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Dr. Drug Rep
On a blustery fall New England day in 2001, a friendly representative from W yeth Pharm aceuticals cam e intom y office in Newburyport, Mass., and m ade m e an offer I found hard to refuse. He asked m e if I’d like to givetalks to other doctors about using Effexor XR for treating . He told m e that I would go around todoctors’ offices during lunchtim e and talk about som e of the features of Effexor. It would be pretty easy. W yethwould provide a set of slides and even pay for m e to attend a speaker’s training session, and he quicklyfloated som e num bers. I would be paid $500 for one-hour “Lunch and Learn” talks at local doctors’ offices,or $750 if I had to drive an hour. I would be flown to New York for a “faculty-developm ent program ,” whereI would be pam pered in a Midtown hotel for two nights and would be paid an additional “honorarium .” I thought about his proposition. I had a busy private practice in , specializing inpsychopharm acology. I was quite fam iliar with Effexor, since I had read recent studies showing that it m ightbe slightly m ore effective than S.S.R.I.’s, the m ost com m only prescribed : the Prozacs,Paxils and Zolofts of the world. S.S.R.I. stands for selective serotonin reuptake inhibitor, referring to the factthat these drugs increase levels of the neurotransm itter serotonin, a chem ical in the brain involved inregulating m oods. Effexor, on the other hand, was being m arketed as a dual reuptake inhibitor, m eaning thatit increases both serotonin and , another neurotransm itter. The theory prom oted by W yethwas that two neurotransm itters are better than one, and that Effexor was m ore powerful and effective thanS.S.R.I.’s. I had already prescribed Effexor to several patients, and it seem ed to work as well as the S.S.R.I.’s. If I gavetalks to prim ary-care doctors about Effexor, I reasoned, I would be doing nothing unethical. It was a perfectlyeffective treatm ent option, with som e data to suggest advantages over its com petitors. The W yeth rep wassim ply suggesting that I discuss som e of the data with other doctors. Sure, W yeth would benefit, but so wouldother doctors, who would becom e m ore educated about a good m edication. A few weeks later, m y wife and I walked through the luxurious lobby of the Millennium Hotel in MidtownManhattan. At the reception desk, when I gave m y nam e, the attendant keyed it into the com puter and said,with a dazzling sm ile: “Hello, Dr. Carlat, I see that you are with the W yeth conference. Here are yourm aterials.” She handed m e a folder containing the schedule of talks, an invitation to various dinners and receptions andtwo tickets to a Broadway m usical. “Enjoy your stay, doctor.” I had no doubt that I would, though I felt agnawing at the edge of m y conscience. This seem ed like a lot of m oney to lavish on m e just so that I couldprovide som e education to prim ary-care doctors in a sm all town north of Boston. The next m orning, the conference began. There were a hundred or so othe from different partsof the U.S. I recognized a couple of the attendees, including an acquaintance I hadn’t seen in a while. I’dheard that he m oved to another state and was m aking a bundle of m oney, but nobody seem ed to know exactlyhow. I joined him at his table and asked him what he had been up to. He said he had a busy private practice andhad given a lot of talks for W arner-Lam bert, a com pany that had since been acquired by His talks wereon , a drug that was approved for but that m y friend had found helpful in his practice. (In 2004, W arner-Lam bert pleaded guilty to illegally m arketing Neurontin forunapproved uses. It is illegal for com panies to pay doctors to prom ote so-called off-label uses.) I knew about Neurontin and had prescribed it occasionally for bipolar disorder in m y practice, though I hadnever found it very helpful. A recent study found that it worked no better than a placebo for this condition. I asked him if he really thought Neurontin worked for bipolar, and he said that he felt it was “great for som epatients” and that he used it “all the tim e.” Given m y clinical experiences with the drug, I wondered whetherhis positive opinion had been influenced by the m oney he was paid to give talks.
