Epidemiological evidence about the relationship between ptsd and alcohol abuse

Addictive Behaviors, Vol. 23, No. 6, pp. 813–825, 1998 Copyright © 1998 Elsevier Science Ltd Printed in the USA. All rights reserved 0306-4603/98 $19.00 1 .00

Pergamon

PII S0306-4603(98)00098-7

EPIDEMIOLOGICAL EVIDENCE ABOUT THE RELATIONSHIP BETWEEN PTSD AND ALCOHOL ABUSE: THE NATURE OF THE ASSOCIATION A. C. MCFARLANE University of Adelaide

Abstract — This article uses the Bradford Hill criteria for assessing causal associations to examine the nature of the relationship between PTSD and alcohol abuse. A series of studies are presented which examine this relationship. A cross-sectional study of 2,501 subjects in a community sample examined the relationship between at-risk drinking and 11 types of traumatic events. The traumatic events associated with at-risk drinking were involvement in life threatening accidents, witnessing severe injury, rape, being the victim of serious physical assault using the CIDI. In a longitudinal study of 469 firefighters exposed to a natural disaster, PTSD was associated with both an increase and decrease in alcohol consumption and PTSD rather than exposure accounted for the changes in drinking behaviour. In three other populations, psychiatric inpatients, motor accident victims and female prisoners, the association between PTSD and alcohol abuse emphasised the clinical and public health importance of this relationship. The available evidence does nevertheless support the causal nature of this relationship. Other risk factors are necessary to predict alcohol abuse following exposure to traumatic events, although exposure to traumatic events can be caused by alcohol abuse. © 1998 Elsevier Science Ltd

The relationship between posttraumatic stress disorder (PTSD) and alcohol abuse is an issue of practical importance for several reasons. Firstly in compensation settings, the comorbid problem of substance abuse is often presented as being caused by the associated PTSD. The resolution of this question is important as it can significantly influence the damages awarded because of the contribution of substance abuse to the associated disability and handicap. Second, there is often a debate in treatment settings about the relationship (Brown & Wolfe, 1994). The conclusions have a significant impact on the structure of treatment services. The argument arises as to whether the substance abuse problem needs to be treated before the PTSD can be treated. This presents a particular quandary because if the alcohol abuse represents a form of self-medication, it seems paradoxical if the individual has to give up this source of symptom relief before they receive any alternate assistance. From a public health perspective there is the broader question about the role of traumatic stress as a cause of substance abuse. If there is a significant contribution of traumatic stress to the onset of substance abuse, it suggests that populations who are traumatised may be worthwhile targets for intervention to prevent substance abuse. The complex nature of this relationship has led to the formulation of a series of competing and overlapping hypthotheses about the relationship between alcohol abuse and PTSD. Professor McFarlane is President-Elect of the International Society for Traumatic Stress Studies and is President of the Australian Society for Traumatic Stress Studies. The Sercis data were collected by the epidemiology unit of the South Australian Health Commission. The data are used with their permission. E. Rafalowicz, P. Papay, and J. Eden assisted in the collection of the data in the firefighters study. M. Atchison collected the data in the study of 200 motor accident victims. C. Bookless assisted in the collection of the data on the 143 psychiatric inpatients. T. Air analysed the data for this article. Requests for reprints should be sent to A. C. McFarlane, University of Adelaide, Department of Psychiatry, Queen Elizabeth Hospital, Woodville Road, Woodville 5011, Australia. 813

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Hypothesis 1: PTSD is a significant risk factor and causes higher rates of alcohol abuse. This arises from the notion that alcohol is a method of self-mediation (Khantzian, 1985). The evidence for this argument comes from a variety of data. Firstly there are high rates of comorbidity of these two disorders. This is particularly observed in populations which have significant levels of disability associated with their psychiatric disorder, such as psychiatric patient populations, substance abuse clinics and prisoners. Similar relationships emerge in epidemiological samples, but generally speaking the relationship is not so strong. This points to the need for a risk factor model where traumatic stress is only one of a series of contributing variables. Hypothesis 2: Alcohol abuse causes an increased rate of traumatisation because of the association between alcohol use and accidents, violence and rape (Cottler, Compton, Mager, Spitznagel, & Janca, 1992). There is little doubt that there is a significant relationship between alcohol and accidents and violence. This begs the questions as to the extent that this represents secondary victimisation where there is a cycle of traumatisation. This would suggest that there are high rates of alcohol abuse amongst those who are traumatised and that this is not just congregated in the group with PTSD. Hypothesis 3: PTSD leads to an increase or decrease in alcohol use rather than there being a simple linear relationship. This possibility emerges to explain some of the conflicting findings which provide contradictory evidence about the nature of this relationship. A corollary of this hypothesis is that traumatic life events are associated with high or low rates of alcohol use. Hypothesis 4: An extension of the self-medication hypothesis suggests that alcohol abuse is associated with fewer traumatic memories in the short and long term. PTSD in those with substance abuse is more likely to go into remission than those who do not use alcohol. There is a series of articles which have extensively reviewed these and related questions (Brems & Johnson, 1997; Brown, Recupero, & Stout, 1996; Keane, Gerardi, Lyons, & Wolfe, 1988; Kofoed, Friedman, & Peck, 1993; Stewart, 1996; Zaslav, 1994; Zweben, Clark, & Smith, 1994). Rather than reexamining this evidence in detail, this article will use the Bradford Hill criteria to examine the nature and plausibility of this relationship (Hill, 1965). Data which have been collected as an adjunct to a series of studies will be presented to elucidate these various criteria. The Bradford Hill criteria were developed to examine some of the complex questions which emerge about causality. These causal criteria were attributed to Sir Austin Bradford Hill and assist in clarifying observed associations from causal relationships. Often there are different types of evidence from distinct domains which can be brought to bear on these issues. A conclusion emerges out of the counterbalancing of these various arguments, which depends both on the importance of epidemiological data and the existence of plausible hypotheses about the mechanisms which might account for these relationships. These criteria were developed to allow some counterbalancing of different types of information that can be presented in the public health domain. A P P L I C A T I O N

