Skip to main content

Abstract

Objective:

The authors sought to clarify the etiology of the association between pregnancy and reduced risk of alcohol use disorder.

Methods:

The authors used data from longitudinal population-wide Swedish medical, pharmacy, and criminal registries to evaluate whether rates of alcohol use disorder are lower during pregnancy. They compared pregnant women born between 1975 and 1992 (N=322,029) with matched population controls, with female relatives discordant for pregnancy, and with pre- and postpregnancy periods within individuals. They further compared rates of alcohol use disorder between pregnant women and their partners.

Results:

Pregnancy was inversely associated with alcohol use disorder across all analyses (odds ratios, 0.17–0.32). In co-relative analyses, the strength of the association increased among more closely related individuals. Within individuals, rates of alcohol use disorder were substantially decreased during pregnancy relative to the prepregnancy period (odds ratios, 0.25–0.26), and they remained reduced during postpartum periods (odds ratios, 0.23–0.31). Results were similar for second pregnancies (odds ratio, 0.23). The partners of pregnant women also exhibited reductions in alcohol use disorder (odds ratio, 0.45). Among women who became pregnant at earlier ages and those with a history of criminal behavior, the negative association between pregnancy and alcohol use disorder was especially pronounced, but no moderation was observed for a personal or maternal parental history of alcohol use disorder.

Conclusions:

The findings suggest that pregnancy plays a critical, and likely causal, motivational role in reducing alcohol use disorder risk among women and, to a lesser extent, their partners. These results extend our understanding of the relationship between pregnancy and alcohol use, demonstrating that even a severe condition such as alcohol use disorder is subject to the protective effects of pregnancy.
Alcohol consumption during pregnancy increases the risks of miscarriage, stillbirth, and a variety of physical and neurodevelopmental effects in offspring, collectively known as fetal alcohol spectrum disorders (1). The World Health Organization (WHO) notes that “there is no safe level of alcohol use during pregnancy” (2). WHO and the U.S. National Institute on Alcohol Abuse and Alcoholism have developed guidance for prevention or reduction of alcohol consumption during pregnancy to reduce alcohol-related harms due to prenatal exposure. However, while discouraged by much of the medical community and socially stigmatized in some environments, alcohol use during pregnancy persists.
In a national survey in the United States (3), nearly 10% of pregnant women in the age range of 15–44 years reported alcohol use, with more than 2% reporting binge drinking; alcohol use was reported to be more common earlier in the pregnancy, and less common than among nonpregnant women. Attitudes toward alcohol consumption during pregnancy vary widely across Europe. In a multinational European study, 28.5% of U.K. women reported drinking during pregnancy, while Swedish women more closely resembled American women, with 7.2% continuing to drink (4). Some evidence suggests that drinking during pregnancy is underreported (5).
Although a nontrivial proportion of pregnant women continue to drink, the majority abstain, suggesting that pregnancy serves as a strong incentive to abstain from alcohol. During the economic recession of 2008–2009, when binge drinking prevalence increased overall in the United States, pregnancy was one of the strongest predictors of a decreased likelihood of binge drinking (6). Even as past-30-day alcohol consumption and binge drinking have increased among nonpregnant U.S. women, these behaviors have decreased among pregnant women (7). As noted in the context of prenatal illicit substance use (8), women who misuse substances may be more likely to have an unplanned pregnancy (9, 10), which would result in a positive association between pregnancy and alcohol misuse. However, the drive to protect one’s offspring from the adverse effects of alcohol is likely a counteracting factor, resulting in a negative association between pregnancy and alcohol misuse.
Drinking during pregnancy is associated with a variety of maternal characteristics. Swedish women with lower educational attainment, and those who live in smaller cities, are more likely to abstain during pregnancy (4, 11). Those who smoked (4) or exhibited heavier or more frequent drinking before pregnancy (1113) reduced their drinking during pregnancy to a lesser degree than nonsmokers or light drinkers, respectively. Cognitive factors are also relevant. Women who report having used alcohol to enhance social interactions before pregnancy and those who perceived that small amounts of alcohol were not problematic were less likely to abstain (13). In contrast, women who received a pamphlet detailing the negative effects of alcohol during pregnancy were more likely to reduce their drinking than those who received standard care (14).
Alcohol consumption is distinct from, although correlated with, alcohol use disorder. Light or moderate, but nondependent, drinkers may abstain during pregnancy without undue effort. In contrast, problem drinking frequently involves motivational and volitional components, potentially because of neurobiological adaptations that reduce cognitive control over substance use (15, 16). Indeed, the diagnostic criteria for alcohol use disorder include an inability to stop or reduce drinking despite one’s intentions and drinking for longer periods or in greater quantities than intended (17). Thus, pregnancy may not be a sufficient incentive for women with alcohol use disorder to cease drinking. However, contingency management for alcohol use disorder—although used less commonly than for other substance use disorders (18)—has demonstrated some success in increasing alcohol abstinence rates relative to standard care (1921), suggesting that volitional capacity can be improved by extrinsic factors. Pregnancy is a qualitatively different motivator than the monetary incentives typically used in such programs. Rather than implicitly relying on immediate positive outcomes of monetary value to oneself, pregnancy-based motivation would rely on avoidance of distal negative outcomes for one’s offspring. This difference may mitigate the effectiveness of the “reward” (22) and may be particularly relevant to alcohol use disorder, given its association with impulsivity and delay discounting (2326).
Where pregnancy and alcohol misuse are negatively associated, it remains unclear whether this is due to a causal process or to other factors contributing to the coincidence of pregnancy and decreased alcohol misuse. In this study, we used Swedish national registries to investigate the potential causal association between pregnancy and alcohol use disorder. Although observational data preclude definitive conclusions about causality, we applied a range of analytic methods, in a statistically powerful sample, to clarify the nature of this association. First, we examined rates of alcohol use disorder in pregnant women relative to matched population-based control women. Second, given the prominent genetic influences on risk for alcohol use disorder (27), we employed co-relative designs that enabled us to control for a degree of genetic liability while examining rates of alcohol use disorder in female relative pairs in which one member was pregnant and the other was not (i.e., discordant pairs). Third, we capitalized on the longitudinal nature of the registries to apply within-individual designs, comparing rates of alcohol use disorder registrations during pregnancy and nonpregnant time frames. Finally, we compared rates of alcohol use disorder in spouses before and during the pregnancy. Our study thus extends previous studies focused on alcohol consumption to address whether pregnancy may play a direct role in reduced incidence of alcohol use disorder.

