FREDRIC SCHIFFER, M.D.
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OF TWO MINDS
scientific papers with some full text articles



WHAT ARE THE CAUSES OF ANXIETY, DEPRESSION, PSYCHOSIS, AND/OR ADDICTION?

     When you push any of these buttons (anxiety, depression, psychosis, or addiction) you will arrive at this same page-- because it is my belief that they are each variants of the same problem as I feel are all (or certainly in my view) most psychological problems.  I want to stress that these are my views, and they may be at odds with some of my colleague (as well as allied with others).  Since this is my page, I’ll offer my opinions.  But, I only have opinions; no one has a monopoly on the truth.  I believe my opinions to be true (at least I do today), but that doesn’t make them true.  You can read my views if you like and consider them.

     It is my view that abuse causes the great majority of psychological problems.  By abuse I use a very wide definition which includes neglect and rejection, even perceived neglect or rejection, and, of course, I include more severe forms of abuse such as severe neglect, harsh chronic rejections, as well as a large catalog of mental, physical and sexual abuses.  There is no question that the human being perpetrates much harm and abuse.  The human being can be splendid and he can be horrific, just look at your newspaper, and see how many people in this world are trying to ethnically cleanse, dominate, rob, betray, murder, and/or subvert some one or some people.

     I believe that when abuse is greater than a person’s capacity to bear the situation, emotional problems develop.  Because children are the least able to protect themselves and have the least capacity to bear, they are the most vulnerable members of our species, and they are often harmed by the people who are trying (or not trying very hard) to care for them, their parents.  It is for this reason that almost all the people I see in my practice come to discover that they were exposed to some distressing life situations as children and that their symptoms usually come from their failed attempts to cope with those situations.

     As parents, we all have some limits and foibles, but we do have a responsibility to try our best to correct or limit them.  Children, especially as they get older, have more ways of trying to protect themselves.  Some children are more creative and more effective than others.  Some situations defy coping.  As I discuss further in the section below, I believe we do not really know the relative importance of genetics in this area, but it is my personal belief that all or almost all of us are quite fragile ultimately, and even if our genetics play a role along with our environment and their interactions (as they must to some extent), still in the wrong situation we all can fail.

     Anxiety is a biological property of the human being.  It is evoked by perceived danger, and is best relieved by the removal of the threat or correction of the perceived threat (if the perception is mistaken).  All human beings experience anxiety.  It is normal and it is helpful.  It makes us more vigilant and spurs us on to attend to the threat.  However, when the threat is not able to be met, not able to be adequately addressed, it causes continued and usually increasing degrees of anxiety to the point that the anxiety is apt to become destructive as it interferes with the person’s comfort and functioning.  When anxiety becomes too severe, it interferes with our thinking and tends to mentally paralyze us.  If it continues unabated, it leads to panic.  Intense anxiety and/or panic, themselves, are destructive and evoke further anxiety and/or panic.

     The best way to deal with anxiety or panic is to eliminate the threat and achieve safety.  If the anxiety emanates from a past severely threatening situation (which may or may not be remembered or appreciated as the source, even if remembered) which is now resolved in reality but not in some place in the brain or mind, then the correction of the anxiety involves the correction of the inaccurate perceptions of danger.  We’ll discuss briefly how to do that in the next section on treatment.

     I see depression as much the same as anxiety, that is as a human emotion, but this time evoked not just by a sense of threat, but further by a sense of defeat, a sense that the battle has been lost.  We often feel depressed after a loved one has died because death is a defeat against which we have no recourse, except to grieve, to try to bear it.  Like anxiety depression too interferes with functioning, and when it severely impairs functioning, it tends to promote an even greater sense of defeat.

     In the DSM, the official diagnostic manual (which I will blast in a moment), psychiatrists have gone to great lengths to differentiate between anxiety and depression syndromes or disorders, but in reality they almost always occur together.  This is because if we are defeated we are very likely to be threatened and when chronically threatened, often defeated.

