Robert See-Hoong Tan (born 1959) is a physician, author and medical director. He currently lives in Houston, Texas. He has written & lectured extensively on aging and men’s health issues including andropause. He is a pioneer in testosterone replacement therapy and effects on the brain.

Dr. Tan completed his early education at Anglo Chinese School and National University of Singapore. In the late 1980s he went to London, U.K. to complete his studies in Geriatric Medicine at the Royal Postgraduate Medical School/Hammersmith Hospital. His further medical training was completed at Case Western Reserve University in Cleveland, Ohio. He is noted to be one of the rare physicians in the world to hold multiple board certifications in different countries (Australia, UK, USA), and also an MBA. He is still in active clinical practice with more than 25 years experience and also founded the OPAL Medical Clinic, a unique center dedicated to wellness and men’s health. He is Clinical Professor with University of Texas Houston & Associate Professor with Baylor College of Medicine and a board member of Men’s Health Network. He has been elected to the Best Doctors in America for several consecutive years.

Adapted from the Wikipedia article Robert Tan, under the G. N. U. Free Documentation License. Please also see http://en.wikipedia.org/wiki

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In humans Irritable Male Syndrome is referred to as the andropause, defined as symptomatic of hormonal, physiological, and chemical changes that can occur in all men. These changes are considered to affect physical, psychological, interpersonal, sexual, and nutritional aspects of men’s health. Stress tends to be a common trigger, especially when combined with rapid hormone changes later in life.

Symptoms

Symptoms, in humans, caused by a drop in the male hormone testosterone include:

* anger and social withdrawal

* irritability

* hypersensitivity

* anxiety

* mood swings

* depression

* stomach cramps

* hot flashes

* lack of libido

* back and head aches

External causes

External factors that can cause testosterone levels to fall include certain forms of medication, poor diet, excessive alcohol consumption, illness, lack of sleep, stress or surgery.

Adapted from the Wikipedia article Irritable male syndrome, under the G. N. U. Free Documentation License. Please also see http://en.wikipedia.org/wiki

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Routes of administration

There are many routes of administration for testosterone. Forms of testosterone for human administration currently available include injectable (such as testosterone cypionate or testosterone enanthate in oil), oral, buccal, transdermal skin patches, and transdermal creams or gels.

In the pipeline are “roll on” methods and nasal sprays.

Indications

The original and primary use of testosterone is for the treatment of males who have too little or no natural endogenous testosterone production—males with hypogonadism. Appropriate use for this purpose is legitimate hormone replacement therapy (testosterone replacement therapy [TRT]), which maintains serum testosterone levels in the normal range.

However, over the years, as with every hormone, testosterone or other anabolic steroids has also been given for many other conditions and purposes besides replacement, with variable success but higher rates of side effects or problems. Examples include infertility, lack of libido or erectile dysfunction, osteoporosis, penile enlargement, height growth, bone marrow stimulation and reversal of anemia, and even appetite stimulation. By the late 1940s testosterone was being touted as an anti-aging wonder drug (e.g., see Paul de Kruif’s ”The Male Hormone”). Decline of testosterone production with age has led to interest in androgen replacement therapy.

To take advantage of its virilizing effects, testosterone is often administered to transsexual men as part of the hormone replacement therapy, with a &

Testosterone patches are effective at treating low libido in post-menopausal women. Low libido may also occur as a symptom or outcome of hormonal contraceptive use. Women may also use testosterone therapies to treat or prevent loss of bone density, muscle mass and to treat certain kinds of depression and low energy state. Women on testosterone therapies may experience an increase in ”weight” without an increase in body fat due to changes in bone and muscle density. Most undesired effects of testosterone therapy in women may be controlled by hair-reduction strategies, acne prevention, etc. There is a theoretical risk that testosterone therapy may increase the risk of breast or gynaecological cancers, and further research is needed to define any such risks more clearly.

