Archive for June, 2013

Diseases of Altitude/ Ascent of Kilimanjaro

Tuesday, June 25, 2013 // Uncategorized

The New England of Journal recently had a review article on Acute High Altitude Illnesses, those problems that people develop when they ascend to high altitudes.  I wanted to write a letter to the editor extolling it’s advice to a theoretical patient who was about to climb Mount Kilimanjaro.   I could have used it when I started researching for practical advice before I climbed Mount Kilimanjaro thirty years ago.  The problem is that no one writes fan letters to the New England Journal of Medicine.  The letter writers are  always taking to task the authors of the research articles which are published weekly in the journal.  It is medical combat over study design , interpretation of data and it’s implications for society.  No one writes a letter saying thank you, I wish someone had told me that thirty years ago.  Back then we went to the library, perused the Index Medicus, a medical Reader’s Guide to Periodic Literature, and then looked through bound journals.  Upon finding the article in question we would take it to the copying machine and pay 10 cents a page to copy it.  Now all the pertinent information was laid out before me with the references.

While it is very high, 19340 feet at the summit, Kilimanjaro has become a very popular climb because it involves no technical climbing. The theoretical patient is ascending in 5 days and descending in 2-3 days, a leisurely pace.  Back then a ascent in 3 1/2 days and descent in 1 1/2 days was the norm.  The problem is that a quicker ascent increases the risk of problems such as acute mountain sickness the symptoms of which are headache, nausea and lassitude.   A slow ascent and the taking of acetazolamide, a drug formerly used to treat glaucoma, can reduce the risk.  Our group of sojourners, a ten dollar word used to describe mountain climbers, included 4 recovering residents and a dozen other climbers of various backgrounds with whom we were bundled.  Ages ranged from mid twenties to late forties.  We all took acetazolamide 500 mg twice a day and all reached the summit. The only person who had any medical problems was the youngest, a mid twenties university fundraiser.  She complained of blurred vision which improved as we descended.  We didn’t realize the severity of her visual loss until a few years later when we had a reunion and looked at photographs.  She remarked that she didn’t remember that because she couldn’t see it.  Aside from that the only problems we had were irritating paresthesias, intense numb feelings in the hands and feet caused by the acetazolamide, and a member of our group whose passport and airline tickets fell down the long drop, a mountainside privy, which involved a unforgettable wade through the bottom of the outhouse for retrieval.  The final ascent takes place under moonlight while the scree (gravel0 slopes are frozen for better footing which results in watching the sunrise from Gilman’s point at 18,650 feet before moving around the crater and the summit.

Once I took photographs at the summit, it dawned on me that now I had to go down.  I was unprepared for that task which involved completely different muscles than the ascent.  At one point we “skied” down the gravel slopes.

Since I had been chosen the  default leader of our group by the owner of the small hotel in Moshi, I was in charge of gathering and distributing gratuities to our guides, cook, assistant cook and porters.  I was the last one to shower and by then the little hotel had run out of hot water, something I had been thinking of for 5 days.

It was an extraordinary event, but my swan song for mountain climbing.

I have advised many people over the last 30 years who were preparing for the same climb and in the last 18 months five of my patients have made the ascent.

Here is everything you wanted to know about diseases of altitude:

Acute High-Altitude Illnesses

Peter Bärtsch, M.D., and Erik R. Swenson, M.D.

N Engl J Med 2013;  368:2294-2302June 13, 2013DOI:  10.1056/NEJMcp1214870

This Journal feature begins with a case vignette highlighting a common clinical problem. Evidence supporting various strategies is then presented, followed by a review of formal guidelines, when they exist. The article ends with the authors’ clinical recommendations.

A 45-year-old healthy man wishes to climb Mount Kilimanjaro (5895 m) in a 5-day period, starting at 1800 m. The results of a recent exercise stress test were normal; he runs 10 km 4 or 5 times per week and finished a marathon in less than 4 hours last year. He wants to know how he can prevent becoming ill at high altitude and whether training or sleeping under normobaric hypoxic conditions in the weeks before the ascent would be helpful. What would you advise?

The Clinical Problem

Persons who are not acclimatized and ascend rapidly to high altitudes are at risk for any of several debilitating and potentially lethal illnesses (Table 1Table 1Symptoms, Signs, and Differential Diagnosis of High-Altitude Illnesses.) that occur within the first days after arrival at high altitudes.1 Traditionally, 2500 m has been used as the threshold for high-altitude illnesses; in rare cases, mild illness occurs in persons who have ascended above 2000 m but below 2500 m.

Acute Mountain Sickness

Headache that occurs with an increase in altitude is the cardinal symptom of acute mountain sickness and is usually accompanied by anorexia, nausea, dizziness, malaise, sleep disturbance, or a combination of these symptoms.2 Acute mountain sickness generally occurs within 6 to 12 hours after a person ascends to 2500 m or higher. Its prevalence and severity increase with increasing altitude. Acute mountain sickness occurs in approximately 10 to 25% of unacclimatized persons who ascend to 2500 m. Symptoms are usually mild at this altitude and have little effect on activity. However, acute mountain sickness occurs in 50 to 85% of unacclimatized persons at 4500 to 5500 m and may be incapacitating.3-5

In a retrospective study, major independent risk factors for acute mountain sickness included a history of acute mountain sickness, fast ascent (≥625 m per day above 2000 m), and lack of previous acclimatization (<5 days above 3000 m in the preceding 2 months).6 A prospective study involving trekkers and climbers who went to altitudes between 4000 and 8848 m showed the same major risk factors for incapacitating acute mountain sickness and other severe altitude illnesses7 (described below). Other possible risk factors include female sex, an age younger than 46 years, and a history of migraine. Exercise may exacerbate acute mountain sickness, but good physical fitness is not protective.6-8 Symptoms usually resolve within 1 to 2 days when appropriate measures are taken (see below).

