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SOCIAL INTERVENTION IN SCHIZOPHRENIC FAMILIES
1275 SOCIAL INTERVENTION IN SCHIZOPHRENIC FAMILIES
SIR,-Your Nov.
13 editorial reviewed studies done in our unit than two decades and did so fairly. Unfortunately, we cannot say the same for your coverage of our latest study, a controlled trial of social intervention in families7 of schizophrenics. You claim that we concluded that the differences in outcome between our experimental and control groups "were due to specific aspects" of our intervention, and dissented from this conclusion. Your phrasing blurs distinctions that were clearly made in our over more
paper. We set up clear aims for our intervention in the families: reduction of relatives’ criticism and overinvolvement and/or lowering of social contact with the patients. These targets were met in three-quarters of the experimental families, who showed a substantial and highly significant fall in criticism and a nearsignificant drop in overinvolvement. The control relatives showed virtually no change in these indices. Hence we felt justified in concluding that these differences between the groups stemmed from our
intervention.
Among the families in which we achieved our therapeutic aims, no patient relapsed. If the effect on the patients of our intervention was non-specific, we would expect an equally low relapse rate in the 3 experimental families in which we did not reach our targets. Unfortunately the size of this group (3) allows very little room for variation in outcome. As we reported, the single experimental patient who relapsed came from this group. Subsequently this patient has had several further relapses, while 1 other patient committed suicide, and the third made a serious suicidal attempt which has left her brain-damaged. The tragic and disastrous outcome for this group strongly suggests that, regardless of how much attention is paid to these families, there is no therapeutic gain for the patients unless the specific targets we set up are met. We stated clearly that we could not identify the element or elements in our therapeutic package which were responsible for our success in altering the family environment. We were aware from the start that the design of our study did not allow us to address this issue, and saw our trial as the first stage in a series of intervention studies. The next stage has already begun and consists of a comparison of family therapy with a relatives’ group, in which equivalent attention is given to both samples of families. M.R.C. Social Psychiatry Unit, Institute of Psychiatry, London SE5
University Psychiatric Clinic, Munich, West Germany Mental Health, School of Medicine, University College London
J. LEFF L. KUIPERS R. BERKOWITZ R. EBERLEIN-FRIES
Department of
D. STURGEON
HEPATIC ALDEHYDE DEHYDROGENASE AND ALCOHOLISM
SIR,-Dr Thomas and colleagues (Nov. 13, p. 1057) report that the low liver cytosolic aldehyde dehydrogenase (AIdDH) activity previously reported in alcoholicsI remains low after abstinence, and they suggest that this may represent a primary abnormality predisposing to alcoholism. We too have investigated this possibility in a prospective study, but with some important differences and with contrasting results. 29 patients with a history of alcoholic liver disease were studied. Every patient had two liver biopsies six months apart. Hepatic AIdDH activity was measured2 on each occasion. After the first liver biopsy the patients were seen regularly and their alcohol consumption was assessed independently. 17 continued to drink 1
alcohol (more than 80 g daily) as before; 10 significantly reduced their alcohol intake, to below 40 g daily; and 2, who had not been drinking to excess at the time of their first liver biopsy, began drinking heavily (over 80 g daily) before the second biopsy. In those patients who continued to drink to excess there was no significant change in hepatic AldDH activity; in those who reduced their alcohol intake significantly there was a uniform rise in activity (p<0 01), and 6 of the 10 values rose to within the normal range (12-2±1 mU/mg protein, mean±SEM). In contrast, in the 2 patients who were virtually abstinent at first but who began drinking heavily before their second liver biopsy, there was a marked fall in hepatic AldDH activity from within the normal range (see figure). This was associated with a striking increase in hepatic excess
Jenkins WJ, Peters TJ. Selectively
reduced hepatic acetaldehyde dehydrogenase in alcoholics. Lancet 1980; ii: 628-29 2. Palmer KR, Jenkins WJ. An improved method for determination of aldehyde dehydrogenase in human liver biopsies using gas chromatography Clin Chim Acta 1981; 155: 359-62.