     A person suffering anxiety and/or depression then must try to achieve safety.  Sometimes through cleverness, perseverance, courage and other virtues we are able to do so, but often in spite of our best efforts we fail to achieve the safety we seek.  Sometimes we get some help, perhaps from a therapist, a relative, a peer, or a teacher, and that alliance can aid our quest for safety.  Sometimes we make wise choices; sometimes out of nothing more than dumb luck or out of seeing and taking a passing opportunity, we discover a way to true safety.  For example, a child from a dysfunctional family may discover school and studying and promote the support of teachers and peers as well as gain the personal power and pleasure that intellectual pursuits can offer.  This discovery may lead the child to eventual safety.  But, another child may not make that discovery, and in fact, may find no constructive solution to his predicament, a predicament he usually doesn’t appreciate as harmful.  This child may experiment with his mind and discover fantasy and withdraw into an inner world.  I believe (and I think I stand in a minority with this belief) that such children may become prone to perfect such withdrawal from the world to the point that they learn how to leave reality and enter their own inner world.  When pursued too far, I believe this may be the ground work for a psychosis, a sustained period of unrealistic thinking and chaotic feeling.  Drug abuse serves a similar purpose, that of helping a person escape a life situation which is perceived to be intolerable.  Like psychosis, drug abuse does not achieve safety, and actually leads to greater danger, more tendencies toward anxiety and depression, more dysfunction, and greater needs to escape further into psychosis, drug abuse or both.  Notice too that both psychosis and drug abuse are almost never without profound depression and profound anxiety.  And this is why in my view, the vigorous efforts of many of my colleagues to try to separate these states into distinct, unrelated conditions, is misguided.

     I include here a section from my book, OF TWO MINDS, which my editor wisely deleted.  It doesn’t belong in the book, but I think it goes nicely here.


 Within the psychiatric profession there is no question that depression has become a biological disease, often compared with pneumonia.

 "It may be useful to compare the pneumonias and the depressions. Both disorders are diagnosed on the basis of clinical data, and both are treated more effectively using information gleaned from clinical tests. In the case of pneumonias, the physician makes a diagnosis on the basis of the history and physical examination (including a chest X-ray). After the diagnosis is made, sputum cultures are obtained to aid in determining the specific type of pneumonia that the patient may have and the specific antibiotic or other forms of treatment that may be most effective, irrespective of why the pneumonia developed. Similarly, in the case of depressions, the physician diagnoses depression on the basis of the clinical history and findings on physical and mental status examinations. Having made a diagnosis of depression, a physician can then use specialized clinical laboratory tests to obtain further information to assist in determining the type of depression the patient may have and the forms of treatment most likely to be effective in the care of that patient."(1)

 Do I have a problem with that?  Yes.  Nowhere in this scientific approach is the patient's life experience, past or present, considered.  This omission is called malpractice.  And unfortunately, this practice has become the standard treatment in just about all psychiatric hospitals throughout the country and even the world.

 As I described in Chapter 3, when I was a resident in psychiatry in 1973, psychodynamic psychotherapy was well regarded and practiced.  When the biological wards came into existence around that same time, I witnessed that depending on which ward a patient was assigned to, his treatment would be dramatically different.  If he went to a so called "dynamic" ward, he received the type of care I was administering.  If he were assigned to a "biological" ward, his treatment consisted of a diagnostic interview (a symptom check list) to ascertain his correct biological diagnosis, and he was then treated with the appropriated medication.  The patient's life history was now irrelevant, for the problem was in his genes and his chemical imbalances.  Good mothers were no longer to be blamed.  And, of course, psychotherapy was irrelevant also for only a fool would talk to chemicals.

 As the years passed more and more wards became biological.  If a patient were thought to be depressed he was sent automatically to the "depression" unit which unfortunately was already converted to a biological unit.  These patients did receive a superficial, supportive psychotherapy from therapists unskilled in dynamic psychotherapy.

 Well, do I mean to say I don't believe in psychotropic medications?  No, I don't believe in them.  I simply use them.  I do not practice the religion of biological psychiatry, but I do prescribe medications when I feel they may be helpful.  My gripe with biological psychiatry is not that it uses medications, it is not that it attempts to discover who will benefit from which medication, and it is not that it seeks to understand the biology of depression.  I too am fascinated with the biology of depression, and study it.  My gripe is that modern biological psychiatry has discarded its inheritance of psychological knowledge, and that disposal is tragic for those who need to be helped with depression.

 Has this science succeeded in discovering the chemical imbalances which cause depression, and has it like the Galileo's telescope corrected the misconceptions of the dynamic psychiatrists who preceded them?  Not at all.  Yes, we know that there are many more chemicals and receptors than we thought before.  And now we know that a number of hormones are intertwined with the neurochemicals.  But, we still are no closer to knowing if ordinary clinical depressions are ever caused as a primary brain disease.  Certainly, strokes or other brain injuries can cause depression.  And certainly, imbibing alcohol and other chemicals can cause depression.  In fact, the biological revolution began with two important observations.  Reserpine a drug given for high blood pressure, which blocks noradrenalin, often caused depression in patients as a side effect, and amitriptyline a drug which among other things tends to increase norepinephrine, was found to relieve depression in some depressed patients.  These two observations led to the hypothesis that a low level of norepinephrine causes depression, and that theory was bantered around for decades until it was finally discredited by the biological psychiatrists themselves.  They learned that depression doesn't correlate with noreprineprhine levels, and that the real picture is too complicated to be deciphered at this time.