Hormone replacement therapy

Testosterone levels decline gradually with age in human beings. The clinical significance of this decrease is debated (see andropause). There is disagreement about when to treat aging men with testosterone replacement therapy. The American Society of Andrology’s position is that:

The American Association of Clinical Endocrinologists says:

There is not total agreement on the threshold of testosterone value below which a man would be considered hypogonadal. (Currently there are no standards as to when to treat women.) Testosterone can be measured as “free” (that is, bioavailable and unbound) or more commonly, “total” (including the percentage which is chemically bound and unavailable). In the United States, male total testosterone levels below 300& ng/dL from a morning serum sample are generally considered low. However these numbers are typically not age-adjusted, but based on an average of a test group which includes elderly males with low testosterone levels. Therefore a value of 300& ng/dL might be normal for a 65-year-old male, but not normal for a 30-year-old. Identification of inadequate testosterone in an aging male by symptoms alone can be difficult. The signs and symptoms are non-specific, and might be confused with normal aging characteristics, such as loss of muscle mass and bone density, decreased physical endurance, decreased memory ability, and loss of libido.

Replacement therapy can take the form of injectable depots, transdermal patches and gels, subcutaneous pellets, and oral therapy. Adverse effects of testosterone supplementation include minor side effects such as acne and oily skin, and more significant complications such as increased hematocrit which can require venipuncture in order to treat, exacerbation of sleep apnea and acceleration of pre-existing prostate cancer growth in individuals who have undergone androgen deprivation. Exogenous testosterone also causes suppression of spermatogenesis and can lead to infertility. It is recommended that physicians screen for prostate cancer with a digital rectal exam and PSA (prostate specific antigen) level before starting therapy, and monitor hematocrit and PSA levels closely during therapy.

Benefits

Appropriate testosterone therapy can prevent or reduce the likelihood of osteoporosis, type 2 diabetes, cardio-vascular disease (CVD), obesity, depression and anxiety and the statistical risk of early mortality. Low testosterone also brings with it an increased risk for the development of Alzheimer’s Disease.

A small trial in 2005 showed mixed results.

Large scale trials to assess the efficiency and long-term safety of testosterone are still lacking.

Adverse effects

Exogenous testosterone supplementation comes with a number of health risks. Fluoxymesterone and methyltestosterone are synthetic derivatives of testosterone. In 2006 it was reported that women taking Estratest, a combination pill including estrogen and methyltestosterone, were at considerably heightened risk of breast cancer. That said, methyltestosterone and Fluoxymesterone are no longer prescribed by physicians given their poor safety record, and testosterone replacement in men does have a very good safety record as evidenced by over sixty years of medical use in hypogonadal men.

One adverse effect that many men complain of is that of the development of gynecomastia (breasts), but this is something that can be prevented by appropriate choice and dosing of medication, and, in required cases, the use of ancillary medications that help lower SHBG or estradiol. Another side-effect is having difficulty urinating.

Athletic use

Testosterone may be administered to an athlete in order to improve performance, and is considered to be a form of doping in most sports. There are several application methods for testosterone, including intramuscular injections, transdermal gels and patches, and implantable pellets.

Anabolic steroids (including testosterone) have also been taken to enhance muscle development, strength, or endurance. They do so directly by increasing the muscles’ protein synthesis. As a result, muscle fibers become larger and repair faster than the average person’s.

After a series of scandals and publicity in the 1980s (such as Ben Johnson’s improved performance at the 1988 Summer Olympics), prohibitions of anabolic steroid use were renewed or strengthened by many sports organizations. Testosterone and other anabolic steroids were designated a “controlled substance” by the United States Congress in 1990, with the ”Anabolic Steroid Control Act”. The levels of testosterone abused in sport greatly exceed the quantities of the steroid that are prescribed for medical use in hypogonadism. It is the supraphysiological doses and ultra high levels of testosterone that bring with it many undesirable effects and potential long term adverse health effects. Coupled with the nature of cheating in sport, this is seen as being a seriously problematic issue in modern sport, particularly given the lengths to which athletes and professional laboratories go to in trying to conceal such abuse from sports regulators. Steroid abuse once again came into the spotlight recently as a result of the Chris Benoit double murder-suicide in 2007, and the media frenzy surrounding it – however, there has been no evidence indicating steroid use as a contributing factor.

