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Family or Fate? a critical evaluation of a Psychogenic and a Genetic theory of Schizophrenia
Is it due to Family or Fate? From fifty years ago and on into the early eighties, a large body of work developed the idea that mental illness could be caused by family circumstances. That idea has (at least in America) now largely been - what? Rejected? Disproven? No, quietly forgotten. Why? Was it actually wrong?
Schizophrenia is a dreadfully disabling and distressing condition for everyone whose life is touched by it; the sufferer, their family, friends, partners. It is the most commonly-diagnosed psychotic disorder; according to Keith et al (1991), more than 1% of the American public is suffering from schizophrenia at any one time (that is, over 2.2 million people); 14% of Americans will suffer at some time in their lives. Keith (1991) estimated the world-wide figure for 1990 as being 20 million. The sheer numbers involved mean that first, questions of the origins, causes and treatment of schizophrenia are in no sense 'academic' but of pressing practical significance and second, there is a very large amount of money (estimated by Rice & Miller (1992) at $16 billion for 1990 for the USA alone) involved in the treatment, maintenance and housing of sufferers from a condition affecting so many. These factors, amongst others, mean that there are, inevitably, entrenched interests surrounding many of the issues concerning the aetiology of schizophrenia, the control of policy concerning it and the manufacture of drugs to treat it. This essay will examine just two of the opposing claims.
It is not at dispute that schizophrenia tends to run in families. One interpretation is that schizophrenia is a reaction to a morbid family environment. Fromm-Reichmann (1948) identified the schizophrenogenic mother, who, by her behaviour, alienated the child and induced psychosis. The mother's behaviours were described as 'rejecting, imperviousness to the feelings of others, rigid moralism concerning sex and fear of intimacy'. Bateson et al proposed (1956) the double-bind hypothesis, that schizophrenic behaviour is a reaction to intolerable stress within the family. The specific nature of the double-bind was that conflicting injunctions were placed by the authority cum power figures in the family in such a way as for it to be impossible for the 'victim' to satisfy one without breaking another. Bowen (1960) built on this in the observation that schizophrenic patients often improved in hospital but deteriorated when returned to their families. On this basis the idea of the schizophrenogenic family was postulated - a family that caused or induced schizophrenia in one of its members.
Wynne et al (1958) found that disturbed families maintained a fašade of internal familial harmony together with a denial of problems. This they labelled pseudomutuality. Research by Brown et al (1966), which has been replicated several times since, clearly demonstrated that the quality of the family environment into which discharged patients returned is strongly predictive of their return to hospital. Brown introduced the term expressed emotion ('EE') to describe the level of criticism, hostility and emotional dependency connected to the patient. Patients from low-EE homes were about one-sixth as likely to return to hospital as those from high EE homes (10% versus 58%).
Norton (1982) found that communication difficulties in families predicted the later onset of schizophrenia, but this was not specific; the same occurred with later onset of manic patterns of behaviour (Miklowitz 1985). Recent work by Tienari et al (1991) has shown that adopted children of schizophrenic mothers show more psychopathology if they are raised in a disturbed family, and more than controls did when raised in a similarly disturbed family. [NOTE 1]
All of this represents quite a weight of evidence, yet what is the picture generally portrayed to the public?
"Schizophrenia - Fact and Fiction. Fact: Schizophrenia is a real physical illness. Many people do not have a clear understanding of schizophrenia. Schizophrenia is a physical illness, just like diabetes or a broken leg. Schizophrenia has typical signs and symptoms that are recognizable in patients with this illness, and like all illnesses, the symptoms vary from person to person... ...Fact: Schizophrenia is a treatable illness. Being diagnosed with any life long illness can be difficult to accept. It is important to remember that schizophrenia is a treatable illness. With medication and treatment, the symptoms of schizophrenia can often be controlled. Once the symptoms improve, people can continue to have productive lives."
(http://www.healthguide.com/Schiz/ published by Clinical Tools Inc)
How is this argument sustained against the evidence previously given here? In this case, it is not; the bald statement is made, and that is that. Let us look at a more academic site: the department of Social Psychiatry, University of Groningen. Here we find:
"The cause of schizophrenia is not definitely known. Hereditary aspects certainly are a factor of importance, as twin-studies have shown. First degree relatives have a higher risk of acquiring the disorder. The notion that rearing styles or upbringing causes schizophrenia has been entirely abandoned [author's emphasis]. Though causes per se are not known, those afflicted by the disease are thought to have a congenital vulnerability for decompensating under stressful circumstances. Indeed, stress may precipitate the first onset of the psychosis or cause a relapse."