Methods

Identification of Alcohol Use Disorder

We used several different Swedish population-based registers with national coverage, linking them with each person’s unique identification number, which was replaced by a serial number to preserve confidentiality. We secured ethical approval for the study from the Regional Ethical Review Board of Lund University (No. 2008/409). Alcohol use disorder was defined either by ICD codes for main and secondary diagnoses from Swedish medical registers (see the online supplement for a list of the ICD codes used) or by registrations of individuals in the Swedish Crime Register. Each individual could have several registrations in the criminal or medical registers. To avoid double-counting registrations, within each type of register (criminal and medical), we allowed for a 90-day period after each registration in which a new registration was not counted.

Sample

We selected all women born in Sweden between 1975 and 1992 who had at least one child registered in the Swedish multigenerational register for which the mother was likely first aware of being pregnant between the ages of 18 and 35. As in a previous study (8), we estimated that women became aware of being pregnant 242 days before the birth.

Statistical Analysis

We matched each mother (N=322,029) to five unrelated control women (N=1,610,145) who had the same year and month of birth. The control women had to be alive and registered in Sweden at the time of the case subject’s pregnancy and not themselves registered as being mothers or having had a child within 9 months after the date of birth of the case subject’s child. For all control subjects, we examined alcohol use disorder during the same period as the case subject. We next replicated the matching approach but instead of using unrelated random individuals as controls, we matched on female cousins and full siblings, and we allowed for up to 3 years’ age difference between the case subject and the relative control subject. We matched 120,938 control cousins to 104,550 case subjects and 41,567 control siblings to 40,045 case subjects. By matching on cousins and siblings, we accounted for unmeasured genetic and environmental factors shared among cousins and siblings. Finally, we examined alcohol use disorder in a within-individual model comparing a 242-day period prior to the pregnancy to the pregnancy period.
We used conditional logistic regression, with a separate stratum for each case subject and their control(s), in which we compared alcohol use disorder in the case subject (i.e., alcohol use disorder during pregnancy) with alcohol use disorder in the control subjects (i.e., alcohol use disorder during a nonpregnant period). Model 1 was only a crude model, whereas in model 2 we adjusted for average parental educational (≤9 years, 10–11 years, ≥12 years) and school achievement of the individual (see reference 28 for how school achievement was defined). Odds ratios between 0 and 1 would indicate a reduced risk for alcohol use disorder during pregnancy (i.e., a protective effect of pregnancy), and odds ratios >1 would indicate an increased risk.
We then combined the population, full sibling, and cousin data sets and performed two co-relative analyses. The first allowed all coefficients for each sample to be independent. In the second, we modeled the genetic resemblance assuming that it equaled 0 for the population, 0.125 for cousins, and 0.5 for full siblings. We compared this model with the previous model, using Akaike’s information criterion, a model-fit statistic that balances goodness of fit and parsimony. If the second model fit the data well, we obtained improved estimation of the association between alcohol use disorder and pregnancy among all types of relatives. In this model we are also able to extrapolate an odds ratio for monozygotic twins (there were no monozygotic twins registered for alcohol use disorder while pregnant).
In additional analyses, we investigated whether the association between pregnancy and alcohol use disorder was moderated by the following variables: the average educational status across the individual’s parents; the individual’s school achievement; lifetime registration of alcohol use disorder in a parent of the mother (dichotomized as yes or no); alcohol use disorder registration of the individual prior to pregnancy; criminal registration of the individual prior to pregnancy (for a definition of criminal registration, see reference 29); drug abuse registration of the individual prior to pregnancy (for a definition of drug abuse, see reference 8); psychiatric registration of the individual prior to pregnancy; age at pregnancy (dichotomized as ≤25 years and >25 years); marital status (dichotomized as married or not married; in the analyses of married people, individuals who married during the control or hazard period were excluded); alcohol use disorder registration of the child’s father prior to pregnancy; and alcohol use disorder registration of the child’s father during pregnancy. These moderation analyses were performed only on the within-individual sample, using an interaction term (using the logit link) between the covariate of interest and the mother’s alcohol use disorder status. In the within-individual sample, we also tested whether the decrease in alcohol use disorder rates between control and pregnancy periods was the same for mothers and fathers. This was done by including an interaction term between a dummy variable indicating mother or father and alcohol use disorder status in mother and father.
Finally, we examined, using within-individual analyses only, the rates of alcohol use disorder in postpartum periods. Our control was the 242-day period prior to pregnancy, and we examined three 242-day postpartum risk periods: 0–242 days, 243–484 days, and 485–726 days after childbirth. We eliminated from these analyses mothers whose child died during the risk period. We included mothers who were no longer cohabiting with their child (the Ns were 1,088, 3,604, and 4,898, respectively, for the three postpartum risk periods) because these mothers had substantial elevations in rates of alcohol use disorder, suggesting that in some cases the child had been removed because of their problematic behavior. Excluding them would bias downward the postpartum alcohol use disorder rates.
In all these models, the within-individual and within-family clustering were taken into consideration. In models that included information on fathers, the father had to cohabit with the mother at the end of the year the child was born. All statistical analyses were performed using SAS, version 9.3 (SAS Institute, Cary, N.C.).

