Antisocial Symptoms Decrease to Normal Levels in Long-Term Abstinence

Abstract

Background

We have previously shown highly elevated antisocial symptoms and measures of social deviance proneness and antisocial disposition in long-term abstinent alcohol dependence versus non-substance-abusing controls (NSAC). Current antisocial symptoms were reduced to subdiagnostic levels in long-term abstinence; however, the number of current symptoms was not measured beyond its being subdiagnostic.

Methods

Here we measured social deviance proneness, antisocial disposition, and both lifetime and current antisocial symptoms in short-term and long-term abstinent substance-dependent and NSAC samples.

Results

Lifetime antisocial symptoms (and diagnoses) and social deviance proneness and antisocial disposition were highly elevated in both short- and long-term abstinence, replicating earlier findings. Current antisocial symptoms were dramatically reduced in long-term versus short-term abstinent samples, close to levels in controls. In contrast, social deviance proneness and antisocial disposition remain highly elevated in long-term abstinence.

Conclusions

These findings suggest that antisocial behavior is reduced in extended abstinence, despite continued elevated social deviance proneness an antisocial disposition. This suggests a top-down model in extended abstinence, whereby executive control inhibits deviance-prone tendencies.

In 2007, we showed that a lifetime antisocial personality disorder (ASPD) diagnosis was more prevalent in a long-term abstinent alcohol-dependent sample than non-substance-abusing controls (NSAC) (Di Sclafani et al., 2007). Lifetime ASPD symptoms were higher in long-term abstinent alcoholics (LTA) than controls, even when individuals with an ASPD diagnosis were excluded, demonstrating that a dimensional versus diagnostic assessment of ASPD problems was more sensitive to the difference between alcoholics and controls. No individuals had a current ASPD diagnosis, consistent with current ASPD behavior decreasing to subdiagnostic levels in long-term abstinence. Psychological measures of deviance proneness remained highly elevated in LTA versus controls, suggesting that behavior changed despite unchanged dispositional antisociality. An important limitation was that we did not have data on current ASPD symptoms. We used the computerized diagnostic interview schedule (C-DIS) (Blouin et al., 1988) for ASPD diagnosis and symptom assessments. The C-DIS determines currency of symptoms only when diagnostic criteria are met, reinforcing a diagnostic versus dimensional bias through the data that it collects. We also did not determine which individuals had adult antisocial behaviors only (AABO) or ASPD without conduct disorder (CD), an important ASPD subtype that is often ignored. Finally, our sample excluded individuals with comorbid lifetime substance use disorders (SUDs), providing data only on LTA in “pure” alcoholics. In this study, we address these limitations of the earlier study.

ASPD is more prevalent in SUDs and alcohol use disorders (AUDs) than controls (Compton et al., 2005; Goldstein et al., 2007). A 2010 paper (Grella et al., 2010) found that 30% of individuals (n = 578) with an opioid use disorder had a diagnosis of ASPD. In a study of psychiatric comorbidity among 629 drug users in Barcelona, Torrens and colleagues (1980) found that 16.5% had a lifetime diagnosis of ASPD. In a 2007 article, Ralevski and colleagues (2007) stated that ASPD is the most frequently diagnosed personality disorder among individuals with alcohol and other drug dependence, with ASPD rates ranging from 15 to 50%.

A large body of the literature suggests that individuals with an ASPD diagnosis are less likely to achieve long-term abstinence than those without ASPD. Clinicians often consider patients with ASPD as not responding well to treatment for SUDs (Arndt et al., 1994; Brochu et al., 2002; Favrat et al., 2002; Nurco et al., 1984). Hesselbrock (1991), in a study of 266 alcoholics, reported that alcoholics with ASPD reported poorer 1-year treatment outcomes than non-ASPD alcoholics. A Veterans Administration (VA) study found that, among 255 alcoholic men, only antisocial personality characteristics were consistently associated with worse long-term drinking outcomes (Hunter et al., 2000). Another VA study on 360 men hospitalized for alcoholism from 1980 to 1984 found that one of the best predictors of poor long-term outcome was an ASPD diagnosis (Powell et al., 1998). Westermeyer and Thuras (2011) evaluated 606 individuals in university SUD treatment programs and found that morbidity (as measured by the number and types of substance-related problems and other treatment variables) was greater in those that also had co-occurring ASPD. However, it is important to note that there are also studies that suggest that pessimism for treatment success in SUDs with comorbid ASPD may not be warranted (Alterman and Cacciola, 1991; Cacciola et al., 1995; Longabaugh et al., 1994). Longabaugh and colleagues (1994), for example, suggest that poor prognosis to treatment has been confounded by not covarying on pretreatment drinking measures.

To meet Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (DSM-IV) ASPD diagnostic criteria, a childhood and adult components are required (evidence of CD with onset before age of 15 years is necessary). A 1995 study of 405 drug users (Cottler et al., 1995) evaluated AABO, or ASPD without CD, and found that a full ASPD diagnosis ignored 33% of men and 42% of women in the AABO subtype. A similar study of opioid injectors found that 24% had AABO, but not ASPD (Brooner et al., 1992). These findings support the importance of studying both ASPD and AABO in AUDs/SUDs.