Let us note the differences between this and the previous portrayal. First, instead of the (frankly ridiculous) statement '...schizophrenia is a physical illness, just like diabetes or a broken leg' there is a more tentative '...the cause of schizophrenia is not definitely known'. However, we still find that the schizophrenogenic theory has '...been entirely abandoned'. Why? The reader will note the sudden absence of references in the forthcoming text; despite preparing this essay over several weeks, the author could not find any cogent and clear explanation as to why the schizophrenogenic theory has been abandoned.
There are many possible criticisms that can be made of any sort of study, on various different grounds. For example, it may be possible to argue:
None of these sorts of criticisms of the studies mentioned above appeared anywhere in the reading done by this author. Certainly, the early proponents of schizophrenogenic theories were of the psychoanalytic orientation, which has been extensively criticised for being 'non-scientific', in that its claims are difficult to test or impossible to falsify [NOTE 2] . Kalat (1995) says (p.573): "This [schizophrenogenic parent] hypothesis is now considered obsolete. The main reason for its downfall was the results of adoption studies" but without giving any references; generally, the text is thick with them. Davison & Neale (1997) say (p.283):"Controlled studies evaluating the schizophrenogenic mother theory have not yielded supporting data" - oddly, though, again there is a complete lack of references. Sarason & Sarason (1996) perhaps give us a clue as to some reasons why this may be in their 'First Person' feature (p.359) entitled "Lessening a Family's guilt over schizophrenia". Here we find (in part) "...learning that schizophrenia has a biological basis 'made me feel better, made my ex-husband feel better. Even my youngest son is starting to accept it now. And it's made me feel easier with Malcolm to realize that this is just an illness'...". Davison & Neale go on to say, editorially, "...the experience of the Lees shows the importance of helping family members understand that there are biological causes of schizophrenia in order to avoid needless and crippling guilt...".
If schizophrenia indeed has a biological cause, is nothing to do with the family environment, then such a move could only be applauded for its humanity. But let us for a moment see what Miller (1991) has to say, admittedly in the context of the abused child: "...if the abused daughter does eventually arrive at a clinic suffering from schizophrenia and is treated ... with massive doses of medication, then she will know less than she did before, she will never find out that it was her father's behavior that drove her into madness...to salvage his image...she must not know the truth. She would rather 'lose' her mind..."(p.63) "...parents are permitted to destroy the lives of their children with impunity...all that is forbidden is to call it a scandal..." (p.22) and "...in leafing through my early books, I am struck by my constant efforts to avoid blaming parents...I could not reproach the parents..." (p.25).
Miller is somewhat controversial; she has abandoned psychodynamic psychotherapy, without adopting another 'recognised' approach. So let us just note that she, at least, is certainly not in agreement with the general biological/genetic hypothesis put forward in the textbooks mentioned above. It's time to examine the case for the genetic theory of schizophrenia, to see if, with Kalat, we can regard the adoption studies as rendering the schizophrenogenic theory 'obsolete'.
The hypothesis of the Genetic theory is simply put; schizophrenia is due to a physical disorder of the brain, it is genetic in origin, caused by a gene or synergy between various genes in combination, and it is inherited from the parent or parents [NOTE 3] (see, for example, Gross (1996, p. 12-13)). For brevity in this discussion, let us label this gene or set of genes as the 'schizophrenogenic gene' [NOTE 4] .
If this hypothesis is true, then we can predict that schizophrenia will run in families; that there will be a high concordance rate, higher the closer the relationship; that given the proclivity there will be a tendency for the disorder to develop; that we should be able to find physical results of the developmental disorder; and that once developed, the disorder will be incurable, and therefore chronic.
The principal evidence adduced for the genetic theory is statistical and comes from family studies. Gottesman (1991), given as a source in Kalat (1995) and Sarason & Sarason (1996), suggests that 48% of monozygotic twins [NOTE 5] , whose twin has developed schizophrenia, will develop it themselves. This compares with 17% of dizygotic twins [NOTE 6] , 17% of children of schizophrenic mothers raised by non-schizophrenic mothers, 9% of siblings and 13% of children. Similar figures are given in Davison & Neale (1997), Gross (1996) and Hayes (1995).
Overall it would appear that the risk of developing schizophrenia increases if a very close relative has it. This evidence is solidly scientific and completely objective - or is it? The biological hypothesis rests on genetic studies. The genetic studies rest upon monozygotic twin studies. The concordance rates [NOTE 7] rest upon statistics, which in their turn rest upon accurate assignment of subjects to categories. 'Being a twin' is not an imposed category [NOTE 8] ; however, schizophrenia as a diagnosis is (at least to some extent) in the eye of the beholder. Is this a doubtful proposition? Let us look at the evidence for it.