But I put those questions aside as we gulped down our coffees and took seats in a large lecture room . On theagenda were talks from som e of the m ost esteem ed academ ics in the field, authors of hundreds of articlesin the m ajor psychiatric journals. They included Michael T hase, of the and theresearcher who single-handedly put Effexor on the m ap with a m eta-analysis, and Norm an Sussm an, aprofessor of psychiatry a, who was m aster of cerem onies. Thase strode to the lectern first in order to describe his groundbreaking work synthesizing data from m orethan 2,000 patients who had been enrolled in studies com paring Effexor with S.S.R.I.’s. At this tim e, with hisEffexor study a topic of conversation in the m ental-health world, Thase was one of the m ost well known andwell respected psychiatrists in the United States. He cut a captivating figure onstage: tall and slim , dynam ic,incredibly articulate and a m aster of the research craft. He began by reviewing the results of the m eta-analysis that had the psychiatric world abuzz. After carefullypooling and processing data from eight separate clinical trials, Thase published a truly significant finding:Effexor caused a 45 percent rem ission rate in patients in contrast to the S.S.R.I. rate of 35 percent and theplacebo rate of 25 percent. It was the first tim e one antidepressant was shown to be m ore effective than anyother. Previously, psychiatrists chose antidepressants based on a com bination of guesswork, gut feeling andtailoring a drug’s side effects to a patient’s sym ptom profile. If Effexor was truly m ore effective than S.S.R.I.’s,it would am ount to a revolution in psychiatric practice and a potential windfall for W yeth.
One im pressive aspect of Thase’s presentation was that he was not content to rest on his laurels; rather heraised a series of potential criticism s of his results and then rebutted them convincingly. For exam ple, skepticshad pointed out that Thase was a paid consultant to W yeth and that both of his co-authors were em ployeesof the com pany. Thase responded that he had requested and had received all of the com pany’s data and hadnot cherry-picked from those studies m ost favorable for Effexor. This was a significant point, becausecom panies som etim es withhold negative data from publication in m edical journals. For exam ple, in 2004, was sued b, who was then the New York attorney general, for suppressingdata hinting tha causes thoughts in children. The com pany settled the case and agreed tom ake clinical-trial results public.
Another objection was that while the study was billed as com paring Effexor with S.S.R.I.’s in general, in factm ost of the data com pared Effexor with one specific S.S.R.I.: . Perhaps Effexor was, indeed, m oreeffective than Prozac; this did not necessarily m ean that it was m ore effective than the other S.S.R.I.’s incom m on use. But Thase announced that since the original study, he had analyzed data on Paxil and otherm eds and also found differences in rem ission rates. For his study, Thase chose what was at that tim e an unusual m easure of antidepressant im provem ent:“rem ission,” rather than the m ore standard m easure, “response.” In clinical antidepressant trials, a “response”is defined as a 50 percent im provem ent in depressive sym ptom s, as m easured by the Ham ilton depressionscale. Thus, if a patient enters a study scoring a 24 on the Ham ilton (which would be a m oderate degree ofdepression), he or she would have “responded” if the final score, after treatm ent, was 12 or less. Rem ission, on the other hand, is defined as “com plete” recovery. W hile you m ight think that a patient wouldhave to score a 0 on the Ham ilton to be in rem ission, in fact very few people score that low, no m atter howdeliriously happy they are. Instead, researchers com e up with various cutoff scores for rem ission. Thasechose a cutoff score of 7 or below. In his study, he em phasized the rem ission rates and not the response rates. As I listened to his presentation,I wondered why. W as it because he felt that rem ission was the only really m eaningful outcom e by which tocom pare drugs? Or was it because using rem ission m ade Effexor look m ore im pressive than response did?Thase indirectly addressed this issue in his paper by pointing out that even when rem ission was defined indifferent ways, with different cutoff points, Effexor beat the S.S.R.I.’s every tim e. That struck m e as a prettyconvincing endorsem ent of W yeth’s antidepressant. The next speaker, Norm Sussm an, took the baton from Thase and explored the concept of rem ission in m oredetail. Sussm an’s job was to system atically go through the officially sanctioned “slide deck” — slides providedto us by W yeth, which we were expected to use during our own presentations. If Thase was the riveting academ ic, Sussm an was the engaging populist, translating som e of the drierresearch concepts into term s that our prim ary-care-physician audiences would understand. Sussm an exhortedus not to be satisfied with response and encouraged us to set the bar higher. “Is the patient doing everythingthey were doing before they got depressed?” he asked. “Are they doing it even better? That’s rem ission.” Tofurther persuade us, he highlighted a slide showing that patients who m ade it all the way to rem ission are lesslikely to relapse to another depressive episode than patients who m erely responded. And for all itsm ethodological lim itations, it was a slide that I would becom e well acquainted with, as I would use it over andover again in m y own talks. W hen it cam e to side effects, Effexor’s greatest liability was that it could cause , a side effectnot shared by S.S.R.I.’s. Sussm an showed us som e data from the clinical trials, indicating that at lower doses,about 3 percent of patients taking Effexor had hypertension as com pared with about 2 percent of patientsassigned to a placebo. There was only a 1 percent difference between Effexor and placebo, he com m ented,and pointed out that treating high blood pressure m ight be a sm all price to pay for relief from depression.