High-Altitude Cerebral Edema

High-altitude cerebral edema is characterized by truncal ataxia, decreased consciousness, and usually mild fever.2,9 Without appropriate treatment, coma may evolve rapidly, followed by death from brain herniation within 24 hours. Headache that is poorly responsive to nonsteroidal antiinflammatory drugs (NSAIDs) and vomiting indicate probable progression of acute mountain sickness to high-altitude cerebral edema, but the absence of headache and other symptoms of acute mountain sickness does not rule it out. High-altitude cerebral edema usually develops after at least 2 days at altitudes above 4000 m. The prevalence is estimated to be 0.5 to 1.0% among persons at 4000 to 5000 m.10 Magnetic resonance imaging in patients with high-altitude cerebral edema shows vasogenic edema11 and microhemorrhages that are located predominantly in the corpus callosum.12

High-Altitude Pulmonary Edema

High-altitude pulmonary edema is characterized by loss of stamina, dyspnea, and dry cough with exertion, followed by dyspnea at rest, rales, cyanosis, cough, and pink, frothy sputum.13 Deterioration in gas exchange also increases the risk of high-altitude cerebral edema. This condition develops 2 or more days after exposure to altitudes above 3000 m and is rare in persons at altitudes below 2500 to 3000 m. The risk increases with increased altitude and faster ascent. For example, the incidence among persons with an unknown history of high-altitude pulmonary edema is 0.2% if they ascend to 4500 m in 4 days and 2% if they ascend to 5500 m in 7 days; the incidence increases to 6% and 15%, respectively, when these altitudes are reached within 1 to 2 days. The risk is further increased among persons with a history of high-altitude pulmonary edema (e.g., the risk of recurrence is 60% among persons who ascend to 4500 m in 2 days).14 The estimated mortality among persons with untreated high-altitude pulmonary edema is 50%. This disorder is a noncardiogenic pulmonary edema caused by exaggerated hypoxic pulmonary vasoconstriction and abnormally high pulmonary-artery pressure and capillary pressure.15 These high pressures lead to a noninflammatory and hemorrhagic alveolar capillary leak that secondarily may evoke an inflammatory response.16

Strategies and Evidence

Risk Assessment

Risk assessment (Table 2Table 2Risk Assessment for Acute High-Altitude Illnesses.) should start with a clinical evaluation directed toward any cardiopulmonary diseases that might worsen during a sojourn involving high altitude. Although a discussion of the effect of altitude in persons with preexisting disease is not within the scope of this article, reviews of this topic are available.17,18 Given that previous altitude illness is a strong predictor of recurrence, detailed information about the person’s history with respect to visits to high-altitude areas, acclimatization before previous ascents, maximum altitudes for climbing and sleeping, rates of ascent, and any altitude illness should be obtained. The estimation of risk is most reliable for persons with previous rates of ascent and final altitudes that were similar to those planned.

Other Assessments

The assessment of ventilation in response to exposure to hypoxic conditions at rest or during exercise has been proposed as a means of refining risk prediction for altitude sickness. The increase in ventilation at rest or during exercise while breathing 11.5% oxygen,19 as well as arterial oxygen saturation after the first 30 minutes of exposure to an altitude of 3000 m or to corresponding normobaric hypoxic conditions,20 is on average significantly lower in persons who are susceptible to acute altitude sickness than in those who are not. However, considerable overlap between groups classified as susceptible and those classified as not susceptible in a retrospective study20 and between a group classified as having acute mountain sickness and a group classified as unaffected in a prospective study19 makes it impossible to define cutoff values that are sufficiently sensitive and specific to be useful in practice. A multivariate analysis of risk factors for severe high-altitude illness7 showed that the hypoxic ventilatory response and other physiological measurements under hypoxic conditions add little to the discrimination provided by patient characteristics and history (i.e., sex, level of physical activity, rate of previous ascent, and status with respect to previous severe high-altitude illness and migraines).

Persons who are considered to be susceptible to high-altitude pulmonary edema because of two previous episodes of high-altitude pulmonary edema have abnormally high systolic pulmonary-artery pressure (>40 mm Hg) under hypoxic conditions (12% oxygen in ambient air at sea level).21 In a study of a western European population, exaggerated hypoxic pulmonary-artery pressure was detected in about 10% of study participants,22 but high-altitude pulmonary edema develops in only 15% of persons with exaggerated hypoxic pulmonary-artery pressure responses who make a rapid ascent (unpublished data). For this reason and because of a very low pretest probability of high-altitude pulmonary edema (e.g., an incidence of 1 to 2% among trekkers to the Mount Everest base camp), measurement of pulmonary-artery pressure under hypoxic conditions cannot be recommended as a means of identifying persons who are susceptible to high-altitude pulmonary edema.

Although athletic persons are more likely to reach the summit than persons who are not athletic,19 physical fitness appears to have no association8,19 or at most a modest association7 with susceptibility to acute mountain sickness and high-altitude pulmonary edema. Thus, an exercise test is not indicated to assess the risk of acute high-altitude illness. Information about the amount and intensity of the person’s regular exercise as well as his or her level of athletic performance is helpful in estimating whether there is sufficient reserve to cope with the expected loss of exercise capacity at high altitudes of about 1% for every 100 m above 1500 m.23 Persons without athletic training should be encouraged to begin regular physical exercise several weeks to months before the planned ascent, particularly when rigorous outdoor activities are planned at high altitudes.


Nonpharmacologic Approaches

Although data are lacking from prospective studies that systematically assess the influence of the rate of ascent (defined as the gain in altitude between the altitudes at which one sleeps on 2 consecutive nights) on prevention of acute high-altitude illnesses, guidelines for ascents to altitudes above 3000 m24,25 recommend ascent rates of 300 to 500 m per day and a day of rest every 3 to 4 days (Table 3Table 3Prevention of High-Altitude Illnesses.). However, there are large differences among persons with respect to ascent rates that are not associated with poor outcomes. A person without previous experience in high altitudes should follow the ascent rates recommended by these guidelines. If the planned ascent rate is faster, additional measures, such as acclimatization strategies before the ascent or prophylactic medications, should be considered.

Mountaineering or residence with regular physical activity at altitudes above 3000 m in the weeks preceding a climb to 4500 m is associated with a reduced incidence of acute mountain sickness that is independent of the person’s susceptibility to this condition and the rate of ascent.6 An ascent made after 1 week at an altitude of 2000 m or higher, as compared with an ascent from near sea level, reduces both the incidence and severity of acute mountain sickness at 4300 m by 50%.26 It has been hypothesized that exposure to normobaric hypoxic conditions before an ascent might provide protection against acute mountain sickness. In double-blind, placebo-controlled trials, however, repeated intermittent exposure to normobaric hypoxia equivalent to an altitude of 2500 to 4500 m for 60 to 90 minutes27,28 or continuous exposure to normobaric hypoxia equivalent to an altitude of 2500 to 3000 m during 8 hours of sleep on 7 consecutive nights29 did not significantly reduce the incidence or severity of acute mountain sickness at altitudes of 4300 to 4559 m. On the basis of these data, a recommended strategy to reduce the risk of high-altitude illness is to remain at an altitude between 2000 and 3000 m for about a week6,26 and to include day hiking or climbing at higher altitudes. This should be done as close in time as possible to the trek or expedition, since it is not known how quickly acclimatization diminishes with time.30