O F

T H E

B R A D F O R D

H I L L

C R I T E R I A

Strength of association Traumatic events lead to alcohol abuse independent of PTSD. The relationship between alcohol and PTSD could be accounted for by two pathways, assuming a causal relationship. Firstly there could be a direct relationship between trauma and alcohol abuse

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independent of the existence of a PTSD. The reanalysis of the North Carolina data set of the Epidemiological Catchment Area (ECA) suggested that there was a significant relationship between substance abuse and traumatisation, particularly when this had occurred in adolescents (Davidson, Hughes, Blazer, & George, 1991). This study suggested a similar relationship between traumatic stress and suicidal thinking. The heavy rates of substance use in Vietnam also indicated that while traumatic exposure continued this pattern of usage remained, suggesting that it was a method of coping with the sense of threat and associated fear (Sapol & Roffman, 1969; Wedding, 1987). The advantage of alcohol in this setting may be that it changes the individual’s state of mind and creates some relief from the enduring feeling of tension. This question was examined in a telephone survey of a stratified sample of people in the city of Adelaide who had listed telephone numbers (Centre for Population Studies in Epidemiology, 1997). A total of 2,501 were contacted. The history of traumatisation was examined using the PTSD section of the Composite International Diagnostic Interview (CIDI) and the drinking pattern was measured to ascertain both the frequency and quantity of alcohol usage (National Heart Foundation, 1989). A specific measure of PTSD was not used although the GHQ (Goldberg, 1972) was used as a measure of general psychiatric morbidity and the pattern of disability was examined using the SF12 (McCallum, 1994). In this population, 19.5% of the population were cases according to the GHQ which is in the lower range of morbidity found in Australian populations using this scale (Clayer, McFarlane, & Bookless, 1997). Using the SF12, 11.8% of the population were defined as having severe depression. Using a 3/4 score on alcohol risk as cutoff, 4.7% of the population had high-risk drinking characterised by more than 13 drinks per drinking session and more than three or four drinking sessions a week. The data in Table 1 show that there is no uniform association between substance abuse and psychiatric morbidity. This suggests that the relationship between PTSD and alcohol abuse is not just a nonspecific effect accounted for by a general relationship with all types of psychiatric morbidity. Both anxiety and depression in this sample were significantly related to prior traumatic exposure, in particular severe depression on the GHQ which is made up of questions biased toward suicidal thinking. In this population the relationship between the different types of traumatic life events examined in the CIDI was investigated (Table 2). This indicated that there was a significant relationship between some but not all traumatic life events and at-risk drinking. The traumatic events associated with at-risk drinking were involvement in life-threatening accidents, witnessing severe injury, rape, being the victim of serious

Table 1. Relationship between high-risk drinking and psychiatric morbidity

Severe Depression (SF-12) Physical Disorder (SF-12) GHQ Casea GHQ Somaticb GHQ Anxietyb GHQ Social Dysfunctionb GHQ Severe Depressionb a 4/5

cutoff for caseness definition. 1/2 cutoff.

b Using

Sample size (n 5 2,501)

% high-risk drinkers (n 5 119)

x2

Sig

295 (11.5%) 825 (33.0%) 488 (19.5%) 534 (21.3%) 486 (19.4%) 366 (14.7%) 127 (5.1%)

24 (20.2%) 32 (27.0%) 30 (25.2%) 29 (24.4%) 37 (31.1%) 14 (11.8%) 12 (10.1%)