It was an accurate reading of the data, and I rem em ber finding it a convincing defense of Effexor’s safety. AsI look back at m y notes now, however, I notice that another way of describing the sam e num bers would havebeen to say that Effexor leads to a 50 percent greater rate of hypertension than a placebo. Fram ed this way,Effexor looks m ore hazardous. And so it went for the rest of the afternoon. W as I swallowing the m essage whole? Certainly not. I knew that this was hardly im partial m edical education,and that we were being fed a m arketing line. But when you are treated like the anointed, wined and dined inManhattan and placed am ong the leaders of the field, you inevitably put som e of your critical faculties on hold.
I was truly im pressed with Effexor’s rem ission num bers, and like any physician, I was hopeful that som ethingnew and different had been introduced to m y quiver of therapeutic options. At the end of the last lecture, we were all handed envelopes as we left the conference room . Inside werechecks for $750. It was tim e to enjoy ourselves in the city. II. The Art and Science of Detailing
Pharm aceutical “detailing” is the term used to describe those sales visits in which drug reps go to doctors’offices to describe the benefits of a specific drug. Once I returned to m y Newburyport office from New York,a couple of voice-m ail m essages from local W yeth reps were already waiting for m e, inviting m e to give som epresentations at local doctors’ offices. I was about to begin m y speaking — and detailing — career in earnest.
How m any doctors speak for drug com panies? W e don’t know for sure, but one recent study indicates thatat least 25 percent of all doctors in the United States receive drug m oney for lecturing to physicians or forhelping to m arket drugs in other ways. This m eant that I was about to join som e 200,000 Am erican physicianswho are being paid by com panies to prom ote their drugs. I felt quite flattered to have been recruited, and Iassum ed that the rep had picked m e because of som e special personal or professional quality. The first talk I gave brought m e back to earth rather quickly. I distinctly rem em ber the awkwardness of walkinginto m y first waiting room . The receptionist slid the glass partition open and asked if I had an appointm ent.
“Actually, I’m here to m eet with the doctor.” “Oh, O.K. And is that a scheduled appointm ent?” A light went on. “Oh, are you part of the drug lunch?” Regardless of how I preferred to think of m yself (an educator, a psychiatrist, a consultant), I was nowclassified as one facet of a lunch helping to pitch a drug, a convincing sidekick to help the sales rep.
Eventually, with an internal wince, I began to introduce m yself as “Dr. Carlat, here for the W yeth lunch.” The drug rep who arranged the lunch was always there, usually an attractive, vivacious wom an with plattersof gourm et sandwiches in tow. Hungry doctors and their staff of nurses and receptionists would filter into thelunch room , grateful for free food.
Once there was a critical m ass (and crucially, once the s arrived), I was given the go-ahead by the W yethreps to start. I dove into m y talk, going through a handout that I created, based on the official slide deck. Idiscussed the im portance of rem ission, the basics of the Thase study showing the advantage of Effexor, howto dose the drug, the side effects, and I added a quick review of the other com m on antidepressants. W hile I still had som e doubts, I continued to be im pressed by the 10 percent advantage in rem ission rates thatEffexor held over S.S.R.I.’s; that advantage seem ed significant enough to overcom e Effexor’s m ore prom inentside effects. Yes, I was highlighting Effexor’s selling points and playing down its disadvantages, and I knewit. But was m y salesm anship going to bring harm to anybody? It seem ed unlikely. The worst case was thatEffexor was no m ore effective than anything else; it certainly was no less effective.
