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Old 09-05-04, 09:05 AM
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Jane Pauley shares her story: Former Dateline NBC co-host talks @ struggle w/illness

In a new autobiography, Jane Pauley reveals that several years ago she was diagnosed with bipolar disorder. It's a revelation that surprised her fans and colleagues alike. Most at NBC didn't know about her illness or that during a leave from the network, she'd been admitted to a psychiatric clinic. Jane says she decided if only one good thing came out of her experience, it would be the opportunity to raise awareness about bipolar disorder. You can read an excerpt of her new book, "Skywriting: A Life Out of the Blue."

The assumption that the etiologies of DSM-IV disorders are fundamentally related to "chemical imbalances" is challenged. While the chemical imbalance model may eventually be empirically shown to be unequivocally accurate in specific disorders, this is not presently the case for any disorder. The attempt to correct chemical imbalances through medication is at the heart of modern psychiatric treatment, as are evidence-based protocols which follow from the establishment of an accurate diagnosis. There is much to be said for this approach, but the downside is that other medication treatment strategies are rendered illegitimate. Instead of correcting imbalances, it is argued that pharmacological agents may be viewed as inducing particular psychological states which though not specifically related to diagnosis, are nonetheless the basis for the usefulness of the medication. This perspective provides justification for using medications in clinical situations that may not even be DSM-IV defined. To properly use medications in this way, patients must more often be viewed in the complexity usually associated with psychotherapy. A case is made against the widespread use of medications by non-psychiatrists as well as the 15-minute, once-a-month medication visits that have become standard psychiatric practice, both the product of the chemical imbalance model.

Over the last 10-20 years a particularly appealing way of presenting mental illness has been found. Axis I disorders are boldly portrayed as "chemical imbalances" in patient brochures, news articles, and other educational materials. While it is acknowledged that DSM-IV, the officially designated diagnostic manual used in the United States, is currently not based on etiology, it is, for now, an operationally defined diagnostic system based on the clustering of symptoms. The implicit premise of the chemical imbalance perspective is that this will be temporary. The working assumption of many researchers using the "chemical imbalance" model is that certain DSM-IV defined "disorders" are deficient in a particular neurotransmitter in a particular part of the brain that is causally related to the disorder. In the gray area are expansions of the basic illness with so-called spectrum disorders. Presumably, in this case, differences in symptoms are more apparent than real. A genetic or biological link explains the usefulness of certain medications across the entire spectrum of the related disorders.

The attractiveness of this model to patients is undeniable. By removing psychiatric illness from the realm of psychology, it removes blame, especially pejorative implications that weakness of character, poor upbringing, or lack of will are issues in bringing on the illness or combating the symptoms. It places psychiatry firmly under the umbrella of science and modern medicine. This is a crucial element in convincing patients to seek treatment and to be compliant with the treatment plan. In the United States, the chemical imbalance argument has proven to be important in winning legislative support for improved insurance coverage that gives psychiatry parity with other medical conditions. One other byproduct of the chemical imbalance model: its simplicity has led to a great deal of comfort, on the part of physicians other than psychiatrists, to dispense psychotropic medications. Believing that they are operating within the logic of cause and effect, they merely have to focus on the improvement of the symptoms of the disorder in question and watch for side effects from the medication. A majority of psychiatrists also work within these parameters. They typically see patients for med checks and that is all.

There are fundamental crucial problems with this perspective that need to be aired. First and foremost is that, while some day we may accumulate the knowledge to demonstrate the particulars of the chemical imbalance model, no such imbalances have been unequivocally demonstrated for any disorder. We are offered interesting conjectures, educated guesses that are forever shifting as the latest data is accumulated. The continual construction of new hypotheses is how science should proceed. But good science is normally modest. It clearly distinguishes between soft knowledge and what is known. It does not trumpet a few pieces of a jigsaw puzzle that have been brilliantly put in place, as the solution to the entire puzzle. The public (including practitioners) and the media are being misinformed about the state of our knowledge.

It isn't that researchers are unaware of the difficulties of integrating current knowledge with theory. Frustration with the "chemical imbalance" neurotransmitter model has, for instance, led certain authors (e.g. Duman, Henninger, Nestler (1997)) to propose an intracellular hypothesis to explain the effectiveness of various medications. Even more to the point, despite the widespread respectability of the chemical imbalance hypothesis it has all along been met with skepticism in some very important places. Thus, the 1992 edition of The Pharmacological Basis of Therapeutics states flatly regarding the "neurotransmitter hypothesis of mood disorder" that "the data are inconclusive and have not been consistently useful either diagnostically or therapeutically."