Prophylactic Medication

Randomized, placebo-controlled trials have shown a significant reduction in the risk of headache with the use of acetylsalicylic acid at a dose of 320 mg taken three times at 4-hour intervals, starting 1 hour before ascent,31 or ibuprofen at a dose of 600 mg three times per day,32,33 starting a few hours before ascent to altitudes between 3480 and 4920 m. Headache is a defining symptom of acute mountain sickness, and the incidence of this condition was reduced in all these trials, which lasted 1 or 2 days only. A risk associated with these medications is gastrointestinal bleeding, which may be increased at high altitudes,34 but studies were not powered to assess this risk.31-33

When risk assessment indicates a high probability of the development of acute mountain sickness (Table 2), acetazolamide is recommended. In a large, prospective, observational study, the use of acetazolamide was associated with a 44% reduction in the risk of severe high-altitude illnesses.7 A meta-analysis of randomized trials of various doses of acetazolamide initiated before ascent likewise showed a significantly reduced risk of acute mountain sickness; the authors of this meta-analysis concluded that the lowest effective dose for prevention is 125 mg twice per day.35 This dose has been shown to be effective in reducing the incidence of acute mountain sickness associated with rapid ascent from a baseline altitude of 1600 to 4300 m36 or during further ascent to 4900 m among trekkers who have ascended to 4200 m without illness.37 However, a study that showed acute mountain sickness in more than 50% of persons who received acetazolamide at a dose of 250 mg twice per day during a rapid ascent of Mount Kilimanjaro (5895 m in 5 days)38 suggested that low-to-moderate doses may be inadequate with more rapid ascents and higher final altitudes; it is not known whether higher doses are more effective in persons at these altitudes. Acetazolamide should be started 1 day before the ascent and discontinued after 2 days at the final altitude or during the descent. A meta-analysis showed that acral paresthesias occurred in 35 to 90% of persons receiving acetazolamide, and polyuria occurred with the first several doses in 8 to 55%, with distaste for carbonated beverages in 4 to 14%.35 Nausea and tiredness developed in about 20% of persons who received 250 mg of acetazolamide three times per day at low altitudes.39 Thus, testing for side effects of the drug before the ascent might be useful to avoid confusion of a side effect with a symptom of acute mountain sickness. If side effects occur, the person should be advised not to use this prophylactic agent.

If there is a contraindication to acetazolamide or if it has intolerable side effects, an alternative is dexamethasone at a dose of 4 mg two or three times per day. In a randomized, placebo-controlled trial, dexamethasone was associated with a significant reduction in the incidence and severity of acute mountain sickness among persons who ascended to 2700 m.40 Several smaller randomized trials, including one head-to-head trial,39 have also shown these results at 4300 to 4570 m, with a magnitude of effect similar to that of acetazolamide.10 Given the potential adverse effects of dexamethasone (e.g., hyperglycemia, adrenal suppression, and psychosis), its use for prevention of acute mountain sickness should be limited to persons with unequivocal indications, and it should be administered for less than 1 week.

Since there appears to be a continuum from acute mountain sickness to high-altitude cerebral edema, drugs that prevent the first condition will probably also reduce the risk of the second one. However, systematic data are lacking to confirm this theory.

Small randomized trials involving persons with a history of high-altitude pulmonary edema have shown that the risk of recurrence can be reduced with the use of medications that lower the high pulmonary-artery pressure that is typical in susceptible persons. Nifedipine in a slow-release formulation at a dose of 30 mg twice per day,41 tadalafil (a phosphodiesterase-5 inhibitor) at a dose of 10 mg twice per day, and dexamethasone at a dose of 8 mg twice per day42 appear to be similarly effective in lowering pulmonary-artery pressure and reducing the incidence of high-altitude pulmonary edema from approximately 70% to approximately 10% or less. Although it has not been compared directly with these agents, inhaled salmeterol, a long-acting β2-agonist, at a high dose of 5 puffs (125 μg) twice per day, appears to be less effective; in a placebo-controlled trial, it was associated with a reduction in the incidence of high-altitude pulmonary edema from 74% to 33%.43


The treatment of mild-to-moderate acute mountain sickness (Table 4Table 4Treatment of Acute High-Altitude Illnesses.) generally consists of a day of rest, NSAIDs for headache, and possibly antiemetic drugs. One small, placebo-controlled, crossover trial showed that ibuprofen reduced headache significantly in affected persons.44 Treatment with oxygen and acetazolamide may also facilitate more rapid recovery, although there are only limited data from randomized trials to support the benefit of acetazolamide in persons in whom acute mountain sickness has already developed.45 In remote areas, a descent of 500 to 1000 m is indicated if symptoms of acute mountain sickness persist despite a day of rest and symptomatic treatment. If descent is not possible because of logistical constraints or the person’s condition, improvement sufficient to allow descent can be achieved with one or a combination of the following interventions: administration of dexamethasone at a dose of 4 to 8 mg every 6 hours,46 provision of supplemental oxygen (2 to 4 liters per minute), or treatment in a manually pressurized, body-length, portable hyperbaric bag.47

Immediate descent is lifesaving when severe symptoms suggest the onset of high-altitude cerebral edema or high-altitude pulmonary edema. In persons with high-altitude pulmonary edema, pulmonary-artery pressure should be lowered by means of supplemental oxygen (2 to 4 liters per minute), descent to a lower altitude, or pulmonary vasodilators (of which only nifedipine has been tested in a prospective study, which was uncontrolled).48 Anecdotal reports describe a benefit of phosphodiesterase-5 inhibitors for the treatment of high-altitude pulmonary edema, but they do not provide support for the use of dexamethasone.49 Although descent to a lower altitude is the primary goal for the management of high-altitude pulmonary edema in remote areas, allowing a fully conscious person with mild-to-moderate high-altitude pulmonary edema to remain in a mountainous resort area is reasonable when supplemental oxygen and oral pulmonary vasodilators can be provided under the supervision of a local physician or in an emergency facility.50 There is no role for diuretics in the treatment of high-altitude pulmonary edema.

Areas of Uncertainty

Since high-altitude cerebral edema and high-altitude pulmonary edema occur infrequently in remote areas, rigorous data are lacking to guide their management. Although numerous trials provide support for the use of acetazolamide for prophylaxis against acute mountain sickness, the appropriate dosage for persons planning an ascent to higher altitudes (above 4500 to 5000 m) or a rapid ascent is uncertain; data are lacking from randomized trials comparing dexamethasone with high doses of acetazolamide in these circumstances. The magnitude and duration of a reduced risk of acute mountain sickness associated with various forms of exposure to high altitudes before an ascent remain unclear.