During m y first few talks, I worried a lot about m y perform ance. W as I too boring? Did the doctors see m e assleazy? Did the W yeth reps find m e sufficiently persuasive? But the day after m y talks, I would get a call oran e-m ail m essage from the rep saying that I did a great job, that the doctor was im pressed and that theywanted to use m e m ore. Indeed, I started receiving m ore and m ore invitations from other reps, and I soon hadtalks scheduled every week. I learned later that W yeth and other com panies have speaker-evaluationsystem s. After m y talks, the reps would fill out a questionnaire rating m y perform ance, which quickly becam eavailable to other W yeth reps throughout the area. As the reps becam e com fortable with m e, they began to see m e m ore as a sales colleague. I received faxesbefore talks preparing m e for particular doctors. O ne note inform ed m e that the physician we’d be visiting thatday was a “decile 6 doctor and is not prescribing any Effexor XR, so please tailor accordingly. There is alsoone m ore doc in the practice that we are not fam iliar with.” The term “decile 6” is drug-rep jargon for a doctorwho prescribes a lot of m edications. T he higher the “decile” (in a range from 1 to 10), the higher theprescription volum e, and the m ore potentially lucrative that doctor could be for the com pany. A note from another rep rem inded m e of a scene from “Mission: Im possible.” “Dr. Carlat: Our m ain target, Dr.
, is an internist. He spreads his usage am ong three antidepressants, Paxil, at about 25-30percent each. He is currently using about 6 percent Effexor XR. Our access is very challenging with lunchessix m onths out.” This doctor’s schedule of lunches was filled with reps from other com panies; it would be vitalto m ake our sales visit count.+ Naïve as I was, I found m yself astonished at the level of detail that drug com panies were able to acquire aboutdoctors’ prescribing habits. I asked m y reps about it; they told m e that they received printouts tracking localdoctors’ ery week. The process is called “prescription data-m ining,” in which specializedpharm acy-inform ation com panies (like IMS Health and Verispan) buy prescription data from local pharm acies,repackage it, then sell it to pharm aceutical com panies. This inform ation is then passed on to the drug reps,who use it to tailor their drug-detailing strategies. This m ay include deciding which physicians to aim for, asm y W yeth reps did, but it can help sales in other ways. For exam ple, Shahram Ahari, a form er drug rep forthe m aker of Prozac) who is now a researcher at the University of California at San Francisco’sSchool of Pharm acy, said in an article in The W ashington Post that as a drug rep he would use this data tofind out which doctors were prescribing Prozac’s com petitors, like Effexor. T hen he would play up specificfeatures of Prozac that contrasted favorably with the other drug, like the ease with which patients can get offProzac, as com pared with the hard tim e they can have withdrawing from Effexor. The is also a key player in prescription data-m ining. Pharm acies typicallywill not release doctors’ nam es to the data-m ining com panies, but they will release their Drug Enforcem entAgency num bers. The A.M.A. licenses its file of U.S. physicians, allowing the data-m ining com panies to m atchup num bers to specific physicians. The A.M.A. m akes m illions in inform ation-leasing m oney. Once drug com panies have identified the doctors, they m ust woo them . In the April 2007 issue of the journalPLoS Medicine, Dr. Adriane Fugh-Berm an of G eorgetown team ed up with Ahari (the form er drug rep) todescribe the m yriad techniques drug reps use to establish relationships with physicians, including inviting themto a speaker’s m eeting. These can serve to cem ent a positive a relationship between the rep and the doctor.
This relationship is crucial, they say, since “drug reps increase drug sales by influencing physicians, and theydo so with finely titrated doses of friendship.” III. Uncom fortable M om ents
I gave m any talks over the ensuing several m onths, and I gradually becam e m ore com fortable with theprocess. Each setting was som ewhat different. Som etim es I spoke to a crowded conference room with severalphysicians, nurses and other clinical staff. Other tim es, I sat at a sm all lunch table with only one otherphysician (plus the rep), having what am ounted to a conversation about treating depression. My basic Effexorspiel was sim ilar in the various settings, with the focus on rem ission and the Thase data. Meanwhile, I was keeping up with new developm ents in the research literature related to Effexor, and not allof the news was positive. For exam ple, as m ore data cam e out com paring Effexor with S.S.R.I.’s other thanProzac, the Effexor rem ission advantage becam e slim m er — m ore like 5 percent instead of the originallyreported 10 percent. Statistically, this 5 percent advantage m eant that only one out of 20 patients wouldpotentially do better on Effexor than S.S.R.I.’s — m uch less com pelling than the earlier proportion of one outof 10. I also becam e aware of other critiques of the original Thase m eta-analysis. For exam ple, som e patientsenrolled in the original Effexor studies took S.S.R.I.’s in the past and presum ably had not responded well. Thism eant that the study population m ay have been enriched with patients who were treatm ent-resistant toS.S.R.I.’s, giving Effexor an inherent advantage. I didn’t m ention any of this in m y talks, partly because none of it had been included in official com pany slides,and partly because I was concerned that the reps wouldn’t invite m e to give talks if I divulged any negativeinform ation. But I was beginning to struggle with the ethics of m y silence. One of m y m ost uncom fortable m om ents cam e when I gave a presentation to a large group of psychiatrists.