In our prior study, we examined psychological measures of social deviance. We found that the LTA had much higher MMPI Psychopathic Deviance scores and lower socialization scores on the California Psychological Inventory than controls (Fein et al., 2006). In other words, they showed a much higher propensity toward social deviance than controls, even though they did not meet criteria for a current diagnosis of ASPD. Decreasing disinhibitory behavior in the face of a continuing psychological tendency toward social deviance may be critical in achieving long-term abstinence.

In this study, we focus on ASPD (and AABO) diagnoses and symptoms in LTA, short-term abstinent alcoholics (STA), and NSAC (n = 262). Alcohol-dependent samples included individuals with and without comorbid SUD. We expanded the C-DIS interview, with follow-up questions ascertaining currency of all endorsed symptoms. To meet a diagnosis of ASPD or AABO, an individual had to meet at least 3 of 7 criteria (see Table 3 for a list of the criteria). We also examined symptom counts for each of the 7 ASPD criteria.

Materials and Methods

Participants

A total of 262 individuals 35 to 60 years of age were recruited for the study from the Honolulu area by postings at AA meetings, bars and clubs, community centers, treatment centers, Craigslist, and participant referrals. The study had 5 groups: 2 LTA groups, 1 with lifetime dependence on alcohol only (ALC) and 1 with lifetime dependence on alcohol and another drug of abuse (ALC+DRG); 2 STA groups, similarly defined as the LTA groups; and a control group. All groups had both men and women.

The LTA and STA ALC groups met DSM-IV (American Psychiatric Association, 2000) criteria for lifetime alcohol dependence, but not for lifetime abuse or dependence on any other drug (other than nicotine or caffeine). The LTA and STA ALC+DRG groups met DSM-IV lifetime criteria for alcohol dependence and dependence on another drug of abuse. LTA samples were abstinent from alcohol and drugs (other than nicotine and caffeine) for at least 18 months; STA samples were abstinent from 6 to 15 weeks. Inclusion criteria for the control group was a lifetime drinking average of <30 standard drinks per month with no periods of drinking more than 60 drinks per month, and no lifetime history of alcohol or substance abuse or dependence.

Exclusion criteria for all groups were as follows: (i) significant history of head trauma or cranial surgery, (ii) history of diabetes, stroke, or hypertension that required medical intervention, (iii) history of significant neurological disease, (iv) laboratory evidence of hepatic disease, (v) clinical evidence of Wernicke–Korsakoff syndrome, and (vi) lifetime or current diagnosis of schizophrenia or schizophreniform disorder (as determined during the C-DIS interview).

Procedures

All participants completed 4 sessions consisting of clinical, neuropsychological, electrophysiological, and neuroimaging assessments, administered by trained research associates. Controls were asked to abstain from alcohol for 24 hours prior to any laboratory visit. A breathalyzer test (Intoximeters, Inc., St. Louis, MO) and a rapid oral fluid drug screen test (Innovacon Inc., San Diego, CA) for THC, amphetamines, methamphetamines, cocaine, opioids, and PCP were administered to all participants, with a negative result required for all participants at all sessions. Participants were compensated for their time and travel expenses and were given a bonus for completing the entire study. The data presented here were from the first-day clinical psychiatric and psychological assessments. The study was reviewed and approved by an independent human subjects research review committee (E&I Review Services, LLC, Corte Madera, CA), and signed informed consents were obtained from all participants.

Alcohol-, Substance-, and Nicotine-Use Measures

Participants were interviewed on their lifetime use of alcohol and each drug that they had taken (including nicotine) using a timeline follow-back assessment (Skinner and Allen, 1995; Skinner and Allen, 1982; Sobell and Sobell, 1988; Sobell et al., 1982).

Family History of Problem Drinking and Drug Problems

The Family Drinking Questionnaire was administered based on the methodology of Mann and colleagues (1985) with regard to drinking and with regard to other drug use. Participants rated family members as abstainers, users with no problem, or problem users. The family history density of alcohol problems was the proportion of first-degree relatives identified as problem drinkers. The family history density of drug problems was the proportion of first-degree relatives that were problem substance users.

Antisocial Personality Disorder, Adult Antisocial Behaviors Only Diagnoses, and Symptom Counts

ASPD disorder and AABO symptoms and diagnoses were obtained using the C-DIS (Blouin et al., 1988; Robins et al., 1995). For each ASPD symptom the subject endorsed, we asked about currency. AABO consisted of individuals who met all criteria for ASPD except for a CD diagnosis.

Measures of Antisocial Disposition

Deviance proneness was assessed using the Socialization Scale of the California Psychological Inventory (Gough, 1969) and the Psychopathic Deviance Scale of the MMPI-2 (MMPI-PD) (Hathaway and McKinley, 1989). These measures have been used as measures of antisocial disposition in many prior investigations. (Burger and Collins, 1982; Gizer et al., 2010; Lilienfeld, 1996; Sutker et al., 2009).