Results

Association Between Pregnancy and Alcohol Use Disorder Registration

Rates of alcohol use disorder among pregnant women were considerably lower than among matched control women (odds ratio=0.32, 95% CI=0.27, 0.37) (Table 1). This association became stronger (that is, the odds ratio was closer to 0) after controlling for mean parental education and school achievement. These findings corresponded closely to the negative association between pregnancy and alcohol use disorder among cousins discordant for pregnancy (odds ratio=0.31, 95% CI=0.23, 0.42); similarly, accounting for potential confounders strengthened the observed association. When comparing alcohol use disorder rates in pregnant women and their discordant biological full sisters, the negative association was even more pronounced (odds ratio=0.22, 95% CI=0.13, 0.36).
TABLE 1. Observed association of first pregnancy with registration for alcohol use disorder in the general population, in cousin and sibling pairs discordant for pregnancy, and within individuals
  Frequency of Alcohol Use Disorder Registration      
  PregnancyControl PeriodModel 1, UnadjustedModel 2, AdjustedaModel 1, Unadjusted
GroupNN%N%Odds Ratio95% CIOdds Ratio95% CICohen’s d95% CI
Population322,0291550.052,4520.150.320.27, 0.370.260.22, 0.310.630.55, 0.72
Cousins112,457550.051990.150.310.23, 0.420.210.15, 0.300.650.48, 0.81
Siblings40,005170.04820.200.220.13, 0.36  0.830.56, 1.12
Within individual           
 Control period 242 days prior to the start of pregnancy332,4361650.055590.170.250.21, 0.30  0.760.66, 0.86
 Control period ending 6 months prior to start of pregnancy332,4361650.055530.170.260.21, 0.31  0.740.65, 0.86
 Control period ending 12 months prior to start of pregnancy332,4361650.055870.180.250.21, 0.30  0.760.66, 0.86
 Second pregnancy, control period 242 days prior to the start of pregnancy197,383400.021300.070.230.15, 0.35  0.810.58, 1.05
a
Adjusted for mean parental education and school achievement.
We used unadjusted results from the discordant cousin and sibling analyses to fit a co-relative model, extending to estimated odds ratios for discordant monozygotic twins. As shown in Table 2, the estimated odds ratios decline monotonically, from 0.32 to 0.17, as a function of relatedness. These findings are illustrated in Figure 1. The fit of the predicted model is superior to that of the observed model, as indicated by a lower Akaike’s information criterion value (Table 2).
TABLE 2. Association between pregnancy and alcohol use disorder in the general population and in cousins, siblings, and monozygotic twins discordant for pregnancy, as estimated from a co-relative modela
SampleEstimated Odds Ratio95% CI
Population0.320.28–0.37
Discordant cousins0.300.26–0.34
Discordant siblings0.240.16–0.35
Discordant monozygotic twins0.170.08–0.38
a
The observed and predicted Akaike’s information criterion values were 1431449.1 and 1431448.0, respectively.
FIGURE 1. Association between pregnancy and risk for alcohol use disorder in the general population, cousins, siblings, and monozygotic twins discordant for pregnancy, and within individuals (comparing matched periods before and during pregnancy) for a first and second pregnancya
a Odds ratios are from the predicted model and are estimated from models without covariates. Sample sizes are based on individuals with alcohol use disorder registrations within each group (see Table 1); for cousins and siblings, these are from discordant pairs. Error bars indicate confidence interval.
We conducted a series of within-individual analyses, first using periods prior to pregnancy as the control. Regardless of the control time frame—the 242 days prior to the estimated beginning of the pregnancy, 6 months prior to start of pregnancy, or 12 months prior to start of pregnancy—the risk of alcohol use disorder was consistently and substantially reduced during pregnancy (odds ratios, 0.25–0.26) (Table 1). We next tested whether rates of alcohol use disorder were similar in the first and second halves of a pregnancy, and found no significant difference (odds ratio=1.08, 95% CI=0.78, 1.49). We also examined whether the negative association was observed during a second pregnancy, and obtained comparable results (odds ratio=0.23, 95% CI=0.15, 0.35) (Table 1). Finally, we examined the persistence of the observed negative association during a range of postpartum periods (Table 3). We found a gradual decrease in the protective effect of pregnancy across time, with the prevalence of alcohol use disorder in the immediate postpartum period (0–242 days after childbirth) only half that in the third period (485–726 days after childbirth). Even so, the confidence intervals for the odds ratios in the third period remained far below one.
TABLE 3. Within-individual analyses of rates of alcohol use disorder in the pre-pregnancy and postpartum periods
  Prevalence of Alcohol Use Disorder (%)  
Risk PeriodNControl PeriodaRisk PeriodOdds Ratio95% CI
0–242 days after childbirth294,6230.170.030.170.13–0.21
243–484 days after childbirth273,1570.170.040.230.19–0.29
485–726 days after childbirth250,8550.170.060.310.25–0.38
a
The control period was 242 days prior to childbirth.