Detection of abuse

A number of methods for detecting testosterone use by athletes have been employed, most based on a urine test. These include the testosterone/epitestosterone ratio (normally less than 6), the testosterone/luteinizing hormone ratio and the carbon-13 / carbon-12 ratio (pharmaceutical testosterone contains less carbon-13 than endogenous testosterone). In some testing programs, an individual’s own historical results may serve as a reference interval for interpretation of a suspicious finding.

Adapted from the Wikipedia article Testosterone, under the G. N. U. Free Documentation License. Please also see http://en.wikipedia.org/wiki

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In clinical testing

* Ostarine – affects both muscle and bone, intended mainly for osteoporosis but also general treatment for andropause

* BMS-564,929 – mainly affects muscle growth, intended as general treatment for symptoms of andropause

Pre-clinical

* AC-262,356

* JNJ-28330835.

* LGD-2226 – affects both muscle and bone

* LGD-3303

* S-40503 – selective for bone tissue, particularly low virilization, intended for osteoporosis and may be suitable for use in women

* S-23 – under development as a male hormonal contraceptive

Examples no longer being developed

* Andarine (“S-4″) – partial agonist, intended mainly for treatment of benign prostatic hypertrophy

Adapted from the Wikipedia article Selective androgen receptor modulator, under the G. N. U. Free Documentation License. Please also see http://en.wikipedia.org/wiki

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Although there is disagreement over whether or not andropause is a condition to be “diagnosed” and “treated”, those who support that position have made several proposals to address andropause and mitigate some of its effects.

* Morley emphasizes the importance of response to treatment, as well as testosterone level and identifiable symptoms.

* Mintz, Dotson, & Mukai include an emphasis on hormones other than testosterone. They also focus upon diet, and exercise.

* Diamond (a lay person) believes that depression is one of the most common problems of middle-aged men, and feels it is greatly under-diagnosed, sometimes with serious consequences.

The following treatments have been found to be effective. These include:

*Hormone replacement therapy

*Exercise, dietary changes, stress reduction

Selective androgen receptor modulators have also been proposed.

Adapted from the Wikipedia article Andropause, under the G. N. U. Free Documentation License. Please also see http://en.wikipedia.org/wiki

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House makes a shocking revelation in a bid to save himself from jail time; a firefighter chooses to have a risky, radical treatment on his brain in order to avoid dealing with his affection for a colleague.

Derek, a firefighter, has just escaped a burning building when he begins to have trouble breathing and becomes delirious. He then staggers over to the burning building before being stopped by fellow firefighter, Amy. Derek complains that he is freezing even though he is within yards of the burning building.

The first diagnosis is MRSA to which Derek asks if that is what makes him see blue. Dr. Cameron realizes that this is something entirely different and House suggests male menopause (high estrogen, low testosterone levels). House orders a hormone panel. The team tests for this latest theory but Derek becomes disturbed and begins to strangle Cameron. Meanwhile, House visits Tritter and although House apologizes, Tritter ignores him and says he only cares about House’s actions.

Back at the hospital, Foreman insists it must be neurological and asks to CT the brain and give a lumbar puncture to test for meningitis. House agrees and leaves and reveals that he is checking himself into rehab. Derek begins to have trouble breathing and it is discovered that he is having another heart attack. The team goes to House for advice who tells them to look at what was in common during this attack and the previous two he had: Amy was present. To test this, the team brings Amy in with Derek. Both confused, Derek suddenly goes into another heart attack. Derek reveals that his brothe

The procedure is performed successfully. When Amy and Derek’s brother walk in, he has no idea who they are. Outside the room, Cameron apologizes to Amy for the burden of caring for Derek landing so soon before her wedding. However, Amy has no idea what she is talking about as she’s not even dating Derek’s brother. Meanwhile, House and Wilson meet in rehab. House apologizes to Wilson for everything.

The team calls House who is at trial and says that the engagement was a fabricated memory and wasn’t true. House rushes out of court (risking being held in contempt by the judge) back to the hospital. The team diagnoses Derek with a spinal meningioma that restricted blood to his brain, creating the false memories.

