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Journal of Affective Disorders, 4 (1982) 1-8 Elsevier .Biomedical Press
Disease, Distress and Depression
A comment George W. Brown and Tirril Harris Depurtment
o/Sociologv
(Fruser Lodge), Bedford College, Inner Circle, Regents J’urk, London N WI 4NS (Great Britain) (Received (Accepted
16 July 1981) 20 July, 1981)
Summary Bebbington et al. (1981) in their paper in the present number of this Journal suggest that psychiatric disorders in the community are likely to be cases of distress and base this assertion on the fact that very few out-patients have a significant life event preceding onset. A review of 7 recent studies of depressive patients, using a broadly comparable lifeevent instrument, gives a quite different picture: an average of 56% had an important life event before onset, compared with 18% in the general population. It is concluded that the authors arrive at their conclusion because they have failed in a number of critical respects to replicate previous analyses. The ‘distinction between disease and distress is discussed in the light of these results.
Introduction Bebbington et al. (1981) in their paper in a recent number of this Journal, conclude that they have found a consistent trend in favour of their claim that disorders seen in patients differ from those seen in the community in their relationship to adversity, and go on to claim: ‘This difference supports the suggestion that disease theories are more likely to be required to explain the occurrence of the more severe affective disorders, whilst less severe disorders often have a ready explication as understandable and unmysterious responses to adversity’. The all-or-none distinction between disease and distress has always seemed misguided to us, but its application in the conclusions of this pa&cular study-seem to warrant comment lest certain misconceptions about research in this area become established.
0165/0327/82/0000-0000/$02.75
@ 1982 Elsevier Biomedical Press
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(A) The independent variable - adversity Bebbington and his colleagues have used the same research instruments as our earlier work in the same South London population, where we reached a very different conclusion - in a study of 114 in- and out-patients, 75% were found to have had a severe event or major difficulty in the 32 weeks before onset, and we concluded that at least 61% of the conditions had been brought about by such a provoking agent *. (Comparable figures for severe events alone are 61% and 49%, respectively.) However, in spite of these impressive relationships, we also made the point that the strength of the association was somewhat less than in the general population, where the great majority of depressive onset conditions had such a provoking agent. But while there was a difference, it was merely one of degree, and certainly not one that would support the claim of Bebbington and his colleagues. To our knowledge there have been 7 recent studies of treated depressed patients which have used an interview-based measure of life events of comparable status to that used by Bebbington and his colleagues. In practice, all have utilised either an instrument developed by Paykel and his colleagues in New Haven, or by Brown and his colleagues at Bedford College - or some derivative of both instruments. The results are summarised in Table 1. It will be seen that every study shows a high rate of important events before onset of depression. For a total of 613 patients the average is 56% with a much lower rate in the general population comparison series supplied by a number of the studies. Looked at in broad terms the findings certainly confirm our claim that about half of all onsets among patients treated by psychiatrists have been brought about by a severely threatening life event in the 6 months or so before onset. A few further comments are perhaps in order. The rate of ongoing major difficulties is not given in this table as they were not considered in most of the studies. The early version of the Paykel instrument almost certainly tends to understate the aetiological role of events, and the later version, used by Fava and his colleagues, is much closer in form to the Bedford College instrument and gives a higher proportion of patients with an ‘event’ **. In the face of this evidence, it is necessary to ask why the Institute of
* This 61% is derived from an index, x, which allows for the chance juxtaposition of event and onset (see Brown and Harris 1978a, pp. 120-121). ** We have not devoted time to discussing some early studies (e.g. Hudgens et al. 1967), a number of which were apparently negative, or to discussing results obtained by the SRE instrument as a measure of life events (Holmes and Rahe 1967). This is partly for reasons of space, but also because along with Bebbington et al. (1981) we have grave reservations about the meaning of data collected by the existing alternative instruments. It is, however, worth stating that a recent review of the earlier findings does raise strong doubts about whether any have really shown negative results (Finlay-Jones, unpublished manuscript).
257
672
613 45
40
40
30
89
40 -
-
130 25
382
114
25
185
Comparison group
185
Patients
--
Number of
a Manic-depressive, bipolar sample. b Includes some anxiety states.
