1 1 NO. 90-CI-06033 JEFFERSON CIRCUIT COURT DIVISION ONE 2 3 4 JOYCE FENTRESS, et al PLAINTIFFS 5 6 VS TRANSCRIPT_OF_THE_PROCEEDINGS __________ __ ___ ___________ 7 8 9 SHEA COMMUNICATIONS, et al DEFENDANTS 10 11 * * * 12 13 14 TUESDAY, OCTOBER 18, 1994 15 VOLUME XVII 16 17 * * * 18 19 20 21 _____________________________________________________________ REPORTER: JULIA K. McBRIDE 22 Coulter, Shay, McBride & Rice 1221 Starks Building 23 455 South Fourth Avenue Louisville, Kentucky 40202 24 (502) 582-1627 FAX: (502) 587-6299 25 2 1 2 I_N_D_E_X _ _ _ _ _ 3 4 WITNESS: DOCTOR_PETER_BREGGIN - Continued _______ ______ _____ _______ 5 Examination by Mr. Smith.................................6 6 7 * * * 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 3 1 2 A_P_P_E_A_R_A_N_C_E_S _ _ _ _ _ _ _ _ _ _ _ 3 4 FOR THE PLAINTIFFS: 5 PAUL L. SMITH Suite 745 6 Campbell Center II 8150 North Central Expressway 7 Dallas, Texas 75206 8 NANCY ZETTLER 1405 West Norwell Lane 9 Schaumburg, Illinois 60193 10 IRVIN D. FOLEY Rubin, Hays & Foley 11 300 South, First Trust Centre Louisville, Kentucky 40202 12 13 FOR THE DEFENDANT: 14 EDWARD H. STOPHER Boehl, Stopher & Graves 15 2300 Providian Center Louisville, Kentucky 40202 16 JOE C. FREEMAN, JR. 17 LAWRENCE J. MYERS Freeman & Hawkins 18 4000 One Peachtree Center 303 Peachtree Street, N.E. 19 Atlanta, Georgia 30308 20 * * * 21 22 23 24 25 4 1 The Transcript of the Proceedings, taken before 2 The Honorable John Potter in the Multipurpose Courtroom, Old 3 Jail Office Building, Louisville, Kentucky, commencing on 4 Tuesday, October 18, 1994, at approximately 9:05 A.M., said 5 proceedings occurred as follows: 6 7 * * * 8 9 SHERIFF CECIL: The jury is now entering. All 10 rise. The Honorable Judge John Potter is now presiding. 11 Court is now in session. You may be seated. 12 JUDGE POTTER: Please be seated. Ladies and 13 gentlemen of the jury, I take it did anybody have any 14 difficulty with staying away from the newspapers and your 15 family and whatnot last night? How about you, Ms. Whitehouse? 16 We're going out of order. 17 JUROR WHITEHOUSE: No problem. 18 JUDGE POTTER: Okay. Let me mention one other 19 thing to you. The documents that you-all are getting, as I 20 told you either yesterday or last week, you will be allowed to 21 keep. The initial thought was that at some point we'd collect 22 them back up from you just because of the bulk, but I realize 23 as you were going along it's helpful for you to mark on them 24 or use them. So as I told you, they will not be taken away 25 from you when you go to the jury room. Because it's getting 5 1 kind of bulky, what we're going to do later today is my 2 clerk -- my secretary is preparing up some boxes, you know, 3 about -- not one of those huge banker's boxes but one -- I 4 hate to say it -- about the size of a case of whiskey. Maybe 5 some of you-all have seen that. And it will be just plain 6 boxes. It will have your name on it and that way you can 7 store older stuff in there if you want to. And your box is 8 your box, just like in kindergarten. Nobody is supposed to 9 mess with your box. 10 Okay. I've also told the attorneys this and so 11 I told them that if they want to, at the beginning of a day, 12 if they look ahead and they say, you know, "Gee, I think it 13 would be good if the jury had a certain exhibit number," 14 they'll tell my sheriff and, of course, you don't have to 15 bring it out. You can keep bringing everything you want. You 16 can bring nothing or bring it all or whatever, but on certain 17 days my sheriff might alert you that a previous exhibit, one 18 of the attorneys thinks it would be helpful if you had it. 19 Okay? Okay. 20 Doctor Breggin, I remind you you're still under 21 oath. 22 Mr. Smith. 23 24 25 6 1 EXAMINATION ___________ 2 3 BY_MR._SMITH:(Cont'd) __ ___ ______ 4 Q. Doctor Breggin, we were in a little rush last 5 night and I may have gone through your past history a little 6 too quick. Let's back up a little bit and let me ask you 7 about some other things that you've done since you've become a 8 medical doctor. All right, sir? 9 JUDGE POTTER: Doctor Breggin, the microphone 10 that comes out in the courtroom is not the one that's there. 11 But you see the little brown one; that's the one that you need 12 to have out in front of you and, also, don't put papers and 13 things over it because it makes noise. 14 Go ahead, Mr. Smith. I didn't mean to 15 interrupt. 16 Q. Once you began your psychiatric practice and 17 started speaking at various seminars and meeting with various 18 professionals on issues of psychiatry and drug treatment in 19 psychiatry, did there come an occasion when you started an 20 entity known as the Center for the Study of Psychiatry? 21 A. Yes, sir. I founded that in the early '70s, the 22 center. 23 Q. Tell the jury about the reason for that and what 24 it is. 25 A. Well, the center is a network of professional 7 1 people. We have about 25 psychiatrists, 30 or 40 2 psychologists, some members of the United States Congress are 3 on the board of directors and actively involved over the 4 years, and it's a network of people who have similar concerns, 5 similar interests to my own philosophy that have kind of 6 collected as a network over the years. We have a newsletter 7 that comes out 4 times a year, and we make occasional reports 8 on issues of concern to us. I've made some reports through 9 the center on Prozac, for example. 10 Q. And is that an organization that is examining 11 topical issues in psychiatry as they come up? 12 A. Yes, very much so. It's a nonprofit 13 organization. It's a tax-exempt organization. It's for 14 educational purposes. 15 Q. Have you served as an adviser on any committees 16 or things of that nature? 17 A. Well, currently I'm a consultant to the research 18 committee of the American Academy of Psychotherapists. I 19 don't think I mentioned the academy. That's a national 20 organization that you have to be elected to for having certain 21 credentials as a psychotherapist and it has psychiatrists 22 psychologists, social workers, anyone who does talking therapy 23 can be elected to the American Academy of Psychotherapists. 24 Q. And what is your status? 25 A. Well, I'm a member, but I'm also a consultant to 8 1 the research committee. 2 Q. Research into new techniques or existing 3 techniques in psychotherapy? 4 A. Well, a whole variety of issues. Right now we 5 have a research project to see the viewpoint of the members on 6 medication treatment and psychotherapy treatment and the 7 balance between the two. That's our current research project. 8 Q. And is that ongoing? 9 A. Yes. It's ongoing. 10 Q. Are you on the editorial boards or are you a 11 peer review editor for any publications or journals, Doctor 12 Breggin? 13 A. Yes. I'm a peer reviewer on several journals. 14 The way a peer review works is that when you submit an article 15 to a journal, if it's a peer review journal, a peer meaning 16 your colleagues or equals, review the article, give opinions 17 on it before it's accepted for publication or rejected for 18 publication. So professionals on various journals make up a 19 panel in a sense or a committee in a sense of reviewers, and I 20 am a reviewer of four, five or six journals. 21 Q. International Journal of Risk and Safety in 22 Medicine? 23 A. Yes, sir. 24 Q. Review of Existential Psychology and Psychiatry? 25 A. Yes, sir. 9 1 Q. What does existential mean? I've seen that a 2 lot. 3 A. Existential means with emphasis on human values 4 and human ethics and the role that values and ethics and 5 ideals play in mental health. 6 Q. The Psychotherapy Patient. What is that? You 7 are on the editorial board of that publication? 8 A. That's a journal that four times a year or so, 9 actually it's a little less frequently, puts out a volume of 10 research on a topic in psychotherapy. For example, sometime 11 in the next year -- it should be coming out soon -- I'll be 12 actually editing one of the volumes, actually the work's been 13 done. And that particular volume will be on working with very 14 disturbed or upset patients and I'll be editing that 15 particular volume. 16 Q. Have you during your practice, since we're 17 talking about disturbed and upset patients -- and certainly 18 Mr. Wesbecker presents a picture of that, does he not, sir? 19 A. At different times he does; at other times he 20 does not. I mean, there's vast periods of time when he does 21 not appear that way. 22 Q. But have you in your experience had one-on-one 23 dealings with patients who are disturbed and upset? 24 A. Yes. It's in a way a specialty of mine to do 25 that. It's just evolved over the years by people coming to me 10 1 and being referred to me for that purpose. That's one of the 2 reasons why I'm doing the special -- editing the special 3 volume on working with disturbed patients, and I give 4 workshops to psychiatrists, psychologists, mental health 5 professionals on how to do that. 6 Q. I see here you're also on the editorial board of 7 The Psychotherapy Patient. What is that, sir? 8 A. I think you just asked me about that one. That 9 was the one I was talking about where I have the volume coming 10 out in the next year. 11 Q. I'm sorry. I need to be checking these off as 12 we go. How about the publication, Changes in International 13 Journal of Psychology and Psychotherapy? 14 A. Yes. Changes is the official journal of the 15 major psychotherapy association in Great Britain, and I am on 16 that board; yes, sir. 17 Q. Reviewing articles that are being submitted by 18 other psychiatrists and psychotherapists for publication in 19 that journal; is that correct? 20 A. Yes. Reviewing. Also discussing in general 21 with the editor about directions the journal might take and 22 contributing to it, as well. 23 Q. I see that you're also involved in the Journal 24 of Mind and Behavior. Can you identify that, sir? 25 A. The Journal of Mind and Behavior is a very 11 1 research-oriented journal and I do the same thing there. I'm 2 on the editorial board and I'm published in it, too. 3 Q. And I see also listed the Journal of Hospital 4 and Community Psychiatry. What is that publication, sir? 5 A. That's a publication of the American Psychiatric 6 Association that deals with -- often with the more disturbed 7 population, and I'm a reviewer. That means occasionally they 8 send me an article to look at and to give an opinion on for 9 publication. 10 Q. In addition to serving as a member of various 11 editorial and peer review positions, have you given 12 professional seminars, lectures and papers, Doctor Breggin? 13 A. Yes, I have. 14 Q. And give us a rundown of some of the places that 15 you've given seminars and presented papers. 16 A. Well, just to organize it, I started with my own 17 home area. I've given talks at the University of Maryland 18 psychiatric center. These are usually -- most of these are 19 seminars where doctors, nurses, psychologists can get 20 professional training credit by having an outside person come 21 in and give a talk and some of them are just invited without 22 that, but often they have that credit training program flavor 23 to them. But I've given that kind of presentation at the 24 University of Maryland psychiatric facility, at two or three 25 local state mental hospitals, Saint Elizabeth's Hospital, very 12 1 famous place, on several occasions. Also given grand rounds 2 at these places; that's where you're invited in as the outside 3 doctor or sometimes the inside doctor to review a case or to 4 review a subject for the doctors present. I've done that at 5 Saint Elizabeth's, at Suburban Hospital. I've given talks at 6 the Walter Reed Army Hospital psychiatric training program. 