I will try to show later in this article that despite the ad nauseam use of the term "expert" to refer to treatment protocols and the like, (which in itself should arouse suspicions that we are dealing with a "Wizard of Oz" phenomenon) adherence to this model in what has become standard psychiatric practice, the once-a-month, 15-minute med check, is not only not "expert" care, but is grossly inadequate care. And, if this is the case, even if one shares a distaste for the hype and psychobabble, "the therapy cures all" excesses that once characterized the worst of psychiatry, the current cursory lip service given in training programs to the role of psychological and social factors in mental illness, is producing psychiatrists unequipped to properly treat patients. That is true even when medications are justifiably the main treatment strategy. Moreover, despite insistence on empirical data, and infatuation with the toys of science, the technological wonders available in modern laboratories, there has not been enough of the most crucial hallmark of "science," rigorous critical thinking about the basic model. What are the most glaring difficulties with the chemical imbalance model?

1) Medications such as the Selective Serotonin Reuptake Inhibitors (SSRIs) are finding usefulness in so many Axis I and Axis II disorders (e.g. OC Disorder, Depression, Panic Disorder, Eating Disorders, phobias of many varieties, Borderline Personality, PTSD, Body Dysmorphic Disorder, Fibromyalgia, in selected cases Intermittent Explosive Disorder, Pathological Gambling, Kleptomania, not to mention OC Personality, Avoidant Personality, Dependent Personality) that to consider all of these forms of misery part of the same biological spectrum is stretching credulity. Occam's razor demands a more parsimonious approach.

2) Medications that work in completely different ways are effective for the same disorder. For example, antidepressants such as desipramine and bupoprion have little serotonin effect yet are just as effective agents for depression as SSRIs. To keep the chemical imbalance hypothesis alive speculations are offered to explain the effectiveness of noradrenergic agents as ultimately influencing serotonin receptors downstream. This is not impossible but it is only a guess. A completely different hypothesis is offered by Petty (1995) who argues that GABAnergic drugs are fundamentally related to mood.

In Obsessive Compulsive Disorder (OCD) similar problems emerge. Originally, the fact that serotonin enhancing drugs were uniquely effective led to a belief that there was a causal connection, but as early as 1991 there was confounding evidence. Thirty mg. of dextroamphetamine was found to ameliorate OCD symptoms (Joffe 1991). Moreover, while I am not advocating this as treatment, I have had patients report to me that intoxicants such as marijuana, alcohol, and cocaine have given them temporary relief from OCD symptoms. Indeed, a recent study has shown that oral morphine is reasonably effective (Franz, 2001). Once again it is possible to speculate that there is a downstream effect on serotonin, but if we use this argument we have come full circle in a tautological trap. The original reason for the serotonin-OCD chemical imbalance model was that serotonergic agents were believed to be unique in their effectiveness.

With so called "mood stabilizers" we are faced with similar difficulties in integrating theory with the facts. There is a murkiness in reasoning which can only be explained by the attractiveness of the idea that somehow a chemical imbalance is being corrected, and hence bipolar disorder is being treated on a fundamental, etiological level. However, the various "mood stabilizers" work through different chemical mechanisms. Thus, valproic acid and gabapentin have been hypothesized to work on GABAdenergic receptors, whereas (for example) the proposed mechanism of action for carbamazepine and lamotrigine is voltage dependent inhibition of Na+ currents. The latest speculations about lithium is that it is affecting G proteins, that it exerts a push/pull effect on the neurotransmitter glutamate. (Dixon And Hokin, 1998: Lenox et al., 1998), or that it alters sodium transport in nerve and muscle cells and effects a shift toward intraneuronal metabolism of catecholamines. (Physician Desk Reference, 1999). Even the definition of what constitutes a mood stabilizer is controversial. (Sobo, 1999). Originally, the idea was that a mood stabilizer had both anti-depressant and anti-manic qualities. When it has so far been difficult to demonstrate anti-depressant effectiveness for the anti-seizure medicines, Sachs (1996) replaced this concept with a new definition, an agent which will "decrease vulnerability to subsequent episodes of mania or depression" and not exacerbate the current episode or maintenance phase of treatment. So gripping is the appeal of the original mood stabilizer concept that despite the lack of double blind evidence for the effectiveness of any anti-seizure medication for bipolar depression, they are, nevertheless, recommended in the APA's expert consensus protocol as a first line treatment for bipolar depression. Indeed, as soon as an agent has been shown to have antimanic properties it is invariably labeled as a "mood stabilizer."

