3 times higher than in the steroids only group.

When their cycles ended, the bodybuilders had their hearts examined. The table below summarizes some results. The control group consisted of fifteen young males with active life styles who didn’t engage in weight training.


Steroids + GH
Heart rate 66 bpm 65 bpm 65 bpm
Systolic blood pressure 131 mmHg 131 mmHg 130 mmHg
Diastolic blood pressure 77 mmHg 76 mmHg 89 mmHg
Left ventricular weight 167 g 257 g 342 g
Ratio left ventricular weight: length 93 g/m 141 g/m 191 g/m
Relative wall thinkness 0,37 0,42 0,53
Ratio early peak flow velocity: peak atrial flow velocity (E/A ratio) 1,66 1,72 1,29

Steroids and the combination of steroids and growth hormone change the structure of the heart, the table suggests. But that doesn’t have any consequences for the cardiovascular health of at least the steroid users. Their diastolic blood pressure – reported to rise phenomenally in some steroid related medical horror-stories – was fine, and more interestingly, their E/A ratio improved. Cardiologists use the E/A ratio to measure the hearts efficiency. According to the table, in the steroids only group deterioration of the heart muscle didn’t occur.

But growth hormone, well, that is another story. The table speaks for itself. The higher steroid doses that the GH-users took can only explain a small part of the serious ventricular hypertrophy, the Finnish stress. They suspect that the lowering effect of androgens on the IGF-1-binding protein 3 concentrations causes the ventricular growth.


So far not so good. But there is more. The Finnish discovered something very interesting about the nature of the relationship between anabolic aids and hypertrophy of the heart: it’s direct. For example, the Finnish asked their subjects for how many years they had been using steroids. The answers varied from one to twelve years. Statistically the relationship between lifetime steroid use and the E/A ratio was weak. On the other hand, the mean steroid dose of the present cycle was a strong predictor of variables like E/A ratio, ventricular weight of relative wall thickness.

This means that cycles don’t have a cumulative effect on heart hypertrophy. The Finnish discovered that even the pronounced impact of cycles with added growth hormone wears off. That became evident when they investigated an athlete three times: when he just finished a five weeks cycle of steroids and growth hormone, after a wash out period of 237 days, and just after he completed a steroids only cycle. The results are in the figure below.

E/A Ratio and RWT

Of course a study with twenty users is not conclusive. But the study suggests that

  1. just like the Australians proved before, steroids are not as disastrous for the heart morphology as some agencies want you to believe;
  2. the combination with growth hormone does however add considerable cardiovascular risks to steroid cycles; and
  3. the deleterious effects wear off during wash out periods.

Especially athletes in their late thirties and older should take their wash out periods seriously. The age of the subjects in the Finnish study ranged from 25 to 43. In this population age was the strongest predictor of the E/A ratio. The older they were, the lower their ratio ratio. (The Pearson’s correlation coefficient was –0.70. The coefficient of mean steroid dose and E/A ratio was –0.42.)


Anabolic Androgenic Steroids (AAS) are prohibited substances in sport due to their ability to improve muscle strength and power. Usually athletes who abuse these substances dose in cycles of up to 8-12 weeks. Whether the effects require this length of time to manifest is unknown. Also unknown is the minimum dose required and whether sports drug testing laboratories are able to detect all cases of AAS use by athletes.

PURPOSE: To determine if the AAS, testosterone enanthate could increase strength and athletic performance in 3-6 weeks and the use the T/E ratio screening measure could detect the use of the steroid over that period.

METHODS: Eighteen healthy young males (25+4.0 yrs) were match-paired and randomly assigned in a double blind manner to either a testosterone enanthate or a placebo group. All subjects performed a structured heavy resistance-training program while receiving either testosterone enanthate (3.5 or saline intramuscular injections once weekly for six weeks. 1RM strength measures (bench press and leg press) and 10-second cycle sprint performance were monitored at the pre- (week 0), mid (week 3) and post (week 6) time points. Body mass and the urinary testosterone/epitestosterone (T/E) ratio were measured at the pre (week 0) and post (week 6) time points. Urine samples collected at week 0 were analysed for the presence of WADA prohibited substances. ANOVA with repeated measures was used for statistical analysis.

RESULTS: When compared to baseline (pre), 1RM bench press strength and total work during the cycle sprint increased significantly at week 3 (p <0.01) and week 6 (p <0.01) in the testosterone group but not the placebo group. At week 3, 1RM bench press increased 9% from baseline whilst at week 6 the increase was 15%. No significant differences were found between groups for 1RM leg press or peak power. Body mass at week 6 was significantly greater (7%) than at week 0 in the testosterone group (p <0.01) but not the placebo group. Despite the clear performance enhancing effects of testosterone in as little as three weeks, four of the nine subjects in the testosterone group (44%) had a T/E ratio of < 4. T/E ratios for the testosterone group ranged from 2 to 37. T/E ratios for the placebo group remained unchanged between week 0 and week 6.

CONCLUSIONS: The AAS, testosterone enanthate, enhances 1RM bench press and 10-second cycle sprint performance in 3 weeks in a dose that is used therapeutic ally. Using the T/E ratio of 4:1 (currently used to screen urine samples), not all subjects could be detected who were being administered the steroid and gaining performance enhancement from it.

Suggested Citation

Deakin, GB, Rogerson, S, Meir, RA, Coutts, RA, Zhou, S, Marshall-Gradisnik, SM & Weatherby, RP 2006, ‘Performance enhancement and urinary detection after short-term testosterone enanthate use’, American College of Sport Medicine annual meeting, Journal of Medicine and Science in Sports and Exercise, vol. 38, supplement 5, Denver, CO, 31 May -3 June, American College of Sports Medicine, Indianapolis, IN, p. S405.