7 Q. Walter Reed, is that -- 8 A. That's the big army medical facility in 9 Washington. We have a number of those, and just looking at 10 where I talk locally, it's been at most of those places. I've 11 given invited presentations to the National Institutes of 12 Health, National Institute of Mental Health, National 13 Institute of Neurological Disease and Stroke, although that 14 one's gone back a few years. A variety of different medical 15 places. And also many universities. Johns Hopkins, not long 16 ago, the health students invited me to give a talk. Harvard 17 University. A lot of places around the country. 18 Q. How about Georgetown University School of 19 Medicine? 20 A. I've given a number of talks there, as well. I 21 don't want to give the impression that's what I do all the 22 time; that's spread out over a number of years. 23 Q. You're not currently speaking at all of those 24 places and here at once, are you? 25 A. Right. 13 1 Q. Anything else about your education and training 2 on what you've done, Doctor Breggin, in your field of medicine 3 that you think would be helpful to the jury in understanding 4 your credentials and where you're coming from here, sir? 5 A. I think the only thing I can think of off the 6 top of my head is that the kind of presentation I've been 7 giving you is actually quite similar to one that I've given 8 many times to professionals, as well, often using the same 9 simplified language, sometimes more complex. So it is 10 something I'm familiar with doing. The reason why I may be 11 able to appear to do it with relative ease is because I've 12 done it before professional audiences in so many occasions. 13 Q. In connection with reuptake, the serotonin 14 system and specific serotonin reuptake inhibiting? 15 A. Yes. And also a variety of other medications, 16 as well. 17 Q. Have you published medical books, Doctor 18 Breggin? 19 A. Yes, sir. 20 Q. Tell us about -- just give us a list of a few of 21 the books you've published concerning psychiatry or medicine. 22 A. My first two medical books -- well, my first 23 goes back to -- well, actually back to college, really I 24 mentioned to you from the mental hospital program, we did 25 publish a book that was published as a professional book about 14 1 the volunteer program but my -- that was co-authored. In '79 2 I published a book on the brain dysfunction associated with 3 electroshock treatment. Then in 1983, I published a book on 4 psychiatric medication, both of these by Springer Publishing 5 Company, which is a professional publisher, not a lay 6 publisher. 7 Q. In addition, I've published several books which 8 are crossover books, that is, they're intended for both 9 professional audiences and lay audiences. Toxic Psychiatry is 10 an overview of all psychiatric medications from a scientific 11 viewpoint, but also from my own philosophy, which is that they 12 are often overused or more hazardous than we realize. That 13 book is in the general bookstores, but it's also listed as a 14 basic medical textbook at the National Library of Medicine, 15 and it's been a selection of the professional book club. So 16 in recent years, I've written several books like that which 17 are read by the general public but also are in professional 18 book clubs or used in courses, often introductory courses in 19 psychology, for example, or in abnormal behavior at different 20 universities. 21 Q. How about Talking Back to Prozac? 22 A. That's one of my more recent books. That was 23 co-authored with my wife. I actually did the writing, but she 24 has done so much on the maintenance of the files and helping 25 with research. She's not a professional person, but she's 15 1 such an integral part of the whole organization of my life 2 that she's been co-author of the last two books that I've 3 written. And Talking Back to Prozac was definitely written 4 for the general audience, but it too has been a selection now 5 of the Psychotherapy Book Club, which is a professional book 6 club. So, again, as kind of a crossover. I'm trying to write 7 books that are understandable to both professionals and the 8 public. 9 Q. Have you written a book since Talking About 10 Prozac? 11 A. Our most recent book, yes, is about some 12 government programs that we've been critical of called The War 13 Against Children. We're very critical of the overmedication 14 of children. It's a very big concern of mine that too many 15 children in America are being medicated. 16 Q. Well, let's make it clear, Doctor Breggin, you 17 have as a philosophy criticism of the administration of 18 psychiatric drugs generally, and specifically you have some 19 criticisms in connection with fluoxetine hydrochloride, 20 Prozac; is that correct? 21 A. Yeah. I'm trying to separate out my general 22 philosophy from the very specifics of this particular 23 medication. This is the only time I've written a book, one 24 book about one medication, for example. And while, in 25 general, I myself prefer not to treat people with medication, 16 1 I certainly think it's one of the options that people should 2 have. And there's many, many doctors, of course, providing 3 that medication, providing medications, but I do separate out 4 my general feeling about medication from the specific 5 criticisms or analysis here today of Prozac. 6 Q. All right. Now, I think it might be helpful, 7 Doctor Breggin, if we do a quick review of this serotonin 8 system generally and reuptake in this -- where it works in the 9 synaptic cleft specifically. 10 A. All right. 11 Q. And I'm not going to put this on the easel, but 12 just to refer back to this diagram of the brain. 13 A. Should I come on down again? I guess I have to, 14 don't I? Okay. 15 Q. You talked about the serotonin system affecting 16 a number of different areas of the brain; is that right? 17 A. Yes. What I pointed out is that the beginning 18 of the cell, the body of the serotonin cells are clustered in 19 several clusters here that are in the dark color called the 20 raphe nuclei and that that's where it starts, but then the 21 long arm or axon of each individual cell reaches sometimes 22 into the spinal cord a shorter distance into the cerebellum 23 and on up in particular into the centers of the brain that 24 have to do with mental life and emotional life, and they 25 spread throughout and through that, develop elaborate, 17 1 elaborate, elaborate connections, somewhat kind of like the 2 complex roots of a tree with the fibers. You can see -- if 3 you've taken out a tree from a transplant, you see all the 4 branches of the fibers and the same process happens here 5 throughout the brain. It's a system that we don't even begin 6 to understand what it's doing all these many places in the 7 brain. We have very, very little understanding of what it's 8 doing. We know that it can, to some extent, regulate the 9 pituitary functions and therefore the glandular functions of 10 the body. We know it's influencing the areas that have a lot 11 to do with motion and thinking, but it's all in a very general 12 way. We have no specific knowledge that in this part of the 13 brain it affects this nerve and that affects visualization or 14 thinking certain kinds of thoughts or having certain kinds of 15 feelings. We have no such knowledge like that. It's much too 16 widespread. It's the part I used in the analogy. It's part 17 of the orchestra of the brain and we're not able to decipher 18 what particular tunes it's playing, what in particular it's 19 doing. 20 Q. Now, again, is it true that the serotonin system 21 that you've depicted here is only one of dozens of 22 neurotransmitter systems within our brain? 23 A. Yes. And one of about six or eight that has 24 been studied very, very extensively and we're only beginning 25 to get a sense of, we really don't have a -- we don't know how 18 1 our brain relates to thought and to feeling. It's still a 2 very enormous mystery. 3 Now, one very basic theory that's important is 4 that the system has something to do with the regulation of 5 impulses. 6 Q. All right. Is that generally accepted? 7 A. That is generally accepted and was the basis of 8 exploring Prozac, exploring a whole variety of substances that 9 eventually became Prozac. The theory is that this system 10 regulates our control of impulses and, in particular, either 11 violent impulses towards others or toward self, and that this 12 is one package physiologically that violence towards self and 13 others is a single entity that has a lot to do with this 14 system. And one of the reasons that's thought to be so is 15 that the by-products of this system, the by-products which we 16 attempt to measure to see how active the system is, the system 17 appears to be sluggish or slow, not putting out as much waste, 18 as much product in some people who are violent or suicidal or 19 delinquent. And this has been done in studies of children, 20 adults and a variety of animals and, in particular, rhesus 21 monkeys. 22 Q. Are these by-products, is that what has earlier 23 been referred to as metabolites? 24 A. Metabolites, yes. Metabolites. The major 25 metabolite is called 5-hydroxyindoleacetic acid, not something 19 1 you have to remember, and it's measured generally in the 2 spinal fluid, which is a fluid that encases the brain. That's 3 a very rough measure. 4 Q. Why? 5 A. In a way, it's like measuring the exhaust of a 6 car to try to figure out how hard the engine is working and 7 how fast it's going, when there are so many things that can 8 control the car, the catalytic converter, for example. Unlike 9 the car, the brain itself is using up some of the products and 10 they aren't even getting into the spinal fluid, so it's a very 11 indirect measure, but there's been hundreds of articles, 12 suggest -- sometimes supporting the view, sometimes not, but 13 hundreds of articles that tend to suggest that in some people 14 this system is low, sluggish, whatever term to describe that, 15 less active when people are lacking in impulse control. And, 16 again, it's a unitary idea. It's violence and suicide, it's 17 not just one or the other. 18 Q. You know, Doctor -- 19 A. Let me take the other end for a second. The 20 other end is there's a lot of information of what happens when 21 the system is jacked up too high so disruption of its being up 22 or down is likely to cause impulse control problems, and 23 Prozac's overall tendency is to increase the output of the -- 24 the activity of the system, increase the activity of the 25 system, and that is what probably -- and there's general 20 1 agreement on this -- produces the agitation, the 2 hyperactivity, the overstimulation, that irritability, that 3 whole agitation syndrome. And some people think that when the 4 system is hyperactive it tends to produce anxiety and upset 5 and agitation and when it's low it tends to produce 6 depression, but all of this is I would say hypothetical. It's 7 the beginning attempts, very rudimentary attempts to 8 understanding it. We can say the consensus is this system has 9 to do with impulse control. 10 Q. Would that include depression and feelings of 11 lows and high? 12 A. Definitely. 