3) With all that is unknown about the chemistry of mental illness, using the chemical imbalance model, researchers are not shy about concluding that a given disorder is "really" something else on the basis of the effectiveness of a medication. Thus Donovan, SJ (as reported by Sherman, C) 1998 proposed that a new diagnosis, "Explosive Mood Disorder" be created and replace Conduct Disorder and Oppositional Defiant Disorder, for "children with irritable mood swings" because Depakote helped his cohort of inner city, out of control, kids. Similarly all kinds of problems with impulse control (called compulsions by laymen) such as overeating, gambling, paraphilias, various patterns of alcohol and drug abuse, and so forth have been labeled Obsessive Compulsive spectrum disorders because SSRIs are sometimes effective. The reason these "compulsions' were originally excluded from OCD was that they revolved around giving in to temptation, over indulgence of a forbidden pleasurable activity. The fact that SSRIs can be useful here should change nothing regarding etiology or nosology.

4)The chemical imbalance model is not an important part of the basic (animal) research being done to test new potential anxiolytics and anti-depressant agents. The chemical imbalance model might or might not stimulate a search for agents that effect given neurotransmitters, but while there is some research on genetically predisposed strains of mice and guinea pigs, who may be wired differently, or chemically different, most research is done on ordinary animals that are environmentally stressed and then relieved of this stress by potentially useful chemical agents. For example, the FST (forced swimming test) tests the ability of drugs to postpone hopelessness in animals forced to swim and swim and swim to remain alive. SSRIs do this. So do noradrenergic agents (which interestingly enough, are more likely to cause the rats to try to climb out of their test environment (Detke 1995)). More pointedly, for the purposes of my argument, rat pups that are isolated from their mother and litter mates produce "ultrasonic sounds" that are indicative of stress. SSRIs reduce these sounds. (Oliver, 1994) Recently, there was excitement that substance P antagonists may be useful psychotropic agents because they were shown to reduce "stress induced vocalizations" in guinea pig pups (once again separated from their moms). A drug successfully screened in this manner will certainly not be presented to patients as a drug that is so good at shutting off distress that it even works to subdue what might be considered the prototypical model of terror, a helpless infant separated from its mother. A patient told he is being given a drug that will kill his reaction to what has been upsetting him will approach that treatment very differently than a patient given a different spin, one told that his medication is treating the chemical imbalance that is causing his ailment. Similarly, primary care physicians and psychiatrists will be far more enamored with the thought that an agent has been tested (and even better, FDA approved) for a specific DSM-IV disorder if the mindset is that the effectiveness is due to fixing faulty synapses, rather than that the patient is being drugged out of his suffering.

I would like to suggest a different approach to explaining how SSRIs affect individuals, and why they are so clinically useful for so many psychiatric conditions. A case can be made that SSRIs are efficacious in conditions as disparate as borderline character, depression, obsessive compulsive disorder, anorexia nervosa, panic disorder, social phobias, and so forth because increasing serotonin has a psychological impact that is nonspecific to the disorders in question. Alcohol will produce inebriation in a person with schizophrenia, obsessive compulsive disorder, depression, or someone with no psychiatric diagnosis. Analogously, SSRIs typically impact individuals in ways that are not specific to diagnosis. What is that effect?

The most frequent description of the effects of SSRIs that I have heard from my patients are "It doesn't matter." or "Don't sweat the small stuff." or "What's the big deal?" It is this "Don't sweat the small stuff" perspective that I believe is SSRIs unique blessing and curse. It means relief from worry, relief from the feeling that something is missing, something needs to be done, something needs to be fixed, "my makeup isn't right, the sky is falling, I won't be able to pay my bills, I'm not smart enough, I won't be able to tolerate the loneliness if I leave my lover" (even if he/she is abusive).

SSRIs supply, if not always happiness, a nice contented feeling that all is well and will be well. They can allow parents to be able to play with their children more, fret less over the details, appreciate what is, actually want to do the proverbial modern mantra, stop and smell the roses. They are the answer to existential angst. Perhaps Sisyphus, if he had only been born in the 90's, could have left that rock alone and had a nice snooze.

On the other side of the equation, I have a psychiatrist colleague who took Prozac to relax and enjoy his vacation. It worked very well. He told me that he tried it at home when he returned. He quickly stopped it when he found himself thinking, "Who cares?" when his patients described their problems.