Our recommendations are generally concordant with the guidelines of the Wilderness Medical Society for the prevention and treatment of high-altitude illnesses.45

Conclusions and Recommendations

The person described in the vignette has planned a rapid ascent of Mount Kilimanjaro (5895 m over a period of 5 days). In addition to the need for region-specific prophylaxis against infectious disease such as malaria, he should be advised that his plan involves a 40% risk of the development of acute mountain sickness that would be severe enough to prevent him from reaching the peak, as well as a small risk of high-altitude pulmonary edema or high-altitude cerebral edema. To improve his chances of staying relatively symptom-free and reaching the summit, we would recommend that he spend several days hiking and living at intermediate altitudes of 2000 to 3000 m near his home before departure; consider climbing Mount Meru, a 4500-m neighboring peak, in 3 or 4 days before ascending Mount Kilimanjaro; or plan a flexible timetable to allow additional stops at intermediate altitudes according to his clinical condition. Since randomized trials have shown no significant reduction in the incidence of high-altitude illness with athletic training in hypoxic conditions, such training should not be recommended, but we would encourage regular endurance training, since good aerobic performance will help to make mountaineering less strenuous. There are currently no reliable tests to predict susceptibility to high-altitude illnesses during an ascent. If acclimatization before the ascent or a slower ascent rate is not possible, we would recommend that prophylaxis with acetazolamide, at a dose of 250 mg two or three times per day, be initiated at the mountain base after testing for side effects of the drug at home. However, the efficacy of acetazolamide for particularly high and fast climbs such as this one is uncertain. It would be reasonable to provide the patient with dexamethasone for use as rescue medication during descent, if severe acute mountain sickness or high-altitude cerebral edema develops suddenly, and he should be advised not to delay the descent, if it is indicated.

Anyone climbing to a high altitude should be educated about high-altitude illnesses and the steps that should be taken if symptoms develop. Good sources of information include and Steps include resting for a day if acute mountain sickness develops and descending if there is no improvement in symptoms with the use of NSAIDs and antiemetic agents within 1 day, and descending immediately at the first appearance of symptoms or signs of high-altitude pulmonary edema or high-altitude cerebral edema.

Dr. Bartsch reports receiving lecture fees from Merck Sharp & Dohme and Bayer HealthCare and payment to his institution for meeting expenses from the Linde Group. No other potential conflict of interest relevant to this article was reported.

Disclosure forms provided by the authors are available with the full text of this article at

We thank Ingrid Slater of Division VII: Sports Medicine, Department of Internal Medicine, University Hospital, Heidelberg, Germany, for her assistance with the preparation of the manuscript.

Source Information

From the University Clinic, Department of Internal Medicine, Division VII: Sports Medicine, Heidelberg, Germany (P.B.); and Pulmonary and Critical Care Medicine, Department of Medicine, Veterans Affairs Puget Sound Health Care System, University of Washington, Seattle (E.R.S.).

Address reprint requests to Dr. Bärtsch at the University Clinic, Department of Internal Medicine, Division VII: Sports Medicine, Im Neuenheimer Feld 410, 69120 Heidelberg, Germany, or at [email protected].

Key Clinical Points


Acute high-altitude illnesses occur in persons who are not acclimatized during the first days at an altitude of 2500 m or higher, with wide variation in the incidence according to patient characteristics and history.
Headache is the major symptom of acute mountain sickness. If acute mountain sickness is not treated adequately, it can progress to life-threatening high-altitude cerebral or pulmonary edema.
High-altitude illnesses can be prevented by ascending 300 to 500 m per day at altitudes above 3000 m and including a rest day every 3 to 4 days.
Risks of acute mountain sickness and high-altitude cerebral edema are reduced with the use of acetazolamide or dexamethasone; the risk of high-altitude pulmonary edema is reduced with the use of nifedipine, phosphodiesterase-5 inhibitors, or dexamethasone.
Acute mountain sickness may be treated by a day of rest and nonsteroidal antiinflammatory drugs for headache, but when it is severe, descent or supplemental oxygen is indicated. Dexamethasone is indicated for severe acute mountain sickness or high-altitude cerebral edema, and nifedipine or phosphodiesterase-5 inhibitors are indicated for high-altitude pulmonary edema; treatment with these agents should be followed by descent as soon as possible.
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Low T Marketing Part 2

Wednesday, June 5, 2013 // Uncategorized

The following is an editorial in JAMA from the same edition that hasd the essay by the medical ghostwrite.  It outlines the marketing of a treatment for a pseudodisease.  It’s worth a billion dollars.

Invited Commentary | ONLINE FIRST

Low “T” as in “Template”: How to Sell Disease:  Comment on “Promoting ‘Low T’” ONLINE FIRST

Lisa M. Schwartz, MD, MS; Steven Woloshin, MD, MS
[+-] Author Affiliations

Author Affiliations: VA Outcomes Group, Department of Veterans Affairs Medical Center, White River Junction, Vermont; the Center for Medicine and the Media, Dartmouth Institute for Health Policy and Clinical Practice; and the Norris Cotton Cancer Center, Lebanon, New Hampshire (Drs Schwartz and Woloshin).


JAMA Intern Med. 2013;():1-3. doi:10.1001/jamainternmed.2013.7579.
Text Size: A A A
Published online June 3, 2013

A man on TV is selling me a miracle cure that will keep me young forever. It’s called Androgel . . . for treating something called Low T, a pharmaceutical company–recognized condition affecting millions of men with low testosterone, previously known as getting older.
The Colbert Report,1 December 2012

Mr Ferguson, a healthy 55-year-old man without active problems, is in your office for his annual checkup. He tells you that he has no problems and feels fine.

“Well,” his wife chimes in, “he has been a little grumpy. Especially since Sammy—our son—starting beating Shaun here in their one-on-one basketball games.”

“Of course, I’m grumpy. We bet on a game and now I have to do the lawn,” Shaun says, shaking his head. “Takes forever, and it’s exhausting.”

“I understand,” you reply, laughing. “So, are you still off cigarettes?”

“Wait,” his wife blurts out before Shaun answers. She stares. “Don’t you think he needs a blood test? Could this be . . . Low T?” She hands you a paper—Shaun has completed the Low T question quiz from the Is It [Low T]? website.2

Testosterone usually brings sex to mind. Curiously, only 2 of 10 quiz questions are about sex: Decreased libido? Erections less strong? Your patient did not check either. But he checked 3 about energy, mood, and sports performance, enough for the quiz to suggest asking his doctor about “Low T” (low testosterone level, aka hypogonadism).