13 Q. All right. Specifically -- let's get this easel 14 because I'm getting tired of holding these charts -- let's 15 look at how Prozac works in connection with, as you say, 16 affecting or jacking up the sluggish system. Now, is that 17 what it was intended to do? 18 A. Yeah. The intention -- the theory is that 19 depressed people may have a sluggish system and so we're going 20 to energize it, energize the system with Prozac. It's not a 21 scientific fact and, in fact, when a person is depressed and 22 comes to the psychiatrist's office, it's not like you're a 23 diabetic and the doctor says, "Hey, your blood sugar is way 24 up, we'll give you some insulin and lower it," it's a 25 hypothesis, a theory, an idea that the depressed person may 21 1 have a low serotonin. It's not something the doctor measures 2 and then gives the right amount of Prozac for. It's just a 3 theory. The doctor gives the Prozac which is digested and 4 then passed through the blood, passed through the liver, 5 eventually getting into the brain in amounts that aren't easy 6 to calculate with no known knowledge whatsoever in that 7 particular patient of what's happening here. So it's not like 8 getting a blood sugar level and adjusting it with insulin. 9 It's a much vaguer, more hypothetical process than that. 10 Q. All right. Why don't you take us through -- and 11 you described it generally yesterday, why don't you take us 12 through again how this -- the anatomy of this, Number One, and 13 then how the -- I've got some better colors, if you'd like. 14 We have black, white, purple. 15 A. We'll try this. This is your basic neuron or 16 nerve cell. Here's its body in biology. You remember I 17 mentioned yesterday it has a nucleus in it and other things in 18 the cell, and this is the long arm or axon and it, too, breaks 19 down into fibers and this is rather infinite. I mean, you get 20 a lot of fibrousness as you look at it under a microscope. It 21 literally looks like the fine hairs on a -- the roots of a 22 tree just spreading everywhere and this is one of the tips, 23 one of the tips of these fibers, and this is the blowup -- 24 this footlike structure is the blowup of this. Is that clear, 25 I hope? This footlike structure, which is one of hundreds or 22 1 more at the end of the cell, is what's blown up here. 2 Now, this particular cell is producing 3 serotonin, which I have labeled as S. And the cell has an 4 impulse, an electrical impulse coming down it and it releases 5 the serotonin into this little tiny, tiny space called the 6 synaptic cleft or synapse, and then the serotonin to be 7 effective has to reach the receivers here on the surface, and 8 they're called receptors. It has to reach and fit. And only 9 serotonin fits. 10 Now, Mr. Smith asked me yesterday if there could 11 be other things in here and I said, well, we don't really -- 12 we think of this synapse as the serotonin synapse, but there 13 could be other things passing through. There could be some 14 other neurotransmitter passing through in this fluid system, 15 there's no walls here. It wouldn't connect. It wouldn't have 16 the effect. But there are no walls here. It's reaching out 17 into the network of the brain. When the serotonin reaches 18 here it fires the nerve impulse of the next nerve. The whole 19 process, serotonergic neurotransmission, the whole process is 20 what Prozac aims to increase on the hypothetical idea that it 21 might be low in some people. 22 Q. And, again, we don't know in any particular 23 individual whether it's high, average or low? 24 A. No. We don't know if it's high, average or low 25 and we don't even know if 50 years from now science will think 23 1 it's a correct theory, because there have been many similar 2 theories over the years that no one now believes is correct. 3 Q. Give us an example of that. That's interesting. 4 A. Well, it was thought for a long time that people 5 with depression had something the matter with their steroidal 6 system, what's called the corticosteroids. And there was a 7 fancy test to see if the brain was reacting right. And it was 8 generally accepted for a long time that this probably played a 9 role in causing depression. It turns out that it's much more 10 an effect of being stressed, so people who have head injury 11 have it, people who are stressed have it physically, people 12 who are depressed sometimes have it. So it hasn't turned out 13 to be a cause, but rather a result of many different kinds of 14 stresses. 15 In medical school, the research that I carried 16 on had to do with the production of adrenaline during anxiety, 17 and one of the questions I researched was did the output of 18 adrenaline at all cause anxiety or was it a result of anxiety 19 and, of course, it's basically a result. If you're anxious 20 you put out adrenaline, it makes you sweat, it makes your 21 pupils get big, so it gets you ready to do something. It 22 scares you, gets you alerted, but it's not the cause. And 23 it's not established that having low 5-hydroxyindoleacetic 24 acid is a cause, although that is a very widely-believed 25 theory right now. But I've been around for 30 years and I've 24 1 seen a lot of widely believed theories. 2 Q. You mean you've been in medical practice for 30 3 years? 4 A. Yes. 5 Q. You're not 30 years old, are you? 6 A. I've been interested in the psychiatric 7 literature since 1954 or '-5, and there's always been a theory 8 and this is the one now. On the other hand, it does seem that 9 this system probably has something to do with impulse control 10 and my own sense of it is the disruption of this system 11 disrupts impulse control, can make it harder to control 12 impulses, that that's very, very possibly true. 13 Now, one of the things that we discussed is how 14 does Prozac work. Prozac does not stimulate this system 15 directly. Fluoxetine does not directly come in and replace 16 the serotonin and stimulate the system; there are drugs that 17 do that but the serotonin does not do that. What serotonin 18 does is block the removal -- and here we see one of the 19 serotonin molecules being taken up to a chemical transporting 20 system made of chemicals and it's transporting the serotonin 21 back in the cell. That process then allows itself to either 22 reuse the serotonin or to break it down into 23 5-hydroxyindoleacetic acid. Now, the theory that the 24 researchers at Lilly developed and worked out was that if they 25 could block the transport system, you'd have more serotonin 25 1 for a longer period of time, even without producing more you'd 2 have more because it wasn't being removed by the shuttle. And 3 I gave you the analogy yesterday of the boxcars. I think of 4 these chain systems that carry stone up a quarry, and imagine 5 that they're competing to see whether the red stones are 6 getting in or whether the Prozac's getting in. And if Prozac 7 is getting into the transport system then there isn't enough 8 room for the serotonin, and that's not too much of an 9 oversimplification. I mean, that's basically what's going on 10 that the Prozac gets into the transport system, uses it and 11 the serotonin stays in here and the measured results -- and 12 this is measured in a variety of ways -- is that in general 13 these nerves start firing more, but it's very complicated 14 abuse; the neuron doesn't like this. This is an intrusion. 15 Q. When you say it's an intrusion, what do you 16 mean? 17 A. The brain was not intended to have Prozac in it. 18 Q. Otherwise, the good Lord would have made Prozac? 19 A. The same with alcohol, the same with many 20 different things that people do with their brains. The brain, 21 in every case just about that we know of, resists a substance 22 coming in, even a natural substance, which Prozac is not, if 23 it's in excess the brain tries to get rid of it. The brain 24 has a process called homeostasis; it's trying to get back to 25 normal. 26 1 Q. Is this controversial? Is this disputed by 2 Lilly? 3 A. I certainly don't think that Lilly could dispute 4 that the brain is trying for homeostasis. What Lilly would 5 dispute, they would say it is good for the brain to have this 6 activity increased; whereas, I would say if the brain thought 7 so it would have done it, but this is an intrusion. So they 8 call it enhancement of neurotransmission because they believe 9 this is a good thing and I view it as a hyperactivity of this 10 system that's unnatural. And the question is does that 11 unnatural hyperactivity sometimes make people feel better? 12 That may be. There are many things that people do that make 13 them feel better by making a system hyperactive. You can do 14 it with other drugs that are more commonly known as 15 stimulants, like amphetamines will make the system hyper. 16 Even make this one a little hyper, not as hyper as Prozac 17 makes it. 18 Q. Why? Why does Prozac cause such sensitivity 19 here? 20 A. Because the drug was so cleverly designed to 21 specifically get at this system. They worked till they got a 22 drug that was pretty specific for this system. Now you'll -- 23 for that reason they call it a selective reuptake blocker or a 24 selective blocker for just this nerve, but it's much more 25 complex than that because once this nerve gets hyperactive 27 1 other nerves react back, so you get reactions in the dopamine 2 systems, you get reactions in the norepinephrine system, and 3 you get reactions in this system as it tries to shut down the 4 hyperactivity. And to try to shut down the hyperactivity it 5 does two things that we know of. I should always put that in. 6 We may find years from now it does one hundred things, but we 7 know of two that it does right now. And Lilly, because 8 they're the lab that works on this, has done some of the 9 research, but it's been done all over the western world and 10 elsewhere in the world. 11 One of the things that happens is that the very 12 first dose -- and this was known by Lilly from the 13 beginning -- the first dose of Prozac, this never shuts down, 14 it stops releasing serotonin. 15 Q. Why? 16 A. Because it has sensed from another feedback 17 mechanism that's not drawing here, there's another feedback 18 mechanism. It senses that there's too much out here. It 19 senses it's not being removed. 20 Q. Do you mean it recognizes the change? 21 A. It recognizes the excess of serotonin. That's 22 indisputable. That's as close as we get to scientific fact in 23 some of what we're talking about. It recognizes there's too 24 much serotonin, so it stops firing. It stops releasing as 25 much serotonin and may even go to a relative almost total 28 1 shutdown for a while. 2 After a time, however, this system just can't 3 hold up and it stops functioning in that manner over a period 4 of a week or two. It begins to gradually stop controlling 5 this nerve. But very quickly, not as sharply and 6 dramatically, but very quickly within days another slower 7 process begins as the nerve again tries to handle what it 8 perceives to be as too much serotonin. And what it does is 9 these receptors begin to disappear. No one knows exactly 10 where they go. No one knows if they're in essence dead or if 11 they've simply turned in a fashion that inactivates them, but 12 they are no longer measurable. They don't exist. And this 13 has been demonstrated on some of -- there are classes of these 14 receptors, some classes but not others. In other words, you 15 might do a chemical study of how much one of the receptor 16 classes is present, you may find 30 to 60 percent of it, 40 17 percent of it is gone, it isn't there anymore. 