Bebbington et al. 1981 b (London)
Fava et al. 1981 (Padua) Benjaminsen 1981 (Odense, Denmark) Vahder and Ndetei 198 1 (London)
PaykeI et al. 1969 (New Haven) Brown and Harris 1978a (London) Barrett 1979 (Boston) Glassner et al. 1979 a (New York)
Source
18
56
67
63
73
56
58
61
44
Patients (%)
8
10
18
-
30
16
-
19
17
Comparison group (%)
Proportion with at least one event
3 months
12 months
6 months
6 months
12 months
6 months
8 months
6 months
Period covered
PATIENTS
“Marked and moderate threat - independent events”
“Severe threat”
“Severe loss”
“Uncontrollable”
“Major role loss”
“Undesirable”
“Severe threat”
“Undesirable”
Type of event
SUMMARY OF RECENT STUDIES OF LIFE EVENTS AND ONSET OF DEPRESSION AMONG PSYCHIATRIC
TABLE 1
w
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Psychiatry study obtained such an extremely low rate of ‘severe’ events in their patient series - only 18% had such an event. Possible reasons are easy to find, since the investigators have not chosen to replicate the earlier Camberwell analysis. We will discuss some of the more important differences and briefly comment on their likely effect. (1) The period covered Only events occurring in the 3 months before onset are analysed, although figure 1 of Bebbington, Tennant and Hurry’s paper suggests that patients show an excess of events in most of the months from 4 to 12 before onset. All the studies, listed in Table 1, have taken at least 6 months. In terms of the Brown and Harris Camberwell patients, about one third with a severe event before onset would have been missed by taking only a 13-week period (Brown and Harris 1978a, table 5: 113). (2) Independence Only results for ‘independent’ events have been given in the paper, although material for ‘possibly independent’ events was collected and apparently was included for some of the later analyses concerning symptomatology. Measurement of independence involves 3 possible ratings: ‘independent’, ‘possibly independent’ and ‘illness-related’. The latter involves any event obviously related to a disorder such as admission to hospital because of a suicide attempt, or giving up work because of tiredness. Illnessrelated events are never included in any aetiological analysis, since they are acknowledged to be results, rather than causes, of illness. Remaining events are then either classified as ‘independent’ or ‘possibly independent’. Events are only rated ‘independent’ if a strong logical case can be made that they could not have been brought by any incipient disorder, because their source is so much outside the volition of the subject - for example, death of a mother from cancer. Ratings are made on the assumption that it is possible for anyone to develop disorder within the period prior to interview and thus can be applied to all populations, both with and without disorders. The reason for presenting a separate analysis of ‘independent’ events is a methodological one - the chance of certain kinds of bias can be fairly confidently ruled out for such events. Thus if a significant case can be made for a causal link using ‘independent’ events alone, such a link will have a greater methodological credibility. However, given positive results from such an analysis, it is essential to include ‘possibly independent’ events at a later stage of any theoretically focussed analysis. There is bound to be an intuitive appeal for purists in research to distrust the aetiological role of any event which has not earned the pedigree ‘independent’, but it is important to stress that the logic behind the concept of ‘possibly independent’ is not that such events’are no longer part of the social stressors in a person’s environment; it hardly makes
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sense that any measure of adversity should ignore that a man’s wife has left him, or that he has been made bankrupt, just because he has played a part in bringing them about. Once the credibility of the impact of adversity has been established analysing ‘independent’ events alone, it is important to go on to examine the total potential impact of adversity by including ‘possibly independent’ events as well. Indeed, Bebbington and his colleagues state that the difference in rates of adversity between community cases and patients is less prominent if ‘possibly independent’ events are also included in the analysis. It is a pity that they have not supplied figures so that readers could make further comparisons with other research. In excluding them, the authors differ from the other published studies and we estimate that their exclusion together with their use of a shorter period, would have reduced the proportion with a severe event among our own total patient series by half from 61% to 33%. (B) The dependent variable (1) Diagnostic syndrome - depression vs. other diagnoses, onset vs. chronic conditions The study by Brown