According to this theory it is the "well whatever" feeling, emotional blunting, that is so useful in the great variety of different syndromes. Thus, for a person with anorexia nervosa to react with "well whatever" after they have gained a pound or two is to get at the heart of the problem. The same can be said for body dysmorphic disorder, a condition in which a person's life is completely distorted by imagined or slight body defects (such as thinning hair, a big nose, and the like). In obsessive-compulsive disorder the ability to treat compulsions and obsessional thoughts in this manner is a godsend. Similarly, a depressed person's preoccupation with the hopelessness of their situation, the gravity of their errors and defects, the inadequacy of their decisions, and so forth will be enormously relieved to regain a less "negative" perspective. In panic disorder, a condition characterized by exquisite sensitivity to body sensations, and a catastrophizing of consequences, (I once had a patient who described a horrible attack of panic because she feared something was going wrong with her vision. Only later, when she removed her glasses did she realize that her dirty eyeglasses had set her off) SSRIs have been found to be effective because the sense of catastrophe leaves. For similar reasons social phobias and bridge phobias and flying phobias often become manageable on SSRIs, as do intermittent explosive disorder which may improve because it is harder to press the patient's button. Alcoholism, pathological gambling, overeating and the like may respond if a sense of frustration has significantly contributed to the pathological behavior. (They may worsen these conditions if a heroic disciplined battle is being waged against temptation, which is then weakened by a "well whatever" letting down of the guard.) SSRIs can help perfectionists ("obsessive compulsive personalities") give themselves a little (or a lot of) slack. They can allow borderline personality disorder patients to cool their heels, to not be tortured, like a wounded lover, when the person, upon whom they have passionately centered their survival, is not reciprocally involved with them. And so we can apply this perspective about SSRIs down a long list of DSM-IV defined disorders that have been empirically found to be treatable by a change in brain chemistry.

This perspective also suggests itself as useful in psychological circumstances where a specific DSM-IV diagnosis is not at issue. Thus, for instance, a not uncommon treatment scenario is teenagers who are having a very rough go of it with their classmates, kids who are picked on precisely because of their vulnerability. The popular students are the ones who are cool; that is, they don't blush easily, are bold with the opposite sex, and so forth. Adolescents often turn to illicit drugs (analogous to adults at cocktail parties), to get rid of their social anxiety. But teenagers are often extremely up front about these issues, meaning they out and out torture the nerds. It is not unusual for adolescents to come to therapy because they feel like misfits and to put it bluntly, the use of SSRIs may be very helpful here to magically assist them in having a thicker skin, which is exactly the quality they needed all along to not get picked on and possibly even have the "cool" to be "popular." How does that differ from drugging oneself out of problems rather than "learning critical skills during the formative years?" Isn't discomfort often a stimulant of growth, (the stutterer who becomes the grand public speaker, the short guy who becomes Napoleonic)? I'm not sure it is different, but that discussion will have to await a different article. The fact is however, that SSRIs are used exactly in this way and a myriad of other analogous ways by clinicians to the tune, according to one estimate, of 65 million people in the United States since their introduction. Right now, when they are found effective, the chemical imbalance perspective leads to the conclusion that the patient must have "really" been depressed, or had a subclinical version of an illness or had a spectrum disorder. I am suggesting we can spare ourselves this pseudo logic and address the more important question raised above. Should we or should we not drug people into subjectively improved states when an officially designated "illness" is not at issue?

On a still more fundamental level the use being made of the DSM-III and IV model of illness is at issue. DSM-II, perhaps out of respect for the underlying psychodynamics believed to be behind patient's symptoms, tended to be loose about how to label patients. What was going on inside was more important. Beginning with DSM-III the decision to cluster symptoms into operational definitions that were consensually agreed upon was a proper step in trying to use scientific models. We were asked to buy into the principle, that regardless of theories about causality, there would be an agreed upon name for the collection of observed symptoms. But it has all too often deteriorated into a Platonic essence model, that is, a belief that there is a "real" version of the illness and actual illnesses are imperfect derivatives. If we truly understood etiology and pathogenesis this approach would be wonderful. It would mean we had arrived at the promised land. But short of this, DSM-IV can actually hinder therapeutic perspectives and treatment approaches.

Let me develop this last point. DSM-IV allows researchers to gather together a group of patients who meet the described criteria for the disorder, try different treatments, and compare the results. Thus, a given percentage of patients with social phobia might be helped by placebo, and if a greater number will be helped by Paxil, or Neurontin, or cognitive behavioral therapy or whatever the treatment in the research design might be, than these treatments can be designated effective if statistical significance is reached. This is a good thing. Evidence-based treatment appeals to the FDA and, more importantly, appeals to common sense. Empirical data is usually far more valuable than theories and controversy that cannot be backed up by a test of the facts.