Comparison With Fathers

We tested whether a similar association was observed among biological fathers, using the 287,292 cases where the father and mother were cohabitating at the end of the child’s year of birth. When examined together, the reduction in risk for an alcohol use disorder registration from the control to the pregnancy period was more pronounced for the mother (odds ratio=0.18, 95% CI=0.14, 0.23) than for the father (odds ratio=0.45, 95% CI=0.41, 0.49). This difference was also reflected in a model that treats mothers and fathers as independent: the reduction in risk in the control period compared with the pregnancy period was stronger in the mother relative to the father (odds ratio=0.56, 95% CI=0.47, 0.68).

Potential Moderating Factors

We considered a range of sociodemographic and psychopathological factors that may moderate the negative association between pregnancy and alcohol use disorder (Table 4). We observed evidence of moderation (p<0.05) for only two factors: a criminal registration in the mother prior to pregnancy and age at pregnancy (<25 years or ≥25 years). Specifically, the negative association between pregnancy and alcohol use disorder was stronger among mothers with a criminal history relative to their counterparts without a criminal history; similarly, the negative association was more pronounced among younger mothers.
TABLE 4. Potential moderators of the effect of pregnancy of risk for alcohol use disorder
  Rate of Alcohol Use Disorder (%)   
VariableNPregnancyControlDifferenceInteraction pOdds Ratio95% CI
General potential moderators
Parental education levela       
 Low103,6730.060.210.150.3090.270.22, 0.34
 Middle173,2380.050.170.39 0.230.18, 0.29
 High18,1630.030.090.06 0.190.12, 0.32
Alcohol use disorder in mother’s parents       
 No293,8920.040.140.100.3290.240.20, 0.29
 Yes38,5440.130.400.27 0.280.21, 0.37
School achievement (SD units)b       
 –2.5 to –1.520,8030.130.490.360.9200.220.18, 0.28
 –1.5 to –0.579,2050.070.240.17 0.220.19, 0.27
 –0.5 to 0.5120,7170.020.100.08 0.230.18, 0.29
 0.5 to 1.582,9130.010.040.03 0.230.16, 0.33
 1.5 to 2.513,5420.000.000.00 0.230.14, 0.38
Prior alcohol use disorder in mother       
 No327,0200.030.120.090.1490.230.19, 0.28
 Yes5,4161.142.821.68 0.300.23, 0.40
Prior crime in mother       
 No309,7650.030.130.100.0090.220.18, 0.26
 Yes22,6710.290.730.44 0.330.26, 0.43
Prior drug abuse in mother       
 No325,8360.030.120.090.1850.230.19, 0.28
 Yes6,6000.942.561.62 0.290.22, 0.38
Prior psychiatric diagnosis in mother       
 No328,7690.050.160.090.5860.250.21, 0.30
 Yes3,6670.250.790.54 0.200.09, 0.45
Age at pregnancy (years)       
 <25135,1870.070.300.23<0.0010.210.17, 0.26
 ≥25197,2490.040.080.04 0.360.28, 0.47
Marriedc       
 No255,6230.060.200.140.6780.250.22 0.30
 Yes38,9490.020.080.06 0.310.13, 0.75
Features of cohabiting biological father’s alcohol use disorder as potential moderators
Prior alcohol use disorder in father       
 No274,2660.020.090.070.2220.160.12, 0.22
 Yes13,0260.120.480.36 0.230.14, 0.38
Alcohol use disorder during pregnancy in father       
 No286,8860.020.110.090.8020.180.14, 0.23
 Yes4060.741.981.24 0.150.05, 0.49
a
Parental education was used as a continuous term in the models, hence there is only one interaction term; the odds ratios reported here are an illustration of the odds ratios at different levels of parental education.
b
School achievement was used as a continuous term in the models, hence there is only one interaction term; the odds ratios reported here are an illustration of the odds ratios at different levels of school achievement.
c
In the analyses of married people, individuals who married in the control or hazard period were excluded (for these individuals, we could not separate whether the effect was due to marriage or to pregnancy).