18 Q. Is that a study you did? 19 A. No. That requires being in a laboratory. These 20 are studies done at Lilly and other places in Canada and North 21 America. 22 Q. All right. 23 A. And these are facts. This is in the factual 24 area that we have a shutdown mechanism here and we have this 25 which is called subsensitivity, it becomes less sensitive. So 29 1 what happens to the patient who takes Prozac is complicated, I 2 think, beyond our ability to predict, really complicated 3 because you have the system doing different things. Now, most 4 measures show that the system is getting more active despite 5 the attempts to shut it down, that Prozac is so powerful that 6 if you measure the activity of these nerves, which you can 7 actually do directly electrically, you can put in a measuring 8 electrode and do it other ways, do it indirectly by what the 9 system is doing, what it's putting out, that this system as a 10 whole is getting hyperactive. And Lilly would call it 11 enhanced. At the same time, we don't know if it's going down 12 in some places, whether some places -- because the brain is so 13 complex -- the compensation is stronger than the Prozac. But 14 the overall effect generally seems to be the hyperactivity 15 production and that's what is responsible, surely responsible 16 for the anxiety, the tension, the insomnia, this whole complex 17 of things that are stimulant in nature. That is produced by 18 this excess of serotonin making this system go. And in the 19 extreme, it produces a degree of stimulation which is 20 psychotic in level, that is, the person loses touch with 21 reality. They're so overstimulated they may think that 22 they're God or may think they're some incredible person, know 23 incredible people. Typically, when someone is that high they 24 may take off their clothes and run outside and try to direct 25 traffic. And that happened on these studies. On just the 30 1 short-term patients four, five weeks or so, this happened in 2 approximately 1 out of 100 people got that high. 3 Q. Why -- if you have this hyperstimulation, why 4 doesn't everybody react the same way every time all the time, 5 Doctor Breggin? Is that a reasonable question? 6 A. Well, it's a reasonable question and it plays 7 some role in this suit because he, this gentleman, Mr. 8 Wesbecker got Prozac twice. One of the questions that's 9 raised is he seemingly got fatigued the first time he took it 10 and then seemingly agitated, I think obviously agitated the 11 second time he took it, in the Doctor's opinion or 12 observations. Well, there's many reasons that can happen. In 13 this case we don't need the complicated reasons because I 14 looked over the chart and it's very simple what happened the 15 first time. It's really simple why he got fatigued. He was 16 toxic on lithium. At the moment that he is experiencing 17 himself as fatigued, the Doctor has discovered he has a serum 18 level of 1.5 milliequivalence of lithium, which is a generally 19 acknowledged toxic level. And the Doctor calls him on the 20 phone, this is in the middle of his taking Prozac the first 21 time. The Doctor calls him on the phone and says, "Your 22 lithium is up, your level is up." He says -- he wonders if he 23 took the test at the wrong time of day. That is, whether he 24 through a complicated -- you're not supposed to have your 25 lithium the morning you take the blood level; you're supposed 31 1 to skip the morning and check the blood level. He asked him 2 did you skip the morning, he wasn't sure because he had such a 3 high level on the test. So the Doctor says cut back on your 4 lithium. 5 Q. And I want you to get into that in some detail 6 later, Doctor Breggin. My question simply was: If you have 7 this definitely, I mean, in every neuron you're going to have 8 by virtue of the intake of Prozac an increase in the serotonin 9 availability or volume in the synaptic cleft, if this is bad, 10 why isn't it bad for everybody? 11 A. There are many reasons why people react 12 differently, why some people feel good and some people feel 13 bad on a drug, and often we don't know the answer. In this 14 case it turned out to be another drug he was taking that was 15 probably making him fatigued, not the Prozac. But if you 16 think about diabetes, which many of us have some familiarity 17 with that, a person is taking a certain number of insulin 18 units a day, one day that produces low blood sugar, another 19 day it's not enough and the blood sugar is too high. So even 20 in a very gross system like the pancreas attempting to control 21 the blood sugar, which is a much more gross system than this, 22 this is like the fine tuning of human life, whereas insulin, 23 animals, everybody shares that kind of a system, they don't 24 have the complexity of this brain system. So even in a system 25 as comparatively rough as the insulin system, the doctor who's 32 1 studying the blood sugar can't always know how much insulin is 2 going to do it on any given day. 3 Q. Even when he can measure it? 4 A. Even when he can measure it. Even when the 5 patient is walking around with insulin testing kits now. You 6 may have friends who before they eat, after they eat are 7 taking a little blood or testing their insulin. They're 8 testing their blood sugar. I took the same amount of insulin 9 today, but it's up. Why would that happen. There are so many 10 reasons. 11 In the case of Prozac it's even more complex 12 than insulin because Prozac is a pill, so it's got to go 13 through the stomach; it's got to be digested; it's got to go 14 in the bloodstream indirectly; it's got to pass through the 15 liver, and what the liver does to it will determine how much 16 of it is put out, and this system, unlike most brain systems, 17 also responds to how much of the building blocks are 18 available. 19 The building block, the serotonin is something 20 you may have heard of because it's a basic amino acid called 21 tryptophan. It's something that you used to be able to buy on 22 the market till there was a bad batch of it in Japan. The 23 amount of the food substance that's available affects 24 production in the system. Usually these systems protect 25 themselves from the vagaries of how much you ate that day, but 33 1 this system is responsive to that. 2 There are just a whole variety of things. Your 3 mood, your attitude will affect your brain, so it's very 4 common for people to react differently one time when they get 5 a psychiatric drug and another time when they get it. And, of 6 course, the second time a person gets it the brain has had 7 experience with it once, so maybe the brain is set differently 8 and waiting differently for the effect of the drug, but it is 9 very, very common for a person to respond differently to 10 insulin, to alcohol, to any substance that affects the brain 11 in the body. But in this case, as I said, we don't have to 12 get that complicated because when I look at the record, he was 13 getting a drug in toxic dose that would make him fatigued at 14 that moment, and that was cut back and we can go into that 15 with the dates and all that later. 16 Q. Do you think there's anything else that's 17 relevant that we need to know about the serotonin system, the 18 synaptic interchange and this reuptake blocking of serotonin 19 by Prozac? 20 A. Well, just to reemphasize, the general idea that 21 it is impulse controlled, that this has something -- I'm sure 22 it does many other things. I've already told you it helps 23 control the pituitary and that when it goes up that it 24 produces anxiety, agitation, mania and those things can be 25 accompanied by violence. We know that mania, agitation can be 34 1 accompanied by violence and sometimes by suicide, and then 2 when it goes down, it's more like depression. That's a 3 general theory. But really at this point I'd say this: 4 Systems involved with impulse control, disrupting it disrupts 5 impulse control. 6 Q. Okay. Let's get into more specifics of what 7 you've done and what you've reviewed. 8 A. Okay. 9 Q. Let me begin, Doctor Breggin, by asking you what 10 you did to -- I assume you have some opinions in this case? 11 A. Yes, sir. 12 Q. What did you do to -- what did you review to 13 formulate your opinions in this case? 14 A. I reviewed masses of materials. I have many, 15 many, many cartons, cartons of materials that I reviewed. One 16 whole batch of a number of cartons and microfiche are 17 materials I obtained from the Food and Drug Administration of 18 the United States, the FDA, and I obtained them directly 19 through something called FOIA, the Freedom of Information Act. 20 It entitles any citizen, you could do this, anyone can do 21 this, to write to the government and say, "I want basic 22 information about the inner workings, paper work of your 23 agency on a particular subject. I want the paper work in this 24 case on the approval process of Prozac." Now, if you wrote 25 them that they might write back and say, "We have hundreds of 35 1 cartons of material on that. What particular do you want on 2 Prozac?" So I would send in individual requests on material 3 on Prozac, and that and the Prozac approval process. And I 4 did that on my own before, actually, I became involved as an 5 expert in this case and then afterward, as well. 6 Then in addition, Mr. Smith had -- and his 7 colleagues had gathered information from the Food and Drug 8 Administration, too, and you shared that with me, although, I 9 think I probably had more volumes of that. In addition, Mr. 10 Smith obtained information from the corporation, from Eli 11 Lilly, cartons and cartons of information, and he sent me 12 large batches of that material, memos, research, letters, all 13 kinds of things surrounding the internal process at Lilly. So 14 I had fairly good coverage of the processes at Lilly during 15 approval of the drug and the processes of the FDA during 16 approval of the drug. 17 In addition, over the years I have gone to 18 conferences sponsored by Lilly in which it has people speaking 19 on the subject of medication and Prozac, and recently I went 20 to what I think is the first FDA full-day training program for 21 physicians and other people to understand -- and industry to 22 understand the postmarketing evaluation of drugs, the 23 evaluation of drugs after they're already approved. I have 24 interviewed a number of FDA officials over the years and 25 former officials as to how the Food and Drug Administration 36 1 works. 2 Q. Okay. You've interviewed FDA officials 3 generally on the approval process, but have you talked with 4 FDA officials specifically in connection with the approval of 5 Prozac, Doctor Breggin? 6 A. Yes. I've spoken with them both generally as to 7 how the FDA works and specifically about the approval process 8 for Prozac. 9 Q. How were you able to do that? We weren't able 10 to talk with or take the depositions of any FDA employees in 11 this case, not a one. It was disallowed by law for us to do 12 that. 13 A. Well, I wasn't involved in the case at that time 14 with you, and I just called people. I said, "Hi, I'm Peter 15 Breggin, I'm a psychiatrist here in Bethesda. You may know 16 about my work generally." I got a general acknowledgment that 17 they either heard my name or at least in one case specifically 18 familiar with things I had done, and then I went in one case 19 and I had extensive interviews with the man who was in charge 20 of the study of Prozac's side effects. His name is Richard 21 Kapit, and he was no longer with the FDA at the time, although 22 he's back there now, he was with another government agency. 