Statistical Analysis

Diagnosis rates were compared using chi-square statistics, while symptom counts were examined using the general linear model within SPSS (SPSS Inc., 2009). For all analyses, STA and LTA were first combined to compare alcohol-dependent samples with controls. This was followed by comparisons between STA and LTA and between ALC and ALC+DRG. All analyses included sex as a factor. We used the Wilcoxon–Mann–Whitney odds ratios (O'Brien and Castelloe, 2006) as the effects size measure for demographics and the standard odds ratio for diagnoses. The Wilcoxon–Mann–Whitney odds ratios is the ratio of the odds that the variable for a random individual in the first group is larger than the variable for a random individual in the second group. If the test compares A with B, a value >1 means A>B, a value <1 means A<B; thereby giving direction of the effect. For symptom counts, we used partial eta-squared as the effect size measure because we did not expect the hypothesized reduced current symptom counts for LTA to be reflected in more LTA having fewer symptoms than controls, but rather in the magnitude of the difference from controls being much less in LTA than STA, which would be reflected in the proportion of variance accounted for by the effect (partial eta-squared) when comparing LTA or STA with controls. Associations between family history density measures and ASPD diagnoses and measures were examined with analysis of variance and nonparametric correlations, but were not corrected for multiple comparisons.

Results

Demographic and Alcohol Use Variables

Table 1 presents demographic and alcohol use data. LTA were older than STA. STA and LTA were comparable in years of education but had less education than controls. There were no education effects of sex or between ALC versus ALC+DRG. STA and LTA also had more first-degree relative problem drinkers than controls with no difference between individuals with ALC and ALC+DRG, and with women having a higher family density of alcohol problems than men. STA and LTA had more first-degree relatives who were problem drug users than controls. Women had a somewhat higher family density of drug problems than men, and ALC+DRG had a higher family density of drug problems than ALC. The alcohol-dependent groups drank more alcohol than controls, and men drank more than women. In the STA ALC+DRG sample, 51% had lifetime cocaine dependence, 59% methamphetamine dependence, and 31% marijuana dependence. For the LTA ALC+DRG sample, 67% had lifetime cocaine dependence, 57% methamphetamine dependence, and 44% marijuana dependence. The rate of lifetime and current cigarette smoking was much greater in both STA and LTA than controls. A randomly chosen alcoholic was almost 16 times more likely to be a current smoker than a randomly chosen control. There were no significant differences between STA and LTA, between ALC and ALC+DRG, or between men and women in the rate of current smoking.