Aging is associated with reduced GH, IGF-I, and sex steroid axis activity and with increased abdominal fat. We employed a randomized, double-masked, placebo-controlled, noncross-over design to study the effects of 6 months of administration of GH alone (20 microg/kg BW), sex hormone alone (hormone replacement therapy in women, testosterone enanthate in men), or GH + sex hormone on total abdominal area, abdominal sc fat, and visceral fat in 110 healthy women (n = 46) and men (n = 64), 65-88 yr old (mean, 72 yr). GH administration increased IGF-I levels in women (P = 0.05) and men (P = 0.0001), with the increment in IGF-I levels being higher in men (P = 0.05). Sex steroid administration increased levels of estrogen and testosterone in women and men, respectively (P = 0.05). In women, neither GH, hormone replacement therapy, nor GH + hormone replacement therapy altered total abdominal area, sc fat, or visceral fat significantly. In contrast, in men, administration of GH and GH + testosterone enanthate decreased total abdominal area by 3.9% and 3.8%, respectively, within group and vs. placebo (P = 0.05). Within-group comparisons revealed that sc fat decreased by 10% (P = 0.01) after GH, and by 14% (P = 0.0005) after GH + testosterone enanthate. Compared with placebo, sc fat decreased by 14% (P = 0.05) after GH, by 7% (P = 0.05) after testosterone enanthate, and by 16% (P = 0.0005) after GH + testosterone enanthate. Compared with placebo, visceral fat did not decrease significantly after administration of GH, testosterone enanthate, or GH + testosterone enanthate. These data suggest that in healthy older individuals, GH and/or sex hormone administration elicits a sexually dimorphic response on sc abdominal fat. The generally proportionate reductions we observed in sc and visceral fat, after 6 months of GH administration in healthy aged men, contrast with the disproportionate reduction of visceral fat reported after a similar period of GH treatment of nonelderly GH deficient men and women. Whether longer term administration of GH or testosterone enanthate, alone or in combination, will reduce abdominal fat distribution-related cardiovascular risk in healthy older men remains to be elucidated.



The Testosterone:Cortisol Connection
By Dan Gwartney, MD
In the humorous parody periodical, Mad Magazine, a recurring feature is “SPY vs. SPY.” Two spies, identical except for their coloring (one is black and the other is white), attempt to thwart each other by devising all sorts of creative and hilarious booby traps. Of course, readers over the decades have never seen these two actually accomplish any worthwhile spying as the efforts serve merely to cancel each other out. Despite the extreme measures taken, neither spy gains an advantage in the man-to-man battle.
The Battle Within
A similar battle rages every day within the human body. Two nearly identical molecules are pitted against each other in a seemingly futile war to shift the balance of power from one side to the other. In fact, a stalemate is  maintained unless something occurs in the environment to create an advantage for either side. The two molecules are testosterone and cortisol.Testosterone, an intimately familiar hormone to all bodybuilders, is considered an anabolic steroid due to its positive effects on muscle and sex-related glands. Cortisol is often referred to as a catabolic steroid as it has the reverse effect when present in excess; high cortisol levels lead to a breakdown of muscle, loss of lean mass and strength. Though they appear to be complete opposites, the two molecules are very similar in physical structure and are linked in a reciprocal fashion; meaning when one is up (elevated), the other is often down. It’s the hormonal equivalent of Superman and Bizzaro, an arch-nemesis to the cartoon  superhero who was the exact opposite, despite having nearly identical super powers. The relationship between testosterone and cortisol is important to clinicians and critical to athletes. Exercise, when performed at a suitable intensity and volume, can increase the anabolic stimulus, resulting in stronger and larger muscles.1 However, as many have discovered the hard way, exercising to excess can result in a weakened, catabolic state known as the overtraining syndrome.2-4 Numerous examples exist in the scientific literature, confirming that moderate-volume, high-intensity training can increase testosterone, growth hormone, IGF-1 and other anabolic signals, resulting in improved exercise performance.4,5Other studies show how high-volume, high-intensity exercise leads to increased inflammatory and catabolic hormones levels.6 Persisting in the overtrained state often leads to impaired long-term performance, muscle loss and decreased mental function.
The Anabolic-to-Catabolic Balance
Fortunately, the body appears to be able to recover from excess exercise with rest. One study examining rugby players over the course of a tournament found that though testosterone lowered and cortisol rose by the end of the tournament, a compensatory anabolic state occurred during the following days of rest, returning to normal after five days. The researchers concluded that intense competition should be followed by a minimum of one week’s rest to avoid overtaxing the body’s ability to recover from extreme exertion.8In a hospital setting, it’s been documented that stressed individuals have a greater reaction to ACTH (the pituitary hormone responsible for stimulating cortisol secretion) than normal persons.9 Prolonged illness or  chronic poor health results in high levels of catabolic hormones and low levels of anabolic hormones, including a low testosterone-to-cortisol ratio, with an accompanying loss of muscle.10Even more data has been collected relating to this issue in the field of aging. As people grow older, testosterone levels fall and cortisol levels rise, creating a hormonal environment that doesn’t support the muscle mass attained during young adult years.11Clearly, paying attention to the anabolic-to-catabolic balance is vital over the long term. The most often cited measure of this balance is the testosterone-to-cortisol ratio. Bodybuilders are quite adept at increasing testosterone levels. This is easily achieved through the use of exogenous anabolic steroids, resulting in impressive gains in muscle mass and strength. However, during intense training, especially under the hypocaloric conditions encountered as bodybuilders are cutting up for a competition, stress levels rise and catabolic conditions set in. Pounds of hard-earned muscle can disappear in a matter of days, leaving one with a depleted appearance. To avoid this, some bodybuilders try to control cortisol levels pharmaceutically.