 Certainly, depression, as a state of mental defeatedness, will change brain chemistry as must any change in mental state.  The psychopharmacologist do have a cadre of blood tests for depression, but none has yet been reliable or clinically useful.  I still outdatedly think it is easer to simply ask the patient if he's depressed.

 And what about genetics?  Hasn't it been established that depression is a genetic illness?  And doesn't that prove a biochemical, organic cause for depression?  Well, yes, if depression were shown to be inherited like Huntington's Disease, a clearly inheritable neurologic disorder with psychiatric manifestations, it would, like Huntington's Disease be a biological illness.  If I were referred a patient suffering Huntington's Disease, I would not attempt to do in depth psychotherapy.  I might like the biological psychiatrists offer some superficial, supportive therapy to try to help him adjust to the physical loss of his mental capacities, but I wouldn't hunt for past abuses and their mental consequences.

 But, depression after decades of study has been definitively shown to be not inheritable like Huntington's Disease.  Are there any inheritable features of depression as is popularly believed?  Lets look at what a biologically minded geneticist concluded in a recent review of the field published in the major comprehensive textbook of psychiatry.

 In a field plagued by complexity of expression and lack of valid definitions of discrete disorders, coupled with the little progress in uncovering the cause of psychiatric disorders, the application of molecular biological approaches has provided a renewed opportunity for researchers to identify markers for psychiatric disorders. Such markers may serve as vulnerability or disease indicators with which to circumvent the exclusive reliance on clinical signs and symptoms to diagnose psychiatric illness. However, the initial enthusiasm engendered by the potential yield of these methods has diminished after five years of inconsistent and disappointing results involving labor-intensive and costly research.

 But, let's not just take the word of an expert, let's examine the evidence for ourselves.  First of all, there has been no research on the inheritability of ordinary, every day depressions.  Research has been conducted on patients with Major Depression, which is a very profound depression often requiring hospitalization.  For Major Depression the evidence does not suggest much in the way of inheritability.  For instance, when identical twins (with identical genes) were compared to fraternal (non-identical) twins (with different genes as in any pair of siblings) in regard to depression, there was little difference between the two types of twins.  One study involving over 1000 twins showed that if one identical twin was depressed then 48% of the time so was the other.  If one fraternal twin was depressed then so was the other 42% of the time.  I don't think there's a big difference between 48 and 42%.  If major depression were inherited you would expect a large difference between the two types of twins.

 Geneticists often use this type of twin study in which the similarities between identical twins are compared with those between fraternal twins.  These studies have certain problems inherent in them.  For instance, identical twins probably have more similar environments than fraternal twins; they get dressed identically and are constantly mistaken for one another, and so one might find differences between the groups on the basis of environmental as well as genetic factors.  I have always regarded these studies with caution, and the finding in one such study, that identical twins both with heart disease differed substantially in their smoking habits, demonstrating that cigarettes do not pose a risk for heart disease, gives me further confidence in my caution.

 Better twin studies are obtained by examining identical twins who were adopted and reared apart, but I know of no such studies.  There are 2 studies of adopted children who were not twins.  The first study looked at how many biological parents of 56 depressed, adopted children living separately were also depressed.  They found that 5 of the biological parents suffered depression, in contrast to 3 of the adoptive parents.  This study suggests that depression is not inherited.

 The second adoptive study looked at 8 depressed biological parents and found that 38% of their adopted away children suffered depression.  Of 43 biological parents who were not depressed only 9% of their adopted away children suffered depression.  Though 38% is much larger than 9%, because there were only 8 depressed parents, the results could be due to chance alone since they did not pass the mustard of statistical analysis.  These authors did report that known environmental factors were very important in inducing the depressions in these children.  I think this study leaves open the possibility that inheritable factors are important in depression, but it certainly proves nothing of the sort.

 Another serious test of hereditability would be to see if we could find the actual genes which cause depression.  This has not happened.  The next best thing would be to see if known inheritable traits such as eye color or blood type could be consistently associated with depression.  Such known inherited traits are referred to as "genetic markers," meaning that if an association between a known trait such as eye color and depression can be established then eye color would become a genetic marker for depression.  Over the last few decades a plethora of studies have attempted to find such genetic markers for depression.  On many occasions such genetic markers have been found, but, in each case so far, the findings were not confirmed by repeated study, and to dated no accepted genetic markers for depression have been discovered.