7.73 2.14 2.94 0.68 10.88 0.74 6.14

**

*** **

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physical assault and other types of traumatic events. The fact that combat and natural disasters were not associated suggests that the nature of the relationship is not clear. In particular, these events are independent of the individual (could not be caused by the person’s own behaviour) and did not appear to have a direct association. Thus the association could either be that at-risk drinking increased the risk of these events occurring or that these types of traumatic events were independent risks factors for substance abuse. One factor which would favour the latter direction of causality is that it was a lifetime history of these events which was documented and the drinking behaviour was that currently present. The work of Breslau and Davis (1992) suggests that both factors are likely to be contributing. There is other evidence to suggest that the patterns of comorbidity vary for different types of stressor (Deering, Glover, Ready, Eddleman, & Alarcon, 1996). Thus alcohol abuse probably is a risk factor for traumatic exposure and traumatic exposure predicts substance abuse. The fact that many of those who did have exposure to traumatic events were not abusing alcohol indicated that this is a relatively weak association, given that 4.7% of the population demonstrated high risk drinking whereas 53% of the population had exposure to a traumatic event. At the most, 10% of those who had been seriously assaulted had levels of alcohol use which made them at risk. Of those who had at risk drinking, 74.1% had experience a traumatic event, which suggests that although alcohol abuse is not a very common association of traumatic exposure, it has a strong correlation. The relationship between PTSD and alcohol abuse. The issue arises as to whether the relationship between traumatic exposure and alcohol abuse is stronger in the subgroup of those exposed who develop PTSD. This question was examined in a population of 469 firefighters who had an intense exposure to a bushfire disaster (McFarlane, 1988, 1995). The psychiatric morbidity of this population has been described in detail elsewhere (McFarlane & Papay, 1992). At 29 months after the disaster, their pattern of drinking behaviour was examined. At 42 months a PTSD diagnosis was made using the Diagnostic Interview Schedule (DIS) and alcohol abuse was measured using the CAGE. A total of 68 firefighters had no prior disorder and developed a PTSD. Of the 141 high-risk group members and controls interviewed at 42 months, 41.8% (n 5 68) were abusing alcohol according to the CAGE. Of these, 37 also had a PTSD which was a significant association (x2 5 8.52, df 5 1, p , .01). This demonstrated that PTSD was

Table 2. Traumatic experience and relationship to drinking

Combat Life-threatening accident Natural disasters Witnessed severe injury Rape Sexually molested Serious assault Threatened with weapon Torture victim Other events No event

Sample size (n 5 2,501)

% high-risk drinkers (n 5 119)

x2

119 (4.8%) 445 (18.1%) 358 (14.3%) 739 (29.5%) 67 (2.7%) 186 (7.4%) 266 (10.6%) 313 (12.5%) 22 (0.9%) 731 (29.2%) 941 (37.6%)

6 (5.0%) 33 (27.7%) 23 (19.3%) 56 (47.1%) 8 (6.7%) 13 (10.9%) 27 (22.7%) 20 (16.8%) 2 (1.7%) 49 (41.2%) 34 (28.6%)

0.13 7.96 2.68 18.09 9.49 2.7 19.94 2.33 0.79 8.16 4.61

Sig ** *** ** *** ** *

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significantly associated with the existence of alcohol abuse diagnosed by the CAGE. At 29 months the firefighters were asked about the changes in their drinking pattern. Those who developed a PTSD (n 5 63) were likely to either increase or decrease their drinking (n 5 29) in the 6-month period which preceded the diagnosis of their PTSD (x2 5 6.26, df 5 1, p , .01), in contrast to the no-PTSD subjects where only 18 out of 71 reported a change in their drinking pattern. This was not a significant change in the drinking pattern of the PTSD group (n 5 24) compared with those without PTSD (n 5 25) in the period immediately prior to the 42-month assessment (x2 5 0.2, df 5 1, p . .05). Thus the mental state associated with PTSD seemed to either discourage or increase the alcohol consumption of these men in the early stages of the disorder, suggesting that there may be either a self-medication effect or a dysphoric effect of alcohol in this disorder. This may minimise the association between alcohol abuse and PTSD where there is a propensity to use alcohol to sooth aversive mental states. This bidirectional effect may negate this association because there may be a group whose decreased drinking is equally indicative of their psychological distress. In terms of the Bradford Hill criteria this is an argument for the strength of the association between PTSD and alcohol abuse. McFall (1992) similarly suggested that PTSD rather than combat stress per se is linked to the severity of substance abuse. These findings support the hypothesis that there is a significant relationship between PTSD and alcohol and that this is a relationship which is clinically significant. This population had substantial exposure to subsequent trauma as most remained in the volunteer fire service and were involved in fighting minor fires and in motor vehicle accident retrievals. Thus a kindling effect may have been involved. Many had to cope with the stress of rebuilding their homes which had been destroyed or damaged. Many were farmers who had substantial repairs to complete. Also, the possibility exists that the strength of this relationship will differ in different trauma-related disorders, such as posttraumatic depression which emerges in the absence of PTSD, in a subgroup of those with traumatic exposure. Our group conducted a study of 200 motor accident victims who were recruited at the time of admission to hospital with their injuries (McFarlane, 1997). They were interviewed on the first day after the accident and again on the 10th day. They were interviewed again at 6 months and 12 months postaccident. This allowed exploration of the relationship between the emergence of PTSD in a setting where there was an accurate assessment of pre-existing disorders and associated alcohol abuse. There were a total of 35 subjects who developed a PTSD, and 5 of these were positive for substance abuse 6 months after the accident according to the DISSI (Robins & Marcus, 1987). This was a significantly lower rate of substance abuse than would have been anticipated if alcohol abuse was the presumed cause of PTSD in this population. In fact only 3 subjects who developed a PTSD had a prior history of alcohol abuse. Thus while there was a significant rate of PTSD in this population only a small percentage developed alcohol abuse. There were more cases of substance abuse which preceded these people’s accident. The weakness of this association was significantly less than that expected, given the rates of comorbidity in the National Comorbidity Study (Kessler, Sonnega, Bromet, & Nelson, 1995) and Vietnam Veterans Readjustment Study (Kulka et al., 1990). This was particularly noteworthy because of the earlier data presented which associated accidents with alcohol abuse and raised the possibility of the accident being due to substance abuse (Cottler et al. 1992). Another possibility is that alcohol abuse emerges later than the first 2 years after the trauma which this study investigated. Thus, alcohol abuse may represent a late rather than an