and his colleagues excluded patients with depression secondary to other disorders and also those with manic symptoms. In order to obtain a series with an onset in the year before admission a considerable number of patients with a more a distant onset were excluded and a special interview used to establish onset and course of symptomatology designed in collaboration with John Copeland. Bebbington, Tennant and Hurry only excluded those with a diagnosis of schizophrenia, alcoholism and dementia, and those who had seen a psychiatrist in the previous 6 months. It therefore appears possible that the 45 acute patients contain other diagnoses such as anxiety state, phobia or obsessional. There is some confirmation for this point - 2% of the original 69 patients were anxiety conditions (Wing et al. 1981) and, although it is not possible to calculate it directly, it is possible that the study is based on only some 40 depressed patients. In our experience many affective disorders which reach psychiatric treatment, particularly those involving anxiety, tend to have had their onset long before the final referral and it would therefore not be at all suprising to find that, even among persons who had not seen a psychiatrist during the previous 6 months, the symptoms were chronic and the period taken for causal investigation was thus not really ‘pre-onset’. Unfortunately, Bebbington, Tennant and Hurry do not say whether or not they controlled for this, let alone give an indication of by what means. If, indeed, some of the symptoms were chronic, it would hardly be suprising to find that by questioning about more recent events, they have missed those more distant events which had played the original aetiological role, thus emerging with a lower overall rate for patients than should really be the case. Barrett carried out a special com-
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parison of out-patient depressive (=130) and anxiety disorders (=72) and found that anxiety states had significantly fewer with ‘undesirable events’ (58% vs. 42% - op. tit: 93). This could have due to the same factor namely that more of the anxiety states than depressive conditions are chronic before receiving treatment, and that such chronic conditions had not all been excluded from his series. It is probably much easier to select patients with new anxiety conditions in general practice and certainly here a high rate of severe events characterised by ‘danger’ can be found before onset (FinlayJones and Brown 1981). (2) Severity
of depression
Bebbington, Tennant and Hurry mention that Brown and Harris’ study gives no data as to severity of disorder in the patients. Although we did not use the Index of Definition, we did assess severity of disorder by a measure developed with John Copeland. A chapter of our book is devoted to discussion of how this did not relate to adversity before onset, but to various other factors which we call symptom-formation factors. A few final comments may be useful. The distinction that the authors make between a distress and disease model seems to us basically misguided. Although it is never fully spelt out, the authors appear to imply that a disease could not be seen as caused by stress, and it is this which distinguishes it from distress which is, by definition, so caused. Such a perspective is reminiscent of a search for a single final cause, instead of an approach which sees disease as the result of many factors, among which stress could certainly be numbered. Besides, there could, for example, be other conclusions drawn on the basis of the data presented than that the cases in the general population are examples of distress, and the patients examples of disease. They might both be examples of disease, but of diseases which differed either in intensity or kind. If Bebbington and colleagues had distinguished patients from cases in their table 6 we might have some clue about this. In fact, at the end of their paper, they seem to be moving towards such a position when discussing the neurotically depressed patients, despite the fact that the logic of their earlier position would demand that they be considered distressed rather than sick. The women we have characterised as cases in our population surveys experienced essentially comparable symptoms to the women studied in outpatient clinics and we are convinced that psychiatrists would not have hesitated to see them as psychiatrically ill if seen in an out-patient clinic, and treated them accordingly (Finlay-Jones et al. 1980). The only way they differ as a group from those seen in out-patient clinics is in length of time of their disorders. Many probably clear up within several months of their onset - although we would remind the reader that at least half of the case conditions found in the general population are chronic in the sense of having lasted at least one year.