The main problem with this is that it can lead to conclusions that make no sense whatsoever, when viewed in light of later understanding of what is truly occurring. For the purpose of illustration let us consider heart failure as a model. An important aspect of treatment is to focus on a manifest symptom such as edema, especially pulmonary edema and pleural effusions. The strain on the heart from excessive fluid demands the use of diuretics (which, of course, do not act on the heart at all but on the kidneys). Unencumbered by fluid in the lungs shortness of breath and orthopnea will improve. The treatment addresses pathophysiology without taking etiology into account. The actual diseases that brought about the heart failure are once removed from the focus of treatment. Heart failure might be due to muscle damage from an MI or a viral cardiomyopathy. There might be valvular damage from rheumatic fever, or subacute bacterial endocarditis and so forth. A clinician focusing on presenting symptoms is proceeding rationally because regardless of etiology, when the heart doesn't do its job, when it is not pumping blood efficiently, the final common pathway manifested by the accumulated fluid may be of more immediate concern than the underlying cause of the illness. One hundred years ago congestive heart failure could be described without an understanding of its many causes and that description remains therapeutically relevant today even after we can now better understand underlying causality.

But there is a problem with congestive heart failure as a diagnosis. For argument's sake let us say our knowledge base remained at the turn of the 20th century and atrial fibrillation were causing the heart failure of a given patient. A treatment aimed specifically at the fibrillation would fail miserably when tested in a larger population of patients whose "disorder" had been defined as "congestive heart failure." For example a beta blocker could, in those cases with atrial fibrillation, be the proper treatment for cases of heart failure caused by atrial fibrillation but otherwise this drug might worsen the illness of the other patients in a larger test group of heart failure patients. Viewed from the perspective of the heart failure diagnosis ("disorder"), the few patients it might help might then be described in individual case studies but would probably be dismissed as anecdotal if proponents argued that it should be used as a general treatment for congestive heart failure. Indeed it would be seen as harmful to the treatment of congestive heart failure, even though it was the proper treatment for the subgroup whose heart failure was due to the fibrillation. And let us say the fibrillation were due to hyperthyroidism. Then what? My point is obvious: As reasonable as evidence-based treatment protocols for symptom defined "disorders" might seem to be, they are, in fact, pathetic compared to what is possible when a true understanding of etiology can be used to provide rational care. We are simply not there yet.

Given that DSM-IV does not represent an advanced understanding of the actual causes and pathogenesis of the disorders in question my focus on the psychology of these disorders and the psychology of psychopharmacological agents should have remained and still be a focus of study. Van Praag (1990) in his "Nosological Tunnel Vision in Biological Psychiatry, A Plea for a Functional Psychopathology" made this point a decade ago. His description of the psychological effects of serotonergic and noradrenergic agents may not exactly correspond to my own, but the model is similar. Most psychotropics ameliorate component psychological functions that are misfunctioning rather than "cure" specific syndromes at the etiological level. As noted we use diuretics for congestive heart failure, and, sometimes edema due to liver and kidney disease, not because they are all part of the same disease or "spectrum disorder", but because we are addressing an aspect of the pathophysiology. There is no mystery in the fact that a drug that affects the kidney helps a failing heart.

Or, to use a different parallel, penicillin cures strep throat, pneumococcal pneumonia, gonorrhea, syphilis--all very different diseases, but all caused by bacteria. Clearly SSRIs are helpful in ameliorating a common characteristic of many DSM-IV defined disorders. If they consistently worked as well as penicillin, we might validly consider them to be correcting "the" etiology of the illness, but SSRIs aren't always as effective as we might like. That doesn't mean, however that adding evidence-based augmentation strategies (a second, third, fourth or fifth medication) based on empirical data tabulated for a specific drug and a specific DSM-IV diagnosis will finally fix the elusive chemical imbalance. A feel for what the various drugs do is often far more effective for the skillful clinician.

Thus, it is no mystery that gabapentin or benzodiazepines might ameliorate both agitated depression and social phobia. Anxiety is an important component in both disorders, and targeting this is more relevant than research that exclusively correlates DSM-IV disorder with a given medication. It might be more productive, for example, to study the role of anxiety (or fear!) in schizophrenia, depression, alcoholism, borderline characters, social phobias and so forth and how the relief of anxiety improves symptoms in these illnesses. Interestingly, there was recent soft evidence that SSRIs administered to a group of "at risk" adolescents (for developing schizophrenia), may have had some efficacy in heading off the disease (Cornblatt, 2000). Sticking to the chemical model might lead to all kinds of elaborate chemical pathways to explain this strange finding. But if the model for explaining what leads to psychosis is a different one, if for instance a premorbid period of emotional isolation or intense forbidden conflicts, overwhelmingly intense (possibly "limbic") level cognitively disruptive emotions, and factors such as these play a role in pushing a genetically primed vulnerable person over the edge into psychosis (never to return to normalcy again) then SSRIs would make perfect sense because of their powerful effect in calming (in my model) stormy emotions.

Similarly, using the model of SSRIs giving a "thicker skin," I tried them with two delusional disorder patients (with paranoia) in addition to antipsychotic medications. They were very helpful. Once again my model was the psychological effects of the medications not concern with a particular neurotransmitter. I am confident that if others were using this model they would develop other useful applications for medications that might be helpful.