The site also offers strategies for spouses to “motivate the men in their lives to talk to their doctors.” For example, if the man says “I don’t have much energy anymore,” “[his spouse might think] he’s just making excuses.” But the site tells her that Low T may be the real issue because it can affect energy levels—never suggesting other explanations such as stress, depression, or other medical problems.

The Low T website is part of a broader disease awareness campaign run by Abbott Laboratories, maker of Androgel, the leading testosterone replacement product (>3 million prescriptions and >$1 billion in sales in the United States in 20123).

Whereas traditional drug promotion such as direct-to-consumer ads, physician samples, gifts, and detailing has received much attention, far less is known about disease awareness campaigns—much broader efforts to influence how physicians and the public think about what constitutes disease and when drugs are needed. These well-coordinated campaigns are more subtle than drug-specific campaigns, and they blur the line between public health or professional education and marketing.

The article by Braun4 on the promotion of Low T is a fascinating and troubling first-hand look inside the kitchen of industry disease awareness campaigns. Braun exposes how industry used ghostwritten magazine articles under a celebrity physician’s byline. This is on top of educational campaigns, television and magazine ads, and mobilizing industry-funded advocacy groups. The campaigns also target physicians through special journal supplements, consensus statements, and continuing medical education, as Braun also highlights.

The Low T campaign provides a template for understanding how disease awareness campaigns work. Like other campaigns (eg, Bipolar Disorder and Restless Legs Syndrome), the Low T campaign uses 3 basic strategies: lower the bar for diagnosis (turning ordinary life experiences into conditions that require medical diagnoses), raise the stakes so that people want to get tested, and spin the evidence about drug benefits and harms.

Health exists along a spectrum. At one end, people are clearly well; at the other, clearly sick. What about the big gray zone in between? When do bothersome experiences become symptoms? Where do you draw the line? For Low T, the location of the line is implausible. Everyone feels a little tired—or sad or grumpy—sometimes. And everyone slows down a bit over time (it is called aging). Recent US endocrinology5 and European urology6 guidelines actually recommend against using such Low T–type quizzes because they are unreliable and unvalidated. The Endocrine Society guideline goes even further, recommending against general population screening for Low T “because of the lack of consensus on a case definition and the extent to which androgen deficiency is an important health problem.”5(p2543)

Interpreting laboratory values is all about lines—often determined statistically: lines are typically drawn, for example, 2 standard deviations beyond the mean, defining 5% of the population as abnormal. If the lines are drawn closer to the mean of normally distributed values, the proportion defined as abnormal expands rapidly. For testosterone, a serum level of 230 ng/dL (to convert to nanomoles per liter, multiply by 0.0347) defines 7% of men 50 years and older as abnormal; moving the line to 350 ng/dL (the cutoff for “normal” used in the consensus recommendation coauthored by Braun4) increases the abnormal proportion to 26%.

Ideally, the line would be drawn to maximize benefit and minimize harm. Unfortunately, lines are often drawn not because of evidence but to expand the market. Whether or not broad disease definitions are in the public’s interest, they do serve the financial and professional interests of industry, specialists, and advocacy groups.

It is one thing to tell men that Low T can make them grumpy; it is another to say that it can kill them. Messages raising the stakes about Low T have appeared regularly in scientific meeting reports and journal articles7 and often make their way into the news (“Low testosterone could kill you,” according to ABC News8).

Because Low T becomes more common with aging, associations with death are inevitable. But these associations come from inherently weak observational studies that cannot exclude residual confounding or establish causality. To his credit, Braun4 was able to highlight these fundamental limitations in the consensus recommendations that he coauthored. Ironically, the same report asserts that Low T increases the risk of heart disease even though this finding is based on similarly limited research (in fact, a randomized trial of testosterone therapy in elderly men was stopped early because it increased the risk of cardiovascular disease9).

The implicit message of the Low T awareness campaign is that testosterone therapy will improve men’s energy, mood, and sex life. Neither the Low T website, nor the consensus recommendation, nor the magazine articles published using unnamed ghostwriters4 tell readers which outcomes are likely to improve with testosterone therapy—let alone the magnitude of the changes. The focus is on getting a diagnosis and on which form of treatment to take.

Physicians and patients who assume that treatment has an important effect on all or most symptoms may be surprised by the evidence from randomized trials (Table): Testosterone therapy results in only small improvements in lean body mass and body fat, libido, and sexual satisfaction, and has inconsistent (or no) effect on weight, depression, and lower extremity strength. Whether these effects are big enough to matter to patients is unknown. Nor is it known whether they are big enough to outweigh the harms of testosterone therapy, ie, polycythemia that may increase thromboembolic events, edema, serious hepatotoxic effects, gynecomastia, worsening of sleep apnea, prostate enlargement, and rise in prostate-specific antigen level (and potential increased risk of prostate cancer).10

Table Grahic Jump LocationTable. Claims and Supporting Evidence About Testosterone Therapy for Low T

There are a lot of American men. Some are grumpy. Some are tired. Some may not even be interested in sex at the moment. And all of them are aging. This is the intended audience for the Low T campaign. Whether the campaign is motivated by a sincere desire to help men or simply by greed, we should recognize it for what it is: a mass, uncontrolled experiment that invites men to expose themselves to the harms of a treatment unlikely to fix problems that may be wholly unrelated to testosterone levels.

We agree with Braun that there is a strong analogy between the marketing of testosterone therapy for men and estrogen therapy for menopausal women. Ignoring the lessons of estrogen therapy is scandalous. Before anyone makes millions of men aware of Low T, they should be required to do a large-scale randomized trial to demonstrate that testosterone therapy for healthy aging men does more good than harm.

Correspondence: Dr Woloshin, Department of Veterans Affairs Medical Center, White River Junction, VT 05009 ([email protected]).

Published Online: June 3, 2013. doi:10.1001/jamainternmed.2013.7579

Conflict of Interest Disclosures: None reported.

Disclaimer: The opinions expressed by the authors of this Invited Commentary are their own, and they should not be interpreted as official positions of the Department of Veterans Affairs.

Additional Information: Drs Schwartz and Woloshin are members of the Steering Committee for the Preventing Overdiagnosis conference cosponsored by the Geisel School of Medicine at Dartmouth in September 2013.

Additional Contributions: We thank Stephen Colbert for bringing needed attention to the selling of Low T and Victor Montori, MD, for reviewing the Table.