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As we have noted elsewhere, whatever the relationship of length of disorder and severity turns out to be (at present it is quite unclear), it is obviously important to include ‘short-lived’ conditions if we are to understand more about factors that help to perpetuate psychiatric conditions and whether or not such episodes increase the chance of subsequent breakdown (Brown and Harris 1978b). A more relevant distinction between community cases and psychiatric patients may well prove to be the fact that a general practitioner has to decide to refer the person for specialist treatment. It is not impossible that even beyond considerations of the intensity and duration of symptoms, general practitioners tend to feel that with modern psychotropic drugs they can cope themselves with depression which are ‘understandable’, but that those disorders which are less understandable present more of a risk if not given specialist treatment. Clearly the presence of obvious adversity would make a depression seem more understandable and thus any tendency for a patient series to have a somewhat lower experience of adversity may be less a matter of disease versus distress, or even of different types of disease, than of general practitioner attitudes to the treatability of different women with essentially the same kind of disorder. But whatever turns out to be of relevance, most present research suggests that any difference between patients and community cases in the role of adversity will be merely one of a modest difference in proportions, rather than one of kind. We also believe that the distress-disease comparison exhibits a more profound misjudgement. An important aetiological role for social stressors does not rule out in any way biologically based influences - it becomes increasingly clear that a multi-factorial model for conditions such as depression and anxiety is essential. There is no reason why some biological predisposition does not increase the chance of a major depressive disorder following a stressor. Moreover, it becomes also obvious that we must consider the possibility that once a major depressive disorder has occurred, the chance of a subsequent episode is probably increased - and such subsequent attacks may well occur without the kind of obvious stressor present at the first attack. This is not the place to spell out the many possibilities. What does seem clear is that existing evidence suggests that the simple juxtaposition of terms such as distress and disease in psychiatry is not useful - although by its rhetorical appeal it is probably able to arouse strong feelings and a sense of allegiance in a medically-based discipline such as psychiatry, many of whose members yearn for the comforting security of a disease-based model. Even conditions such as schizophrenia now appear to be open to a surprising amount of influence from ‘stress’, both in terms of onset and course, and the affective disorders, perhaps not surprisingly, appear to have even more important links. We do not doubt that a fair amount of the depressive disorders seen by psychiatrists will ultimately be shown to have significant somatic links - however, this is unlikely to be established without taking seriously the possibility that ‘stress’ plays a significant role in the aetiology of the whole range of depressive disorders - short-cuts, based on indifferent analysis of material, are likely to delay this final appraisal.
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References Barrett, J.E., The relationship of life events to the onset of neurotic disorders. In: J.E. Barret (Ed.), Stress and Mental Disorder, Raven Press, New York, 1979, pp. 87-110. Bebbington, P.E., Tennant, C. and Hurry, J., Adversity and the nature of psychiatric disorder in the community, J. Affect. Dis., 3 (1981) 345-366. Benjaminsen, S., Stressful life events preceding the onset of neurotic depression, Psychol. Med., 11 (1981) 369-378. Brown, G.W. and Harris, T., Social Origins of Depression - A Study of Psychiatric Disorder in Women, Tavistock Publications, London, 1978a. Brown, G.W. and Harris, T., Social origins of depression - A reply, Psychol. Med., (1978b) 577-588. Fava, G.A., Munari, F., Pavan, L. and Kellner, R., Life events and depression -A replication, J. Affect. Dis., 3 (1981) 159-165. Finlay-Jones, R., Brown, G.W., Duncan-Jones, P., Harris, T., Murphy, E. and Prudo, R., Depression and anxiety in the community - Replicating the diagnosis of a case, Psychol. Med., 10 (1980) 445-454. FinlayJones, R., Showing that life events are a cause of depression - A review, Unpublished manuscript. Glassner, B., Haldipur, C.V. and Dessauersmith, J., Role loss and working-class manic depression, J. Nerv. Ment. Dis., 167 (1979) 530-541. Holmes, T.H. and Rahe, R.H., The social readjustment rating scale, J. Psychosom. Res., 11 (1967) 213-218. Hudgens, R.W., Morrison, H.R. and Barchaa, R.G., Life events and onset of primary affective disorders, Arch. Gen. Psychiat., 16 (1967) 134-145. Paykel, E.S., Myers, J.K., Dienelt, M.N., Klerman, G.L., Lindenthal, J.J. and Pepper, M.P., Life events and depression - Controlled study, Arch. Gen. Psychiat., 21 (1969) 753-760. Tennant, C., Bebbington, P. and Hurry, J., The role of life events in depressive illness Is there a substantial causal relation? Psychol. Med., 11 (1981) 379-389. Vadher, A. and Ndetei, D., Life events and depression in a Kenyan setting, Brit. J. Psychiat., 139 (1981) 134-137. Wing, J.K., Bebbington, P., Hurry, J. and Tennant, C., The prevalence in the general population of disorders familiar to psychiatrists in hospital practice. In: J.K. Wing, P. Bebbington and L.N. Robins (Eds.), What is a Case? The Problem of Definition in Psychiatric Community Surveys, Grant McIntyre, London, 1981. pp. 52-61.