Discussion

We used national registry data to examine the potential causal relationship between pregnancy and reduced risk for alcohol use disorder among Swedish women. We considered a variety of contextual perspectives: matching to population controls, comparison with female relatives discordant for pregnancy, within-individual control periods, and comparisons between mothers and fathers. We consistently observed markedly lower rates of alcohol use disorder registrations during pregnancy, with the reduction in risk among mothers ranging from ∼70% to 80% across analyses. The findings are suggestive of “inverse confounding,” such that adjustment for potential sociodemographic or genetic confounders strengthened the observed association. These results are consistent with previous reports that women reduce their alcohol consumption during pregnancy (6, 30, 31). We extend those findings to demonstrate that the observed association applies to a clinically relevant outcome, indicating that even among women at elevated genetic risk for or with a personal history of alcohol use disorder, pregnancy can be a critical motivating factor for modifying alcohol misuse.
We first compared pregnant women with matched control women and, accounting for covariates, found that the odds of an alcohol use disorder registration were reduced by 74% among pregnant women. When controlling for confounding factors by applying a co-relative design, we found that pregnancy was even more strongly protective against risk for alcohol use disorder, with the odds of alcohol use disorder reduced by 83% in the pregnant member of a discordant monozygotic twin pair. While the unique nature of pregnancy precludes comparison with other circumstances in which changes to drinking are expected (e.g., contingency management programs), these reductions are objectively substantial. Notably, previous studies have demonstrated that clear communication from clinicians, such as provision of a pamphlet or interpersonal discussions about the risks of prenatal alcohol use, may further reduce alcohol misuse, beyond the effects of pregnancy alone (13, 14). Pregnancy may therefore present an important window of opportunity for intervention (32).
Longitudinal data and the temporally discrete nature of pregnancy enabled us to use women as their own controls, comparing rates of alcohol use disorder during pregnancy and during periods preceding and following pregnancy. This approach is not subject to potential confounders that may complicate observed associations between pregnancy and alcohol use disorder. Given that many pregnancies are planned and women may modify their alcohol use in anticipation, we used a range of time frames as the reference; the quite stable results suggest that even if pregnancy is planned 6 to 12 months in advance, the actual pregnancy still represents a period of substantial reduction in risk of alcohol use disorder. This relationship was borne out in the postpartum periods as well. In the period immediately following pregnancy, the odds of alcohol use disorder were identical to those predicted for discordant monozygotic twins. In the next two successive periods, the odds increased but remained substantially lower than 1. Thus, the protective effect potentially conferred by pregnancy persists over time, with only minor decreases in strength; additional analyses could clarify the extent to which risk stabilizes. Previous work indicates that parenthood itself is inversely associated with risk of alcohol use disorder (33, 34), and thus long-term decreases in risk relative to the prepregnancy period are likely.
We evaluated potential moderation of the association of pregnancy and alcohol use disorder by a variety of factors. We found that the risk of alcohol use disorder decreased during pregnancy more sharply among women with a history of criminal behavior. Similarly, women who became pregnant before age 25 exhibited a more pronounced reduction in risk of alcohol use disorder than those who became pregnant at a later age. These findings suggest that pregnancy may be an especially powerful motivator for healthful behavior among women who are otherwise at higher risk for alcohol use disorder. Interestingly, we observed no interaction between pregnancy and personal history of alcohol use disorder. Parental history of alcohol use disorder, an indicator of genetic and environmental alcohol use disorder risk, also did not moderate the association between pregnancy and alcohol use disorder. In conjunction with our co-relative analyses, this suggests that while genetic factors may inversely confound the observed association, the protective effect of pregnancy is robust even to the pronounced genetic component of alcohol use disorder liability. Indeed, the paucity of moderating factors underscores the consistency of pregnancy’s motivational capacity.
Pregnancy is also associated with reductions in alcohol use disorder among partners, although to a lesser extent than among mothers. Again, this suggests that factors other than fetal alcohol exposure contribute to the observed association; a previous study found that changing social contexts and concern for the mother motivated decreased alcohol consumption among the partners of pregnant women (35). The discrepancy in risk reduction across mothers and fathers may be attributable to concerns about alcohol’s direct effect on the fetus: Brief interventions that educate pregnant women about alcohol’s teratogenic effects have been shown to decrease consumption (14, 36). Notably, partner alcohol use disorder, prior to or during the pregnancy, did not moderate mothers’ alcohol use disorder risk. A Dutch study of pregnant women found that women drank less if their partner more strongly disapproved of drinking during pregnancy or if the partner drank less during the pregnancy (37). Taking these findings together, it is possible that health-promoting partner behavior may discourage adverse outcomes in the mother, while the inverse may not be true: pregnant woman are unlikely to be differentially affected by “risky” partner behavior.
We note a number of limitations to this study. Our analyses were conducted on native-born Swedes and may not generalize to other populations; while we have no reason to believe that Swedish women are substantially different from women in other industrialized countries, the social resources available to pregnant Swedish women may facilitate decreases in alcohol misuse. We selected a birth cohort to maximize data availability during the time frame relevant to childbirth; this may come at the expense of detecting long-term changes in rates of alcohol use disorder, or specifically changes in the association between alcohol use disorder and pregnancy. Our use of registry data may be more likely to capture more severe cases of alcohol use disorder and therefore may be subject to false negatives; however, false negatives are a pitfall of nearly any study design, and registry records are less subject to recall or reporting bias than self-reports. The reliance on registry records also precludes examination of intra- or interpersonal factors, such as personality, motives for changes in alcohol use or misuse, quality of the relationship with one’s partner, and so on.
In summary, these findings suggest that pregnancy plays a pivotal motivational role in the reduction of alcohol use disorder. Our results are consistent with a causal role for pregnancy in alcohol use disorder risk reduction, although this should not be considered definitive, given the observational nature of the data. Negative associations were strong and consistent across all analyses and, overall, were robust to moderation by an array of factors that are otherwise reliable predictors of risk of alcohol use disorder. Both parents benefit from the reduction in alcohol use disorder risk during the pregnancy, with the association more pronounced for mothers, among whom it persists, with modest attenuation, into the postpartum period. In conjunction with evidence from alcohol use disorder treatment programs that include cash or prize rewards for abstinence, this putative protective role of pregnancy suggests that qualitatively different factors have the potential to motivate reduction in alcohol misuse, which may broaden the possibilities for intervention in alcohol use disorder treatment. These findings further suggest that the reduction in volition often associated with substance use disorders may be superseded by especially salient circumstances.