Effect of alcohol
consumption on hepatic AIdDH-activity. (A) 17 patients continuing to drink >80 g alcohol/day; (B) 10 patients who significantly reduced their alcohol intake to <40 g/day; and (C) 2 patients who increased their alcohol intake to >80 g/day. steatosis. Thus, our results show that hepatic AldDH activity in alcoholic patients rises if alcohol intake is reduced, remains low if alcohol excess continues, and falls if alcohol intake is increased. We have previously reported the lack of an association between reduced hepatic AldDH activity in alcoholics and the histological severity of the liver damage,3and this led us to suggest that reduced activity of this enzyme might represent a primary abnormality in these patients. However, this intriguing possibility seems unlikely since our present study clearly demonstrates that alcohol consumption itself depresses hepatic AldDH activity. It is not clear why our results differ from those of Thomas et al. Although the serum liver function tests had improved before their 6 patients underwent a second liver biopsy, it is notoriously difficult to obtain accurate drinking histories, and their patients may have consumed more alcohol than they admitted before the follow-up biopsy. Also, the interval between the two biopsies was shorter (mean 15 weeks) than it was in our study and variable (4-34 weeks). Furthermore, the wide range of liver cytosolic AldDH activity found at the time of the second biopsy (9 - 3±3 - 5 mU/mg protein, mean ±SEM) suggests that at least some of the values must have fallen within the normal range (20±2’ 2 mU/mg protein, mean ±SEM), if their data were normally distributed. Although our major finding differs from that of Thomas et al. we confirm that in 87 alcoholic patients, in whom hepatic AldDH activity was significantly reduced, the reduction was greater for the cytosolic than for the mitochondrial isozyme. Also, we found no evidence of missing hepatic isozymes of AldDH in alcoholics, but rather one or two extra cytosolic isozymes demonstrated by isoelectric focusing in most of these alcoholic patients. We
plan
to
publish our results
in full elsewhere.
Royal Free Hospital School of Medicine, London NW3 2QG Middlesex London 3. Palmer
Hospital,
W. J. JENKINS K. CAKEBREAD K. R. PALMER
KR, Jenkins WJ. Impaired acetaldehyde oxidation in alcoholics. Gut 1982; 23:
729-33.
SIR,-Your Nov.
13 editorial reviewed studies done in our unit than two decades and did so fairly. Unfortunately, we cannot say the same for your coverage of our latest study, a controlled trial of social intervention in families7 of schizophrenics. You claim that we concluded that the differences in outcome between our experimental and control groups "were due to specific aspects" of our intervention, and dissented from this conclusion. Your phrasing blurs distinctions that were clearly made in our over more
paper. We set up clear aims for our intervention in the families: reduction of relatives’ criticism and overinvolvement and/or lowering of social contact with the patients. These targets were met in three-quarters of the experimental families, who showed a substantial and highly significant fall in criticism and a nearsignificant drop in overinvolvement. The control relatives showed virtually no change in these indices. Hence we felt justified in concluding that these differences between the groups stemmed from our
intervention.