In this same vein, if drug manufacturers were doing research based on Van Praag's model they might convince the FDA to sanction medications for broader usage rather than force studies verifying effective use for one diagnosis at a time. DSM-IV is doing a disservice if it distracts researchers, clinicians, and journal editors away from its originally carefully defined purposes and toward the chemical imbalance model as the exclusive etiology for psychiatric disorders. It is doing a disservice regarding potential uses of medications if there is practically no discussion of this approach in the literature and little if any discussion in training programs.
Other important implications for treatment

The specificity and empirical nature of the chemical imbalance perspective loans itself better to the brevity of scientific articles. Perhaps, this is part of the reason that it has gained a measure of legitimacy for psychiatry in the world of science. But I don't know of any other way to present the data necessary to illustrate that it has led to poor therapeutics other than through a series of short case illustrations (with commentary) which emphasize the subtleties required to adequately deliver care. Unfortunately this approach is shamelessly "anecdotal". It is in the language of the humanities, the arts, the very opposite of science, the very defect that has plagued psychiatric literature from the very beginning. But there is no other choice if the true acceptable goal, that we share, is trying to gain as accurate a glimpse of the nature of things as we can. If these case illustrations can be viewed by the critical reader as analogous to photographs and pictorial illustrations, than perhaps we can venture into less rigorous territory.
Case 1:

Mrs. L. had originally required 40 mg of Paxil to recover from a postpartum depression. After 12 months on the meds, an incident happened which disturbed her. She was visiting her one year old at his daycare center during her lunchtime when one of the workers began screaming at another infant without picking her up. The next day Mrs. L went shopping during her lunch break. Later that week a coworker became tearful during the course of a conversation with Mrs. L. regarding her own child's daycare center. Only then did Mrs. L. wonder about her decision to go shopping the day after she had witnessed the daycare worker's inappropriate reaction. She wondered if her Paxil had made her indifferent when ordinarily she would have reacted and worried about such a thing.

We decided to taper the dose of medicine to 20 mg. Sure enough on less medicine there was a dramatic change in her perspective about many things. For the first time I learned about the pressures she had been under at the time of her original hospitalization. Mrs. L. had tried to find time to be the powerhouse worker at her job that had brought her so many promotions in the past, an ideal mother for her newborn infant and responsive to her husband's very exacting standards about her housekeeping. Suddenly, without the higher doses of Paxil her fury poured out. She described, in detail, episode after episode in which her husband stood to the side and supplied her with a never ending critique of her adequacy as a mother. The higher doses of medication had muted her responsiveness, allowed his criticism to go in one ear and out the other, but now there would have to be change "or else". Mrs. L. also acknowledged that she had not been doing her job as carefully as in the past and eventually the company would discover her drug induced "what the hell" attitude. At home, she had bounced several checks, something that had never happened before she was on medication.

Therapy now turned to how her life would have to change. She seriously considered stopping her job. She loved being a mother and didn't want to miss out on her son's crucial early years. She demanded changes in her husband (with the threat of divorce). Her new assertiveness had rapidly put him on good behavior even before marriage counseling started. A few times during her sessions she became tearful about her dilemmas. Although we discussed the possibility of returning to higher doses of medication should the need arise, she was not eager to do this. She felt her tears were about real things and did not consider herself depressed. She did not feel hopeless nor helpless. Her sleep was not as restful. She sometimes tossed and turned. But she was okay. We joked that we might go up on the Paxil temporarily if and when she needed a vacation from her stresses. In fact, throughout I was concerned that her greater emotionality might be a prelude to the return of her original symptoms. But our perspective was quite different than an automatic increase of medicine at the first sign of tears. As it happens she did not need to return to higher doses. She did quite well, eventually deciding to work part time. Three months after making that decision she was the happiest she had been in years.

It is noteworthy that when she was reduced to 10mg (at her urging) there was another improvement (depending on perspective). She again noticed dust on her furniture. She noticed that the pictures on her table had been placed haphazardly. She arranged them more aesthetically. She did not feel driven to take better care by the internalized monster described in obsessives by Shapiro in Neurotic Styles, by an unending "I should, I should I should." She took pride in her newly regained "attention to detail." She also regained a degree of empathy for her husband. There certainly was the danger that she was returning to a dynamic of taking care of everyone and everything, of offending no one, a role that she had assigned herself from early on in childhood. This pattern may have played a part in her original postpartum depression as she tried to juggle her responsibilities and became overwhelmed, consequently generating forbidden anger at her newborn. Certainly, her regained empathy for her husband might be the beginning of permission for him to begin carping again but she thought she "would be able to handle that."
Case 2