Acknowledgments

The authors thank the Swedish Twin Registry at the Karolinska Institute, which provided the twin data for this study.

Footnote

Drs. K. Sundquist and Kendler jointly supervised this work.

Supplementary Material

File (appi.ajp.2018.18050632.ds001.pdf)

References

1.
Sokol RJ, Delaney-Black V, Nordstrom B: Fetal alcohol spectrum disorder. JAMA 2003; 290:2996–2999
2.
Schölin L: Prevention of Harm Caused by Alcohol Exposure in Pregnancy: Rapid Review and Case Studies From Member States. Copenhagen, World Health Organization, 2016
3.
Substance Abuse and Mental Health Services Administration: Results from the 2013 National Survey on Drug Use and Health: Summary of National Findings. Rockville, Md, Substance Abuse and Mental Health Services Administration, 2014
4.
Mårdby AC, Lupattelli A, Hensing G, et al: Consumption of alcohol during pregnancy: a multinational European study. Women Birth 2017; 30:e207–e213
5.
Alvik A, Haldorsen T, Groholt B, et al: Alcohol consumption before and during pregnancy comparing concurrent and retrospective reports. Alcohol Clin Exp Res 2006; 30:510–515
6.
Bor J, Basu S, Coutts A, et al: Alcohol use during the great recession of 2008–2009. Alcohol Alcohol 2013; 48:343–348
7.
Slater ME, Haughwout SP, Castle I-JP: Trends in Substance Use Among Reproductive-Age Females in the United States, 2002–2013. Washington, DC, US Department of Health and Human Services, Public Health Service, National Institutes of Health, 2015
8.
Kendler KS, Ohlsson H, Svikis DS, et al: The protective effect of pregnancy on risk for drug abuse: a population, co-relative, co-spouse, and within-individual analysis. Am J Psychiatry 2017; 174:954–962
9.
Kirby D: Looking for Reasons Why: The Antecedents of Adolescent Sexual Risk-Taking, Pregnancy, and Child-Bearing. Washington, DC, National Campaign to Prevent Teen Pregnancy, 1999
10.
Salas-Wright CP, Vaughn MG, Ugalde J, et al: Substance use and teen pregnancy in the United States: evidence from the NSDUH 2002–2012. Addict Behav 2015; 45:218–225
11.
Skagerström J, Alehagen S, Häggström-Nordin E, et al: Prevalence of alcohol use before and during pregnancy and predictors of drinking during pregnancy: a cross sectional study in Sweden. BMC Public Health 2013; 13:780
12.
Comasco E, Hallberg G, Helander A, et al: Alcohol consumption among pregnant women in a Swedish sample and its effects on the newborn outcomes. Alcohol Clin Exp Res 2012; 36:1779–1786
13.
Nilsen P, Skagerström J, Rahmqvist M, et al: Alcohol prevention in Swedish antenatal care: effectiveness and perceptions of the Risk Drinking Project counseling model. Acta Obstet Gynecol Scand 2012; 91:736–743
14.
Bortes C, Geidne S, Eriksson C: Preventing alcohol consumption during pregnancy: a randomized controlled trial. Health 2015; 07:289–299
15.
Kalivas PW, Volkow ND: The neural basis of addiction: a pathology of motivation and choice. Am J Psychiatry 2005; 162:1403–1413
16.
Koob GF, Volkow ND: Neurocircuitry of addiction. Neuropsychopharmacology 2010; 35:217–238
17.
American Psychiatric Association: Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5). Washington, DC, American Psychiatric Association, 2013
18.