Testosterone’s Effect on Cortisol

Before getting into more specific drugs that lower cortisol and its catabolic effects, it’s important to realize that the drug-enhanced athlete often doesn’t need to be overly concerned about cortisol, as long as he’s not  overtraining with high volume exercise. Exercise, fitness, and many of the drugs used to build mass also have a fortunate consequence of lowering cortisol levels. Exercise builds muscle and improves the condition of the body. One component of the effects of exercise is an improvement in insulin sensitivity; a measure of how well the body handles sugar. Though the relationship between the two is unclear, it’s been shown that for males, a decrease in testosterone is experienced with a coinciding rise in cortisol.This pattern of low testosterone and high cortisol is associated with insulin resistance.12 It’s unclear whether the insulin resistance causes the shift to a catabolic balance or if a catabolic hormonal environment inhibits insulin’s actions. Regardless, the beneficial effects of exercise on insulin sensitivity appear to favor an anabolic balance.Obesity is often related to a low testosterone:cortisol ratio. The hypothalamic-pituitary-adrenal axis is overactive in obese men
and elevated cortisol levels are seen in people with central obesity (predominantly abdominal fat).13 It’s known that central obesity is predictive of other metabolic diseases and an altered testosterone:cortisol ratio is prevalent in people with type 2 diabetes, hypertension and cardiovascular disease.14Testosterone, and likely other androgens, has a suppressive effect on the adrenal glands– the source of cortisol. Cortisol is produced and secreted under the influence of the hypothalamic-pituitary-adrenal gland axis. The hypothalamus (a region in the brain) sends a chemical messenger called CRH to the pituitary (a gland located near the base of the brain) to release another hormone called ACTH. ACTH travels through the bloodstream to the adrenal glands, stimulating the production and secretion of cortisol. Testosterone inhibits the adrenal glands’ response to ACTH, resulting in lower cortisol output.15 Interestingly, human chorionic gonadotropin (hCG) stimulates the release of both testosterone and cortisol, though the impact on testosterone persists for a longer period.16
Drugs Affecting Cortisol Levels
Another anabolic hormone frequently used is growth hormone (GH). GH is well known for its fat reducing properties, in addition to increasing lean mass. GH promotes tissue growth primarily through the actions of IGF-1, but its fat burning properties appear to be more direct. One function of GH that may explain this is its effect on an enzyme called 11β- hydroxysteroid dehydrogenase (11β-HSD). This enzyme has two forms, type 1 and 2, which are involved in cortisol metabolism. Type 1 11β-HSD reactivates cortisol from its inactive form– cortisone. GH inactivates type 1 11β-HSD, preventing cortisol from being reactivated from the inactive form, cortisone. This effect occurs at very low dosages (0.17 milligrams per day) and isn’t dependent on changes in fat mass, IGF-1 or insulin sensitivity.17,18 It appears that two of the most potent anabolics, testosterone and GH, derive some of their ability to shift metabolism to an anabolic balance from their abilities to lower the catabolic signal of cortisol.One class of drugs used by bodybuilders to cut up is associated with muscle wasting if used to excess, these being thyroid hormone drugs. Thyroid hormone appears to activate the hypothalamic-pituitary-adrenal axis, resulting in greater cortisol output.19 Elevated cortisol levels can certainly result in muscle wasting and a loss of strength, symptoms of thyroid hormone excess.Aside from drugs with incidental effects on cortisol levels, there are drugs with more specific actions against cortisol. The most well known and commonly used of this group is aminoglutethimide (Cytadren®).20 Aminoglutethimide is a drug affecting the production of many steroids by blocking the actions of several enzymes involved in steroid synthesis.21,22 Bodybuilders typically only take
aminoglutethimide for short periods, during the most catabolic period of pre-competition training as it may cause a number of side effects, including anorexia, nausea, vomiting, weakness and electrolyte  mbalances.23Aminoglutethimide is taken during this catabolic phase due to its presumed ability to lower cortisol, resulting in less muscle loss and lower fluid retention. However, much of the physique-enhancing effect of the drug may be due to another property of the drug used clinically, that being aromatase inhibition.24Aromatase is an enzyme complex that converts androgens into estrogens, promoting fat and water retention. By lowering
aromatase, and thus estrogens, many bodybuilders walk on stage harder and leaner, attributing the look to lower cortisol. In fact, aminoglutethimide is more efficient at lowering aromatase activity and estrogen levels than affecting cortisol. It appears that the body is able to compensate for partial suppression by low doses of aminoglutethimide by increasing ACTH stimulation of cortisolsecretion.21 The aromatase inhibition occurs at lower doses, possibly as low as 125 milligrams per day, whereas a minimum of 750 milligrams per day is required to lower cortisol levels.25 This combination of aromatase inhibition and cortisol suppression is
seen with other drugs, but these drugs have lost favor as more potent and specific aromatase inhibitors have been developed which don’t affect cortisol levels.26

Cortisol Suppression
In the clinical world, there are several other options for suppressing high cortisol levels, such as is seen in the disease Cushing’s syndrome. All of these drugs act by blocking enzymes involved in the production of steroid hormones, with some being more potent and selective, whereas others are weak or non-specific: trilostane is a weak option; aminoglutethimide is effective, but requires high dosages with frequent side effects; metyrapone inhibits 11β- HSD  recycling, but carries many side effects; ketoconazole is a potent inhibitor, but suppresses androgen production, more so than cortisol, and causes liver toxicity; etomidate is the most potent agent, but requires intravenous injections.27,28 Some other interesting drugs that may affect cortisol’s effects exist, but there’s no experience base from which to judge their actions.

RU-486, known as the morning after pill because it’s used to prevent pregnancies after unprotected sex, decreases cortisol receptor activity.29 Cortisol is metabolized in the body by a variety of enzymes, but two are of interest. 11β- HSD, which recycles cortisol from its inactive metabolite cortisone, is easily suppressed by a component found in licorice root extract.30 Oral use of licorice root may result in a loss of potassium and high blood pressure if overconsumed, but one study has shown that topical use of licorice extract may stimulate loss of subcutaneous fat.31 Another metabolic path of cortisol is 5α- and 5β-reduction. 5α-reduction is the process responsible for converting testosterone to the more potent androgen DHT. Though 5α-reduction  is associated with lower cortisol levels, it’s unclear whether the 5α-reduced metabolite is more  potent, such as in the case with the androgenic effects of testosterone. It’s been shown that high levels of the 5α- and 5β-reduced metabolites are associated with obesity and insulin resistance.32,33Clearly, there are many physical consequences when cortisol levels are high, especially in the setting of low testosterone. Secondarily, there also appears to be negative mental effects to having high cortisol levels. Severe depression is associated with high cortisol levels.34 Several reports describe beneficial responses to cortisol suppression therapy in depressedindividuals.35,36 Many of these individuals appear to be more sensitive to the hypothalamic hormone, resulting in higher ACTH levels.37Treating high cortisol levels improves signs of depression in approximately 70 percent of Cushing’s syndrome patients and depressed patients.38 Even for those not affected by depression, high cortisol levels interfere with information processing, making it more difficult to think or make decisions.39 This cortisol–depression connection may explain the high incidence of depression that occurs after the completion of a cycle, if testosterone levels fall too rapidly.
The Battle All Bodybuilders Face
The anabolic:catabolic balance is the battle all bodybuilders face in their pursuit of developing lean, muscular physiques. It’s important to consider the testosterone:cortisol ratio, as an imbalance quickly shifts the metabolism to favor one side and over the long term can dictate the amount and quality of muscle mass one attains.Cortisol is controlled somewhat by androgens and growth hormone, but there are also several drugs that lower the  hormone. These drugs are not specific and can carry significant side effects if used for long periods. Much of the effect of the more commonly used aminoglutethimide may be ascribed to aromatase inhibition rather
than cortisol suppression. For the drug-using bodybuilder, the anabolic effect of androgens and growth hormone, along with the aromatase suppression of more specific drugs such as Arimidex® or Femara® should provide the same protection with a much lower risk of side effects. It should be noted that a shift in balance favoring cortisol can be expected once a cycle ends, which may induce depression in some individuals. There’s certainly a need to control cortisol levels, but rather than resorting to dangerous, non-specific drugs, monitoring training volume and avoiding prolonged stress is a safer alternative.