Table 1. Demographics and Alcohol Use Variables

	Alcohol dependent										Mann–Whitney Wilcoxon odds ratio
	Short-term abstinent alcoholics (STA)				Long-term abstinent alcoholics (LTA)
	ALC		ALC+DRG		ALC		ALC+DRG		NSAC		STA+LTA vs. NSAC	STA vs. LTA	ALC+DRG vs. ALC (STA+LTA)	Men vs. Women
	(n = 36)		(n = 56)		(n = 47)		(n = 59)		(n = 64)
	Men	Women	Men	Women	Men	Women	Men	Women	Men	Women
	(n = 25)	(n = 11)	(n = 34)	(n = 22)	(n = 27)	(n = 20)	(n = 29)	(n = 30)	(n = 30)	(n = 34)
Effect is significant: *p ≤ 0.05, **p ≤ 0.01, ***p ≤ 0.001. ^a Ethnicity abbreviations: A, Asian; AA, African American; AI, American Indian; B/M, Bi/Multi-Racial; C, Caucasian; L, Latino/Hispanic; O, Other; PI, Pacific Islander. ^b STA: ALC-Men (n = 24), ALC+DRG-Men (n = 33); LTA: ALC-Men (n = 26), ALC+DRG-Men (n = 28), ALC+DRG-Women (n = 28); NSAC: Women (n = 32). Due to adopted participants with unknown family drinking histories. ^c Statistical comparisons of these variables are inappropriate as the depenedent variables are related to the selection criteria. ^d In the past 12 months. ALC, lifetime dependence on alcohol only; ALC+DRG, lifetime dependence on alcohol and another drug of abuse; Dx, diagnosis; NSAC, non-substance-abusing controls; SUD, substance use disorders.
Demographics
Age (y)	46.6 ± 6.8	49.9 ± 6.2	45.1 ± 7.5	44.1 ± 5.3	48.3 ± 6.8	50.1 ± 5.4	49.3 ± 7.0	47.8 ± 7.0	47.8 ± 6.9	49.0 ± 7.9	0.8	0.6**	0.6	0.73
Years of education	13.4 ± 2.2	13.7 ± 2.3	13.2 ± 1.7	13 ± 2.1	13.4 ± 2.2	13.6 ± 2.6	13.8 ± 2.7	13.5 ± 2.0	15.5 ± 4.3	16.4 ± 2.9	0.29***	0.9	0.9	0.7
Ethnicity a	1AI, 2A, 1B/M, 21C	1AI, 2B/M, 1PI, 7C	3A, 10B/M, 2B/AA, 6PI, 13C	2AI, 12B/M, 1L 3PI, 4C	1A, 6B/M, 1B/AA, 3L, 16C	4A, 2B/M, 1O, 1PI, 12C	6A, 8B/M, 4B/AA, 1O, 3PI, 7C	3A, 14B/M, 1B/AA, 1L, 1O, 5PI, 5C	4A, 2B/M, 2O, 1PI, 21C	9A, 6B/M, 3B/AA, 1O, 1PI, 14C	N/A	N/A	N/A	N/A
Prop of first- degree relative problem drinkers b	0.29 ± 0.35	0.35 ± 0.28	0.25 ± 0.25	0.39 ± 0.34	0.25 ± 0.28	0.40 ± 0.26	0.28 ± 0.29	0.48 ± 0.34	0.10 ± 0.14	0.21 ± 0.24	1.89***	0.8	0.9	1.06***
Prop of first- degree relative problem drug usersb	0.11 ± 0.17	0.07 ± 0.14	0.20 ± 0.22	0.28 ± 0.29	0.09 ± 0.2	0.20 ± 0.2	0.21 ± 0.29	0.35 ± 0.30	0.03 ± 0.10	0.07 ± 0.15	2.08***	0.9	1.36***	1.16*
Alcohol use variables
Duration of alcohol use (mo)	356.8 ± 123.4	360.6 ± 96.7	343.8 ± 83.3	295.5 ± 79.8	312.7 ± 116.8	312 ± 111.8	331 ± 94.1	305.4 ± 112.1	239.7 ± 154.9	228.1 ± 157.3	2.19c	1.4**	1.2	1.46
Average alcohol dose (drinks/mo)	252.9 ± 255.3	116.9 ± 77.6	153.9 ± 123.7	174 ± 119.5	223.6 ± 172.5	160.8 ± 170.3	140.3 ± 136.7	127.4 ± 140.2	8.2 ± 10.4	3.9 ± 5.9	10.39c	1.2	0.86*	1.68*
Duration of peak use (mo)	112.9 ± 96.6	105.2 ± 60.7	127.2 ± 105.3	69.5 ± 63.2	101 ± 71.5	104.8 ± 57.9	171.2 ± 110^	135.1 ± 94.6	84.1 ± 70.1	70.5 ± 71.2	2.19c	0.8	1.0	1.07*
Peak dose (drinks/mo)	469.4 ± 483.3	219.6 ± 176.1	278 ± 186.5	360.4 ± 208.8	287.9 ± 234.4	267.2 ± 176	257.1 ± 187.9	219.7 ± 181.8	17.3 ± 16.1	19.2 ± 15.6	274.47c	1.1	1.0	1.69*
Abstinence duration (y)	0.17 ± 0.06	0.21 ± 0.05	0.20 ± 0.05	0.18 ± 0.07	7.6 ± 8.1	7.7 ± 7.2	6.1 ± 5.1	9.0 ± 6.8	N/A	N/A	N/Ac	0.009c	0.3	0.65
SUD Dx variables
Alcohol dependence Dx Age	25.5 ± 7.0	32.6 ± 11.4	22.8 ± 8.5	20.7 ± 5.8	22.8 ± 6.8	26.3 ± 10.7	19.7 ± 5.3	19.4 ± 6.4	N/A	N/A	N/A	1.47*	0.81***	1.23
Cocaine dependence Dx Age	N/A	N/A	25.8 ± 8.3 (n = 16)	25.5 ± 7.9 (n = 10)	N/A	N/A	22.6 ± 5.0 (n = 17)	25.3 ± 8.5 (n = 20)	N/A	N/A	N/A	1.2	N/A	1.1
Meth dependence Dx Age	N/A	N/A	26.6 ± 8.3 (n = 19)	27.8 ± 6.2 (n = 15)	N/A	N/A	25.5 ± 6.8 (n = 13)	27.1 ± 7.1 (n = 18)	N/A	N/A	N/A	1.0	N/A	1.0
THC dependence Dx Age	N/A	N/A	16.3 ± 5.4 (n = 11)	14.5 ± 2.1 (n = 2)	N/A	N/A	18.5 ± 4.7 (n = 13)	15.0 ± 2.8 (n = 9)	N/A	N/A	N/A	0.6	N/A	0.7
Smoking variables
Lifetime nicotine dependence # (%)	6 (24%)	1 (9.1%)	9 (26.5%)	8 (36.4%)	9 (33.3%)	6 (30%)	14 (48.3%)	13 (43.3%)	1 (3.3%)	3 (8.8%)	1.45***	1.01*	1.05	1.10
Current nicotine dependence # (%) d	6 (24%)	1 (9.1%)	6 (17.6%)	6 (27.3%)	3 (11.1%)	5 (25%)	6 (20.7%)	7 (23.3%)	0 (0%)	1 (2.9%)	1.74***	0.76	0.99	0.98

Antisocial Personality Disorder and Adult Antisocial Behaviors Only Diagnoses

Table 2 presents ASPD and AABO diagnoses (both lifetime and current) for all groups. In controls, no individuals had a lifetime ASPD diagnosis; about a third had a lifetime AABO diagnosis, with the remaining two-thirds having no lifetime antisocial diagnosis. The results for STA and LTA combined were different. Less than 10% of alcohol-dependent individuals had no lifetime antisocial diagnosis. About a quarter had a lifetime ASPD diagnosis, while over two-thirds had a lifetime AABO diagnosis. The odds of a control not having a lifetime antisocial diagnosis were 25 times that of an STA/LTA (χ² = 99.7, p < 0.0001). Current antisocial diagnoses had much lower prevalence than lifetime antisocial diagnoses. No controls had a current ASPD diagnosis and just under 5% had a current AABO diagnosis, while for STA/LTA, just over 7% had a current ASPD diagnosis and just over 21% had a current AABO diagnosis. The odds of a current ASPD or AABO diagnosis were 8 times greater in STA/LTA than in controls (χ² = 15.4, p < 0.001). The odds of a lifetime ASPD or AABO diagnosis were no different in STA versus LTA, odds ratio (OR) = 0.6, χ² = 1.2, p = 0.27, but the odds of a current ASPD or AABO diagnosis were reduced in LTA versus STA (OR = 0.18, χ² = 25.6, p < 0.0001). Lifetime diagnosis rates for the aggregate of ASPD and AABO were comparable in ALC+DRG versus ALC (OR = 1.09), but lifetime ASPD diagnoses were higher in ALC+DRG versus ALC (OR = 2.68; χ² = 13.1, p < 0.001); however, ALC+DRG and ALC did not differ when the lower rates of current antisocial diagnoses were examined (χ² = 1.1, p = 0.152). The only associations of family history density with ASPD diagnoses were an effect within STA for individuals with a full current ASPD diagnosis to have a higher family history density of drug problems (n = 11, family density = 0.33 ± 0.37) versus individuals with no current diagnosis (n = 48, family density = 0.13 ± 0.17) or versus individuals with an AABO diagnosis (n = 31, family density = 0.20 ± 0.23), overall test: F(2,87) = 3.66, p = 0.030; Scheffe comparisons both p = 0.035. Diagnosis rates did not differ by sex.