In the courtroom, Cuddy is at the stand and is confronted with the log book that shows House’s signature taking oxycodone in the name of a dead patient. Cuddy then testifies that she replaced the pills with a placebo and had the inventory logs to prove it. The case is dismissed and the judge orders Tritter to stop his investigation on House. However, House is ordered to spend the night in jail for contempt. Cuddy and Wilson both visit him that night and Cuddy is infuriated with House because she was forced to fabricate evidence and commit perjury so that his case would be dismissed. She tells House that she now “owns him” and House agrees. Wilson gives House the pills from the rehab department. Wilson realizes it is Vicodin when House greedily takes them. House has bribed the rehab supervisor (referred to as Voldemort) to give him Vicodin. Wilson says that nothing has changed. When Wilson realizes and remarks that House did not need to apologize to him to maintain his deception, House merely answers ambiguously, “Believe what you want.” In the background plays “Season of the Witch” by Donovan.

Adapted from the Wikipedia article Words and Deeds, under the G. N. U. Free Documentation License. Please also see http://en.wikipedia.org/wiki

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The impact of low levels of testosterone has been previously reported. In 1944, Heller and Myers identified symptoms of what they labeled the “male climacteric” including loss of libido and potency, nervousness, depression, impaired memory, the inability to concentrate, fatigue, insomnia, hot flushes, and sweating. Heller and Myers found that their subjects had lower than normal levels of testosterone, and that symptoms improved dramatically when patients were given replacement doses of testosterone.

Andropause has been observed in association with Alzheimer’s disease.

In one study, 98.0% of primary care physicians believed that andropause and osteoporosis risk were related.

The term “symptomatic late onset hypogonadism” (or “SLOH”) is sometimes considered to refer to the same condition as the word “andropause”.

Some researchers prefer the term “androgen deficiency of the aging male” (“ADAM”), to more accurately reflect the fact that the loss of testosterone production is gradual and asymptotic (in contrast to the more abrupt change associated with menopause .) The “D” is sometimes given as “decline” instead of “deficiency”. In some contexts, the term “partial androgen deficiency in aging males” (“PADAM”) is used instead.

Adapted from the Wikipedia article Andropause, under the G. N. U. Free Documentation License. Please also see http://en.wikipedia.org/wiki

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Proponents

Proponents of andropause as a distinct condition claim that it is a biological change experienced by men during mid-life, and often compare it to female menopause. Menopause, however, is a complete cessation of reproductive ability caused by the shutting down of the female reproductive system. Andropause is a decline in the male hormone testosterone. This drop in testosterone levels is considered to lead in some cases to loss of energy and concentration, depression, and mood swings. While andropause does not cause a man’s reproductive system to stop working altogether, many experience bouts of impotence.

Andropause is usually caused by a very gradual testosterone deficiency and an increase in sex hormone-binding globulin (SHBG) that occurs from age 35 onwards. By contrast, women have a sudden onset of menopause around age 51. Testosterone declines 10% every decade after age 30 (1% per year).

Premature andropause can occur in males who experience excessive female hormone stimulation through workplace exposure to estrogen. Men who work in the pharmaceutical industry, plastics factories, near incinerators, and on farms that use pesticides are high-risk for early andropause.

By their mid-50s, about 30 percent of men experience andropause. About 5 million American men do not produce adequate testosterone, which leads to early andropause. In Australia, about 1 in every 200 men under the age of 60 and about 1 in every 10 men over 60 have low testosterone. Regardless of location, the most likely males to develop early andropause are those with diabetes, h

Some of the current popular interest in the concept of andropause has been fueled by the book ”Male Menopause”, written by Jed Diamond, a lay person. According to Diamond’s view, andropause is a change of life in middle-aged men, which has hormonal, physical, psychological, interpersonal, social, sexual, and spiritual aspects. Diamond claims that this change occurs in all men, generally between the ages of 40 and 55, though it can occur as early as 35 or as late as 65. The term “male menopause” may be a misnomer, as unlike women, men’s reproductive systems do not cease to work completely in mid-life; some men continue to father children late into their lives (at age 90 or older). But Diamond claims that, in terms of other life impacts, women’s and men’s experience are somewhat similar phenomena.

The concept of andropause is perhaps more widely accepted in Australia and some parts of Europe than it is in the United States.