Hilgard, Atkinson and Atkinson (1975), Hayes (1995), and Gross (1996) all give the concordance rates for various studies over the last 70 years. Notably, in these studies concordance rates for monozygotic twins drop from typically 60% pre-1961 to as low as 14% in 1972 (Lewontin, Rose and Kamin, 1984). This is said by Hilgard, Atkinson & Atkinson (1975) to be due to tighter criteria for diagnosing schizophrenia in the later studies.
There are, however, feasible alternate interpretations. The reliability of statistics depends upon reliable source data - and abuse of the data produces false results. A notorious example of such abuse was the invented data in the monozygotic twins studies of Burt (Kamin, 1974). The difficulty is that monozygotic twins are not commonplace, and schizophrenic monozygotic twins, raised apart, much less so. Consequently, many of the meta-studies tend to rely on the same data.
In the early part of this century, Kallman (1946) produced the first evidence of a genetic component in schizophrenia, and found a 69% concordance rate for monozygotic twins. This established a genetic explanation as near certain, and has strongly influenced research since (for example see Hayes, 1995, p.286). However, Lewontin, Rose and Kamin (1984) have heavily criticised, and, at least as far as this author is concerned, largely discredited his data. Some of their criticisms include that:
All this is very reminiscent of the Burt issue. Such malfeasance, though, surely is something of the distant past? Or is it? [NOTE 9] It is interesting to note that most (college-course-level introductory) textbooks on abnormal psychology known to this author originate in the USA, lean heavily towards the genetic/biological/medical model of schizophrenia and quote Gottesman, together with various colleagues, as the source of their statistical data (for example Kalat (1995), Davison & Neale (1997), Sarason & Sarason (1996)). The author has tried without success to get a copy of the original meta-studies; this may or may not reflect on the author's competence, but certainly means that the source of the statistics involved cannot be dealt with here. This is unfortunate; one forceful critic of twin studies as proving a genetic origin for schizophrenia, Breggin (1993), particularly takes the statistics of genetic inheritability to task.
Breggin (1993) examines the adoption study of Kety et al (1975), which was carried out in Denmark but sponsored by the NIMH in the USA. Gross (1996) states (p.809) that this study found greater rates of diagnosed schizophrenia amongst the biological relatives of the adopted children who later developed schizophrenia than amongst the controls. Breggin (1993), though, states that when he finally saw the original report, he found that the data showed no increase in schizophrenia in the close biological relatives. What they did find was that the half-brothers and half-sisters on the father's side did have an increased rate of 'schizophrenia' - in other words, the gene ignored mothers, fathers, sisters, brothers - only half-siblings on the father's side were susceptible, a truly unusual gene (Sarason & Sarason mention some of this: p.335). He puts the word 'schizophrenia' in quotes in his comments relating to the study, because he points out that the actual criteria for schizophrenia were such that four out of six 'schizophrenics' were actually diagnosed as 'latent schizophrenic' under DSM II - a diagnosis which did not require patients to have had an episode of schizophrenia. These assertions are reported here without further comment; as previously stated, it would be interesting to have sight of the original documents in these studies and to see whether the meta-studies include any such data.
A genetic theory has an evolutionary implication. Apart from the statistical questions, the genetic theory of inheritable schizophrenia rests on doubtful evolutionary logic. For a genetic theory to have any relevance to any condition, the condition must be inheritable and must have been inherited. But a clear difficulty for the genetic theory arises here: schizophrenia is a condition with early onset (from 15 years of age; Davison & Neale 1997), and thus would be expected to be in full force by and during the childbearing years. Indeed, it could almost be seen as being triggered by the processes that bring about physical sexual maturity.
If schizophrenia is a maladaptive behaviour, 'abnormal', then would it not be reflected in reduced reproductive success? But we have schizophrenia now, in children of parents who - according to the genetic hypothesis - must have survived in earlier epochs where the schizophrenogenic gene did not reduce their fitness (at least below some critical level). The only reasonable conclusions the author can draw here are:
If this last suggestion should seem an unlikely possibility, we might recall the gene that when inherited in single form confers enhanced resistance to malaria, but when inherited from both parents gives rise to sickle-cell anemia. We could also bear in mind the startling artistic capacities of many schizophrenic patients...
Is there such a thing as 'mental' illness? Do patients create their own symptoms? An often-quoted rejoinder from Meehl (Kimble, Garmezy & Zigler, 1980, p.453) to suggestions that schizophrenia is the result of 'labelling' runs:
"I just stood there and didn't know what to say. I was thinking of a patient I had seen on a ward who kept his finger up his *** 'to keep his thoughts from running out', whilst with his other hand he tried to tear out his hair because it really 'belonged to his father'. And here was this man telling me that he was doing this because someone had called him a schizophrenic. What could I say to him?"