1 +

 Low-T and Low-O. The Colbert Report. Comedy Central television. December 4, 2012.—low-o. Accessed April 21, 2013
2 +
 Abbott Laboratories. Is It [LowT]? Accessed April 12, 2013
3 +
Dobrow L. All-star large pharma marketing team of the year: AndroGel. Medical Marketing & Media. January 2, 2013. Accessed April 29, 2013
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Braun SR. Promoting “Low T”: a medical writer’s perspective [published online June 3, 2013].  JAMA Intern MedLink to Article
5 +
Bhasin S, Cunningham GR, Hayes FJ,  et al; Task Force, Endocrine Society.  Testosterone therapy in men with androgen deficiency syndromes: an Endocrine Society clinical practice guideline.  J Clin Endocrinol Metab. 2010;95(6):2536-2559
PubMed   |  Link to Article
6 +
Dohle GR, Arver S, Bettocchi C, Kliesch S, Punab M, de Ronde W. Guideline on Male Hypogonadism. Anhem, The Netherlands: European Association of Urology; 2012
7 +
Lewis BH, Legato M, Fisch H. Medical implications of the male biological clock.  JAMA. 2006;296(19):2369-2371
PubMed   |  Link to Article
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Bunyavanich S. Low testosterone could kill you. ABC News. June 6, 2007. Accessed April 21, 2013
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Basaria S, Coviello AD, Travison TG,  et al.  Adverse events associated with testosterone administration.  N Engl J Med. 2010;363(2):109-122
PubMed   |  Link to Article
10 +
 AndroGel 1.62% [package insert]. North Chicago, IL: Abbott Laboratories; 2012.
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Confessions of a Low T Ghostwriter

Tuesday, June 4, 2013 // Uncategorized

“Ask your doctor”.  These words  make any physician cringe.  Here is a typical example.  Men come in asking about whether they should be checked for low testosterone levels. It is something that they saw on a commercial on TV.  It is a classic case of a drug looking for a disease.  Testosterone levels decline as a function of aging.  A low testosterone level doesn’t mean that one has a disease or needs a medication.  The symptoms described in the adds are very nonspecific.  They are symptoms that everyone experiences at times.  Occasionally men do have symptomatic low testosterone levels, but they are the exception rather than the rule.  There is a whole industry built on this.  Some company has Low T franchises and one is going to put in a clinic down the block from me.  The following is the confession of a medical ghostwriter.




Promoting “Low T”:  A Medical Writer’s Perspective ONLINE FIRST

Stephen R. Braun, BA
[+-] Author Affiliations

Author Affiliation: Braun Medical Media, Amherst, Massachusetts.


JAMA Intern Med. 2013;():1-4. doi:10.1001/jamainternmed.2013.6892.
Text Size: A A A
Published online June 3, 2013

Despite progress in raising the level of transparency about funding, conflicts of interest, and ghostwriting, drug companies remain free to pursue subtle and, therefore, effective means of marketing. Continuing medical education programs and “consensus” panels continue to be funded by companies selling products directly tied to the messages being conveyed by the resulting “educational” materials. And patient education materials continue to be created that, while factually accurate, subtly shift attitudes by including only selected facts and/or omitting ideas that would undermine the funder’s preferred paradigm.

“Low T” (low testosterone level, aka hypogonadism) is high profile these days. Sales of testosterone replacement therapies (TRTs) for Low T have more than doubled since 2006 and are expected to triple to $5 billion by 2017, according to forecasts by Global Industry Analysts.1 Driving these sales is a sophisticated marketing effort to define low testosterone level as a disease for which the treatment is TRT. I know this because, as a professional medical writer, I have helped craft that message for transmission in a range of media to both physicians and consumers.

This is hardly the first time that an age-related condition has been spun into a disease state when a new product has been developed that is believed to alleviate or attenuate the condition. In fact, the current situation with TRT eerily echoes the way that hormone therapy was, for years, touted as a safe treatment for menopause-related symptoms and the prevention of cardiovascular disease in women.2 Only after the Women’s Health Initiative study found that older women using hormone therapy had small excesses in the incidence of breast cancer, myocardial infarction, cerebrovascular accident, and venous thrombosis did physicians become more cautious about prescribing it and limit its use to appropriate female patients.3

An examination of the current ways that industry is reshaping the paradigm of Low T is warranted now not simply because of the potential public health risks associated with widespread use of TRT in the absence of a Women’s Health Initiative–scale study. Efforts have been made in recent years to curtail the abuses of pharmaceutical influence4 and encourage greater transparency in medical communications.5 As this article demonstrates, these efforts, although salutary, do not fundamentally alter the influences of drug company funding on the content and tone of messages directed at physicians and consumers.

In 2009, a well-known endocrinologist was contacted by the public relations firm HealthSTAR Communications. The firm had been hired by a pharmaceutical company to place articles in popular magazines that would appear under the byline of physicians who could talk about the “hazards” of low testosterone levels and the availability of new forms of TRT. The endocrinologist forwarded me the e-mail from the public relations firm requesting that he write a short article for Life After 50 magazine. The e-mail included a “Facts for Women” sheet that encouraged women to “diagnose” their male partners and urge them to seek medical attention (because men, demonstrably, do not seek such attention as much as they should). The fact sheet included the URL for a consumer-oriented website created by Abbott Laboratories.6

I wrote a brief, neutral-sounding article, put the physician’s name on it, and sent it off. In the following months, the physician was contacted by HealthSTAR Communications for more articles, or just quotes that could be passed on to a magazine writer. I generated versions of the original article, also to appear under the physician’s byline, for Woman’s Day, Business Week, Positive Change, and Health View. (I was paid for all of these articles by the physician himself—I do not know whether he was being paid by either the public relations firm or a drug company.) Although these articles were relatively neutral in tone and did not mention specific products, none were skeptical, none questioned the reliability of the data on which claims were being made, and none included the views of clinicians who dissented from the emerging paradigm about Low T. In part, that was because I was just learning about the issue myself and had not dug deeply into the literature. But I also knew what I was getting paid to do: trumpet the party line. As a result, the articles adhered nicely to the new paradigm of Low T as a potentially serious condition for which new treatments were available. The fact that the articles appeared under the byline of a physician and appeared in trade magazines with no mention of the funder behind the overall effort raised the marketing value of the pieces considerably because it is likely that readers trust information that appears to be objective and free of industry influence.

In 2010, I was hired by a medical communications company to write a consumer-level booklet about low testosterone levels and TRT. The project was funded by Solvay, original maker of AndroGel testosterone gel, 1.62% (later purchased by Abbott Laboratories). To my surprise, Solvay did not try to blatantly spin the copy to favor Androgel. Quite the opposite. The Solvay team reviewing the first draft often made changes that made the booklet more neutral.