Higgins ST, Sigmon SC, Heil SH: Contingency management in the treatment of substance use disorders: trends in the literature, in Lowinson and Ruiz’s Substance Abuse: A Comprehensive Textbook, 5th ed. Edited by Ruiz P, Strain E. Philadelphia, Lippincott Williams & Wilkins, 2011, pp 603–621
19.
McDonell MG, Leickly E, McPherson S, et al: A randomized controlled trial of ethyl glucuronide–based contingency management for outpatients with co-occurring alcohol use disorders and serious mental illness. Am J Psychiatry 2017; 174:370–377
20.
Petry NM, Martin B, Cooney JL, et al: Give them prizes, and they will come: contingency management for treatment of alcohol dependence. J Consult Clin Psychol 2000; 68:250–257
21.
Barnett NP, Celio MA, Tidey JW, et al: A preliminary randomized controlled trial of contingency management for alcohol use reduction using a transdermal alcohol sensor. Addiction 2017; 112:1025–1035
22.
DePhilippis D, Petry NM, Bonn-Miller MO, et al: The national implementation of contingency management (CM) in the Department of Veterans Affairs: attendance at CM sessions and substance use outcomes. Drug Alcohol Depend 2018; 185:367–373
23.
Bailey AJ, Gerst K, Finn PR: Delay discounting of losses and rewards in alcohol use disorder: the effect of working memory load. Psychol Addict Behav 2018; 32:197–204
24.
Mole TB, Irvine MA, Worbe Y, et al: Impulsivity in disorders of food and drug misuse. Psychol Med 2015; 45:771–782
25.
Mitchell SH: The genetic basis of delay discounting and its genetic relationship to alcohol dependence. Behav Processes 2011; 87:10–17
26.
Businelle MS, McVay MA, Kendzor D, et al: A comparison of delay discounting among smokers, substance abusers, and non-dependent controls. Drug Alcohol Depend 2010; 112:247–250
27.
Verhulst B, Neale MC, Kendler KS: The heritability of alcohol use disorders: a meta-analysis of twin and adoption studies. Psychol Med 2015; 45:1061–1072
28.
Kendler KS, Ohlsson H, Sundquist J, et al: School achievement, IQ, and risk of alcohol use disorder: a prospective, co-relative analysis in a Swedish national cohort. J Stud Alcohol Drugs 2017; 78:186–194
29.
Kendler KS, Larsson Lönn S, Morris NA, et al: A Swedish national adoption study of criminality. Psychol Med 2014; 44:1913–1925
30.
DeVido J, Bogunovic O, Weiss RD: Alcohol use disorders in pregnancy. Harv Rev Psychiatry 2015; 23:112–121
31.
Kitsantas P, Gaffney KF, Wu H, et al: Determinants of alcohol cessation, reduction, and no reduction during pregnancy. Arch Gynecol Obstet 2014; 289:771–779
32.
Svikis DS, Reid-Quiñones K: Screening and prevention of alcohol and drug use disorders in women. Obstet Gynecol Clin North Am 2003; 30:447–468
33.
Chilcoat HD, Breslau N: Alcohol disorders in young adulthood: effects of transitions into adult roles. J Health Soc Behav 1996; 37:339–349
34.
Fergusson DM, Boden JM, John Horwood L: Transition to parenthood and substance use disorders: findings from a 30-year longitudinal study. Drug Alcohol Depend 2012; 125:295–300
35.
Högberg H, Skagerström J, Spak F, et al: Alcohol consumption among partners of pregnant women in Sweden: a cross sectional study. BMC Public Health 2016; 16:694
36.
O’Connor MJ, Whaley SE: Brief intervention for alcohol use by pregnant women. Am J Public Health 2007; 97:252–258
37.
van der Wulp NY, Hoving C, de Vries H: Partner’s influences and other correlates of prenatal alcohol use. Matern Child Health J 2015; 19:908–916