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early association of PTSD. This is consistent with the suggestion that there is a progressive increase in the severity of symptoms of PTSD, particularly in the first 6 months after the traumatic exposure (McFarlane, 1997). Furthermore the severity of the physical injury in this population may have had an effect of modifying their use of alcohol in the acute postinjury period. These findings from three different populations indicate that the strength of the association between alcohol abuse and PTSD is hidden by the complexity of the longitudinal emergence of the PTSD and the use of alcohol to modify the symptoms. This can readily hide the strength of the association if these complicated relationships are not taken into account. Consistency of association There is a series of epidemiological studies which show the comorbidity of PTSD and substance abuse, particularly alcohol. The only debate emerges as to whether this is due to the pre-existence of this behaviour or whether it has emerged in the aftermath of the event. This issue has been examined in most detail in the Vietnam Veterans study (Kulka et al., 1990). The data suggest that there was a pattern of polysubstance abuse which emerged in many soldiers while in Vietnam as a way of dealing with the enduring stress of combat (Wedding, 1987). Only a minority of these servicemen went on to develop substance abuse on return to the U.S. This indicates that there is a series of other risk factors necessary to explain the existence of alcohol abuse in association with PTSD. These are the same general risk factors which exist in other population settings. This suggests that this association needs to be understood in the context of a multifactorial model (Helzer, 1984). This raises the question as to what the role of the traumatic stressor is, in contrast to the other risk factors present. Firstly, the evidence is that veterans with higher levels of combat exposure were more likely to abuse alcohol than those who saw considerably less combat (Keane et al., 1988). There is also evidence from several studies indicating that the level of combat predicted both the current and lifetime prevalence of comorbid alcohol abuse (Fisher, 1991; Jordan et al., 1991). The ability of this evidence to generalise is an important issue. In contrast to other traumatic stressors, combat occurs over a period of months and occurs in a highly structured social setting. Much of the comradeship of the military is built around the mess and alcohol. These factors have less ability to play a role in traumatic events which have a very brief duration of effect such as witnessing a violent assault or being involved in a life-threatening accident which are generally confined to one individual or small group. Cottler et al. (1992) using the Epidemiological Catchment Area study suggested that the onset of substance abuse preceded the onset of posttraumatic symptoms, suggesting that substance abuse predisposes people to traumatic events or vulnerability to PTSD after such exposure. Kofoed et al. (1993) reviewed the evidence about the role of risk factors and suggested that preservice variables were better predictors of alcohol abuse than combat exposure. These included a family history, age at the time of combat and the use of a learned helplessness pattern of attribution. Thus the epidemiological evidence suggests the consistency of the relationship between alcohol abuse and PTSD. The question is as to the nature of the association. There is sufficient evidence to suggest a multifactorial risk factor model. PTSD is present in a significant percentage of those subjects for whom exposure is critical in the initiation of the substance abuse, but there is another group where the alcohol abuse preceded the event with associated risk factors necessary to understand its on-

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set. In this latter group the evidence suggests that PTSD intensifies the abuse and tends to increase its chronicity. The pattern of drinking may be missed in many data sets, particularly those collected cross-sectionally, indicating the importance of longitudinal studies to investigate this question further. The developmental stage of the PTSD is one factor which may influence the consistency of the association found. Given the importance of social and cultural factors in the consumption of alcohol, the consistency of association should be in terms of cohort effects. Specificity of association In a disorder where there is no dispute about a multifactorial model, the issue of the specificity of the association is a complex question. The fact that other variables play a role in the aetiology of substance abuse means that there will not be a one-to-one relationship between substance abuse and either traumatic exposure or PTSD. To begin with, alcohol abuse is also associated with other psychiatric disorders such as major depressive disorder, social phobia and panic disorder (Kaplan & Saddock, 1998). The evidence for the direction of causal relationship is less clear particularly in relation to major depression where the data would suggest that alcohol abuse has the ability to mimic and increase many of the symptoms of major depressive disorder (Kaplan & Saddock, 1998). Thus, although there is not a specificity of association between PTSD and alcohol abuse, the data would tend to indicate that the causal relationship is perhaps more directly established than with other psychiatric disorders. One way of exploring the relative importance of PTSD as a comorbid condition associated with alcohol abuse is to look at the relative specificity of this relationship in a series of different at-risk populations and to look at the patterns of association in contrast with the other disorders present in these populations. The first study is of a series of 143 consecutive admissions to a general hospital inpatient unit. The full range of psychiatric disorders was present in the admission diagnoses given. The patients were interviewed using the DIS (Robins et al., 1982) and WHO Disability Assessment Schedule (World Health Organisation, 1988). PTSD was the diagnosis in only one case. The CAGE (Mayfield, McLeod, & Hall, 1974) was also given. In contrast to the admission diagnosis on the DIS, a total of 27% of the patients were found to have a lifetime history of PTSD and in approximately 80% of these cases, using a lifetime history method, this was found to be the index episode of psychiatric illness. The group who had a lifetime history of PTSD had significantly higher scores on the CAGE indicating that in a general psychiatric patient population, this was an important risk factor for current alcohol abuse. This suggests that in psychiatric patient populations, the importance of PTSD as a risk factor for substance abuse requires further investigation. Many of the studies which have looked at substance abuse in patient populations have not looked at PTSD as a general risk factor, despite its importance. PTSD has also been found to be a very common diagnosis in substance abusing populations, particularly those seeking treatment (Triffleman, Ball, & Rounsaville, 1995). This further indicates that PTSD is a risk factor among the other psychiatric disorders which has greater specificity for substance abuse than the other psychiatric diagnoses. On the other hand, these data suggest that the specificity of the relationship between PTSD and alcohol abuse may be indicative of a more general relationship between substance abuse and PTSD. This relationship was further investigated in a study of 43 female prisoners who reflected the entire incarcerated population of women in the state of South Australia during the period of the study (Raeside, 1994). Of these, 35 had a current PTSD diagno-