 There is considerable evidence reported by the biological psychiatrists for the hereditability for manic psychoses which often alternate with depression in the so called manic depressive or bipolar illness, but I think this is a long way from the typical clinical depression.  But, even for bipolar illness, the data could use continued examination, especially since clinically according to biological psychiatrists about a fourth of patients with a diagnosis of Major Depression are reclassified as Manic Depressive.

 I remember in 1987 being very impressed when Dan Rather announced on the CBS Evening News that a group of scientists essentially located the gene for manic depressive illness by finding that it was linked to a specific known gene on a specific chromosome.  I found this incredible since it contradicted all I had observed about psychiatric illnesses, even manic depressive illness.

 Over time nine different attempts by different groups of scientists were made to replicate these amazing findings, but none could.  The group which originally announced the findings, two years later retracted them.  To the best of my knowledge the retraction was not announced by Dan Rather on national television.

 So the aim of the biological psychiatrists is to be able to specifically determine not only that the person is depressed but also the specific sub-type of depression.  For instance the patient might have a bipolar or a unipolar depression, which could be sub-divided into major depressive episodes, with or without psychotic features, with or without melancholia, atypical depression, dysthymia, or depression not otherwise specified, just to list the most prominent categories.

 But in the real world these divisions melt into each other and cannot really be distinguished.  For example, one of the clearest divisions should be between a Major Depressive Disorder and a Dysthymic Disorder which is considered a relatively mild, though more chronic condition.  The official diagnostic manuel DSM-IV very seriously lists the criteria.  To have this condition one must have 5 or more of the 9 symptoms listed in category "A."  These include: 1. depressed mood, 2. diminished interest, 3. weight change (loss or gain), 4. insomnia or hypersomnia (over sleeping), 5. agitation or motor retardation (lack of movement), 6. fatigue, 7. feelings of worthlessness or guilt, 8. diminished concentration, and 9. thoughts of death.  Interestingly, to have a Dysthymic Disorder you must have 2 or more of the following 6 symptoms: 1. poor appetite or overeating, 2. insomnia or hypersomnia, 3. fatigue, 4. low self-esteem, 5. poor concentration, 6. feelings of hopelessness.

 Not surprisingly, there is a great deal of overlap between these disorders, but there is a partial solution to that problem.  If a person has dysthymia but then develops a major depression, then he is categorized as having a "double depression."

 After the correct diagnosis is made, then the correct specific treatment is given.  For Major Depression, the first line of treatment is Prozac.  For Dysthymic Disorder the first line of specific treatment is Prozac.  If you have an Atypical Depression you can use an MAO inhibitor, but that has death due to a stroke from an induced hypertensive crisis as possible side effect, so most clinicians use Prozac as an alternative.

 Of course in place of Prozac the doctor can choose Zoloft, Paxil, Serzone, Effexor, Elavil, Sinequan, Trazodone, or Wellbutrin, just to name a few, since they are each found to be as effective as any other.  If these don't work the doctor may add lithium or thyroid hormone, and if that doesn't work, electroconvulsive therapy is likely to be recommended.  I have not yet had to make that recommendation.  And for the profoundly unresponsive depression, there is psychosurgery, which reportedly gets positive results a good percentage of the time,.  I have not yet seen such profoundly unresoponsive patients, myself.  I suppose their caretakers know to refer them only to psychiatrists who specialize in such difficult cases.

 Fortuantely, Prozac is often effective.  According to psychopharmacologist William Appleton Prozac is partially effective about in about 70% of patients with Major Depression.  Appleton admits that about 40% of patients getting sugar pills have the same partial improvement.  He reports that only about 28% get an excellent response.  A comparison sugar pill got the same excellent result in 18% of the patients.  Since Prozac is very expensive, it may be that the sugar pill is more cost effective, but this analysis has yet to be carried out.

 I might add that Appleton's figures are a bit more optomistic than a number of actual studies.  For instance, in a major review of multi-center studies, Prozac had a partial improvement in 63% compared with 38% for the placebo group.  The average decrease in the symptom score was 40% for Prozac and 29% for Placebo.  These results, I think, are a testiment to the honesty and courage of the biological psychiatrists and their sponsoring pharmaceutical companies who went ahead and published these data.  The authors, however, did announce that their evidence supported the superiority of Prozac over Placebo, and they were correct 40 is 11 more than 29.  I suppose that if the New England Patriots had beaten the Packers in the Super Bowl, 40 to 29, it would have been a tremendous victory.  But, then again if the Patriots had beaten the Green Bay Placebos, I might not be as impressed.