For example, I had initially written the following sentence in an early draft: “You can increase the positive effects of TRT on your overall health by taking a few basic steps.” The reference to TRT was removed by the Solvay medical-legal reviewing team, and the sentence was changed to “You can improve your overall health by taking a few basic steps.”

This was not altruism, however. It was astute legal caution. Pharmaceutical companies face a real threat of litigation arising from unsubstantiated marketing claims, as well as regulatory discipline from the US Food and Drug Administration. It is in their interest, therefore, to play it safe with all claims and to avoid the overt peddling of a brand or product. Instead, the goal is to raise awareness of a condition and the availability of a treatment, leaving the responsibility for a decision to the patient, who should “talk to your doctor to see if X might be right for you.”

In the end, the patient education booklet was both blandly accurate and effective in transmitting the company’s core messages to tens of thousands of patients. Here, for example, is part of the booklet’s conclusion:

You’ve seen that the hormone testosterone is important throughout life. A simple blood test can show if you have low testosterone, and a visit with your doctor can confirm whether or not you have hypogonadism. If so, you can choose from several options to deliver testosterone to your blood. Doing so may relieve your bothersome symptoms and may help restore your energy, positive mood and sexuality.

The passage is true, primarily thanks to the liberal use of the words “can” and “may,” which are often suggested by legal review teams because they allow the wiggle room required in legal defenses. And yet the passage is also far from the whole truth. Despite my own best intentions (and training as a journalist), it is a shill for the sponsor—an uncritical, unbalanced presentation of “facts” that serves primarily to drive people to their physicians seeking the holy grail of “energy, positive mood, and sexuality” in the form of testosterone.

In 2012, I was hired by a professional physicians’ organization to attend a meeting of experts in the field of hypogonadism and to write a summary of the meeting’s conclusions—a “consensus statement”—to be published as a guide to clinical practice. In this case, consensus was not difficult to achieve because the panel members shared a basic perspective on the value of TRT (although some differences of opinion on technical matters existed).

The meeting was funded by Abbott, and every panel member had served as either a consultant or researcher for Abbott or other companies with TRT products on the market or in the pipeline (ie, Auxilium, Endo Pharmaceuticals, and Lilly). Abbott’s role as sponsor and the potential conflicts of interest of all panel members were acknowledged in the final printed monograph, as was my involvement as writer.

In writing the monograph, I included as much cautionary or qualifying language as I could, based on my now much deeper knowledge about this subject. Some of this language survived the rounds of review and editing that followed. For example, to balance the claim that low testosterone levels are associated with higher mortality (an association that has appeared more than once in the literature), I noted that a recent systematic review and meta-analysis had found large between-study differences in results and methodological problems that cast doubt on the claimed association.7

But other sections or sentences of a cautionary nature were deleted by panel members during the review process. Here are 2 that were cut:

It is worth noting that the quality of the evidence on which current clinical guidelines for TRT are based is low or very low, and that similar guidelines about the alleged benefits of hormone therapy for post-menopausal women have been questioned after high-quality studies of sufficient size and duration were carried out.8

Composite measures of T levels and the symptoms related to low circulating androgens are likely to be fluid and lack stability over long periods of time. This suggests that Symptomatic Androgen Deficiency (SAD) represents a transient, rather than a permanent, state for the majority of the general male population and may cast doubt on the use of SAD or similar constructs as proxies for true age-related hypogonadism.9

If those paragraphs had remained, they would have helped balance the tone of the resulting monograph. That does not mean that the monograph is hopelessly biased. In fact, I believe that it is more cautionary than some guidelines I have read and that it contains an up-to-date summary of treatment options that nonspecialists might find useful. At the same time, I believe that the overall perspective of the piece is, at best, neutral on the potential clinical utility of TRT and on the larger potential risks posed by widespread use of TRT by eugonadal men. I believe that a more sharply skeptical tone is warranted by the existing data—or lack thereof.

A potential weakness of the consensus panel model for generating clinical practice recommendations is that some panelists work harder than others. Some attendees of the hypogonadism meeting, for example, were careful, responsible, and fair minded, both during the meeting and in the reviewing of monograph drafts. Others did a far more cursory job, and 1 member did not participate in the review process at all. Such variability in effort may be inevitable, but it can result in so-called consensus statements that actually reflect only the strongly held views of a minority of the panel. In addition, of course, a panel as a whole may not represent the true range of opinions that exist on a matter of interest, either because the members are suggested by the funder or because the organizers recruit panel members via the personal recommendations of key members. (Some companies that organize consensus panels are attempting to improve transparency. One of my clients, New England Research Institutes, actively seeks a diversity of opinion among panel members and requires the participation of an independent panelist whose role is to flag imbalance or favoritism appearing in the conference itself or whatever papers or materials arise from it.)

A final point: the monograph resulting from the hypogonadism “consensus conference” was published in 2012 and given continuing medical education credit. I created a PowerPoint slide show based on the monograph that was used by physicians who presented Abbot-funded continuing medical education–accredited lectures on the subject at conferences or other types of professional meetings. This is common practice, although, I believe, fundamentally problematic. Physician education programs (regardless of funding source) have been shown to influence physicians’ prescribing behavior, even though the physicians who attend such symposia often deny such influence.10 And the more objective and less obviously biased a program appears, the greater its potential impact because the messages more easily slip through the skepticism that would be aroused by more ham-handed presentations. “Speakers who sound like drug reps alienate physician audiences and thus work against industry interests,” noted the authors of a 2006 article on the subject.11(p413)

In this article I have described how drug companies can pay for the creation of apparently objective physician or consumer education media products while obscuring or minimizing their role and/or the identity of the actual writers or producers of the products. I have also described how industry influence may skew content even when funding sources are nominally identified or acknowledged. I believe that these dynamics are widespread and deserve closer scrutiny by physicians, consumers, and regulators.

Despite progress in raising the level of transparency about funding, conflicts of interest, and ghostwriting, drug companies remain free to pursue subtle—and, therefore, effective—means of marketing. They can continue to hire public relations firms that, in turn, place articles or ideas in popular media with no mention of the funding source. Continuing medical education programs and consensus panels continue to be funded by companies selling products directly tied to the messages being conveyed by the resulting “educational” materials. And patient education materials continue to be created that, although factually accurate, subtly shift attitudes by including only selected facts and omitting (intentionally or unintentionally) ideas that would undermine the funder’s preferred paradigm.