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sis as assessed by the CIDI (World Health Organisation, 1993). Of these, 25 had a history of PTSD and substance abuse. The typical history of these women was that they had been the victims of child abuse and their PTSD had been manifest in their early adolescence. A pattern of substance abuse then emerged which contributed to their criminal behaviour. A cycle of domestic violence, rape and assault followed. Twenty of the 25 with the comorbid disorder had been the victims of intentional violence against themselves. This suggests that in a variety of populations who are at high risk the specificity of the relationship between PTSD and substance abuse (Jordan et al., 1991) appears to hold up and that this is more robust than the relationship between substance abuse and other psychiatric disorders. This is of particular importance in female prisoners because of the high rates of substance abuse (Maden, Swinton, & Gunn, 1994). One of the issues which clouds the examination of this question is the infrequency with which a trauma history has been collected in studies examining the relationship between alcohol abuse and other psychiatric disorders. Thus there is increasing evidence that PTSD is only one of the posttraumatic disorders, both in the immediate period which follows exposure and in the longer term. Alcohol abuse is associated with other psychiatric disorders such as panic disorder, major depression and social phobia. In the first two, the evidence is that the strength of a causal link is less established than in PTSD, as alcohol abuse can cause the symptoms of depression and lead to anxiety particularly when in states of withdrawal. This suggests that although there is an association between alcohol and psychiatric disorders in general, the relationship is more of a causal nature in PTSD than in panic and depression where alcohol abuse can lead to an intensification of symptoms. Temporality of association This issue has already been referred to in several of the longitudinal studies mentioned before and was highlighted by Bremner, Southwick, Darnell, and Charney (1996) in their study of Vietnam veterans. The importance of longitudinal research in investigating the temporality of association is critical in interpreting the available data. There is evidence to support a series of different models of temporality of association which can be summarised as follows: Antecedent models: Alcohol abuse increases the risk of traumatic exposure. Alcohol abuse increases the risk of developing PTSD. Precipitation models: Alcohol abuse emerges following traumatic exposure. Alcohol abuse develops following the development of PTSD following traumatic exposure. Longitudinal models: Alcohol abuse represents a risk factor for chronicity of PTSD. Alcohol abuse may only emerge in the period after initial PTSD symptoms fail to settle with the passage of time. Alcohol abuse remains while the PTSD has gone into remission and may be associated with some other psychiatric disorder which has taken over from PTSD as the primary psychiatric diagnosis. This highlights that there may be a variety of different temporal relationships present in the one population. The one identified may well depend upon the point in

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the longitudinal course when the population is investigated. The existence of these multiple possible relationships also indicates the methodological problems in trying to investigate this question. The sample size necessary to demonstrate these different effects and to take account of the possible interactions is very large and beyond the scope of most research groups. Hence, the possibility of these different aetiological relationships is often not taken into account in the analysis or interpretation of the available data sets. Gradient of effect The evidence for gradient effects and exposure is sparse. Most traumatic events are defined in epidemiological studies as being present or absent, for example, the national comorbidity study (Kessler et al., 1995). This does not allow gradients of effect to be analysed. This can only occur in large data sets which examine a single event. There are many problems about the way in which to quantify the gradients of severity when it comes to combat or natural disasters (McFarlane, 1995). For example, in a quantitative sense, how does one rate the relative trauma associated with the loss of a spouse, near fatal injury and the destruction of a home? This issue has been examined in two settings. In the firefighters study following the Ash Wednesday bushfires, the exposure and losses of these men were documented in detail. When a composite measure of the disaster was entered in to a multiple regression analysis of the CAGE total, the relationship approached significance (F 5 2.1, df 5 5, 113, p 5 .07, adjusted R2 5 .045). The contribution of the individual variables was examined because of the conceptual issues involved in the development of a linear model of the gradient of effect. The CAGE total was correlated with the number of days spent mopping up after the disaster (r 5 .17, p , .05) and the severity of property loss (r 5 .23, p , .01). This suggested ongoing stresses of living with the impact of the disaster on the firefighters’ livelihood and accommodation arrangements. It appears that in this population it was not the severity of the acute sense of threat or the duration of exposure to the fires which predicted later alcohol abuse, but rather the severity of the losses. Thus substance abuse may emerge in the need to control the chronic stresses associated with the disaster. This suggests that there is a gradient of effect. This contrasts to the lack of association between the ranking of stressors in professional firefighters and alcohol consumption (Boxer & Wild, 1993). Keane et al. (1988) demonstrated a relationship between combat exposure and alcohol consumption where Vietnam veterans with high levels of combat were more likely to abuse alcohol. Later work of Jordan et al. (1991) and Fisher (1991) found similar relationships between the severity of combat trauma and the current and lifetime rates of substance abuse. This suggests that there is a contribution of the gradient of effect both to the prevalence and chronicity of alcohol abuse. In summary, despite the scant nature of the data, there does appear to be a gradient effect supporting the role of traumatic stress in the initiation of substance abuse. B I O L O G I C A L