Skin Treatments and Dermatological Procedures to Promote Youthful Skin
Paul G Sator
Department of Dermatology, Municipal Hospital Lainz, Vienna, Austria
The skin, the largest organ of the body, is the organ in which changes associated with aging are most visible. With increasing frequency, patients are requesting information and treatments that improve the appearance of their skin. Corresponding to this trend, there is an increasing number of products and methods available that claim to aid this pursuit. First, a change of the patient’s lifestyle (eg, sun behavior, nicotine abuse, and nutrition) must take place. Only then may other methods be used. This article reflects on the following topics: topical retinoids, peels, botulinum neurotoxin, soft tissue fillers, lasers, topical and systemic endocrinological therapies, and phytohormones. A thorough knowledge of the properties (benefits, limitations, and complications) of the expanding array of possibilities for rejuvenation of the skin is essential for any physician treating patients with cosmetic complaints.
Keywords: skin aging, topical retinoids, peels, botulinum neurotoxin, soft tissue fillers, lasers, topical endocrinological therapies, systemic endocrinological therapies, phytohormones
The skin is one of the largest organs of the body and, like all other tissues, it undergoes degenerative processes during aging. The skin represents the major organ in which aging-related changes are visible (Zouboulis and Boschnakow 2001). Skin aging is associated with increased rates of skin diseases including skin tumors, and with concomitant psychological distress caused by the deterioration in appearance. Although the main focus of public medicine has long been on age-related chronic diseases of other systems, such as arthritis, heart disease, and cancer (Kligman and Koblenzer 1997), skin aging and its diseases have become increasingly important. Most women in developed societies can expect to spend one-third or more of their lifetime in the postmenopausal period (Kligman and Koblenzer 1997) when the external signs of aging are of utmost importance for most.
Skin aging is caused by a combination of factors including genetic disposition and endocrinological background as well as UV light, life habits (nutrition, nicotine, alcohol, and drugs), catabolic (infections and tumors), and further environmental factors. Many women notice a sudden onset of signs and symptoms of skin aging during menopause, such as a rise in skin dryness, loss of firmness, decrease in elasticity, and increase in skin looseness. There is a connection between these clinical signs and such phenomena as decrease in collagen and elastin, changes in basic substance, the ratio of type I/type III collagen, and alterations in vascularization (Brincat 2000). The external signs of skin aging are reflected in the histopathologic findings of the skin (Broniarczyk-Dyla and Joss-Wichman 2001).
Dermatology patients are requesting information and treatments to improve the appearance of their skin with increasing frequency. The number of products and methods claiming to aid in this pursuit are rising. Many different ways may be helpful. Patients look for a prompt improvement while physicians emphasize safety and efficacy.
General procedures
Sun protection
Sun protection is essential for every age and is a necessary addition to all other interventions against skin aging. Chronic low-dose irradiation by the sun causes wrinkles (Kambayashi et al 2001; Gordon 2005). Ultraviolet irradiation reduces production of type I procollagen, the major structural protein in human skin (Quan et al 2004). To avoid photoaging, it is essential to use sunscreens every day and to protect one’s skin against UV A and B rays (a sun protection factor 15 is adequate, but a higher one is better). In addition, it is also important to use protective clothing or hats and to avoid the sun wherever possible.
Skin care
Cleansing and moisturizing the skin is important for many people. Properly cleaned and moisturized skin feels good to most people and looks better than dry skin. Effective products are available from most cosmetic companies and prevent irritant skin reactions and improve barrier functions. Sun protection, avoidance of cigarette smoke, and balanced nutrition is essential for the prevention of skin aging.
Topical retinoids
The topical retinoids, tretinoin and tazarotene, improve mottled hyperpigmentation, fine wrinkles, roughness, and lentigines (Kligman et al 1986; Kang et al 2001; Weiss 2005). One problem is skin irritation. To minimize this problem, it is useful to start with a relatively mild concentration of topical retinoids. If this is not enough, patients should reduce the application frequency. The aim must be to use the highest concentration that can be tolerated without significant irritation of the skin.
There are three categories of peels: deep peels (eg, phenol peel), medium peels (eg, 30% trichloracetic acid peel), and superficial peels (eg, alpha hydroxyl and salicylic acid peel). Creams with alpha hydroxyl and salicylic acid are also available for the everyday use of the patient. Depending on the depth of the peel, peels remove the uppermost layers of the skin.
Botulinum neurotoxin
Botulinum neurotoxin is a paralysing substance. It is used for softening glabellar frown lines, horizontal forehead lines, crow’s feet, perioral smile lines, platysmal bands of the neck, and to elevate the eyebrows and lateral corners of the mouth (Gordon 2005).
A careful history should be taken to avoid complicating neurologic problems or the ingestion of medications that may interfere with the toxin. The toxin diffuses about 1 cm–1.5 cm from the injection site. This must be considered to avoid eyelid ptosis, for example. The patient should not manipulate the treated area after treatment to avoid unintended diffusion of the toxin. The contraction of the treated muscles after treatment may increase toxin uptake and increase the effectiveness of treatment. The effect of the toxin is seen after about a week.
Soft tissue fillers
Physicians have been searching for the ideal filler for more than a century. The use of injected paraffin for cosmetic purposes more than 100 years ago resulted in paraffinomas (Murray et al 2005). Many substances are available today.
Collagen is a fibrous, extracellular, insoluble protein comprising a major component of connective tissues. Injectable collagen consists of varying concentrations of highly purifed bovine or human collagen. Sensitivity reactions and granulomatous responses have occurred in 1%–3% and 0.5% of patients, respectively (Cooperman et al 1985). Minor side effects such as bruising, redness, and swelling are seen after injection, but tend to resolve after a few days. Reimplantation is usually required in 3–6 months.
Bovine collagen
Bovine collagen is available in several formulations for fine lines as well as for deeper lines and folds. Patients must be allergy tested because of the possibility of rare allergic reactions. Two tests must be performed 3 weeks apart and treatment cannot be started until 3–4 weeks after the second allergy test.
Human-based collagen
No allergy testing is required.
Hyaluronic acid