Everyone involved in the creation of drug company–sponsored educational materials for physicians or consumers—myself most certainly included—must constantly guard against these kinds of influences. We must do our own research, ask hard questions, be skeptical about all claims, and question whether our judgment and our words are being subtly skewed by the knowledge that the funder is watching. Physicians, for their part, must be equally vigilant, skeptical, and independent.

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A Physician’s Reflection on the Changes in Medicine

Monday, June 3, 2013 // Uncategorized

This is from the section of the Annals of Internal Medicine entitled, “On Being a Physician”.  These are the reflections of a physician on the changes in academic medicine over the years as a result of changes in reimbursement.  He laments the dumbing down of medicine and the lack of emphasis on critical thinking.


On Being a Doctor | 21 May 2013

When We Became Rich

George A. Sarosi, MD

Ann Intern Med. 2013;158(10):774-775. doi:10.7326/0003-4819-158-10-201305210-00014
It was a rather difficult faculty meeting. The entire time was given to the director of the faculty practice plan, who went over our tenuous financial situation, emphasizing that revenues were down and that we were not likely to get a raise or a bonus at the end of the year. In discussing the possible remedies, he suggested that we consider reducing some of the frills that we currently enjoyed, the number of fellows that the department was paying, or the educational allowance provided each faculty member. Finally, he warned us that unless we turned around the downward trend of the department income, we might need to make some cuts in compensation.

I couldn’t help but think back to how all of this “prosperity” started. When I was in medical school during the early 1960s, there was no talk about health care costs, length of stay, or diagnosis-related groups. We lived in blissful ignorance of the entire issue of who was paying for the care of our patients. We were exposed only to the charity patients on the ward service and had next to nothing to do with patients on the private service. In fact, the only thing I knew about the private service was what my advisor told me—do not apply for a private service internship because “the attending will not let you do anything.” With this advice in mind, I started my medical internship in a hospital that had mostly nonprivate patients.

During our orientation, not a single word was devoted to the cost of medical care. In fact, the only time any discussion involved money was when we (the medical interns) discovered that the hospital administration trainees were paid four times as much as we were. We then sent a deputation to meet with the hospital director about this salary discrepancy. The response was that the hospital had to pay the administration trainees more because they were “college graduates.”

All admitted patients were initially seen by a medical student before the housestaff to ensure that the students would develop adequate history-taking skills. Except in life-threatening emergencies, these rules were inviolate. When the chairman himself was admitted for some diagnostic tests, he insisted that the medical student see him first. He then severely berated the student for not performing a rectal examination.

Attending rounds were of variable length and quality. We had several truly great attendings who challenged us every day to think in terms of pathophysiology and spent time with the students, honing their skills in summarizing and presenting their findings. The students were an integral part of rounds and were expected to read about all of the patients and help with the scut work.

In January 1966, everything suddenly changed. We were never warned about the forthcoming upheaval. We had never heard the term “Medicaid.” The only visible change in our daily life was that I suddenly had many more forms to fill out on recently discharged patients.

Sometime during the latter part of February, a check for $1800 made out to me showed up in my mailbox. It obviously was not mine, because my annual stipend was $3150. The check was from an insurance company that was the local carrier for Medicaid. I took the check to the medicine office and gave it to the senior secretary. As soon as she saw its distinctive color, she immediately knew what it was. Her only comment was, “Oh, it’s one of those!” She then opened a drawer and pulled out a large stack of similar checks, held together by a wide rubber band.

Although I received a few more similar checks, I stopped thinking about them because someone in the medicine office clearly was in charge of the monies. This blissful state of ignorance was suddenly brought to a halt several weeks later during our weekly department meeting. The meeting included the housestaff as well as the faculty and dealt with patient care and medical education issues.

Unlike all previous meetings, the chairman immediately departed from the usual agenda. He brought with him the large stack of checks. He put these on the lectern, saying that the current situation was unprecedented. He asked the audience for their advice on how to dispose of the money. He thought that these funds should be distributed to the housestaff because, in fact, they took care of the patients.

As soon as he finished that sentence, pandemonium broke out—multiple faculty members started to speak at once, and we (the housestaff) sat dumbfounded. The meeting rapidly spun out of control and ended with no resolution relating to the distribution of the newly acquired largesse.

The next week, a group of dark-suited men with expensive briefcases showed up to work out the details of the embryonic faculty practice plan. The housestaff were never again invited to attend faculty meetings that were now devoted exclusively to discussions about money. At first, not much changed in the daily routine of the hospital, but soon we noticed that several young physicians came to visit and gave grand rounds.

By the next year, a few of these visitors joined the faculty in the various subspecialties of internal medicine. After my chief residency, I joined the Centers for Disease Control and Prevention and eventually returned to the faculty 2 years later as a newly minted junior faculty member. The most notable change was the presence of many new faculty members in various subspecialties of internal medicine, more than doubling the size of the previously small faculty. This welcome change came about because of the sudden availability of new funds in the practice plan.

In the 45-plus years after my resident days, the financial aspects of the entire health care system continued to evolve and the changes have been profound and lasting. During these years, we have learned to live with diagnosis-related groups, direct and indirect medical education payments to the hospitals by Medicare, extensive and punitive “fraud and abuse” investigations of university medical centers by Medicare, markedly increased demands for documentation, and the addition of compliance officers to the practice plan to avoid being accused of “fraud and abuse” due to “upcoding.”

These changes were followed by the work-hour limitations for house officers and the implementation of the electronic medical record, where a single keystroke can generate an entire page of standardized (and useless) history designed to milk the maximum reimbursement from the “payer sources,” and where “cut and paste” has led to hundreds of pages of identical, extensive, and uninformative notes from every person in contact with the patient. Although the electronic medical record has markedly improved the quality and efficiency of medical care, it is important to remember that the impetus to develop it was primarily to facilitate billing.

Along with all of these changes, caring for the patient remained the one constant. The development of evidence-based medicine rationalized therapeutic decisions. Ready access to electronic references is now at one’s fingertips, allowing all of us to get and use the best and most recent information available. The development of order sets has assured a degree of consistency in the level of care, but at the cost of eliminating the need for reflection and critical thinking by the house officer.

The relentless pressure for reduced length of stay has created an avalanche of paperwork that has to be completed by the house officer, all too frequently during the hours set aside for teaching rounds, limiting time for discussion of potentially important considerations for patient care. Finally, the typing of extensive and redundant daily notes has replaced the narrative text, which was an important stimulus of critical thinking.

During the past 45 years of making attending rounds, I learned all of the new fads, mastered the use of the computer, became familiar with the lingo of modern statistics, and can even define and calculate “prior probability.” It is just not as much fun …

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