Mrs. D a computer consultant with a terrible foster home past was successfully treated for depression. She had never felt she was as good as a techie as her 5 male partners. She had a never ending need for reassurance, which was embarrassing to her. Every night on her drive home she tortured herself with the things she felt she had mishandled. On Prozac all of this changed. She acknowledged that she wasn't as good a techie as her partners, but she wasn't bad. More importantly, she realized she was indispensable to her team. She was the only one with sufficient social skills to handle their clients. For the first time in her life she was able to ask questions at conferences without feeling like an idiot. No longer hungry for confirmation she was also able to stop a cycle of love affairs which had led nowhere. On the other hand her comments coming off meds was noteworthy. "I feel like I've been drugged for two years. Now I want to take a look at my checkbook." She also reported behavior that now, off the meds, seemed bizarre. She had bought a puppy that she kept in an unfinished basement. While medicated she had not cleaned up the poop, reacting with "well whatever".

Pomerantz has reported a case of a patient on SSRIs who was completely indifferent to speeding tickets he had gathered while on SSRIs, a reaction that was completely out of character for him. Pomerantz attributed it to "overmedication" and indeed it reacted to a reduction in dosage. I've had patients, successfully treated on SSRIs, report many similar phenomenon. One woman, doing well with a phobia that had crippled her for over 40 years, was struck by her medicated lack of reaction to her only son's diagnosis of testicular cancer. I've seen this same reaction do wonderful things for a patient in despair over her hopeless prognosis. She was able to gather her resources, and replace her terror with courage.
Case 3

Mr. K., a lawyer for a large corporation, was overwhelmingly depressed at home and work. The apparent cause was a difficult supervisor at his job. Almost daily his supervisor would criticize some aspect of his work and Mr. K. would be immobilized for the rest of the day. Sometimes he would stare at the wall in a daze... "my father always called me a complainer...you don't have to love your job; you just have to get it done... I'm a loser ... all those years in law school and for nothing..." Placed on Prozac Mr. K. was quickly fixed. His supervisor would enter his office, make his usual derogatory remarks and nothing would happen. Mr. K. could again get his work done in fine form. There were other benefits. His overweight wife lost 35 pounds. For the first time in years, Mr. K. put down the TV remote control. They began having good conversations, the kind of talks they used to have when their relationship was fresh and engaging. Everything became new. Mr. K. realized that for years he had been going out on Sundays because he was irritated by the tumult of his children at home. On Prozac he found himself playing with his children and having a great time. After ten months on the medication we decided to see how he would do without it. Within a few weeks we were back to square one. His supervisor's remarks were again devastating him and he was a grouch at home. He made a quick recovery once he was placed back on the medication. After 16 months on Prozac Mr. K. found a new job. He loved it. He came off the Prozac. He did just fine. There were only a few peculiarities that he commented on when he got off the medication. Although overall he had worked far more effectively on Prozac, for the first time in his life he found himself ignoring deadlines. Once or twice that had caused difficulties. He bought a Mercedes on the medication. He had always wanted a Mercedes, but off of the medication he considered it a budget buster and foolish.

This case is noteworthy not only because his judgment was altered by the meds but because, at ten months, when we first tried stopping the meds, he would have illustrated the statistics often replicated in studies, of patients who have a recurrence without their meds, thus providing one more piece of evidence confirming the biological basis of his illness. But at 16 months, with the apparent cause of his depression eliminated (his critical supervisor), he did just fine without an SSRI. This doesn't diminish the almost miraculous effectiveness of his original meds, or even that Prozac may very well have helped him gain the initiative to find a new job. However, it does highlight the kind of questions that clinicians should ask themselves about the particulars involved in a specific patient's illness, as opposed to exclusively focusing on the operative factors in a specific diagnosed illness. This perspective is in contrast to the clinical practice guideline issues by the U.S. Department of Health and Human Services which flatly states that where there has been a prior episode(s) of major depression "maintenance of antidepressant medication treatment should be for at least one year"

The fact that on follow up recurrences are found so frequently in unmedicated, as opposed to medicated, patients does not automatically prove biological origin. Generally speaking the issues involved in a depression are deeply woven into a patient's character or the fabric of his life. Miraculous transformations are the stuff of melodrama not reality. One would not expect a change in the original factors that led to depression eight months or nine months into treatment, or even years later unless the patient or his circumstances changed. Hence depression is going to recur off of meds. But it is not impossible for there to be a dramatic change in circumstances. If a patient has gone into a deep depression because of financial hardship after he/she has been fired from a job, chances are that finding a new terrific job will very effectively keep depression from recurring. Winning the lottery works even better. The same can be said for a person who does not have a neurotic pattern of relationships, who has gone into a depression after being rejected by a spouse or lover. Finding a new mate works wonders whether it is three months or two years after medication was begun.
Case 4

Mr. T. was a thirty-year-old man who was very unhappy in his marriage. He had always pictured a family life with two or three children. His wife, a beautiful woman, whom he had originally been smitten by, had never wanted kids. Mr. T had assumed she would change her mind. But now six years into the marriage, he had realized that there would be no change of heart. She was to be the project of the marriage, her vulnerabilities, her needs, the vicissitudes of her emotions. It had gotten old. Over the years, he had noticed his impatience with her grow into indifference and then sarcasm. He came for help when he had become depressed. He couldn't sleep. He couldn't eat. He couldn't concentrate at work.