Table 2. Antisocial Personality Disorder (ASPD) and Adult Antisocial Behaviors Only (AABO) Diagnosis

	Alcohol dependent										Diagnoses	Odds ratios
	Short-term abstinent alcoholics (STA)				Long-term abstinent alcoholics (LTA)				NSAC
	ALC		ALC+DRG		ALC		ALC+DRG
	Men	Women	Men	Women	Men	Women	Men	Women	Men	Women		STA & LTA vs. NSAC	Men vs. Women	STA vs. LTA	ALC+DRG vs. ALC	LTA ALC vs. NSAC	LTA ALC+DRG vs. NSAC
	(n = 25)	(n = 11)	(n = 34)	(n = 22)	(n = 27)	(n = 20)	(n = 29)	(n = 30)	(n = 30)	(n = 34)
Effect is significant: *p ≤ 0.05, **p ≤ 0.01, ***p ≤ 0.001. ALC, lifetime dependence on alcohol only; ALC+DRG, lifetime dependence on alcohol and another drug of abuse; Dx, diagnosis; NSAC, non-substance-abusing controls.
ASPD Dx
Lifetime
None	1 (4%)	4 (36%)	4 (12%)	0 (0%)	3 (11%)	2 (10%)	1 (3%)	0 (0%)	16 (53%)	27 (79%)	ASPD vs. None or AABO	∞	1.4	0.7	3.46***	∞	∞
AABO	21 (84%)	7 (64%)	20 (59%)	17 (77%)	19 (70%)	16 (80%)	17 (38%)	19 (63%)	14 (47%)	7 (21%)	ASPD or AABO vs. None	25.0***	1.9*	0.6	3.0*	17.20***	118.8***
ASPD	3 (12%)	0 (0%)	10 (29%)	5 (23%)	5 (19%)	2 (10%)	11 (59%)	11 (37%)	0 (0%)	0 (0%)
Current
None	13 (52%)	9 (82%)	19 (56%)	9 (41%)	24 (89%)	18 (90%)	25 (86%)	25 (83%)	27 (90%)	34 (100%)	ASPD vs. None or AABO	∞	2.1	4.7**	1.9	∞	∞
AABO	9 (36%)	2 (18%)	10 (15%)	10 (45%)	2 (4%)	2 (10%)	3 (10%)	4 (13%)	3 (10%)	0 (0%)	ASPD or AABO vs. None	8.0***	1.5	5.5***	1.6	2.4	3.7*
ASPD	3 (12%)	0 (0%)	5 (29%)	3 (14%)	1 (7%)	0 (0%)	1 (4%)	1 (4%)	0 (0%)	0 (0%)

Antisocial Personality Disorder Symptoms

Table 3 presents the total lifetime and total current symptom counts for all groups. The number of lifetime ASPD symptoms was over 4 times as large for alcoholics compared with controls, F(1, 258) = 162.7, p < 0.0001, with the difference between groups accounting for 38.7% of the variance of the total lifetime symptom count, with no differences between STA and LTA, F(1, 190) = 0.5, p = 0.46, es (effect size) = 0.3%, nor between sexes, F(1, 258) = 42.8, p = 0.27, es = 0.5%, with about 60% higher lifetime symptom counts in ALC+DRG versus ALC, F(1, 190) = 42.8, p < 0.0001, es = 18.1%. For both STA and LTA, individuals with a lifetime diagnosis of ASPD had much higher lifetime ASPD symptom counts than individuals with a lifetime diagnosis of AABO, F(1, 179) = 21.1, p < 0.0001, es = 10.6%, and this effect was the same for STA and LTA, F(1, 179) = 0.1, p = 0.77, es = 0.1%. In STA, the number of lifetime ASPD symptoms was positively correlated with the family history density of drinking problems (R = 0.295, p = 0.005). The number of current ASPD symptoms was 5 times as large for STA versus controls, F(1, 152) = 38.0, p < 0.0001, es = 20.0%, current symptoms in LTA were 60% lower than in STA, F(1, 190) = 27.0, p < 0.0001, es = 12.2%, and just twice as large as controls, F(1, 166) = 7.8, p = 0.006, es = 4.5%, with no difference by sex, F(1, 258) = 1.3, p = 0.25, es = 0.5%, but with symptom counts being about 50% higher in ALC+DRG versus ALC, F(1, 190) = 5.2, p = 0.024, es = 2.60%. When LTA ALC are compared with controls, the difference becomes smaller and nonsignificant, F(1, 107) = 3.2, p = 0.075, es = 2.9%. For both STA and LTA, individuals with a lifetime diagnosis of ASPD had roughly the same number of current ASPD symptoms as individuals with a lifetime diagnosis of AABO, F(1, 179) = 0.6, p = 0.44, es = 0.3%.