23 And he and I sat and talked for a few hours specifically about 24 Prozac. And he was the key person in all of the FDA I wanted 25 to talk to because he wrote the evaluations, the summary 37 1 evaluations of adverse reactions to Prozac. 2 There are two basic reviewers for any drug, one 3 reviewer inside the FDA looks at all of the studies on 4 efficacy, on whether the drug works. Then another reviewer 5 looks at all the studies on what the dangers of the drug are 6 and that was Kapit, and he was very important because he was 7 in basic agreement with me that this drug is like a stimulant. 8 He himself, in fact, in his reports had compared it to 9 amphetamine, the classic amphetamine stimulant and I had 10 already concluded the same. It was very, very good to be able 11 to talk with him about that. I also talked to a couple of his 12 bosses and other people on the telephone. He was the one 13 lengthy face-to-face interview. I just called people, they 14 talked to me. That's almost always been the case. 15 Then I had the depositions of a number of the 16 Lilly employees, so when an attorney would interview the Lilly 17 employee, such as Doctor Heiligenstein or Doctor Beasley, I 18 would then have the opportunity to read, study, what the Lilly 19 employees said. 20 Q. For instance, Doctor Breggin, we've read 21 portions of the deposition of Doctor Fuller, portions of the 22 depositions of Doctor Stark and Doctor Slater. Have you read 23 those same depositions? 24 A. Yes. Doctor Wong. I mean, there was quite a 25 number, and others, as well. 38 1 Q. All right. 2 A. Including the experts. 3 Q. What do you mean, the experts? 4 A. Three or four of the experts. 5 Q. The experts that Lilly designated in this case? 6 A. Lilly designated, yes, and also two experts that 7 you designated. I read one of their depositions, one of the 8 two experts' depositions. 9 Q. Okay. 10 A. Then I read the family member depositions, which 11 are quite large, and skimmed or read various other 12 depositions. Read carefully, in particular, James' deposition 13 because he was one of the few people who actually spent some 14 time -- his son James, who spent some time with him right 15 around when he was getting agitated on Prozac; and I read 16 James Lucas, the friend, I read his deposition carefully; and 17 the diary of his wife, the people who were right there at the 18 moment. 19 Then I had a number of important depositions, 20 several different depositions that Doctor Coleman gave 21 because, again, I wanted to see what did the person who was 22 there and who knew the most and was the most skilled and 23 trained, what did he observe at the time. 24 Then -- I mean, there's so much I literally need 25 notes to keep track of it all. The medical records. I read 39 1 all the medical records that were made available to me and 2 they at least covered his -- the psychiatrists he saw and his 3 three psychiatric hospitalizations and a variety of other 4 materials, and they were the complete records as far as I 5 could tell. Then there was a coroner's inquest. After the 6 death, the coroner got together -- 7 MR. STOPHER: May we approach the bench, Your 8 Honor? 9 (BENCH DISCUSSION) 10 JUDGE POTTER: You-all have to decide who's 11 going to speak for Lilly on this witness. 12 MR. FREEMAN: I will. 13 JUDGE POTTER: All right. Okay. 14 MR. STOPHER: I apologize, Your Honor. 15 JUDGE POTTER: That's all right. It just works 16 better. 17 MR. FREEMAN: We object to this line of 18 testimony in that the Court has previously ruled out anything 19 in connection with the coroner's inquest or anything of that 20 kind, particularly the finding that I anticipate he's going to 21 get into. 22 MR. SMITH: I just was trying to get him to 23 identify what he'd read and, obviously, there's a transcript 24 of that. 25 JUDGE POTTER: As long as he just said he's read 40 1 witness's testimony or whatever, then the objection is 2 overruled. 3 (BENCH DISCUSSION CONCLUDED) 4 Q. All right. You've told us about reading 5 testimony from the coroner's inquest. Anything else you did 6 in connection with reviewing the facts of this case to form 7 opinions? 8 A. Yeah. The coroner's inquest was important 9 because we got -- 10 Q. That's all we want to say about the coroner's 11 inquest. 12 A. Yes, sir. Looked at -- over the years I've 13 looked at the FDA regulations. I went over them a little bit, 14 not for this particular moment, but I've seen them over the 15 years. I've read over the years and for this case a number of 16 the FDA's advisory committee meetings. The FDA has an outside 17 advisory committee of experts that itself is appointed by the 18 FDA, it has no power, the committee, but it makes 19 recommendations to the FDA. It makes a recommendation of 20 whether to approve a drug or not after the information is 21 submitted to it, for example, and I read two of the FDA 22 committee meetings pertinent to Prozac. I reviewed some 23 others out of interest to do some comparisons in my own mind 24 on others that I had in my possession for other medications. 25 Q. Specifically, Doctor Breggin, did you look at 41 1 the September 1991 PDAC committee transcript? 2 A. Yes, I did. 3 Q. All right. Go ahead. I've interrupted you 4 about three times now. 5 A. I read some of the trial testimony, Lilly pieces 6 of the trial testimony here, I think. Did you give me some of 7 that? 8 Q. I think so. 9 A. And that's -- that's the basic materials I went 10 over, and I don't know if I mentioned scientific literature, 11 books, treatises, that's an ongoing process with me. 12 Q. Did you go back specifically and review what you 13 considered all of the pertinent scientific literature in 14 connection with the serotonin system, Prozac, around matters 15 that would be of scientific importance in formulating your 16 opinion in this case? 17 A. Well, I don't think any human being could read 18 all the pertinent literature in a sense because the literature 19 on Prozac and related issues, like impulse control, is huge, 20 but I did review hundreds of articles in the last year, 21 hundreds and hundreds, maybe into the thousands of articles to 22 one degree or another relevant to this issue in the past 23 couple of years. 24 Q. All right. Can you give the jury an estimate of 25 the amount of time you spent studying this case and studying 42 1 Prozac to come to conclusions in this case, Doctor Breggin? 2 A. Well, because of center reports I've been doing 3 and other writings and this case and other -- 4 Q. I'm talking about this case. 5 A. Just this case it is -- oh, it's certainly 6 hundreds, I would guess. 7 Q. Hundreds of hours? 8 A. Must be by now. I don't have a real good count 9 in my head. It's a lot, a lot of hours, a lot, a lot of time. 10 Q. Can you give the jury any estimate of how many 11 documents you reviewed? 12 A. I would say thousands. 13 Q. In connection with this case? 14 A. I would say thousands. 15 Q. Based on the time that you spent reviewing these 16 documents, based on your years of experience as a psychiatrist 17 who sees and treats people and based on your experience as 18 training as a medical doctor and specifically knowledgeable of 19 psychiatry, do you have opinions as to whether or not Prozac 20 caused Joseph Wesbecker to do what he did on September 14th, 21 1989? 22 MR. FREEMAN: Objection, Your Honor. 23 JUDGE POTTER: Let me see you-all again. 24 (BENCH DISCUSSION) 25 MR. FREEMAN: We'd like to be heard in chambers 43 1 and take a break, please. 2 JUDGE POTTER: We'll just take the morning 3 recess a little early. 4 MR. SMITH: I can go on to something else. You 5 know, I can -- 6 JUDGE POTTER: Well, what is it? Let me just 7 get that straight. Because I'd hate to go back and find out 8 it's just a rephrasing of the question. Are we getting to the 9 motion in limine? 10 MR. FREEMAN: The motion in limine and the 11 relevancy and the basis for his opinions, he's clearly in the 12 minority view on all of these issues. 13 JUDGE POTTER: Mr. Smith, knowing that's going 14 to be the objection, is there any other evidence you want to 15 put in before the jury before we take a recess and talk about 16 that? 17 MR. SMITH: I could put in some more stuff. 18 JUDGE POTTER: It's up to you. 19 MR. SMITH: How are you going to rule, Judge. I 20 mean -- 21 JUDGE POTTER: Okay. It's just up to you. Do 22 you want to take the break now? 23 MR. SMITH: That's fine. 24 (BENCH DISCUSSION CONCLUDED) 25 JUDGE POTTER: Ladies and gentlemen, we're going 44 1 to take our morning recess a little early this morning. As 2 I've mentioned to you-all, do not permit anyone to speak to or 3 communicate with you in connection with this trial. Do not 4 discuss it among yourselves and do not form or express any 5 opinions about it, and we're going to take a half an hour. 6 The recess will be a half an hour. 7 (THE FOLLOWING PROCEEDINGS OCCURRED 8 OUTSIDE THE PRESENCE OF THE JURY) 9 JUDGE POTTER: Mr. Freeman, Mr. Stopher, why 10 don't you go ahead and make the motion that you want to make. 11 MR. FREEMAN: We'd like to excuse the witness 12 while we're making the motion. 13 JUDGE POTTER: Wait just a second. It's my 14 understanding, then, that you do not want to elicit any 15 testimony from the witness to support your motion; is that 16 right? 17 MR. FREEMAN: No, sir. We'll rely on the record 18 as it stands. 19 JUDGE POTTER: The record as it stands is his 20 testimony in the courtroom today. Doctor, could I ask you 21 just to wait out front? 22 DOCTOR BREGGIN: Yes, sir. 23 JUDGE POTTER: Okay. Thank you. 24 (DOCTOR BREGGIN LEAVES THE COURTROOM) 25 JUDGE POTTER: Mr. Smith, is there anything you 45 1 want to say before they make their motion? 2 MR. SMITH: Number One, I thought that the 3 Defendants had represented that they were not going to make 4 the motion in order to avoid us reading any deposition 5 testimony, that that was going to be something that was going 6 to be done at a later date. 7 JUDGE POTTER: Okay. What do you say to that, 8 Mr. Freeman? And I did -- I was kind of under the impression 9 that as part of him not reading depositions and putting in his 10 case through cross-examination of some of the live witnesses 11 you were going to get down here, I know there was definitely 12 agreement about the motion for directed verdict. What is your 13 feeling about a motion on Doctor Breggin? 14 MR. FREEMAN: The motion on Doctor Breggin is 15 directed to a number of issues that have nothing whatever to 16 do with him reading additional depositions or otherwise. 17 JUDGE POTTER: Okay. Well, let's see what your 18 motion is and then I'll let Mr. Smith decide whether or not he 19 thinks... 20 MR. FREEMAN: Your Honor, first of all, we'd 21 like to move to prevent this Witness from giving any opinion 22 in this case upon the following grounds, including among the 23 following grounds are the fact that the evidence as it now 24 stands in the case would not support him being able to give 25 any opinion. Now, specifically what I'm talking about is that 46 1 the Witness has talked about medical records. He's talked 2 about FDA documents. He's talked about depositions, he's 3 talked about a number of things. I'm not talking about Lilly 4 employee depositions, but I'm talking about a number of things 5 that he now wishes to summarize and give conclusions about, 6 not with respect to how serotonin specifically works, but to 7 arrive at an opinion on what caused Joe Wesbecker to do what 8 he did on the day in question. Now, to summarize or synopsize 9 matters that are nowhere in the evidence -- for example, the 10 medical records: For example, the FDA information that he 11 claims to have gotten from the FDA by way of microfiche; for 12 example, the documents that he claims he's basing an opinion 13 on as respects the documents that were obtained from Lilly. 