P L A U S I B I L I T Y / C O H E R E N C E

Kosten and Krystal (1988) have proposed a cogent argument as to how alcohol could lessen the symptoms of PTSD given the neurochemical properties of alcohol and the underlying neurobiology of PTSD. Of particular relevance is the impact of alcohol on the locus coeruleus which modulates the alarm reaction (Brick & Poherecky,

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1983; Goddard, 1958; Lynch et al. 1983). Southwick et al. (1993) using yohimbine as a probe have proposed that norepinephrine dysregulation is a central feature of the disorder. The ability of alcohol to decrease the activity of the norepinephrine projections of this nucleus may explain why it appears to be a drug of choice in PTSD. This suggest that there is biological plausibility in the use of alcohol as a drug of abuse in PTSD. E X P E R I M E N T A L

E V I D E N C E

There is considerable debate about what is an acceptable animal model for PTSD. Yehuda and Antelman (1993) argued that many of the models are general models of stress rather than true models of PTSD. This means that there is a paucity of experimental research or models for examining the impact of alcohol on the symptoms of PTSD or the alcohol consumption in animals with an experimentally induced disorder. There is some evidence from inescapable electric shock models that alcohol consumption increases in rodents in a delayed pattern (Kosten & Krystal, 1988). In humans it is not possible, for the obvious ethical reasons, to conduct research looking at the impact of alcohol on the symptoms of PTSD. Fortuitously there is some evidence that alcohol may lessen the severity of distress in acutely traumatised individuals. Alcohol has been used throughout the ages by soldiers to quell their nerves in battle. In the study of motor accident victims, the pattern of acute distress was examined in those who had a current history of alcohol abuse at the time of the accident. This group had lower levels of intrusive thoughts of the accident on Day 2 (t 5 2.35, df 5 185, p 5 .023), Day 10 (t 5 4.31, df 5 183, p 5 .0001) and 12 months (t 5 2.66, df 5 155, p 5 .011) as measured by the Impact of Events Scale. This suggests that alcohol may lessen the intensity of traumatic memories and their chronicity. This implies that there may be some adaptive advantage in using alcohol at the times of exposure to traumatic stressors. In the longitudinal phase of the firefighters study, there was also evidence that those who consumed larger amounts of alcohol were less likely to have persistent chronic PTSD but were more likely to have fluctuating symptoms or for their PTSD to resolve. This suggests that, although there is a series of significant negative health effects with alcohol, there may be some positive benefits in terms of the mitigation of PTSD symptoms. This may explain the high rates of comorbidity in the Veteran populations. A N A L O G Y

The central analogy to explain the association between PTSD and alcohol abuse is a model of self-medication. It is a clinical wisdom that patients with PTSD use alcohol to relieve or control the distress associated with their self-regulation problems. Khantzian (1985) has developed such a model to explain addictive behaviour where alcohol serves to treat the affect deficits, interpersonal difficulties and hyperarousal. Possibly, the creation of an alternate mental state to the hypervigilance of PTSD which has some of the characteristics of dissociation is a state of mind that provides some respite for the traumatised individual. A central hypothesis about the aetiology of PTSD is the disruption of the homeostasis of the individual which has biological and psychological correlates. Pharmacological agents used in the treatment of PTSD have some similarities in effect to the biological effects of alcohol. Within the self-medication model there is some controversy as to whether the positive impact of drug-induced euphoria is critical or whether the negative relief from dis-

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tress plays the central role in the reinforcement of substance abuse. Volpicelli (1987) suggests that the evidence for the tension relief models is inconsistent and that there is more support for the positive reinforcement model. Kofoed et al. (1993) have also suggested that the self-medication model in PTSD and substance abuse is of little help for planning therapeutic approaches. However there is some support for the greater effectiveness of treatment which addresses both domains simultaneously. Another argument is that the choice of drug for abuse in PTSD is too nonspecific for the selfmedication hypothesis to be plausible (Kofoed et al., 1993). In summary, there is sufficient evidence to argue that alcohol abuse is a predictable consequence of PTSD. The relative ineffectiveness of treatments in the more chronic forms of the disorder may explain why there are such high rates of comorbid alcohol abuse. C O N C L U S I O N