Table 3. ASPD Symptom Count by ASPD Diagnosis Criteria and Psychological Measures

	Alcohol dependent				NSAC (n = 64)	Effect size (Partial η²)
	Short-term abstinent alcoholics (STA)		Long-term abstinent alcoholics (LTA)
	ALC (n = 36)	ALC+DRG (n = 56)	ALC (n = 47)	ALC+DRG (n = 59)		STA & LTA vs. NSAC	Men vs. Women	STA vs. LTA	ALC+DRG vs. ALC	LTA ALC vs. NSAC	LTA ALC+DRG vs. NSAC
Effect is significant: *p ≤ 0.05, **p ≤ 0.01, ***p ≤ 0.001. ASPD, antisocial personality disorder; ALC, lifetime dependence on alcohol only; ALC+DRG, lifetime dependence on alcohol and another drug of abuse; NSAC, non-substance-abusing controls; Sx, symptoms..
Lifetime Sx by ASPD criteria
Social norms conformity	0.72 ± 0.94	1.8 ± 1.1	1.0 ± 1.2	2.1 ± 1.3	0.08 ± 0.32	22.7***	0.1	1.2	1.7***	26.3***	52.2***
Deceitfulness	0.22 ± 0.42	0.30 ± 0.46	0.28 ± 0.45	0.47 ± 0.50	0.00 ± 0.00	10.5***	0.2	1.4	2.2*	18.1***	32.0***
Impulsivity	1.4 ± 1.0	1.6 ± 1.1	0.98 ± 0.90	1.6 ± 1.1	0.31 ± 0.61	18.7***	0.1	0.8	3.9*	16.5***	35.4***
Irritability/aggressiveness	0.47 ± 0.65	1.3 ± 1.0	0.83 ± 0.89	1.5 ± 1.2	0.13 ± 0.42	17.0***	0.2	1.5	12.1***	22.0***	37.3***
Disregard for safety	1.3 ± 0.79	1.6 ± 0.75	1.2 ± 0.81	1.6 ± 0.89	0.52 ± 0.64	21.6***	1.6*	0.1	3.9**	19.9***	33.8***
Work/financial irresponsibility	2.5 ± 1.6	3.2 ± 1.6	2.1 ± 1.5	3.1 ± 1.5	0.63 ± 1.0	27.0***	1.4	0.7	6.6***	25.8***	47.5***
Lack of remorse	0.92 ± 1.2	1.1 ± 1.1	1.1 ± 1.1	1.3 ± 1.1	0.69 ± 0.85	2.9**	0.4	0.4	0.8	3.9*	7.5**
Total lifetime Sx	10.6 ± 5.1	15.6 ± 6.1	10.8 ± 5.5	16.6 ± 5.8	3.1 ± 3.7	38.7***	0.5	0.3	18.1***	41.4***	66.4***
Current Sx by ASPD criteria
Social norms conformity	0.19 ± 0.47	0.57 ± 0.87	0.04 ± 0.20	0.12 ± 0.38	0.02 ± 0.13	3.3**	0.1	6.8***	4.0**	0.7	3.4*
Deceitfulness	0.14 ± 0.35	0.07 ± 0.26	0.00 ± 0.00	0.03 ± 0.18	0.00 ± 0.00	1.4	0	3.6**	0.1	n/a	1.8
Impulsivity	0.83 ± 0.88	0.61 ± 0.89	0.15 ± 0.36	0.15 ± 0.45	0.13 ± 0.38	2.8**	1.1	15.0***	0.7	0.1	0.1
Irritability/aggressiveness	0.14 ± 0.42	0.39 ± 0.76	0.06 ± 0.32	0.19 ± 0.51	0.05 ± 0.28	2.0*	0	1.6	2.9*	0.1	2.9
Disregard for safety	0.25 ± 0.44	0.57 ± 0.85	0.06 ± 0.25	0.19 ± 0.54	0.11 ± 0.36	1.7*	0	5.5***	3.4**	0.5	0.7
Work/financial irresponsibility	0.94 ± 1.3	1.4 ± 1.3	0.45 ± 0.78	0.69 ± 0.86	0.13 ± 0.49	9.0***	0.2	7.0***	2.5*	6.2**	14.8***
Lack of remorse	0.39 ± 0.80	0.54 ± 0.79	0.40 ± 0.83	0.42 ± 0.68	0.17 ± 0.55	2.4*	0.5	0.1	0.3	2.8	4.1*
Total current SX	3.5 ± 3.0	5.2 ± 5.0	1.6 ± 2.3	2.1 ± 2.2	0.9 ± 1.9	7.3***	0.5	12.2***	2.6*	2.9	7.7**
Psychological measures
CPI Socialization Scale	18.1 ± 3.9	17.5 ± 3.8	17.5 ± 3.8	16.6 ± 4.1	22.1 ± 3.2	23.0***	0.1	0.7	1	29.7***	36.5***
MMPI Psychopathic Deviance Scale	26.5 ± 5.9	26.9 ± 5.2	23.2 ± 5.8	25.1 ± 5.6	16.8 ± 4.8	31.3***	0.6	4.8**	1	26.9***	39.0***

We redid the analyses of current symptom counts adding age as a covariate to control for LTA having a mean age 2.9 years older than STA. There was an age effect, F(1, 189) = 8.7, p < 0.005, es = 4.4%, but a much larger effect of group, F(1, 189) = 19.0, p < 0.0001, es = 9.1%, showing that LTA's lower current symptom counts relative to STA was not a consequence of the small age difference between the groups.