Among the families in which we achieved our therapeutic aims, no patient relapsed. If the effect on the patients of our intervention was non-specific, we would expect an equally low relapse rate in the 3 experimental families in which we did not reach our targets. Unfortunately the size of this group (3) allows very little room for variation in outcome. As we reported, the single experimental patient who relapsed came from this group. Subsequently this patient has had several further relapses, while 1 other patient committed suicide, and the third made a serious suicidal attempt which has left her brain-damaged. The tragic and disastrous outcome for this group strongly suggests that, regardless of how much attention is paid to these families, there is no therapeutic gain for the patients unless the specific targets we set up are met. We stated clearly that we could not identify the element or elements in our therapeutic package which were responsible for our success in altering the family environment. We were aware from the start that the design of our study did not allow us to address this issue, and saw our trial as the first stage in a series of intervention studies. The next stage has already begun and consists of a comparison of family therapy with a relatives’ group, in which equivalent attention is given to both samples of families. M.R.C. Social Psychiatry Unit, Institute of Psychiatry, London SE5
University Psychiatric Clinic, Munich, West Germany Mental Health, School of Medicine, University College London
J. LEFF L. KUIPERS R. BERKOWITZ R. EBERLEIN-FRIES
Department of
D. STURGEON
HEPATIC ALDEHYDE DEHYDROGENASE AND ALCOHOLISM
SIR,-Dr Thomas and colleagues (Nov. 13, p. 1057) report that the low liver cytosolic aldehyde dehydrogenase (AIdDH) activity previously reported in alcoholicsI remains low after abstinence, and they suggest that this may represent a primary abnormality predisposing to alcoholism. We too have investigated this possibility in a prospective study, but with some important differences and with contrasting results. 29 patients with a history of alcoholic liver disease were studied. Every patient had two liver biopsies six months apart. Hepatic AIdDH activity was measured2 on each occasion. After the first liver biopsy the patients were seen regularly and their alcohol consumption was assessed independently. 17 continued to drink 1
alcohol (more than 80 g daily) as before; 10 significantly reduced their alcohol intake, to below 40 g daily; and 2, who had not been drinking to excess at the time of their first liver biopsy, began drinking heavily (over 80 g daily) before the second biopsy. In those patients who continued to drink to excess there was no significant change in hepatic AldDH activity; in those who reduced their alcohol intake significantly there was a uniform rise in activity (p<0 01), and 6 of the 10 values rose to within the normal range (12-2±1 mU/mg protein, mean±SEM). In contrast, in the 2 patients who were virtually abstinent at first but who began drinking heavily before their second liver biopsy, there was a marked fall in hepatic AldDH activity from within the normal range (see figure). This was associated with a striking increase in hepatic excess
Jenkins WJ, Peters TJ. Selectively
reduced hepatic acetaldehyde dehydrogenase in alcoholics. Lancet 1980; ii: 628-29 2. Palmer KR, Jenkins WJ. An improved method for determination of aldehyde dehydrogenase in human liver biopsies using gas chromatography Clin Chim Acta 1981; 155: 359-62.
Effect of alcohol
consumption on hepatic AIdDH-activity. (A) 17 patients continuing to drink >80 g alcohol/day; (B) 10 patients who significantly reduced their alcohol intake to <40 g/day; and (C) 2 patients who increased their alcohol intake to >80 g/day. steatosis. Thus, our results show that hepatic AldDH activity in alcoholic patients rises if alcohol intake is reduced, remains low if alcohol excess continues, and falls if alcohol intake is increased. We have previously reported the lack of an association between reduced hepatic AldDH activity in alcoholics and the histological severity of the liver damage,3and this led us to suggest that reduced activity of this enzyme might represent a primary abnormality in these patients. However, this intriguing possibility seems unlikely since our present study clearly demonstrates that alcohol consumption itself depresses hepatic AldDH activity. It is not clear why our results differ from those of Thomas et al. Although the serum liver function tests had improved before their 6 patients underwent a second liver biopsy, it is notoriously difficult to obtain accurate drinking histories, and their patients may have consumed more alcohol than they admitted before the follow-up biopsy. Also, the interval between the two biopsies was shorter (mean 15 weeks) than it was in our study and variable (4-34 weeks). Furthermore, the wide range of liver cytosolic AldDH activity found at the time of the second biopsy (9 - 3±3 - 5 mU/mg protein, mean ±SEM) suggests that at least some of the values must have fallen within the normal range (20±2’ 2 mU/mg protein, mean ±SEM), if their data were normally distributed. Although our major finding differs from that of Thomas et al. we confirm that in 87 alcoholic patients, in whom hepatic AldDH activity was significantly reduced, the reduction was greater for the cytosolic than for the mitochondrial isozyme. Also, we found no evidence of missing hepatic isozymes of AldDH in alcoholics, but rather one or two extra cytosolic isozymes demonstrated by isoelectric focusing in most of these alcoholic patients. We
plan
to
publish our results
in full elsewhere.
Royal Free Hospital School of Medicine, London NW3 2QG Middlesex London 3. Palmer
Hospital,
W. J. JENKINS K. CAKEBREAD K. R. PALMER
KR, Jenkins WJ. Impaired acetaldehyde oxidation in alcoholics. Gut 1982; 23:
729-33.