14 And to summarize those and to come up with some opinion that 15 these in some way caused this man to do what he did is clearly 16 not permissible. 17 The second part of his testimony is 18 scientifically and under the Daubert decision, in direct 19 conflict with each other. For example, in the first part of 20 his deposition or his testimony, he started talking about what 21 happens when the system gets sluggish, what happens when the 22 neurotransmitter serotonin is sluggish and is not acting in 23 the appropriate way, and then he goes to an analysis of the 24 desensitizing the receptors and what happens then, and then he 25 says in summary all of these things are purely hypothetical, 47 1 they are guesses, and tomorrow the whole premise of what I'm 2 saying may not even be believed by anyone, because we have 3 analyses that have occurred back in the early days as to what 4 happens to cause depression and now we know none of these 5 things in fact ever happened. 6 He also then starts into a debate about what 7 occurs when one takes Prozac, and then he says while some of 8 these things are known by Lilly and based upon Lilly's 9 studies, he doesn't introduce anything to show any Lilly study 10 or any study from anybody whomsoever that support anything. In 11 other words, he's arriving at a conclusion with respect to 12 what happens to the postsynaptic receptors, what happens to 13 the presynaptic production of serotonin. That is all, in his 14 opinion, guess or speculation. 15 There has been no foundation laid in this 16 connection with respect to any of these premises other than a 17 blanket statement made by him without any direct evidence to 18 support the evidence that these matters that he now says are 19 hypothetical are generally accepted by anyone whomsoever. 20 Now, we need to have some basis in the evidence for him to 21 arrive at these opinions that he has earlier stated and we 22 suggest to the Court that by his own testimony they are 23 hypothetical in nature, they are speculative in nature and 24 they do not support him being allowed to give any opinion at 25 this time. I'd like just a brief minute to confer with my two 48 1 counsel. 2 As I did earlier when we came to the bench, Your 3 Honor, both this time and on yesterday, we incorporate in our 4 objections to his testimony all of the matters that we set 5 forth in the motion in limine, which we've done at the bench 6 twice, and now reincorporate in this matter that we're taking 7 up before the Court on causation. 8 JUDGE POTTER: Mr. Smith. 9 MR. SMITH: I think that we've established that 10 the Witness is qualified by virtue of his training and 11 experience and his review of the scientific literature to 12 express opinions in connection with Prozac and in connection 13 with psychiatric medications and in connection with conduct of 14 human beings under the influence of psychiatric medications. 15 I think Doctor Breggin was clear in enunciating what his 16 theory, what is proven, what is unproven and what the 17 scientific literature is in connection with that. 18 I think that what Doctor Breggin has testified 19 to in 89 to 90 percent is uncontroverted from his own 20 testimony concerning serotonin. The problem with Lilly is 21 they don't agree with some of the conclusions reached by 22 Doctor Breggin. That, of course, is specifically addressed by 23 Daubert, which is the controlling case in this situation. And 24 Daubert says if there is a scientific basis for your 25 conclusions, if there is reasonable basis in science to draw 49 1 such a conclusion, it's permissible to make the opinion, 2 regardless of whether or not it's generally accepted within 3 the scientific community. 4 Now, I am prepared to and intend to with this 5 Witness take him through the animal studies, the normal human 6 studies, the clinical trials and the postmarketing experience 7 with this drug to establish scientifically that this drug does 8 produce this particular side-effect profile. I think Doctor 9 Breggin testified to it generally, but he can testify as to it 10 specifically. I intend to and am prepared to take Doctor 11 Breggin through and Doctor Breggin is going to make an 12 analysis of Mr. Wesbecker's psychiatric background and discuss 13 the stressors involved in Mr. Wesbecker and the effects of 14 Prozac scientifically on Mr. Wesbecker generally and 15 specifically. The only problem that Lilly has is that they 16 don't agree with his conclusions. 17 Now, I can back this up and go through that 18 entire analysis. I intend to do it anyway, Your Honor, but I 19 was of the -- under the impression that by virtue of the Court 20 desiring that there be in-person testimony from Lilly 21 witnesses and by virtue of the Court's desire to reduce trial 22 time and to save the jury the boring exercise of us reading a 23 lot of depositions, scientific literature into evidence and 24 depositions into evidence, that this motion would be deferred 25 until the conclusion of not only the plaintiffs' case but the 50 1 defendant's case. 2 JUDGE POTTER: Well, Mr. Freeman, is there 3 anything you want to say before I rule on this point? 4 MR. FREEMAN: Yes. I think the briefs clearly 5 speak to what was held to be in Daubert, and one thing that 6 I'd like to point out in particularly that we're talking about 7 now causation as opposed to anything else. We're talking now 8 about the ability of this man to take this complex situation 9 and scientifically testify that it was caused by Prozac and to 10 be able to support it in the scientific literature as far as 11 predictability, as far as duplicating it and all of the 12 elements that we set forth on Page 17 through 19 of our brief 13 in limine. 14 JUDGE POTTER: In deciding whether or not to let 15 a person testify as to an expert, there are several hoops that 16 a person opposing that witness has to jump through, one, that 17 the witness is qualified as an expert by knowledge, et cetera, 18 and I think that's been done with this gentleman. And the 19 second thing is what can he be allowed to use or rely on in 20 forming his opinion. The Kentucky Rules of Evidence are 21 really very forgiving in that and the fact that he's relying 22 on some things, the depositions, the medical records, a lot of 23 things like that that are not in evidence yet, I don't think 24 prevents him from expressing an opinion on those topics. Mr. 25 Smith did not ask him a magic question you often hear, "Well, 51 1 Doctor, are these the kind of things that a person in your 2 position normally relies on, et cetera, et cetera," whatever 3 it takes to fill in Rule 703P, but I think it's plain that the 4 medical records, the documents, maybe when he's getting down 5 to a conversation with Doctor Kapit, maybe he's getting on the 6 edge there, but I do think that the things upon which he 7 purports to rely are permissible. The -- and I think we get 8 to what you-all call the Daubert problem or whatever it is is 9 whether his opinions rise to the level of scientific knowledge 10 under 702. I think that Kentucky has adopted a rule similar 11 to the federal rule, and that to the extent Kentucky would 12 previously put a harsher test, formerly called I think the 13 Frye test, they would retreat from that and follow the supreme 14 court case of Daubert. 15 People tend to forget Daubert was a plaintiff's 16 case. It was a case where the lower courts, if I remember 17 correctly, had not allowed certain testimony because it wasn't 18 scientifically acceptable enough and the Supreme Court said, 19 "Yes, we're going to permit it." I think in judging Mr. 20 Breggin you have to look at what the other testimony has been 21 and what everybody agrees it is going to be, and when I said 22 going to be I was talking about if it's accepted in a light 23 most favorable to the plaintiffs. As I understand it, they 24 anticipate putting on some testimony, and perhaps already 25 have, that if accepted would say that these statistical 52 1 studies and the behavioral clinical trials and whatnot 2 properly analyzed would indicate that Prozac could cause in 3 people suicide or aggression. I see this gentleman as more or 4 less providing a theoretical framework in which the brain or 5 the chemical could act within a person to produce these 6 results. So even though he can't be very sure about and admit 7 that, you know, some of what he's saying is a hypothesis, it 8 is an explanation for how these things could happen, which Mr. 9 Smith I think intends to show by statistical studies analyzed 10 his way in fact do happen. So I don't think his testimony 11 perhaps has to rise to the level of scientific certainty he 12 would have to have if he were the only witness testifying. 13 So I find that his opinion is scientific 14 knowledge that would assist the trier of fact in understanding 15 this evidence. I think it will be helpful to the jury to have 16 one say -- somebody say yes, we accept Mr. Smith's testimony, 17 the clinical trials show thus. This gentleman's testimony 18 shows a method by which, it may be hypothetical, but as I 19 understand it, it's maybe not more hypothetical than some of 20 the stuff that everybody's accepting in connection with this 21 drug now, his testimony shows how it could have happened. 22 So on the evidence that I've heard so far, I'm 23 going to deny the motion to prevent Doctor Breggin from 24 answering the question: Does he have an opinion as to what 25 caused Mr. Wesbecker, and then go into an explanation of how 53 1 the mechanics of his -- the mechanics of Prozac would operate 2 on a brain to produce that result. So the motion is denied. 3 MR. FREEMAN: While we are out, may I take up 4 one additional matter, please? 5 JUDGE POTTER: Uh-huh. 6 MR. FREEMAN: As you know, we approached the 7 bench earlier about the coroner's inquest. Mr. Smith conceded 8 graciously, as always, to your rulings and instructed the 9 Witness not to go any further. 10 JUDGE POTTER: Just chat with him over the 11 break. 12 MR. FREEMAN: The only other thing I wanted to 13 take up was the proposition that this Witness should not be 14 allowed to go into the content of one-way conversation with 15 any person whomsoever or otherwise. He can testify what he 16 did in response to some of these things, but he can't go in 17 and synopsize certainly what Kapit or any of the other people 18 he talked to at the FDA had to do with this particular 19 conversation. 20 JUDGE POTTER: What's the fellow's name at FDA? 21 MS. ZETTLER: K-A-P-I-T. 22 JUDGE POTTER: K-A-P-I-T. Okay. I take it 23 Doctor Kapit, is he going to be part of what we'll hear the 24 rest of today or not? 25 MR. SMITH: Not a large part. Doctor Breggin 54 1 talked with him on a couple of occasions concerning the 2 warning labels that were proposed and discussions that were 3 had with the FDA. Certainly Lilly's been talking with the FDA 4 since 1978 about this drug. Are they saying that we can't 5 talk -- our expert can't testify concerning what the FDA said 6 to them. You know, the problem is, Lilly gets to talk to 7 them, but we can't even take their depositions. 