Antisocial Personality Disorder Dimensions

Table 3 also presents symptom counts (both lifetime and current) for each of the 7 ASPD criteria. The number of lifetime symptoms for all 7 criteria was greater in STA/LTA versus controls, multivariate Wilks' λ = 0.634, es = 36.6%, F(7, 252) = 20.7, p < 0.0001. Effect sizes varied from 2.9% for lack of remorse to 27.0% for irresponsibility with work or finances. There was no difference for lifetime symptoms of any criteria between STA and LTA, all effect sizes <2.0%; multivariate Wilks' λ = 0.951, es = 4.9%, F(7, 184) = 1.36, p = 0.223, and ALC+DRG had more lifetime symptoms for all criteria except lack of remorse, with effect sizes varying between 4.8% for lack of remorse to 74.3% for reckless disregard for the safety of self and others. For NSAC, the number of lifetime and current symptom counts for impulsivity and failure to plan ahead were positively correlated with family history density of problem drinkers (lifetime R = 0.293, p = 0.021; current R = 0.270, p = 0.034). For LTA, current symptoms for irritability and aggressiveness were negatively correlated with family history density of problem drinkers (R = −0.209, p = 0.034), and current symptoms for irresponsibility at work or financially were negatively correlated with family density of problem drug users (R = −0.221, p = 0.026). For STA, there was a positive correlation between lifetime symptom counts associated with failure to conform to social norms with respect to lawful behaviors, reckless disregard for the safety of self and others, and family history density of problem drug users (R = 0.282, p = 0.007) (R = 0.252, p = 0.017).

There were large differences between STA and LTA in current symptom counts, with STA having higher symptom counts than LTA for all criteria except lack of remorse. Basically, current symptom counts in STA were significantly higher than those of controls for all criteria, with effect sizes varying from 4.0 to 21.6%, while for LTA, current symptom counts were higher than those of controls only for financial irresponsibility, es = 8.8%, F(1, 166) = 16.04, p < 0.0001, and lack of remorse, es = 2.8%, F(1, 166) = 4.71, p = 0.031, with all other effect sizes being less than 1.3%. For LTA ALC, current symptom counts were higher than those of controls only for financial irresponsibility (es = 6.2%). For LTA ALC+DRG, current symptom counts were higher than those of controls for financial irresponsibility (es = 14.8%), lack of remorse (es = 4.1%), and failure to conform to social norms with respect to lawful behavior (es = 3.4%). There was no difference in current symptoms for any criteria between individuals with a lifetime diagnosis of ASPD versus AABO, multivariate Wilks' λ = 0.935, es = 6.5%, F(7, 173) = 1.72, p = 0.11.

Psychological Measures Associated with Antisocial Behavior

Table 3 also presents scores on the measures of social deviance proneness and antisocial disposition. Subjects with alcohol dependence had more deviant scores on both measures compared with controls, es = 23.0 and 31.3%, all F(1, 258) = 59.1, ps < 0.0001. There were no differences between STA and LTA for the Socialization Scale, but a significant lower MMPI-PD Scale scores in LTA versus STA, es = 4.8%, F(1, 190) = 9.7, p = 0.002; however, MMPI-PD scores for LTA were significantly higher than those of controls, es = 31.0%, F(1, 166) = 75.4, p < 0.0001. Finally, we examined the psychological measures as a function of whether individuals met a lifetime diagnosis of ASPD versus AABO and found a trend toward lower Socialization Scale scores in individuals with an ASPD versus AABO diagnosis, es = 1.8%, F(1, 179) = 3.3, p = 0.07, but no difference between individuals with a lifetime diagnosis of ASPD versus AABO on the MMPI-PD Scale, es = 0.2%, F(1, 179) = 0.4, ns. For LTA, the MMPI-PD Scale score was positively correlated with family history density of problem drinking (R = 0.221, p = 0.026). For NSAC, the Socialization Scale score was negatively correlated with family history density of problem drinkers (R = −0.341, p = 0.007).

Discussion

This work replicates and extends the results from our 2006 to 2008 studies. Only 10% of alcoholics had no lifetime antisocial diagnosis, providing additional evidence for the association between antisocial personality problems and AUDs/SUDs. Additionally, our data illustrate the importance of taking into account AABO when examining antisocial problems in AUDs/SUDs; many more of our subjects evidenced AABO than ASPD diagnoses. Moreover, our data support the idea that lifetime ASPD and AABO diagnoses have a comparable impact on current deviance-prone thinking and antisocial behavior in abstinent AUD and SUD individuals. We also note that AABO may be a misnomer for those exhibiting ASPD criteria antisocial behavior as adults, but not meeting CD criteria before age 15. Some of these individuals may have met 1 or more CD criteria before age 15 without meeting full CD criteria; thus, a more accurate description of this group may be adult antisocial behavioral syndrome rather than AABO, which may overstate the lack of childhood and adolescent antisocial behavior.