Hyaluronic acid is a component of all connective tissues and is abundant in the human dermis. It is a naturally occurring glycosaminoglycan biopolymer, which provides a fluid matrix or lattice on which collagen and elastic fibers may develop. Its hydrophilic nature attracts and retains water (Pollack 1999). The incidence of allergic reactions is so low that no allergy testing is required. Corrections with hyaluronic acid generally last longer than with collagen.
There are also several formulations for fine to deep lines. There are products that are manufactured through bacterial fermentation and there are others that are extracted from rooster combs. Patients using the latter must not have an allergy to avian products.
Unusual hypersensitivity and granulomatous foreign body reactions have been reported, but hyaluronic acids are generally safe and practical and need no allergy testing (Murray et al 2005).
Autologous fat
Neuber introduced the use of autologous fat for tissue augmentation in 1893 (Neuber 1893). Over the years, the popularity of Neuber’s method has grown, but there is still no evidence-based gold standard method around. The longest lasting results are seen when used for atrophic skin conditions. Adverse events, such as fat necrosis, are temporary but not uncommon.
Allogenic products
Allogenic material is either obtained from cadaveric dermis or fascia, or engineered by methods using human cell lines and has a high biocompatibility with low antigenicity. These products are similar to the bovine collagens in indication and technique, but do not require allergy tests and have a shorter longevity.
Synthetic products
The production of synthetic products is cheaper and they are semipermanent or permanent implants. One of the first synthetic fillers was silicone. Today there are several substances available such as polylactic acid, polyalkylamide, polyacrylamide, and polytetrafluoroethylene. Adverse reactions with these agents can be serious.
Laser is the acronym for “light amplification by the stimulated emission of radiation”. Schawlow and Townes developed the first laser in 1958 (DiBernardo and Cacciarelli 2005). Lasers use light at various frequencies to attain a specific clinical result. They can be categorized by the medium in which the light energy is produced. Mechanisms of action include selective thermolysis and specific cell stimulation while leaving normal tissue unaffected. The immune system clears the unwanted material. Lasers can be used to cut, destroy, cauterize, and vaporize tissue. Dermatological indications are skin rejuvenation, tattoo removal, hair removal, and improvement in various skin abnormalities. For example, an ablative laser such as CO2 or erbium would be considered for skin rejuvenation. Complications could be pigment changes, superficial skin changes, scarring, infection, bleeding, and accidential eye injury.
Surgical procedures
There are many methods of cosmetic surgery such as facelifts not covered by this article. Space limitations preclude an extensive discussion of this field.
Endocrinological therapies for skin aging
Skin is a target organ for various hormones (Zouboulis 2000). Sex steroids have a profound influence on both skin development and composition; adequate levels are required to facilitate its structural integrity and functional capacity (Raine-Fenning et al 2003). Hormonal action requires the binding of the hormone to specific receptors (Zouboulis 2000). Estrogen and other hormone receptors have been detected, inter alia, in keratinocytes, fibroblasts, sebaceous glands, hair follicles, endocrine glands, and blood vessels (Schmidt et al 1990). The receptors vary in density according to site, with higher concentrations of estrogen receptors in facial skin than in the skin at the pelvis or breast. Decreased sex hormones thus induce a reduction of those skin functions that are under hormonal control.
In clinical terms, many females experience a sudden onset of skin aging symptoms several months after menopause. One of the first signs which women experience is increasing skin dryness followed by a loss of skin firmness and elasticity. The increasing looseness of the skin at that stage outweighs other symptoms such as wrinkles. These symptoms correspond to changes in collagenous and elastic fibers that have been reported to be due to estrogen deficiency (Schmidt et al 1994). A significant decrease in skin collagen starting at menopause has previously been demonstrated (Castelo-Branco et al 1992). This negative effect of the menopausal years on the skin was first described by Albright in 1940, who noted that older women with osteoporotic fractures had a higher incidence of altered skin (Albright et al 1940). Among the various types of collagen, types I and III are of major relevance. Type I collagen represents the predominant collagen type in adult human skin whereas type III collagen, also widely distributed throughout the body, predominates in fetal tissues. Both total collagen content and the ratio of type III to type I collagen decline with age (Sawas et al 1993). Skin collagen contents in adults decreases by 1% every year (Shuster et al 1985). This process is more evident in women than in men. Approximately 30% of skin collagen is lost in the first five years after menopause, with an average decline of 2.1% per postmenopausal year over a period of 20 years. Estrogens reverse this trend and increase skin collagen (Zouboulis 2000). Estrogens also enhance the synthesis of hyaluronic acid and promote water retention (Epstein and Munderloh 1975). Animal studies indicate that estrogens induce several changes in the connective tissue of the dermis, including increased mucopolysaccharide incorporation, hydroxy-proline turnover, and alterations in the extracellular matrix (Holland et al 1994).
Epidermal cells – keratinocytes, Langerhans’ cells, and melanocytes – are also target cells of steroid hormones (Zouboulis 2000). The estrogen receptor complex is able to support the expression of growth factors such as insulin-like growth factor type one (IGF-I), a mitosis-enhancing protein for keratinocytes (Tavakkol et al 1999). The Langerhans’ cells are influenced by progesterone, with their number increasing during the luteal phase. Melanocytes are stimulated by 17β-estradiol (Gruber et al 2002).
Sex steroids are involved in many extragenital organ systems such as the urogenital tract, skin and hair, breast, and cardiovascular, nervous, or skeletal systems. Considering that most women spend one-third of their lives with estrogen deficiency, the potential field of action for hormone replacement therapy (HRT) is becoming increasingly larger.
Topical treatment
A placebo-controlled study examined the effect of a topically applied conjugated estrogen skin care cream (Premarin® 0.625 mg/g ointment) in 54 women (Creidi et al 1994). Evaluation criteria were profilometry and measurements of skin thickness by ultrasound. After a 24-week treatment period there was a significant increase in skin thickness in the Premarin® group as compared to the placebo group. Even in regard to small wrinkles, a significant reduction was observed in comparison to the placebo group after 12 and 24 weeks. No side effects were found.
A study was published on the action of topical 0.3% estriol and 0.01% 17β-estradiol in 59 patients (Schmidt et al 1996). The criteria evaluated by the authors were profilometry, corneometry, and clinical signs. Wrinkle depth was significantly reduced and skin hydration was improved. Apart from a rise in prolactin, no other systemic hormonal effects were detected. Histological tests of collagen parameters in 10 patients showed a significant increase in the collagen III fraction at the end of therapy after 24 weeks.