8 JUDGE POTTER: Well -- 9 MR. SMITH: Doctor Thompson testified many times 10 the FDA says we're the best; the FDA says this; the FDA says 11 this. It's certainly not going to be the cornerstone. 12 JUDGE POTTER: I can see where certain things 13 that he heard from -- if he identifies Mr. Kapit correctly and 14 talks about his position, I should think he would be able to 15 rely on some information that Mr. Kapit gave him. I can think 16 of an awful lot of information that Mr. Kapit might have given 17 him that he couldn't rely on, so I really don't know what to 18 do other than say, Mr. Freeman, you just need to be quick on 19 your feet and if he starts to talk about Mr. Kapit in some way 20 that you think is inappropriate, make an objection and I'll 21 rule on it. 22 But, Mr. Smith, I do think if it gets down to 23 "Mr. Kapit told me his opinion was thus and so," or "Mr. Kapit 24 felt it was a stimulant," or what did he call it? 25 MR. FREEMAN: Yes, sir. A stimulant. 55 55 1 JUDGE POTTER: I think maybe he's probably 2 crossed over there. Before he gets there I don't know when he 3 crosses the line but, I mean, this is his opinion, he needs to 4 base it on stuff he's read and stuff in this record and 5 whatnot, and not what Mr. Kapit told him about what he thinks 6 it is. 7 MR. SMITH: Those conversations certainly aren't 8 the cornerstone of our case, Your Honor. 9 JUDGE POTTER: I didn't think they were, but if 10 they're even a little piece, why don't you see if we can get 11 him to leave it out of his opinion. Why don't we take ten 12 more minutes and then we'll come back. 13 (RECESS) 14 JUDGE POTTER: Doctor Breggin, I remind you 15 you're still under oath. 16 Mr. Smith. 17 Q. Doctor Breggin, I'll repeat my last question. 18 Based on the thousands of pages of material that you reviewed, 19 the hundreds of hours that you've spent in reviewing this 20 case, based on your training and experience, do you have an 21 opinion as to the cause of Joseph Wesbecker's conduct on 22 September 14th, 1989? 23 A. I do. 24 Q. What is that opinion, sir? 25 A. That Prozac was a substantial factor, a cause, 56 1 in the events of that date in the production of violence, in 2 the production of suicide, and that it would not have happened 3 without Prozac. 4 Q. All right. Let's back up, then, Doctor Breggin, 5 and carefully tell us the basis in detail for that opinion 6 that you're giving here. Prozac is a drug; Joseph Wesbecker 7 was a human being. How did you start to come to the opinion 8 that this drug caused this human being to conduct himself in 9 such an unusual, tragic way? 10 A. Before I became aware of this case, I had 11 already realized that the drug has a stimulant profile, that 12 it produces agitation, that it can produce this manic kind of 13 behavior in the extreme and paranoid behavior. I was hearing 14 in the workshops that I gave around the country story after 15 story of patients becoming violent, becoming suicidal -- 16 MR. FREEMAN: Objection, Judge. 17 JUDGE POTTER: Objection is overruled. 18 A. -- of patients becoming violent, becoming 19 suicidal in a very compulsive, unusually unexpected violent 20 manner, and I began to have the opportunity to see some of the 21 case material to interview some of the people and then again 22 to look more intensely into the question, first, is this a 23 stimulant drug, and can it produce these behaviors. 24 And what I'd like to do in some detail, because 25 this is such an important question, in some detail to take you 57 1 through some of the materials I've looked at confirming these 2 opinions. And I want to apologize for using memory prompters 3 because there's just so much, and I'm going to try to make it 4 pithy, but I want to get the material to you. I'd like to 5 start with animal studies. 6 Q. All right. These animals studies, who conducted 7 these animal studies, Doctor Breggin? 8 A. The studies that I'm going to describe were 9 conducted by Lilly I believe almost entirely. I'll check as I 10 go through. 11 Q. All right. Tell the jury about the animal 12 studies that you have reviewed. 13 A. Well, first of all, it's important to test a 14 drug on an animal and on a variety of animals because it gives 15 us a sense, a direction of its effect on people, at least it 16 may. Now, human beings are so much more complex, not only in 17 their brain but in their human experience that gets encoded 18 into the person. We're so much more complex that you just 19 can't go from animal to human on an issue like this, but you 20 can get a direction. Because animals are so much more rigid 21 and limited than human beings, you might get to see the 22 direction better in higher doses than are given to human 23 beings because you get to see the extreme effect on the 24 animal, and it may give you a warning, a signal about human 25 beings. And there were many signals that this drug had a 58 1 particular behavioral effect. 2 Lilly did not study the drug for behavior in 3 large animals. We don't have, as far as I know, at least, any 4 studies by Eli Lilly specifically to look at -- during the 5 drug approval period to look at what a monkey -- how a monkey 6 would respond, for example. What we have instead is to make 7 inferences when they were trying to study something other than 8 behavior. They didn't specifically look at the behaviors of 9 large animals but only of rats and mice, which makes it very 10 hard to extrapolate. 11 Q. Would these have been the same things as the 12 toxicology studies that have been described earlier, Doctor 13 Breggin? 14 A. Well, some are toxicology. Let me start with 15 1978. In 1978, from the Lilly Research Labs, Doctors Slater, 16 Jones and Moore published an article, and I'll read you the 17 paragraph that they wrote describing their findings, their 18 summary paragraph. During the course of these experiments -- 19 these were on cats -- "During the course of these experiments, 20 two unexpected findings were encountered. The present authors 21 are at a loss to explain why cats receiving fluoxetine for 22 several days began to hiss and growl and why this behavior 23 decreased with continued treatment." They go on to say -- 24 this is continuous -- "The subjects who received fluoxetine in 25 Phase 1 clinical trial..." -- that's the very earliest trial. 59 1 Phase 1 is where you're not doing anything very scientific; 2 you're just seeing, to start with, is this drug safe in 3 people. They say people in the Phase 1 clinical trial, and 4 they refer to an unpublished paper so we can't check, have not 5 described any change in blood nor have observed, noted any 6 change in affect. In other words, what they're saying, we 7 have this finding in cats, we don't understand it because 8 people aren't responding this way. We shall find, in fact, 9 people were responding this way in the earliest Lilly trials 10 right -- in the development of the animal research. 11 Another source of information is a report from a 12 man named Brophy, who was a project leader at Lilly, and he's 13 talking now about dogs getting very high doses of the drug. 14 "A total of six dogs, two males and four females from the 15 high-dose group were removed from treatment for periods of 16 1 to 17 days due to severe occurrences of either aggressive 17 behavior, ataxia or anorexia." Now, this is important because 18 anorexia is a part of a stimulant syndrome and aggressivity is 19 a part of a stimulant syndrome. Ataxia simply means imbalance 20 from being toxic on the drug. That could have happened 21 probably on large doses of many different drugs. 22 In addition, according to this report, one of 23 the dogs in the toxic study who died of -- purposely, you 24 know, they were testing the toxic dose. One of the dogs 25 showed, quote, marked aggressive behavior. Technician bit 60 1 attempting dosing. There was also tremor that was anorexia in 2 these animals. This is very early on. This particular memo 3 is from 1981. 4 Q. Doctor, couldn't that behavior in the cats and 5 the dogs -- it said in the article itself that these animals 6 were on large doses. Couldn't the aggression there be 7 attributed simply to the fact that this was large doses? 8 A. Well, no. This is a very specific effect. The 9 doses in the cat findings were not toxic, only the dog study 10 is a toxic level, as far as I recall. I'd have to check the 11 details, but, no. Because if you were giving a drug, for 12 example, that had sedative effects or tranquilizing effects in 13 large doses the dogs would be flaked out, the cats would be 14 flaked out, they would be docile. This is true for a whole 15 variety of medications. But instead, these dogs are getting 16 hyper, the animals as a group are getting hyper and 17 aggressive. So you're seeing another trend, you're getting a 18 signal this looks like a stimulant with the specific dangers 19 associated with amphetamines or PCP or other stimulants. 20 Violent behavior. 21 This study is confirmed in a depo by Doctor 22 Fuller, the highest ranking scientist, who said that 6 of 20 23 dogs in the high-dose study group became aggressive, to his 24 knowledge. It's Page 368 of his deposition. 25 Q. Is that statistically significant, 6 out of 20 61 1 dogs becoming stimulated? 2 A. Well, it certainly looks at -- I'm not a 3 statistician, but it certainly looks like a very significant 4 figure, and I think they thought it was significant. It's a 5 signal. It's a trend. The trend continues in every class of 6 animal. 7 Q. Continue, Doctor Breggin. 8 A. Even earlier with smaller animals in 1974, rats 9 given nonlethal doses developed pronounced hyperirritability. 10 I've worked with rats. That probably means, you know, people 11 start to get wary of these rats, irritable, and some of it 12 disappeared from the rats. 13 Then mice. Now, this is from a report in 1986, 14 but I believe it's on an earlier study, and the report is part 15 of the material Lilly had submitted to FDA, and it says of the 16 mice: "The significant effects were essentially limited to 17 the high-dose group and consisted of mortality, 15 percent, 18 persistent hyperactivity, decreased body weight, and then a 19 variety of other mobile chemical and not-relevant-to-us 20 findings. 21 So, again, we have these two findings, either 22 aggressivity or hyperactivity, and body weight loss, the very 23 amphetamine-like response. And in another source, a 24 pharmacological review that was a part of the approval 25 process, it said that hyperactivity is seen in 11 mice in 62 1 toxic studies and this particular group of mice died. 2 So we have here in the earliest studies, 3 signals; as far as I know, none of these studies were followed 4 up. I don't know. I didn't find anywhere in these volumes of 5 pages anybody saying let's do this again, let's try it on 6 chimpanzees, let's see what's going on here. We're getting 7 hyperactivity, we're getting irritability, we're getting 8 aggression, we're even getting bit on at least one occasion. 9 The early human studies also give these flags, contrary to 10 what Doctor Slater published. 11 Q. Now, if you see, in your opinion, Doctor 12 Breggin, this type of behavior in your early animal studies, 13 should that be taken into account in any way in designing or 14 analyzing the clinical trials to where you're going to be 15 giving the drugs to humans? 