The core finding of this study is that TNA do not evidence more psychiatric diagnoses than NAC, but do evidence substantial psychological differences from NAC in the anxiety, mood, and externalizing domains. TNA showed a strong disposition for more anxiety, mood disturbance (both depressive and hypomanic), and deviance proneness on all psychological measures compared to NAC. The results for symptom counts were intermediate between the lack of findings on diagnosis rates and the strong findings on psychological tests. TNA had higher symptom counts than NAC for symptoms aggregated across all domains, for externalizing symptoms. For mood and anxiety symptoms, there was a trend for male TNA to have more symptoms than male NAC. In sum, with regard to psychiatric disorder in the anxiety, mood, and externalizing domains, we see psychological differences between TNA and NAC, smaller differences in psychiatric symptom counts, and no differences in actual psychiatric diagnosis rates. In other words, the observed psychological abnormality is attenuated with regard to manifestation in behavior (symptoms), seldom resulting in behavior that meets criteria for a psychiatric diagnosis.
Previous research has described the high incidence of comorbid psychiatric mood, anxiety, and externalizing disorders in individuals diagnosed with a substance use disorder (Di Sclafani et al., 2007
; Grant et al., 2004b
; Grant et al., 2004c
; Kessler et al., 1997
). In our study of long-term abstinent alcoholics, in whom a lifetime psychiatric diagnosis was the norm, we demonstrated that the association between an alcohol use disorder and comorbid psychiatric illness also exists for sub-diagnostic symptom counts and for psychological abnormality in the mood, anxiety, and externalizing disorder domains. Those findings indicated that diagnostic status was insensitive as an indicator of comorbid pathology when compared to psychiatric symptom counts and measures of psychological abnormality. In that study, we showed that using only the tail of the symptomatology distribution (i.e., diagnoses) is insufficient to control for psychiatric comorbidity in alcoholics. The results of the current treatment-naive study offer additional support for this conclusion. Without examining sub-diagnostic measures, our findings suggest that the TNA sample is psychiatrically normal. However, the sub-diagnostic data present a very different picture, clearly establishing that the TNA subjects are abnormal compared to NAC in all domains.
The comparisons between the TNA and TAA studies show that these groups of alcoholics are different in regard to psychiatric comorbidity, and add even more support for the use of subdiagnostic measures. Intuitively, we hypothesized that the TAA would have less comorbidity, since they were so successful in maintaining long-term abstinence. However, the TAA compared to the TNA had more symptoms and more lifetime and current diagnoses in all three psychiatric domains. TAA also evidenced more deviance proneness than TNA. In contrast, on the mood and anxiety domain psychological measures, TAA and TNA were comparable. In other words, in the mood and anxiety domains, TNA showed comparable psychological substrate abnormality to TAA, but much less behavioral abnormality. If we had limited our analysis to diagnosis rates, only the lessened psychiatric mood and anxiety comorbidity in TNA versus TAA would have been observed, again missing the abnormal (but less than TAA) TNA symptom counts, and the nearly comparable psychological substrate abnormality in the two study samples.