In a recent study, the effects of a 0.01% 17β-estradiol cream were compared with those of a 15% glycolic acid cream and a combination of both (Fuchs et al 2003). The effects examined in 65 patients after 6 months indicated an increase in epidermal thickness and were most marked in the combination group (38%), followed by the glycolic acid group (27%), and the 17β-estradiol group (23%).
Systemic hormone replacement therapy
A HRT consists of two components: estrogens and progestagens. Estrogens administered as monotherapy may result in undesired hyperplasia of the endometrium. To avoid this event, synthetic derivatives of progesterone and testosterone, known as progestagens, are combined with an estrogen compound and may be applied in a cyclical or continuous mode. An estrogen monotherapy is feasible in hysterectomized women, with a choice of oral, transdermal, and vaginal forms of application available.
Beneficial effects of HRT on the skin have been documented by several studies in respect of skin thickness as a mirror image of collagen content (Brincat et al 1987; Maheux et al 1994; Dunn et al 1997; Sator, Sator, et al 2001). A large retrospective multi-center study, NHANES I, conducted in 3825 women in the USA, showed that women under long-term substitution had one-third fewer wrinkles than non-substituted patients (Dunn et al 1997). Postmenopausal women with an HRT had significantly higher collagen content than untreated women (Brincat et al 1987).
One study examined the effects of three types of HRT in terms of skin aging in menopausal women (Sator, Schmidt, et al 2001): one group was given estrogen only via the transdermal route (Estraderm TTS® 50), the second group received estrogen by transdermal application in combination with vaginally applied progesterone (Estraderm TTS® 50 and 0.4 g progesterone vaginal suppository), and the third group was administered oral estrogen and vaginal progesterone (2 mg Progynova® and 0.4 g progesterone vaginal suppository). One group without treatment served as a control. Treatment was continued for 6 months. Skin surface lipids, epidermal skin hydration, skin elasticity, and skin thickness were measured at monthly intervals. Mean levels of epidermal skin hydration, elasticity, and skin thickness were improved at the end of treatment based on both subjective and objective evaluation in patients with HRT. Skin surface lipids were increased during combined HRT, which may reflect stimulatory effects of the progestagen component on sebaceous gland activity, while estrogen alone has a sebum-suppressive action (Zouboulis 2001). A comparison of skin hydration and elasticity in UV-exposed and non-exposed areas revealed no significant difference. This finding suggests that both photoaged and UV-protected skin benefit equally from HRT. These results were confirmed by animal tests using the skin of rats (Tsukahara et al 2001).
Although the majority of publications consider the influence of HRT on skin aging to be positive, there are some authors who doubt or reject any effect of hormone replacement on skin thickness, collagen synthesis, or elastin (Oikarinen 2000).
Alternatives: phytohormones
The estrogen-like effects of some plants were first described in 1926 (Loewe et al 1927). Phytoestrogens are classified in three categories: isoflavones, coumestans, and lignans. The most thoroughly examined group of substances are isoflavones, which display some similarity to the mammal estrogen molecule and are found, inter alia, in soy, beans, lentils, and red clover. Flavonoids are also contained in wine, especially red wine. The most important isoflavones are genistein and daidecin. The group also includes the precursors formonontein (for daidecin) and biochanin (for genistein). Coumestans only occur in the sprouts of legumes. Lignans have no influence on estrogen receptors. The structural similarity to 17β-estradiol explains the estrogen-like effects, which may be traced back to the interaction of these substances with the estrogen receptor (Wang et al 1996). Nutrition in Asian countries, with its large phytoestrogen content, is thought to be the reason why Asian women rarely suffer from climacteric symptoms. The biological potency of isoflavonoids is significantly inferior to that of synthetic estrogens (Markieicz et al 1993). When phytoestrogens are topically applied, they behave like estrogens by causing a proliferation of the epidermis, supporting collagen synthesis and reducing enzymatic collagen degradation.
A controlled open European multicenter study examined the effect of a cosmetic cream preparation including isoflavone (Novadiol®) on 234 women: maximum age 65 years, at least 3 years since menopause, no HRT or other substances affecting the skin aging process (Bayerl and Keil 2002). The length of therapy was 12 weeks. The isoflavone cream was applied two times daily (in the morning with a concentration of 0.0075% isoflavone and in the evening with a concentration of 0.015% isoflavone) on the face, neck, and one upper arm. The other arm was untreated and served as a control. Skin dryness and roughness were significantly improved at the treated areas by 32.9% and 22%, respectively, in comparison with the untreated skin areas. Facial wrinkles were significantly reduced by 22% and skin looseness was significantly reduced by 24%.
Summary of hormonal therapies
Numerous publications on the effects of sex hormones on the aging process are available today. Without claiming that HRT can or should ever be regarded as an independent treatment of skin aging, these findings are still interesting to note, considering that they indicate a beneficial effect of HRT on the skin despite the fact that the results of the “WHI-Study” (Rossouw et al 2002) and the “Million Women Study” (Beral 2003) have shown negative effects of HRT on other organs. What is clear is that HRT must be rejected when it is solely considered for the prevention of skin aging. As an additional benefit in the treatment of menopausal conditions provided by a dermatologist with sufficient experience in the discipline of endocrinology, however, it is a very effective instrument to control intrinsic skin aging.
While the topical application of hormones is certainly a suitable alternative to a systemic HRT, it must be ensured that such a treatment is also administered by a dermatologist experienced in endocrinology given that concentrations and application areas need to be observed in order to avoid systemic side effects.
Phytoestrogens, topical and systemic, appear to be an effective method in the treatment of intrinsic skin aging. However, further data are still required, especially from controlled studies on long-term results of systemic application.
An increasing number of products and procedures exists to promote youthful skin. First, a change of the lifestyle (eg, sun behavior, nicotine abuse, nutrition) of the patient must take place. Only then can other methods be used. A thorough knowledge of the properties (benefits, limitations, and complications) of the ever-expanding array of possibilities for rejuvenation of the skin is essential for any physician treating patients with cosmetic complaints.