Most importantly, our results provide evidence for the idea from our earlier paper that disinhibitory and socially deviant behavior reflected in a diagnosis of ASPD (or AABO) must decrease for long-term abstinence to be maintained, or, alternatively, that long-term abstinence may reduce disinhibited, socially deviant behavior, even though the underlying core psychological characteristics of deviance proneness do not change. We now show, in a sizable sample, that current ASPD symptom counts in long-term abstinence are closer to control values than are those in short-term abstinence. The number of current ASPD symptoms was 60% lower in LTA compared with STA. Moreover, ASPD symptom counts for LTA ALC were comparable with those in controls. We note that ASPD symptom counts were about 50% higher in individuals with ALC+DRG versus ALC, giving evidence of greater antisocial pathology in individuals with ALC+DRG versus ALC. However, even in LTA ALC+DRG, current symptom counts were much lower than STA ALC+DRG and closer to those of controls than to STA ALC+DRG.

An alternative explanation of the reduction in current antisocial symptoms in long-term abstinence could be that, with age, individuals with ASPD or AABO become less antisocial. Our data does not support this explanation. LTA current symptoms were much lower than STA current symptoms after controlling for age, indicating that something other than age is active in the lower current antisocial symptoms in long-term versus short-term abstinence.

Our data support the idea that ongoing antisocial behavior is not conducive to or consistent with sustained abstinence from alcohol and drugs and that a reduction in such behavior is important, and possibly necessary, in extended abstinence. What is most intriguing about our results is that social deviance proneness, or antisocial dispositionality, is comparably abnormal in both short- and long-term abstinence and that the close to normal level of current antisocial behaviors in long-term abstinence takes place in the context of elevated social deviance proneness or antisocial dispositionality. This suggests a top-down model in extended abstinence, whereby one invokes executive control to inhibit deviance-prone tendencies. A crucial question is whether this increased inhibitory control is specific to reducing substance use or manifests in a general increase in inhibitory control of behavior. We recently (Camchong et al., 2012) examined resting-state synchrony (RSS), comparing 23 of the current LTA ALC subjects with 23 age- and gender-comparable subjects from the current control group. Using seed-based measures, we examined RSS with the nucleus accumbens (NAcc) and the subgenual anterior cingulate cortex (sgACC). All participants were assessed with the intra/extradimensional set shift task outside of the scanner to explore the relationship between RSS and cognitive flexibility. Compared with controls, LTA alcoholics showed (i) decreased synchrony of limbic reward regions (e.g., caudate and thalamus) with both the anterior cingulate cortex seed and the NAcc seed and (ii) increased synchrony of executive control regions (e.g., dorsolateral prefrontal cortex) with both the NAcc seed and the sgACC seed. The magnitude of the RSS differences from controls in executive control regions was significantly correlated with better task performance. The results are consistent with an interpretation of a compensatory mechanism in long-term abstinence, evident during rest, in which decision-making networks show reduced synchrony with appetitive drive regions and increased synchrony with inhibitory control regions, with the greater synchrony with inhibitory control regions being associated with generalized better cognitive flexibility. These resting-state findings indicate a general adaptive mechanism present in long-term abstinence that may facilitate the behavioral control required to maintain abstinence. The RSS data and the ASPD behavioral data presented here are both consistent either with recovery of function in executive control or with individuals with greater executive control being better able to sustain recovery, alternatives that are testable in longitudinal studies.

It also might be that the bulk of the adult antisocial behaviors (symptoms) in the alcoholic samples studied here were associated with alcohol and/or drug use, an addictive lifestyle, and the disinhibiting effects of alcohol and drugs. Remove the alcohol and drugs, change the lifestyle, remove the disinhibition from alcohol and drug use, and you have less disinhibited (i.e., antisocial) behavior. A problem with ASPD or AABO in SUD populations is that the antisocial symptoms may be, in part, a consequence of the alcohol and other drug use. To the degree that this is the case, it helps to explain, but does not change the importance of the basic findings: that ongoing antisocial behavior is not consistent with extended abstinence. This work also raises questions regarding the degree to which a personality disorder such as ASPD or AABO can be modified. Our results suggest that the characteristic social deviance proneness or antisocial dispositions associated with these disorders change little, if at all, but that behavior characteristic of the personality disorder may be modified by the individual. We do not know whether the STA and LTA groups differed on other, unmeasured mediating characteristics that may have affected the results (e.g., the LTA individuals could be married and have good jobs, factors that both encourage abstinence and putting the brakes on antisocial acting out).

It is important to note that this study is cross-sectional in nature and did not measure changes from short- to long-term abstinence. However, given the similarities in diagnosis rates and lifetime symptoms between STA and LTA samples, it is a reasonable hypothesis that the differences we report here do reflect changes from short- to long-term abstinence. Direct assessment of such changes can only be demonstrated in longitudinal studies, and we are in the process of gathering 6-month follow-up data on 20 of the STA sample who stayed abstinent and 20 of the STA sample who relapsed during the 6-month follow-up interval. We are not sure whether the follow-up interval or sample size will have sufficient power to test the finding from the current report in a longitudinal design. Nonetheless, we believe the results reported here are important considerations in any model of those mechanisms of behavior change that are necessary to support long-term abstinence from alcohol and drugs.

Acknowledgments

This work was supported by the National Institutes for Health, NIH grants #AA016944 and #AA013659.