Opponents

Many clinicians believe that andropause is not a valid concept, because men can continue to reproduce into old age. Their reproductive systems do not stop working completely, and therefore they do not exhibit the sudden and dramatic drops in hormone levels characteristic of women undergoing menopause. In some men before the age of 60 there is a complete loss of libido, erectile function, and orgasmic ability.

Others feel that andropause is simply synonymous with hypogonadism or low testosterone levels. There is opposition to the concept of andropause in Europe as well as the U.S.

Some clinicians argue that many of the cited symptoms are not specific enough to warrant describing a new condition. For example, people who are overweight may be misguided into treating a new illness rather than addressing the lifestyle that led to their being overweight. Similarly, energy levels vary from person to person, and for people who are generally inactive, energy levels will automatically be lower overall.

While it is true that active and otherwise healthy men could in theory develop andropause-like symptoms, how common and widespread the phenomenon is, and whether genetics, lifestyle, environment, or a combination of factors are responsible, is not yet known.

Adapted from the Wikipedia article Andropause, under the G. N. U. Free Documentation License. Please also see http://en.wikipedia.org/wiki

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Risk factors for osteoporotic fracture can be split between non-modifiable and (potentially) modifiable. In addition, there are specific diseases and disorders in which osteoporosis is a recognized complication. Medication use is theoretically modifiable, although in many cases the use of medication that increases osteoporosis risk is unavoidable.

Nonmodifiable

The most important risk factors for osteoporosis are advanced age (in both men and women) and female sex; oestrogen deficiency following menopause is correlated with a rapid reduction in bone mineral density, while in men a decrease in testosterone levels has a comparable (but less pronounced) effect. While osteoporosis occurs in people from all ethnic groups, European or Asian ancestry predisposes for osteoporosis. Those with a family history of fracture or osteoporosis are at an increased risk; the heritability of the fracture as well as low bone mineral density are relatively high, ranging from 25 to 80 percent. There are at least 30 genes associated with the development of osteoporosis. Those who have already had a fracture are at least twice as likely to have another fracture compared to someone of the same age and sex.

Potentially modifiable

*Excess alcohol—small amounts of alcohol do not increase osteoporosis risk and may even be beneficial, but chronic heavy drinking (alcohol intake greater than 3 units/day), especially at a younger age, increases risk significantly.

*Vitamin D deficiency—low circulating Vitamin D is common among the elderly worldwide. Mild vitamin D insufficie

*Tobacco smoking—tobacco smoking inhibits the activity of osteoblasts, and is an independent risk factor for osteoporosis. Smoking also results in increased breakdown of exogenous estrogen, lower body weight and earlier menopause, all of which contribute to lower bone mineral density.

*Malnutrition—nutrition has an important and complex role in maintenance of good bone. Identified risk factors include low dietary calcium and/or phosphorus, magnesium, zinc, boron, iron, fluoride, copper, vitamins A, K, E and C (and D where skin exposure to sunlight provides an inadequate supply). Excess sodium is a risk factor. High blood acidity may be diet-related, and is a known antagonist of bone. Some have identified low protein intake as associated with lower peak bone mass during adolescence and lower bone mineral density in elderly populations. Conversely, some have identified low protein intake as a positive factor, protein is among the causes of dietary acidity. Imbalance of omega 6 to omega 3 polyunsaturated fats is yet another identified risk factor.[http://www.ajcn.org/cgi/content/full/81/4/934]

*High protein diet—Research has found an association between diets high in animal protein and increased urinary calcium loss from the bones.

* Underweight/inactive—bone remodeling occurs in response to physical stress, and weight bearing exercise can increase peak bone mass achieved in adolescence. In adults, physical activity helps maintain bone mass, and can increase it by 1 or 2%. Conversely, physical inactivity can lead to significant bone loss. (Incidence of osteoporosis is lower in overweight people.)

*Excess physical activity—excessive exercise can lead to constant damage to the bones which can cause exhaustion of the structures as described above. There are numerous examples of marathon runners who developed severe osteoporosis later in life. In women, heavy exercise can lead to decreased estrogen levels, which predisposes to osteoporosis. In addition, intensive training without proper compensatory increased nutrition increases the risk.