In vivo and in vitro stimulatory effects of Cordyceps sinensis on testosterone production in mouse Leydig cells


Department of Cell Biology and Anatomy, College of Medicine, National Cheng Kung University, 1 University Road, 701 Tainan, Taiwan.


The in vivo and in vitro effects of Cordyceps sinensis (CS) and its extracted fractions on the secretion of testosterone in mice were studied. CS, F2 (water soluble protein), and F3 (poorly water soluble polysaccharide and protein) significantly stimulated in vitro testosterone production in purified mouse Leydig cells. However, F1 (water soluble polysaccharide) had no effect (p>0.05). F2 and F3 stimulated in vitro testosterone production in dose- and time-dependent relationships with maximal responses at 3 mg/ml for 3 h (p<0.05). An in vivo study illustrated that testosterone levels in plasma were significantly increased by CS, F2, and F3, respectively (p<0.05). Because CS, F2, and F3 stimulated both in vitro and in vivo testosterone secretions in mice, it is possible that CS might contribute to an alternative medicine for the treatment of some reproductive problems caused by insufficient testosterone levels in human males.

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[PubMed – indexed for MEDLINE]

BUY hCG 5000 units from us $45

A controversial usage of hCG is as an adjunct to the British endocrinologist Dr. A.T.W. Simeons’ ultra-low-calorie weight-loss diet. Simeons, while studying pregnant women in India on a calorie-deficient diet, and fat boys with pituitary problems treated with low-dose hCG, discovered that both lost fat rather than lean (muscle) tissue. He reasoned that hCG must be programming the hypothalamus to do this in the former cases in order to protect the developing fitus, and proceeded to use low-dose daily hCG injections (125 mg) in combination with a customized ultra-low-calorie (500 cal/day, high-protein, low-carbohydrate/fat) diet to help obese adults lose dramatic amounts of adipose tissue without loss of lean, at a Salvator Mundi International Hospital in Rome, Italy, clinic mainly for celebrities. After Simeons death, the diet started to spread to specialized centers and via popularization by such as the controversial popular author Kevin Trudeau (search for hCG in that article for more details).

The controversy proceeds from warnings by the Journal of the American Medical Association[ and the American Journal of Clinical Nutrition that hCG is not safe, indeed ineffective, as a weight-loss aid on its own; yet its usage as cited above to increase testosterone production contradicts this assertion, since much late-life male obesity is associated with estrogen dominance and deficient testosterone in the mis-named, so-called andropause. Furthermore, in the Simeons protocol, it is, as in any diet, the ultra-low-calorie component (caloric deficit) that results in weight loss, if the protocol is followed strictly. hCGs role is supposedly to trigger the hypothalamic lean-protection mechanisms Simeons thought he saw, thus promoting mobilization and consumption of abnormal, excessive adipose deposits, while protecting normal adipose and lean tissue from being consumed, with the assumption that these protective hypothalamic mechanisms exist in males as well as females, to be acted upon by hCG.

hCG for bodybuilding

hCG is provided as a glycoprotein powder to be diluted with water, and acts in the body like luteinizing hormone (LH), stimulating the testes to produce testosterone even when natural LH is not present or is deficient. It therefore is useful for maintaining testosterone production and/or testicle size during a steroid cycle. Use of this drug in the taper is rather counterproductive, since the resulting increased testosterone production is itself inhibitory to the hypothalamus and pituitary, delaying recovery. Thus, if this drug is used, it is preferably used during the cycle itself. A daily amount of 500 IU is generally sufficient, and in my opinion usage should not exceed 1000 IU per day.

Daily administration is superior to less frequent administration.

Doses over 1000 IU are noted for their tendency to cause or aggravate gynecomastia, and also act to desensitize the testicles to LH.

hCG may be injected intramuscularly, subcutaneously, or in a shallow injection about 1/4″ deep with the needle going straight in. A 29 gauge insulin needle is recommended. Injection speed should be slow.

Some hCG products are diluted 5000 or even 10,000 IU per mL, while others are diluted 1000 IU per mL. So far as I know there is no need to make the preparation so dilute. Once mixed, the preparation should be refrigerated and used within a few weeks. The substance is also somewhat temperature sensitive before mixing and should not be exposed to excessive heat.

hCG does not correct the problem of  progressively-decreasing ejaculatory volume that is typical during a steroid cycle. So far as I know the only cure is to go off-cycle and use Clomid, but it is possible that human menopausal gonadotropin (hMG), a related drug which works analogously to follicle stimulating hormone (FSH) might be useful during a cycle to treat this problem. HMG supports spermatogenesis and is commonly used in conjunction with hCG to treat male fertility problems. (Consider use of HMG to maintain ejaculatory volume to be a strictly past-the-cutting-edge hypothesis: I have not yet had the opportunity to test the matter.)

The athlete who would otherwise fail a urinary ratio test because of low epitestosterone may find hCG useful in increasing epitestosterone and therefore improving this ratio. A 500 IU dose is sufficient, but on the other hand, hCG itself is also banned by the IOC and is readily detected in urine.

hCG can also useful for returning testosterone to normal levels should levels be low post-cycle, or, with care, to increase levels from normal to high normal. Titration of the dose, by measuring T levels and then adjusting the hCG dose accordingly, is recommended for long term use.


Turns out that stanozolol, the good old “Winny”, has unique collagen synthesis stimulating properties, that no other steroid has..