I was in the m idst of wrapping up m y talk with som e inform ation about Effexor and. Referringto a large study paid for by W yeth, I reported that patients are liable to develop hypertension only if they aretaking Effexor at doses higher than 300 m illigram s per day. “Really?” one psychiatrist in the room said. “I’ve seen hypertension at lower doses in m y patients.” “I suppose it can happen, but it’s rare at doses that are com m only used for depression.” He looked at m e, frowned and shook his head. “That hasn’t been m y experience.” I reached into m y folder where I kept som e of the key Effexor studies in case such questions arose. According to this study of 3,744 patients, the rate of high blood pressure was 2.2 percent in the placebo group,and 2.9 percent in the group of patients who had taken daily doses of Effexor no larger than 300 m illigram s.
Patients taking m ore than 300 m illigram s had a 9 percent risk of hypertension. As I went through the num berswith the doctor, however, I felt unsettled. I started talking faster, a sure sign of nervousness for m e. Driving hom e, I went back over the talk in m y m ind. I knew I had not lied — I had reported the data exactlyas they were reported in the paper. But still, I had spun the results of the study in the m ost positive waypossible, and I had not talked about the lim itations of the data. I had not, for exam ple, m entioned that if youfocused specifically on patients taking between 200 and 300 m illigram s per day, a com m only prescribeddosage range, you found a 3.7 percent incidence of hypertension. W hile this was not a statistically significanthigher rate than the placebo, it still hinted that such m oderate doses could, indeed, cause hypertension. Norhad I m entioned the fact that since the data were derived from placebo-controlled clinical trials, the patientswere probably not representative of the patients seen in m ost real practices. Patients who are very old or who have significant m edical problem s are excluded from such studies. But real-world patients m ay well be athigher risk to develop hypertension on Effexor. + I realized that in m y canned talks, I was blithely m inim izing the hypertension risks, conveniently overlookingthe fact that hypertension is a dangerous condition and not one to be trifled with. W hy, I began to wonder,would anyone prescribe an antidepressant that could cause hypertension when there were m any otheralternatives? And why wasn’t I asking this obvious question out loud during m y talks? I felt rattled. That psychiatrist’s frown stayed with m e — a m ixture of skepticism and contem pt. I wonderedif he saw m e for what I feared I had becom e — a drug rep with an M.D. I began to think that the m oney wasaffecting m y critical judgem ent. I was willing to dance around the truth in order to m ake the drug reps happy.
Receiving $750 checks for chatting with som e doctors during a lunch break was such easy m oney that it leftm e giddy. Like an addiction, it was very hard to give up. There was another problem : one of Effexor’s side effects. Patients who stopped the m edication were callingtheir doctors and reporting sym ptom s like severe and lightheadedness, bizarre electric-shocksensations in their heads, sadness and tearfulness. Som e patients thought they were havingstrokes or nervous breakdowns and were showing up in em ergency room s. Gradually, however, it becam eclear that these were “withdrawal” sym ptom s. These were particularly com m on problem s with Effexor becauseit has a short half-life, a m easure of the tim e it takes the body to m etabolize half of the total am ount of a drugin the bloodstream . Paxil, another short half-life antidepressant, caused sim ilar problem s. At the W yeth m eeting in New York, these withdrawal effects were m entioned in passing, though we wereassured that Effexor withdrawal sym ptom s were uncom m on and could usually be avoided by tapering downthe dose very slowly. But in m y practice, that strategy often did not work, and patients were having a very hardtim e com ing off Effexor in order to start a trial of a different antidepressant.
I wrestled with how to handle this issue in m y Effexor talks, since I believed it was a significant disadvantageof the drug. Psychiatrists frequently have to switch m edications because of side effects or lack ofeffectiveness, and anticipating this potential need to change m edications plays into our initial choice of a drug.