The Bradford Hill Criteria provide a matrix which suggests that on these criteria there is an aetiological association between exposure to traumatic stress, PTSD and alcohol abuse. The evidence to examine this relationship comes from a variety of different sources and uses different perspectives in considering the question. There is not a simple relationship, as indicated in the hypotheses proposed (which are generally supported), as alcohol abuse can increase the rates of traumatisation as a result of the association with violence and accidents (Brown & Wolfe, 1994). As well as the possible self-medication benefits of alcohol, it has the capacity to hide the association by modifying the symptoms of the associated PTSD. Future research should aim to use large populations and a lifetime or prospective longitudinal methodology to further clarify the issues highlighted. Given the variations in drinking at different points in the onset and in the chronic phase of the disorder, this is critical to preventing false negative associations. There appears to be sufficient argument to support a causal association in a forensic setting as long as the caveats addressed do not apply, such as the event being secondary to pre-existing abuse. The potential for traumatic events to lead to substance abuse is a major public health issue, given the prevalence of these events and the potential for a spiral of secondary retraumatisation which is most graphically demonstrated in the female prisoner population. This would have major ramifications for the prevention of violence, accidents and rape. Finally, although the self-medication hypothesis has some support, it is the general wisdom that the most successful treatment programs simultaneously treat the substance abuse and the PTSD (Brems & Johnson, 1997). One of the central issues in this field is for the complex interlinking of these problems not to be lost in the public policy domain, where these relationships are easily missed as they fall into the domains of different public authorities such as prisons, child welfare agencies, rape crisis centres and health care. R E F E R E N C E S Boxer, P. A., & Wild, D. (1993). Psychological distress and alcohol use among fire fighters. Scandinavian Journal of Work, Environment, and Health, 19(2), 121–125. Bremner, J. D., Southwick, S. M., Darnell, A., & Charney, D. S. (1996). Chronic PTSD in Vietnam combat veterans: Course of illness and substance abuse. American Journal of Psychiatry, 153(3), 369–375. Brems, C., & Johnson, M. E. (1997). Clinical implications of the co-occurrence of the substance use and other psychiatric disorders. Professional Psychology: Research and Practice, 28, 437–447.

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Breslau, N., & Davis, G. C. (1992). Posttraumatic stress disorder in an urban population of young adults: Risk factors for chronicity. American Journal of Psychiatry, 149(5), 671–675. Brick, J., & Poherecky, L. A. (1983). Ethanol-stress interaction: Biochemical findings. Psychopharmacology, 77, 81–84. Brown, P. J., Recupero, P. R., & Stout, R. (1996). PTSD substance abuse morbidity and treatment utilization. Addictive Behaviours, 20, 251–254. Brown, P. J., & Wolfe, J. (1994). Substance abuse and post-traumatic stress disorder comorbidity. Drug and Alcohol Dependence, 35(1), 51–59. Centre for Population Studies in Epidemiology. (1997). Sercis: mental health survey. Adelaide: South Australian Health Commission. Clayer, J. R., McFarlane, A. C., & Bookless, C. L. (1997). Psychiatric morbidity following a natural disaster—An Australian bushfire. Social Psychiatry & Psychiatric Epidemiology, 32, 261–268. Cottler, L. B., Compton, W. M., III, Mager, D., Spitznagel, E. L., & Janca, A. (1992). Post traumatic stress disorder among substance abusers from the general population. American Journal of Psychiatry, 149, 664–670. Davidson, J. R., Hughes, D., Blazer, D. G., & George, L. K. (1991). Post-traumatic stress disorder in the community: An epidemiological study. Psychological Medicine, 21(3), 713–721. Deering, C. G., Glover, S. G., Ready, D., Eddleman, H. C., & Alarcon, R. D. (1996). Unique patterns of comorbidity in posttraumatic stress disorder from different sources of trauma. Comprehensive Psychiatry, 37, 336–346. Fisher, V. I. (1991). Combat exposure and the etiology of post discharge substance abuse problems among Vietnam veterans. Journal of Traumatic Stress, 48, 207–215. Goddard, P. I. (1958). Effect of alcohol on excretion of catechol aminecs in conditions giving rise to anxiety. Journal of Applied Physiology, 13, 118–120. Goldberg, D. (1972). The detection of psychiatric illness by questionnaire. Oxford, UK: Oxford University Press. Helzer, J. E. (1984). The impact of combat on later alcohol use by Vietnam veterans. Journal of Psychoactive Drugs, 16(2), 183–191. Hill, A. B. (1965). A short textbook of medical statistics (11th ed.). London: Edward. Jordan, B. K., Schlenger, W. E., Hough, R., Kulka, R. A., Weiss, D., Fairbank, J. A., & Marmar, C. R. (1991). Lifetime and current prevalence of specific psychiatric disorders among Vietnam veterans and controls. Archives of General Psychiatry, 48, 207–215. Kaplan, H. I., & Saddock, B. J. (1998). Synoposis of psychiatry. Baltimore: Williams & Wilkins. Keane, T. M., Gerardi, R. I., Lyons, J. A., & Wolfe, J. (1988). The interrelationship of substance abuse and posttraumatic stress disorder: Epidemiological and clinical considerations. Recent Developments in Alcoholism, 6, 27–48. Kessler, R., Sonnega, A., Bromet, E., & Nelson, C. B. (1995). Posttraumatic stress disorder in the National Comorbidity Survey. Archives of General Psychiatry, 52, 1048–1060. Khantzian, E. J. (1985). The self-medication hypothesis of addictive disorders. American Journal of Psychiatry, 142, 1259–1264. Kofoed, L., Friedman, M. J., & Peck, R. (1993). Alcoholism and drug abuse in patients with PTSD. Psychiatric Quarterly. 64(2), 151. Kosten, T. R., & Krystal, J. H. (1988). Biological mechanisms in post traumatic stress disorder: Relevance for substance abuse. In M. Galanier (Ed.), Recent advances in alcoholism (Vol. 6, pp. 49–68). New York: Plenum. Kulka, R. A., Schlenger, W. E., Fairbank, J. A., Hough, R. L. Jordan, B. K., Marmar, C. R., & Weiss, D. S. (1990). Trauma and the Vietnam War generation: Report of findings from the National Vietnam Veterans Readjustment Study. New York: Brunner/Mazel. Lynch, M., Littleton, J., McKernan, R. M., Durcan, M. J., McMillan, T., & Campbell, I. C. (1983). Alphaadrenoceptor number and function in rat cortex after ethanol and immobolization stress. Brain Research, 288, 145–159. Maden, T., Swinton, M., & Gunn, J. (1994). Psychiatric disorder in women serving a prison sentence. British Journal of Psychiatry, 164, 44–54. Mayfield, D., McLeod, G., & Hall, P. (1974). The CAGE questionnaire: Validation of a new alcoholism screening instrument. American Journal of Psychiatry, 131(10), 1121–1123. McCallum, J. (1994). The new ‘SF-36’ Health Status Measure: Australian validity tests. Canberra, Australia: National Centre for Epidemiology and Population Health. McFall, M. E. (1992). Combat-related posttraumatic stress disorder and severity of substance abuse in Vietnam Veterans. Journal of Studies on Alcohol, 53, 357–363. McFarlane, A. C. (1988). The longitudinal course of post-traumatic stress disorders following a natural disaster. Journal of Nervous and Mental Disease, 176, 22–29. McFarlane, A. C. (1995). The severity of the trauma: Issues about its role in posttraumatic stress disorder. In R. Kleber & C. Figley (Eds.), Beyond trauma: Cultural and societal dynamics (pp. 31–54). New York: Plenum. McFarlane, A. C. (1997). The prevalance and longitudinal course of PTSD. In R. Yehuda & A. C. McFarlane (Eds.), Psychobiology of posttraumatic stress disorder (pp. 10–23). New York: New York Academy of Sciences.