Stimulation of collagen synthesis by the anabolic steroid stanozolol

Researchers: Falanga V, Greenberg AS, Zhou L, Ochoa SM, Roberts AB, Falabella A, Yamaguchi Y; University of Miami School of Medicine, Department of Dermatology, Miami, Veterans Affairs Medical Center, Florida, USA.

Source: J Invest Dermatol 1998 Dec;111(6):1193-7

Summary: In this report, we measured the effect of the anabolic steroid stanozolol on cell replication and collagen synthesis in cultures of adult human dermal fibroblasts. Stanozolol (0.625-5 micrograms per ml) had no effect on fibroblast replication and cell viability but enhanced collagen synthesis in a dose-dependent manner. Stanozolol also increased (by 2-fold) the mRNA levels of alpha1 (I) and alpha1 (III) procollagen and, to a similar extent, upregulated transforming growth factor-beta1 (TGF-beta1) mRNA and peptide levels. There was no stimulation of collagen synthesis by testosterone. The stimulatory effects of stanozolol on collagen synthesis were blocked by a TGF-beta1 anti-sense oligonucleotide, by antibodies to TGF-beta, and in dermal fibroblast cultures derived from TGF-beta-1 knockout mice. We conclude that collagen synthesis is increased by the anabolic steroid stanozolol and that, for the most part, this effect is due to TGF-beta-1. These findings point to a novel mechanism of action of anabolic steroids.

Discussion: I must first acknowledge that the commonly held belief is that anabolic steroids predispose an athlete to tendon rupture. This conclusion is drawn from animal studies showing that some steroids produce a larger, stiffer tendon in rats and that these steroid-induced tendons “fail” before the tendons from the control animals. The term fail refers to the breaking point.

The interesting thing about the present study is that the steroid stanozolol (Winstrol) had a different effect than testosterone. If you are a regular reader of MESO-Rx you should be well aware that not all steroids act in the same manner. And that because of subtle differences in there molecular structure they are able to elicit different responses. For example, Deca seems to act primarily through the androgen receptor (AR) where as Dianabol has effects beyond those associated with the AR.

Because synthetic steroids have differ in their chemical properties it should not be surprising that testosterone did not have the same effect as Winstrol. Winstrol increased collagen synthesis as opposed to testosterone which did not in this study. Interpreting the results of this study are more difficult than simply describing them. Other researchers have suggested that steroids cause a rapid increase in protein synthesis within tendon fibroblasts which results in fibroids or fibrous nodules within the tendon (Michna,1988). These fibroids alter the mechanical properties of the tendon perhaps predisposing it to rupture. It is also noted that during short term use of steroids there is an alteration in the alignment of collagen fibers which may also lead to rupture. Interestingly these alterations in collagen metabolism are transient with markers of collagen turnover returning more or less to baseline after 3-4 weeks of steroid administration (Karpakka,1992). These same researchers noted that low dose anabolics effect primarily muscle collagenous tissue with tendon being effected only at higher doses (i.e. 5 times the therapeutic dose) which would more closely represent what is needed by bodybuilders to put on mass.

The question remains, dose this mean that Winstrol will actually help prevent tendon injury or will it lead to bigger yet stiffer tendons prone to injury? It is difficult to take animal research and extrapolate the results to humans. Stanozolol is used therapeutically in humans to treat a variety of connective tissue and vascular disorders and its clinical effects suggest that it can modulate connective tissue breakdown in people. Despite being labeled as “ineffective” by many bodybuilders it is very popular among athletes. As with most hormones, dosage plays a role in what effects are seen, be they positive or negative. Hopefully future studies will shed light on the therapeutic effects of different steroids on tendons in humans.


Michna H Appearance and ultrastructure of intranuclear crystalloids in tendon fibroblasts induced by an anabolic steroid hormone in the mouse. Acta Anat (Basel) 1988;133(3):247-50

Karpakka JA, Pesola MK, Takala TE. The effects of anabolic steroids on collagen synthesis in rat skeletal muscle and tendon. A preliminary report. Am J Sports Med 1992 May-Jun;20(3):262-6


30x 1 mg Finpecia finasteride DHT blocker $28

If you are using a DHT blocker such as finasteride, dutasteride or natural substances like green tea or saw palmetto, fortunately it doesn’t mean that you are blocking the anabolic properties of testosterone.

Inhibition of 5{alpha}-reductase blocks prostate effects of testosterone without blocking anabolic effects

Stephen E. Borst,1,2 Jun Hak Lee,1 and Christine F. Conover2

1Department of Applied Physiology & Kinesiology, University of Florida, Gainesville; and 2Geriatric Research, Education and Clinical Center, Malcom Randall Veterans Affairs Medical Center, Gainesville, Florida

Submitted 12 July 2004 ; accepted in final form 26 August 2004

We studied the effect of the 5{alpha}-reductase inhibitor MK-434 on responses to testosterone (T) in orchiectomized (ORX) male Brown Norway (BN) rats aged 13 mo. At 4 wk after ORX or sham surgery, a second surgery was performed to implant pellets delivering 1 mg T/day or placebo pellets. During the second 4 wk of the study, rats received injections of MK-434 (0.75 mg/day) or vehicle injections. Treatment with T elevated serum T to 75% above that for sham animals (P = 0.002) and did not affect serum dihydrotestosterone (DHT) or serum estradiol. T treatment also caused an elevation of prostate T and a marked elevation of prostate DHT. During the second half of the study, ORX rats lost an average of 18.86 ± 4.62 g body wt. T completely prevented weight loss, and the effect was not inhibited by MK-434 (P produced a nonsignificant trend toward a small (5%) decrease in the mass of the gastrocnemius muscle (P = 0.0819). This trend was also reversed by T, and the effect of T was not blocked by MK-434. T caused a significant 16% decrease in subcutaneous fat that was not blocked by MK-434 (P caused a 65% decrease in urine excretion of deoxypyridinoline, a marker of bone resorption, and again the effect was not blocked by MK-434 (P fivefold increase in prostate mass, and the effect was almost completely blocked by MK-434 (P that 5{alpha}-reductase inhibitors may block the undesirable effects of T on the prostate, without blocking the desirable anabolic effects of T on muscle, bone, and fat.