This rejoinder is very 'clever' or 'smart' -- but it actually begs the question, misses the point and fails to address the issue; it is reminiscent of Dr. Johnson's response to Berkeley. Without for a moment denying the reality of the distress suffered by those diagnosed as schizophrenic, is it actually an illness in the same way that, say, tuberculosis is an illness? Or, absurdly, a broken leg? Or cancer? Do you die of it? Szasz (1974) pointed out that 'mental illness' started out as a metaphor, a suggestion that 'mad' people could beneficially be treated as 'ill' rather than 'mad', but the typical process of reification had transformed the metaphor into a reality - much as has happened with 'gene' and 'DNA'.
This author would argue that another, implicit, set of predictions follow on from the genetic hypothesis. The intention here is to point to the expectations that are likely to be engendered by the firm adoption of theoretical positions. Put oneself for a moment in the place of patient or doctor. If schizophrenia is genetic and chronic, then 'I the patient' cannot be cured; at best my symptoms can be alleviated. If 'I the doctor', believing that schizophrenia is genetic and chronic, am faced with the monozygotic twin of a schizophrenic patient of mine, non-presenting for now, how will I treat them? What would my expectations, as a doctor, be? The power of the self-fulfilling prophecy to produce the result expected has been well established; see, for example, Rosenthal and Jacobson's 'Pygmalion' study (1968) or Dement's arguments with his sleep deprivation study (1960).
At the beginning of this essay mention was made of the immense amount of money that is tied up in and around schizophrenia. Space precludes an analysis of the possible interaction between aetiology and company profits, or aetiology and locus of control (but see Breggin, 1993); we can just point out that if schizophrenia is a disease then it 'belongs' to the medical profession, and treatments that would otherwise be unacceptable are justified. In America the medical profession is also an industry; worldwide, the drugs industry sponsors much research, gives many grants and pays for many seminars - as well as making neuroleptic drugs. Is it conceivable that they may have a self-serving bias? Is it conceivable that they should not?
This essay of necessity represents a high-altitude skim over a massive topic. This distant view does however enable us to see clearly the usual (and essentially false) dichotomy apparent in most attributions: nature or nurture. After centuries of study, we know little about schizophrenia, but we know its truly distressing effects. One thing is certain: there are no easy answers. Those who make an attribution of 'nature' are unlikely to be swayed by the opposing viewpoint; the contrary also applies. This author suggests useful and usable truths may well be found in the middle ground. There is no doubt that there are such things as developmental disorders, and some of them affect the brain and nervous system. Some of these disorders may well produce the symptoms labelled as 'schizophrenia'. Some of these may be chronic and incurable. But the author does not accept the invariant chronic prognosis of mainstream biological psychiatry (and, could it be, the drug companies?) that schizophrenia is for life; this is based on both personal experience of work with mild schizophrenics and from the statistic that schizophrenia for some 30% (Davison & Neale, 1997) of people is an episode, resolvable, survivable -- perhaps even valuable. We can speculate that at some time in the distant future the blanket diagnosis and lumping-together of causes and effects we now call 'schizophrenia' will appear to be as ludicrous as the phlogiston theory of combustion appears now to us.
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[Note 1] Quite why these researchers left children in an environment they characterised as 'disturbed' (if they did indeed do so) is another, perhaps urgent, question.
[Note 2] This is not actually equivalent to stating that they are false, though. It means it's hard to find out if they are true or false.
[Note 3] Of course schizophrenia could be (for example) genetic in nature but a result of a common but spontaneous mutation - but in that case the statistics for inheritance could not be directly relevant in arguing causality. They might be relevant to susceptibility.
[Note 4] It is recognised, of course, that by doing so we are in danger of reifying a gene (which is a section of DNA that codes for a protein) into a condition (schizophrenia). It is hard to avoid potential reification... (n.b. to 'reify' is to turn a 'symbol' into a 'thing'. 'Democracy' 'human rights' or 'justice' might be examples.)(n.m.b. This is not an attack on the laudable actual freedoms symbolised as democracy, human rights and justice).
[Note 5] Mono-zygote-ic means 'one egg-ed' - thus, 'identical' twins.
[Note 6] Similarly, di-zygote-ic is 'two-egg-ed' - or non-identical twins.
[Note 7] Concordance is (more or less) the mutual development of some condition - here, schizophrenia, of course.
[Note 8] Some recent and not fully confirmed data might show that this confident statement is in error: apparently many 'identical' twins actually aren't.
[Note 9] At the time of writing there is a great deal of media fuss (especially in Europe) concerning the human-variant CJD epidemic, and the (perhaps) incomplete and (possibly) inaccurate early reporting on this by (some) government scientists as a result of enormous political and farming-industry lobby-group pressure; it is not inconceivable, then, that erroneous data should be collected and promulgated in other fields...
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