PTSD and alcohol abuse

825

McFarlane, A. C., & Papay, P. (1992). Multiple diagnoses in post traumatic stress disorder in the victims of a natural disaster. Journal of Nervous and Mental Disease, 180, 498–504. National Heart Foundation. (1989). Risk factor prevalence study (Survey No. 3). Adelaide: National Heart Foundation of Australia. Raeside, C. W. J. (1994). Posttraumatic stress disorder in a female prison population. Dissertation, Royal Australian and New Zealand College of Psychiatrists. Robins, L. N., Helzer, J. E., Ratcliff, K. S., et al. (1982). NIMH Diagnostic Interview Schedule: Version III. Rockville, MD: National Institute of Mental Health. Robins, L. N., & Marcus, S. C. (1987). The Diagnostic Screening Procedure Writer. Medical Care, 25(Suppl.), S106–S122. Sapol, E., & Roffman, R. A. (1969). Marijuana in Vietnam. Journal of the American Pharmacology Association, 9, 615–630. Southwick, S. M., Krystal, J. H., Morga, C. A., Johnson, D., Nagy, L. M., Nicolaou, A., Heninger, G. R., & Charney, D. S. (1993). Abnormal noradrenergic function in posttraumatic stress disorder. Archives of General Psychiatry. 504(4), 266–274. Stewart, S. H. (1996). Alcohol abuse in individuals exposed to trauma: A critical review. Psycological Bulletin, 120, 83–112. Triffleman, E., Ball, S., & Rounsaville, B. (1995). Screening for PTSD in substance dependent outpatients. Proceedings of the 56th Annual Scientific Meeting of the Committee for Problems in Drug Dependence, National Institute on Drug Abuse Research Monograph, 153(2), 345. Volpicelli, J. R. (1987). Uncontrollable events and alcohol drinking. British Journal of Addictions, 82, 381– 392. Wedding, D. (1987). Substance abuse in the Vietnam veteran. AAOHN Journal, 35, 74–76. World Health Organisation. (1988). WHO Psychiatric Disability Schedule. Geneva: Author. World Health Organisation. (1993). Composite International Diagnostic Interview. Geneva: Author. Yehuda, R., & Antelman, S. M. (1993). Criteria for rationally evaluating animal models of posttraumatic stress disorder. Biological Psychiatry, 33, 479–486. Zaslav, M. R. (1994). Psychology of comorbid posttraumatic stress disorder and substance abuse: Lessons from combat veterans. Journal of Psychoactive Drugs, 26, 393–400. Zweben, J. E., Clark, H. W., & Smith, D. E. (1994). Traumatic experiences and substance abuse: Mapping the territory. Journal of Psychoactive Drugs, 26, 327–344.