Knowing that Effexor was hard to give up m ade m e think twice about prescribing it in the first place. During m y talks, I found m yself playing both sides of the issue, m aking sure to m ention that withdrawalsym ptom s could be severe but assuring doctors that they could “usually” be avoided. W as I lying? Not really,since there were no solid published data, and indeed som e patients had little problem com ing off Effexor. Butwas I tweaking and pruning the truth in order to stay positive about the product? Definitely. And how did Irationalize this? I convinced m yself that I had told “m ost” of the truth and that the potential negativeconsequences of this sm all truth “gap” were too trivial to worry about. As the m onths went on, I developed m ore and m ore reservations about recom m ending that Effexor be usedas a “first line” drug before trying the S.S.R.I.’s. Not only were the newer com parative data less im pressive,but the studies were short-term , lasting only 6 to 12 weeks. It seem ed entirely possible that if the clinical trialshad been longer — say, six m onths — S.S.R.I.’s would have caught up with Effexor. Effexor was turning outto be an antidepressant that m ight have a very slight effectiveness advantage over S.S.R.I.’s but that causedhigh blood pressure and had prolonged withdrawal sym ptom s. At m y next Lunch and Learn, I m entioned toward the end of m y presentation that data in support of Effexorwere m ainly short-term , and that there was a possibility that S.S.R.I.’s were just as effective. I felt reckless,but I left the office with a restored sense of integrity. Several days later, I was visited by the sam e district m anager who first offered m e the speaking job. Pleasantas always, he said: “My reps told m e that you weren’t as enthusiastic about our product at your last talk. I toldthem that even Dr. Carlat can’t hit a hom e run every tim e. Have you been sick?” At that m om ent, I decided m y career as an industry-sponsored speaker was over. The m anager’s m essagecouldn’t be clearer: I was being paid to enthusiastically endorse their drug. Once I stopped doing that, I wasof little value to them , no m atter how m uch “m edical education” I provided. IV. Life After Drug M oney
A year after starting m y educational talks for drug com panies (I had also given two talks for ForestPharm aceuticals, pushing the antidepressant Lexapro), I quit. I had m ade about $30,000 in supplem entalincom e from these talks, a significant addition to the $140,000 or so I m ade from m y private practice. NowI publish a m edical-education newsletter for psychiatrists that is not financed by the pharm aceutical industryand that tries to critically assess drug research and m arketing claim s. I still see patients, and I still prescribeEffexor. I don’t prescribe it as frequently as I used to, but I have seen m any patients turn their lives aroundbecause they responded to this drug and to nothing else. + In 2002, the drug industry’s trade group adopted voluntary guidelines lim iting som e of the m ore lavish benefitsto doctors. W hile the guidelines still allow all-expenses-paid trips for physicians to attend m eetings at fancyhotels, they no longer pay for spouses to attend the dinners or hand out tickets to m usicals. In an e-m ailm essage, a W yeth spokesm an wrote that W yeth em ployees m ust follow that code and “our own W yethpolicies, which, in som e cases, exceed” the trade group’s code. Looking back on the year I spent speaking for W yeth, I’ve asked m yself if m y work as a com pany speaker ledm e to do bad things. Did I contribute to faulty m edical decision m aking? Did m y advice lead doctors to m akeinappropriate drug choices, and did their patients suffer needlessly? Maybe. I’m sure I persuaded m any physicians to prescribe Effexor, potentially contributing to blood-pressureproblem s and withdrawal sym ptom s. On the other hand, it’s possible that som e of those patients m ight havegained m ore relief from their depression and than they would have if they had been started on anS.S.R.I. Not likely, but possible. I still allow drug reps to visit m y office and give m e their pitches. W hile these visits are short on useful m edicalinform ation, they do allow m e to keep up with trends in drug m arketing. Recently, a rep from cam e into m y office and invited m e to a dinner program on the antipsychotic Abilify. “I think it will be a great program , Dr. Carlat,” he said. “W ould you like to com e?” I glanced at the invitation.
I recognized the nam e of the speaker, a prom inent and widely published psychiatrist flown in from anotherstate. The restaurant was one of the finest in town.
I was tem pted. The wine, the great food, the proxim ity to a fam ous researcher — why not rejoin that innercircle of the select for an evening? But then I flashed tf m yself five years earlier, standing at alectern and clearing m y throat at the beginning of a drug-com pany presentation. I vividly rem em bered m ysensations — the careful m onitoring of what I would say, the calculations of how frank I should be. “No,” I said, as I handed the rep back the invitation. “I don’t think I can m ake it. But thanks anyway.” Daniel Carlat is an assistant clinical professor of psychiatry at Tufts University
School of Medicine and the publisher of The Carlat Psychiatry Report.

Source: http://www.gapacademy.ca/files/NYTimesDrugArticle.pdf

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