*Heavy metals—a strong association between cadmium, lead and bone disease has been established. Low level exposure to cadmium is associated with an increased loss of bone mineral density readily in both genders, leading to pain and increased risk of fractures, especially in the elderly and in females. Higher cadmium exposure results in osteomalacia (softening of the bone).

*Soft drinks—some studies indicate that soft drinks (many of which contain phosphoric acid) may increase risk of osteoporosis; Others suggest soft drinks may displace calcium-containing drinks from the diet rather than directly causing osteoporosis.

*Caffeine—contrary to popular belief, there is no evidence linking caffeine to osteoporosis.

Diseases and disorders

Many diseases and disorders have been associated with osteoporosis. For some, the underlying mechanism influencing the bone metabolism is straight-forward, whereas for others the causes are multiple or unknown.

*In general, immobilization causes bone loss (following the ‘use it or lose it’ rule). For example, localized osteoporosis can occur after prolonged immobilization of a fractured limb in a cast. This is also more common in active patients with a high bone turn-over (for example, athletes). Other examples include bone loss during space flight or in people who are bedridden or who use wheelchairs for various reasons.

*Hypogonadal states can cause secondary osteoporosis. These include Turner syndrome, Klinefelter syndrome, Kallmann syndrome, anorexia nervosa, andropause, hypothalamic amenorrhea or hyperprolactinemia. In females, the effect of hypogonadism is mediated by estrogen deficiency. It can appear as early menopause (1 year). A bilateral oophorectomy (surgical removal of the ovaries) or a premature ovarian failure cause deficient estrogen production. In males, testosterone deficiency is the cause (for example, andropause or after surgical removal of the testes).

*Endocrine disorders that can induce bone loss include Cushing’s syndrome, hyperparathyroidism, thyrotoxicosis, hypothyroidism, diabetes mellitus type 1 and 2, acromegaly and adrenal insufficiency. In pregnancy and lactation, there can be a reversible bone loss.

*Malnutrition, parenteral nutrition and malabsorption can lead to osteoporosis. Nutritional and gastrointestinal disorders that can predispose to osteoporosis include coeliac disease, Crohn’s disease, lactose intolerance, surgery (after gastrectomy, intestinal bypass surgery or bowel resection) and severe liver disease (especially primary biliary cirrhosis). Patients with bulimia can also develop osteoporosis. Those with an otherwise adequate calcium intake can develop osteoporosis due to the inability to absorb calcium and/or vitamin D. Other micro-nutrients such as vitamin K or vitamin B12 deficiency may also contribute.

*Patients with rheumatologic disorders like rheumatoid arthritis, ankylosing spondylitis, systemic lupus erythematosus and polyarticular juvenile idiopathic arthritis are at increased risk of osteoporosis, either as part of their disease or because of other risk factors (notably corticosteroid therapy). Systemic diseases such as amyloidosis and sarcoidosis can also lead to osteoporosis.

*Renal insufficiency can lead to osteodystrophy.

*Hematologic disorders linked to osteoporosis are multiple myeloma and other monoclonal gammopathies, lymphoma and leukemia, mastocytosis, hemophilia, sickle-cell disease and thalassemia.

*Several inherited disorders have been linked to osteoporosis. These include osteogenesis imperfecta, Marfan syndrome, hemochromatosis, hypophosphatasia, glycogen storage diseases, homocystinuria, Ehlers-Danlos syndrome, porphyria, Menkes’ syndrome, epidermolysis bullosa and Gaucher’s disease.

*People with scoliosis of unknown cause also have a higher risk of osteoporosis. Bone loss can be a feature of complex regional pain syndrome. It is also more frequent in people with Parkinson’s disease and chronic obstructive pulmonary disease.

Medication

Certain medications have been associated with an increase in osteoporosis risk; only steroids and anticonvulsants are classically associated, but evidence is emerging with regard to other drugs.