 Further, I see a number of methodological problems with these outcome studies.  For instance, all of studies which evaluate antidepressants are based on the Hamilton Rating Scale for depression.  The difficulty is that this scale consists of only 17 to 21 simple questions, scored by a psychopharmacologist.  Sample questions are, on a scale of 0 to 4, how much does the rater find the patient has 1. Depressed Mood, 2. Guilt, 3. Suicide[al thoughts], 10. Anxiety.  A partial improvement is arbitrarily regarded as a 50% reduction in the score which can still leave the patient quite symptomatic.  A remission is a rating of 7 or less.

 My personal experience with such rating scales came when I evaluated my treatment of a group of cocaine addicts begining with their admission to McLean and continued for a year or two afterward.  I had the impression that each had had a successful treatment, but according to the scrutiny of the rating scales given at admission and at two years follow-up, there was only a meager improvement.  This, of course, was surprising because the patients' lives were in complete disarray upon admission, for why else would they go into an inpatient substance abuse program, and they were all off cocaine and doing apparently well in their lives when the rating scales were repeated.  When I would ask why they didn't score significantly better, I would get answers like, "Well, now I have a morgage." or "Yeah, but my wife complains too much."

 So it is entirely possible that Prozac is much more effective than is scientifically demonstrated.  But, then again it could be less, or it could be the same.  Upon these rating scales lies the multibillion dollar pharmaceutical/antidepressant industry.  And upon them also lies the acusation that psychotherapists have been remiss in not depending upon them to demonstrate their efficacy.

 It is my belief that the biological psychiatrists did not come to power on the basis of their intellectual arguments or the force of their scientific findings or the prowess of their therapeutic interventions.  They have come to dominate our mental health care because they could argue louder and their jargon and reams of data impressed the congress and the public, even many psychodynamic therapists.  (See: BLAMING THE BRAIN by E. Valenstein, The Free Press, 1998 and FROM PLACEBO TO PANACEA by S Fisher, Wiley, 1997; and THE ANTI-DEPRESSANT ERA by D Healy, Harvard Univ Pr, 1998).

References

1 Green AI, Mooney JJ, Posener JA, Schildkraut JJ: Mood disorers: biochemical aspects. In, Comprehensive Textbbok of Psychiatry/VI, Kaplan HI, Sadock BJ, eds. 6th edition. Baltimore, Williams and Wilkins, 1995

2 Ries Merikangas K, Kupfer DJ: Mood disorders: genetic aspects. In, Comprehensive Textbbok of Psychiatry/VI, Kaplan HI, Sadock BJ, eds. 6th edition. Baltimore, Williams and Wilkins, 1995

3 Von Knorring A L, Cloninger C R, Bohman M, Sigvardsson S: An adoption study of depressive disorders and substance abuse. Arch Gen Psychiatry 40: 943, 1983.

4 Cadoret R J, O'Gorman T W, Heywood E, Troughton E: Genetic and environmental factors in major depression. J Affective Disord 9: 155, 1985.

5 Egeland J A, Gerhard D S, Pauls D L, Sussex J N, Kidd K K, Allen C R, Hostetter A M, Housman D: Bipolar affective disorders linked to DNA markers on chromosome II. Nature 325: 783, 1987.

6 Kelsoe J R, Ginns E E, Egeland J A, Gerhard D S, Goldstein A M, Bale S J, Pauls D L, Long R T, Kidd K K, Conte G, Housman D E, Paul S: Re-evaluation of the linkage relationship between chromosome 11p loci and the gene for bipolar affective disorder in the Old Order Amish. Nature 16: 238, 1989.

7 Sweet WH, Meyerson Ba: Neurosurgical aspects of primary affective disorders. In, Neurological Surgery, Youmans JR, ed. Philadelphia, Saunders, 1990

8 Poynton AM: Current state of psychosurgery. Br J Hosp Med 1993;50:408-

9 Appleton WS: Prozac and the New Antidepressants. New York, Penguin, 1997

10 Stark R, Hardison CD: A review of multicenter controlled studies of fluoxetine vs. imipramine and placebo in outpatinets with major depressive disorder. J Clin Psychiatry 1985;46:53-58

11 Schiffer F: Psychotherapy of 9 Successfully treated cocaine abusers:techniques and dynamics.  J Subs Abuse Treatment 5:131-137, 1988


® Copyright by Fredric Schiffer, M.D., 1999


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