I'll put the issue in a nutshell. What if the Prozac worked like a charm and completely rid him of his depression? What if Prozac returned bounce to his life and now he found he could, after all, live happily with the status quo? What if 25 years from now, Mr. T. were to wake up and suddenly realize he had wasted his life? He really had wanted children and a family all along. What if he wouldn't allow a doubling of his Prozac dose at that point? A drug had deceived him, cheating him of what had been meant to be. Would Mr. T. have had major depression if he weren't biologically predisposed? We don't know. (Nor do we know with others.) But even if he would not have gotten as depressed without having a biological predisposition, it is wrong to dismiss his marital situation as merely a precipitant. In this case, the depression was an alarm signal. It told the patient that the life he was living would not do.

I had a patient who was having an affair with a married man who was on Prozac. Every time he came off his medications he couldn't stand his marriage for a moment longer and he intended to marry my patient. As soon as he was back on meds his concern switched to his teen-age daughter who needed him to stay. I've had patients find the courage to ignore their fear of loneliness and leave an unsuitable marriage with the help of SSRIs, others find the courage on meds to have what proved to be an unwise affair. I've seen a medicated patient quit his 9-5 job, use his inheritance and "go for it" as a singer. Was this realistic? I suppose it depended on his talent, connections, luck. He had previously been cautious about his inheritance, recognizing that it was a one-time thing and was his only hope for financial security. Only after he also decided he was going to use this money to develop a solar car did I become concerned. He was not manic or hypomanic, but he was definitely feeling better than he had ever felt. When told he would have to stop the Prozac, so that he could review his choices unmedicated, he stopped therapy and went to a different doctor.

{truncated}



read on... http://video.msnbc.com/id/5887567/ or do a search for Jane Pauley
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Old 09-05-04, 09:19 AM
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Shocked that another person is Bipolar..Even Celebs are human like the rest of us but I can relate to it being a relief...I was when I figured out what was going on with me)
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Old 09-05-04, 09:33 AM
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No, I was more shocked that Dateline took the time to do the story and I missed it more than anything else....sorry for the confusion
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Old 09-05-04, 09:40 AM
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No no...it's Ok...cause yeah that is a .Ya rarely see TV do a story on Bipolar. I'm sorry I am such a ditz that my reading comp sucks..Hugs
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Old 09-05-04, 09:54 AM
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hugs hon...
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Old 09-05-04, 09:55 AM
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Hugsssssss I wonder How many More Celb out there have Bipolar as well...Hmmmm
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Old 09-05-04, 09:58 AM
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Give me enough time and I'll find out...lol
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Old 09-05-04, 09:59 AM
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Woohooo Andi Gotta Love Google...hehe!
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Old 09-05-04, 10:05 AM
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Found and Posted in a New thread already...U wont believe this!!!!!!!
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Old 09-05-04, 10:33 AM
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Omg, I saw it...it's wonderful, sweetie.
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Old 09-05-04, 10:38 AM
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Some of them I figured were Bipolar Like Edgar Allen Poe but Abraham Lincoln & Mark Twain???? WOW!!!!!!! I wondered how they figured that when Bipolar wasn't even discovered then I dont think...especially around Napolean's time.
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Old 09-05-04, 10:39 AM
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Talking

Ty shugga Hugsss
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Old 09-11-04, 09:19 AM
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I really liked reading that article, was really enlightening to see someone like her talk about problems with Bi-Polar and what it is like going through the Manic side.

I am Bi-Polar and it is not easy getting by some days, knowing that things are just not right, I sure wish her the best dealing with her Bi-Polar, I like her work, and think she is a great person.
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Old 09-15-04, 08:12 AM
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She is a great person and an inspiration to us all. Shows us that we can all make it no matter how we are feeling.
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Old 09-15-04, 09:38 AM
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I was watching TV yesterday and seen the lady who played on the Terminator with Arnold Swatenager (sp?) she was saying that she is Bi-Polar as well. I like her she is a nice lady that has had interesting parts, like Beauty and the Beast series that she did as well.
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