* Steroid-induced osteoporosis (SIOP) arises due to use of glucocorticoids – analogous to Cushing’s syndrome and involving mainly the axial skeleton. The synthetic glucocorticoid prescription drug prednisone is a main candidate after prolonged intake. Some professional guidelines recommend prophylaxis in patients who take the equivalent of more than 30& mg hydrocortisone (7.5& mg of prednisolone), especially when this is in excess of three months. Alternate day use may not prevent this complication.

* Barbiturates, phenytoin and some other enzyme-inducing antiepileptics – these probably accelerate the metabolism of vitamin D.

* L-Thyroxine over-replacement may contribute to osteoporosis, in a similar fashion as thyrotoxicosis does. This can be relevant in subclinical hypothyroidism.

* Several drugs induce hypogonadism, for example aromatase inhibitors used in breast cancer, methotrexate and other anti-metabolite drugs, depot progesterone and gonadotropin-releasing hormone agonists.

* Anticoagulants – long-term use of heparin is associated with a decrease in bone density, and warfarin (and related coumarins) have been linked with an increased risk in osteoporotic fracture in long-term use.

* Proton pump inhibitors – these drugs inhibit the production of stomach acid; it is thought that this interferes with calcium absorption. Chronic phosphate binding may also occur with aluminium-containing antacids.

* Thiazolidinediones (used for diabetes) – rosiglitazone and possibly pioglitazone, inhibitors of PPARγ, have been linked with an increased risk of osteoporosis and fracture.

*Chronic lithium therapy has been associated with osteoporosis.

Adapted from the Wikipedia article Osteoporosis, under the G. N. U. Free Documentation License. Please also see http://en.wikipedia.org/wiki

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The dramatic growth in the number of categories of mental illness as explained in the various versions of the DSM (Diagnostic and statistical manual of mental disorders) is a primary area of alleged medicalization. For instance, the current (DSM-IV) version, lists impotence, premature ejaculation, jet lag, and caffeine intoxication. One argument is that medicalization of such conditions can give a veneer of medical importance to otherwise vague and unscientific conditions, for example the most commonly diagnosed “personality disorder” is “309.9 Personality disorder not otherwise specified”. Many socially unacceptable behaviors have been medicalized and assigned disease terms in the 20th century (e.g. alcoholism, obesity, attention deficit disorder) while some behaviors previously considered medical problems have become more acceptable and been de-medicalized (e.g., homosexuality, masturbation, and particular theories such as Samuel Cartwright’s infamous drapetomania – the madness of slaves who try to flee captivity). Medicalization in this area, whether through psychiatry or more specifically biopsychiatry, has been most consistently and radically challenged by the antipsychiatry movement.

The HIV/AIDS pandemic allegedly caused from the 1980s a “profound re-medicalization of sexuality”. The diagnosis of Premenstrual dysphoric disorder has caused some controversy, and psychologist Peggy Kleinplatz has criticized the diagnosis as medicalization of normal human behavior, that occurred while fluoxetine (also known as Prozac) was being repackage

In 2005 an interdisciplinary group of scholars gathered in New York City, USA to discuss the clinical, philosophical, and political implications of medicalization. The group’s central question was whether, in the industrialized world, medicalization remains a viable notion in an age dominated by complex and often contradictory interactions between medicine, pharmaceutical companies, and culture at large. Participants represented a variety of disciplines, including psychiatry, sociology, anthropology, history, critical race theory, and gender studies. As such, topics ranged from the economics of medicalization to the creation and perpetuation of medicalized forms of identity and citizenship. Subjects of debate included, but are by no means limited to, the following:

- the medicalization of childbirth and pregnancy as indicated by the high rate of intensive interventions (according to the CDC, 1/3 of American births are by Caesarean section)

- the medicalization of race via so-called race-based medicine and racially-targeted pharmaceuticals such as Bidil (aimed at preventing serious cardiovascular outcomes in African-Americans)

- whether treatment of depression is an appropriate response to debilitating neurological imbalances, or medicalization of “normal sadness”, or somehow pathologizes a natural and rational reaction to the modern world’s detachment from stable traditional value systems

- and whether menopause, andropause, and aging as a whole should be considered physiological malfunctions or normal life processes

Adapted from the Wikipedia article Medicalization, under the G. N. U. Free Documentation License. Please also see http://en.wikipedia.org/wiki

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