16 A. Yes. 17 Q. All right. Can you explain that, why and how? 18 A. Well, your signal is that we're getting 19 hyperactivity, aggressivity and weight loss. We may have a 20 classic stimulant. With the dangers of a classic stimulant, 21 let's design very early studies. First of all, let's not give 22 it to people, let's start with some animal studies that are 23 more sophisticated than that. The other thing is to begin to 24 think of the early human studies in terms of setting up really 25 an in-depth examination in terms of whether people are getting 63 1 more irritable, getting more agitated, how they respond to 2 you. They're not likely to get, on the average, grossly 3 violent. That may only happen 1 in 100 times, but that's a 4 catastrophe; 1 in 1,000 is a catastrophe; just once is a 5 catastrophe. So you want to look at whether this is a 6 possibility with special tests, with in-depth evaluations. 7 Q. Go ahead, Doctor Breggin. 8 A. The material we have on the very earliest 9 studies from Lilly comes again from their own researchers, 10 from their memos. And here we go back to July 1979, a memo by 11 the chief scientist at Lilly, Ray Fuller, and he's talking 12 about an open-label study. An open-label study is where 13 everybody knows who's getting the drug, you're just beginning. 14 It's not like you're doing a real controlled study and you 15 don't know who is getting what, but giving some patients 16 fluoxetine and seeing what happens. 17 And here's what Doctor Fuller wrote and 18 confirmed in his deposition: "Some patients have converted 19 from severe depression to agitation within a few days." Some 20 patients. Right away, flagging just like the animal studies. 21 I'll continue with the quote uninterrupted. "In one case the 22 agitation was marked and the patient had to be taken off drug. 23 In future studies, the use of benzodiazepines to control 24 agitation would be or was -- I can't quite read that -- will 25 be permitted." 64 1 So very early on they have a catastrophe, 2 serious agitation, they get worried and they start to think 3 we'll combine the drug with a sedative right away. Now, this 4 has enormous implications. I'm not sure if this is the point 5 to get into it, but it has enormous implications. 6 I mean, sedatives are addictive. If the drug is 7 going to be approved is it going to be approved as a drug plus 8 a sedative; that's what they're suggesting. A drug plus a 9 sedative is addictive. You've got a whole other series of 10 problems involved here if from the beginning you're saying 11 this drug is in effect so stimulating as to cause agitation. 12 And, remember, agitation includes irritability. It's the 13 beginning of aggressivity. Then, I mean, there's something 14 very special going on early. 15 Another early memo found in August '79, that one 16 doctor who tried Prozac on just two patients that were still 17 doing this open study, we'll try it, we'll see what happens. 18 He tries it on two patients, one person gets very suicidal and 19 gets a thought disorder, begins to look schizophrenic and has 20 to be put on a neuroleptic antipsychotic medication, and they 21 conclude, well, maybe this person was already schizoaffective, 22 the same diagnosis -- schizophrenic, same diagnosis, 23 schizoaffective as Mr. Wesbecker. So they're getting another 24 signal here that maybe something happens to people with this 25 drug. And the other person they said was just a simple 65 1 failure. 2 Q. Doctor Breggin, is that taken from Doctor 3 Slater's notes and memos and depositions in connection with 4 his experience with Doctor Gosenfeld, I believe, in California 5 somewhere? We have that in evidence. 6 A. I don't know, sir. I don't recall what the 7 source was of this, other than it's a direct quote on 8 August 21st, 1979. So perhaps you could make that connection, 9 but I can't. 10 Q. I think we have that in evidence, Doctor 11 Breggin. 12 MR. FREEMAN: Object to the comment, Your Honor. 13 14 JUDGE POTTER: Okay. Overruled. 15 A. The -- I explained to you earlier who Richard 16 Kapit is, a psychiatrist, a doctor, a published author, and 17 the chief medical officer at the FDA for the specific purpose 18 of writing the safety reviews of Prozac. And I want to take 19 you through his safety reviews. 20 And we start with a very early Phase 2 report. 21 We're out of the Phase 1, now we're into Phase 2, and in Phase 22 2 you begin to do a somewhat larger number of patients. You 23 may do some controlled studies; you may not. You've kind of 24 moved from "Here's a drug, how did you do" to "Let's look a 25 little more carefully, a little more systematically to see if 66 1 we should proceed to the very expensive and more risky 2 increase in numbers to the final approval process. And what 3 Kapit wrote in March '86 was that there were five, quote, 4 serious clinical events in the first 77 patients. Now, first 5 of all, note that he does not report among these first 77 6 patients the stuff that we read about. It doesn't somehow 7 make it into that list of 77 patients given to the FDA. 8 Q. Did you check that to confirm that, Doctor 9 Breggin? 10 A. Well, yes; he's very specific. He says that 11 there was a -- out of the 77 patients there were a number of 12 problems and there were two particular ones, a paranoid 13 psychosis and a manic psychosis, and this is very relevant to 14 the Wesbecker issues because Mr. Wesbecker very well may have 15 had a drug-induced paranoid psychosis, a delusion about things 16 being done to him at his workplace that enrages him and makes 17 him want to take an action. That would be a classic paranoid 18 psychosis in this case, and in the cases here very likely drug 19 induced. Now, out of these 77 patients we have two people 20 with such severe reactions, again, a serious signal. One 21 could raise the issue that it just happened to happen with 22 these upset people and this happened to happen, well, this is 23 certainly a very strong warning signal. 24 Meanwhile, the issue of patients getting 25 agitated was getting more and more documented. Doctor Slater 67 1 authorized the use of diazepam specifically to reduce 2 agitation in patients in the early studies. That's on Page 3 364 of his deposition, and he admits that the drug could cause 4 agitation and that tranquilizers were given for it, and that 5 others, that not himself, were mentioning excessive 6 stimulation and agitation from this drug, and that's on Page 7 379. And he's not sure if that's been reported. He said -- I 8 think he was implying to the FDA. 9 Now, by the time they began to do the protocols 10 for Phase 3, let me explain that to you. We now go into the 11 third phase of FDA testing and this is where they try to do 12 the more elegant scientific studies. These studies have vast 13 limitations that we can talk about later, but they're an 14 attempt to make it scientific. And how do you make it 15 scientific? You make it scientific by not letting the 16 patients or the doctors or the raters or anyone know who is 17 getting what drug. So, in fact, all the pills look alike. 18 You may give a placebo or sugar pill that has no effect, 19 Prozac, you may give another class of antidepressant and 20 compare them and they all look alike and they're given in the 21 same schedule, so you can't tell supposedly who's getting 22 what. Now in fact doctors can usually tell. We'll go into 23 that later, but they can often tell, at least, because the 24 drugs have such different effects, they know if a patient is 25 getting sleepy or agitated from the drug. 68 1 But the important thing is these are the studies 2 that are going to be the more scientifically based used for 3 approval and from the start in two protocols, one of which 4 became a key protocol approval, Protocol 19. It was written 5 in that if the patient got agitated you could give them a 6 sedative drug, one of these literally quite-addictive sedative 7 drugs. Protocol 19 and 22 specifically says -- and this is a 8 specific protocol that was written by Lilly. The FDA or the 9 investigators out in the field don't write the protocol; this 10 is Lilly writing the protocol. Quote, if a patient complains 11 of agitation the dose of study drug should be reduced and the 12 patient may receive a benzodiazepine at the investigator's 13 discretion. 14 Q. What's wrong with that, Doctor Breggin? These 15 people might have been agitated or anxious to start with or 16 they might have even had treatment, emergent anxiety or 17 agitation. What's wrong with helping these people with some 18 type of sedative or sleeping pill? 19 A. Well, there's two things about it, one, just 20 simply the information it gives us. The information it gives 21 us is that they expected the drug was doing it. The drug 22 should be reduced, so they're clearly saying to the clinical 23 investigators if you see agitation cut back on the drug. They 24 never put it in the label. The average psychiatrist didn't 25 know this when it came out that the study was based on looking 69 1 for agitation, cutting back on the drug because it was the 2 cause and then adding a sedative. So that's one of the things 3 the information gives us, but it did not get out to the 4 medical profession at all and had to be learned over time. As 5 one of Lilly's experts said, "We learned over time that you 6 had to be careful about the drug dose, you had to add 7 sedatives." 8 The use, by the way, here of sedation, they 9 don't mean a sleeping pill at night. They don't mean like the 10 Restoril that Mr. Wesbecker got at night, which is a sleeping 11 pill. That's called a hypnotic. That's a short-acting, it 12 gives you a good night's sleep, doesn't affect you in the 13 morning very much and not at all during the day, hopefully. 14 They're talking about a regular regimen of giving drugs, 15 medications during the day to control -- that's what's meant 16 to control anxiety. It's not a sleeping pill, it's very 17 different than the treatment of Mr. Wesbecker. But there are 18 so many other problems with doing this. Basically what 19 they're saying is we are testing a combination drug without 20 telling the public that what got approved wasn't Prozac but 21 Prozac often in combination with the addictive sedatives to 22 control agitation. This was very important. 23 Now, in one of the studies that was used for -- 24 now, as I said, 19 was one of the protocols used for approval; 25 27, they were only allowed to give sleeping pills and yet they 70 1 ended up giving a big percentage of patients daytime 2 tranquilization anyway. We don't know exactly the percentage, 3 it's not fully clear, but the data was not produced. 4 Q. Are you saying, Doctor Breggin, that even though 5 the protocol only allowed sleeping pills, that in fact what 6 occurred was that investigators did indeed administer 7 sedatives during the day for agitation and anxiety? 8 A. Yes. They not only did that, but when Lilly 9 examined later their data they couldn't prove the drug helped 10 people if they took out the patients who had the sedatives. 11 The only way the drug looked good and was statistically 12 effective was when they kept the patients on the tranquilizing 13 or sedating drugs. 14 Q. All right. Continue. 15 A. Now, none of this was lost on Richard Kapit, 16 the -- again, the man doing the main analysis at the FDA. He 17 said from very early on in 1985, when he addressed the PDAC, 18 the committee that approves Prozac or doesn't approve it, he 19 said that the drug's most common side effects or effects, but 20 he said side effects were, quote, anxiet