The efforts to classify alcoholics into clinically meaningful subgroups were advanced by our prior finding that TNA are a different population than TAA with regard to alcoholism severity, having lower doses than TAA during the early period of heavy alcohol use (Fein & Landman, 2005
). We now show that TNA evidence much less psychiatric comorbidity than TAA. This demonstrates that generalization regarding psychiatric comorbidity in alcoholics from studies of treated samples to the population of untreated alcoholics is unwarranted. Our results also affirm once more the very strong association between the externalizing disorders of alcoholism and ASPD. Symptoms of ASPD (e.g., impulsivity, low harm avoidance, boredom susceptibility/thrill and adventure seeking, poor learning from negative consequences, etc.), are very similar to the traits of addiction. In addition, there is a different neural substrate for ASPD compared to mood and anxiety disorders. Mood and anxiety disorders are associated with a oversensitization of the Hypothalamic-Pituitary-Adrenal (HPA) axis resulting in hypercortisolism (Arborelius et al., 1999
; Brady and Sinha, 2005
; Plotsky et al., 1995
). In contrast, there is undersensitivation of the HPA axis (indicated by hypocortisolism) in ASPD, including substance abusers with ASPD (Deroche et al., 1997
; King et al., 1990
; Kosten et al., 2000
; Moss et al., 1995
; Vanyukov et al., 1993
There is considerable research showing that a high family density of alcoholism is strongly associated with a greater severity of both alcoholism and other externalizing psychiatric disorders (Babor, 1996
; Babor et al., 1992
; Hesselbrock and Hesselbrock, 2006
; Moss et al., 2007
; Penick et al., 1999
). At present, it is unclear whether this association arises from strong genetic loading for both alcoholism and antisocial personality, or of a single, heritable, ‘liability’ for externalizing illness (Krueger et al., 2005
). This hypothesized externalizing liability predisposes individuals to express externalizing pathology; whether in one or multiple disorders, and in varying degrees of severity. In a comparison of the fit of categorical and continuous models to the NESARC data (n = 43,093), Markon and Krueger (2005)
showed that both the first and second best-fit models were continuous (such as symptoms) rather than categorical (such as diagnoses), confirming that continuous conceptions of externalizing liability (that are normally distributed) provided substantial gains in fit over categorical conceptions of externalizing liability. Our results support Krueger's hypothesis. Findings were much stronger using subdiagnostic measures rather than diagnoses. Moreover, a single, heritable, externalizing liability is consistent with the data from both TNA and TAA. In both samples, differences from NAC on externalizing symptom counts and psychological measures of deviance proneness were much larger than the results for comparable symptoms and measures in the mood and anxiety domains.
It is likely that some of the TNA will eventually seek treatment (all treated alcoholics were at an earlier time TNA). We believe it is likely that the TNA with the most externalizing psychiatric symptoms, greatest dose, and most dense family histories of problem drinkers are, or will become, the type of alcoholic seen in the TAA study. The TAA had a greater family density of problem drinkers, higher alcohol dose, and more externalizing psychiatric symptoms than TNA.
There are caveats to this research. The decision to compare the two studies, treatment-naive versus treated alcoholics, was post-hoc. Therefore, the samples were not designed to be directly comparable. There are two major differences between the TNA and the TAA study; the TNA are still drinking (as opposed to the long-term abstinent alcoholics in the TAA study), and the TNA are younger than the TAA. (Each study had an age- and gender- comparable control group.) These factors do not invalidate the comparison of the studies because, with regard to drinking, we have already shown that these TNA and TAA come from different populations with regard to alcoholism severity. In addition, there were no correlation between abstinence duration and lifetime or current diagnoses in TAA (there is very strong evidence that psychiatric comorbidity in alcoholics does not arise from alcohol dependence, but is premorbid (Berman and Noble, 1995
; Hesselbrock et al., 1991
; Merikangas and Avenevoli, 2000
; Nurnberger et al., 2004
; Pihl and Peterson, 1991
; Yoshino et al., 2000
). Finally, if current drinking exacerbated psychiatric comorbidity, the bias in this study would be against our findings; that is, the TNA would be more psychologically disturbed. Vis-à-vis the difference in age between the TNA and TAA studies, the ‘original’ age and gender comparable control groups for each study were combined because there were no cohort differences between the control groups in any of the dependent measures. In addition, there were no associations between age and diagnoses, symptoms, or psychological measures in any of the groups.
Improvements could be made in this study regarding 1)
collection of information on current symptoms ( the c-DIS does not yield information on current symptoms, although it does yield information on current diagnoses), 2)
collection of information regarding which symptoms were linked to alcohol-seeking, intoxication, or withdrawal, and which were present not in the context of alcohol-seeking, intoxication, or withdrawal (Collins and Schlenger, 1988
; Hines and Straus, 2007
), and 3)
the addition of an assessment of Borderline Personality Disorder in the externalizing domain. (Borderline Personality Disorder is often comorbid with alcohol use disorders (Bowden-Jones et al., 2004
; Dom et al., 2006
), and is strongly associated with impulsivity (Dowson et al., 2004
) and disadvantageous decision-making (Bazanis et al., 2002
; Bowden-Jones et al., 2004
; Dom et al., 2006