Information & Authors

Information

Published In

Go to American Journal of Psychiatry
Go to American Journal of Psychiatry
American Journal of Psychiatry
Pages: 138 - 145
PubMed: 30486670

History

Received: 31 May 2018
Revision received: 15 August 2018
Accepted: 17 September 2018
Published online: 29 November 2018
Published in print: February 01, 2019

Keywords

  1. Alcohol Abuse
  2. Alcohol Use Disorder
  3. Co-Relative Design
  4. Postpartum
  5. Pregnancy

Authors

Details

Alexis C. Edwards, Ph.D. [email protected]
The Virginia Institute for Psychiatric and Behavioral Genetics, Department of Psychiatry (Edwards, Kendler), and the Departments of Psychology, Psychiatry, and Obstetrics and Gynecology (Svikis), Virginia Commonwealth University, Richmond; the Center for Primary Health Care Research, Lund University, Malmö, Sweden (Ohlsson, J. Sundquist, K. Sundquist); and the Icahn School of Medicine at Mount Sinai, New York (K. Sundquist).
Henrik Ohlsson, Ph.D.
The Virginia Institute for Psychiatric and Behavioral Genetics, Department of Psychiatry (Edwards, Kendler), and the Departments of Psychology, Psychiatry, and Obstetrics and Gynecology (Svikis), Virginia Commonwealth University, Richmond; the Center for Primary Health Care Research, Lund University, Malmö, Sweden (Ohlsson, J. Sundquist, K. Sundquist); and the Icahn School of Medicine at Mount Sinai, New York (K. Sundquist).
Dace S. Svikis, Ph.D.
The Virginia Institute for Psychiatric and Behavioral Genetics, Department of Psychiatry (Edwards, Kendler), and the Departments of Psychology, Psychiatry, and Obstetrics and Gynecology (Svikis), Virginia Commonwealth University, Richmond; the Center for Primary Health Care Research, Lund University, Malmö, Sweden (Ohlsson, J. Sundquist, K. Sundquist); and the Icahn School of Medicine at Mount Sinai, New York (K. Sundquist).
Jan Sundquist, M.D., Ph.D.
The Virginia Institute for Psychiatric and Behavioral Genetics, Department of Psychiatry (Edwards, Kendler), and the Departments of Psychology, Psychiatry, and Obstetrics and Gynecology (Svikis), Virginia Commonwealth University, Richmond; the Center for Primary Health Care Research, Lund University, Malmö, Sweden (Ohlsson, J. Sundquist, K. Sundquist); and the Icahn School of Medicine at Mount Sinai, New York (K. Sundquist).
Kristina Sundquist, M.D., Ph.D.
The Virginia Institute for Psychiatric and Behavioral Genetics, Department of Psychiatry (Edwards, Kendler), and the Departments of Psychology, Psychiatry, and Obstetrics and Gynecology (Svikis), Virginia Commonwealth University, Richmond; the Center for Primary Health Care Research, Lund University, Malmö, Sweden (Ohlsson, J. Sundquist, K. Sundquist); and the Icahn School of Medicine at Mount Sinai, New York (K. Sundquist).
Kenneth S. Kendler, M.D.
The Virginia Institute for Psychiatric and Behavioral Genetics, Department of Psychiatry (Edwards, Kendler), and the Departments of Psychology, Psychiatry, and Obstetrics and Gynecology (Svikis), Virginia Commonwealth University, Richmond; the Center for Primary Health Care Research, Lund University, Malmö, Sweden (Ohlsson, J. Sundquist, K. Sundquist); and the Icahn School of Medicine at Mount Sinai, New York (K. Sundquist).

Notes

Send correspondence to Dr. Edwards ([email protected]).

Competing Interests

The authors report no financial relationships with commercial interests.

Funding Information

Forskningsrådet om Hälsa, Arbetsliv och Välfärd10.13039/501100006636: 2013-1836, 2014-0804
Vetenskapsrådet10.13039/501100004359: 2012-2378; 2014-10134, K2012-70X-15428-08-3
National Institute on Alcohol Abuse and Alcoholism10.13039/100000027: AA023534
Supported by NIH grant R01AA023534 and grants from the Swedish Research Council (K2012-70X-15428-08-3), the Swedish Research Council for Health, Working Life, and Welfare (Forte; Reg.nr. 2013-1836), the Swedish Research Council (2012-2378; 2014-10134), and FORTE (2014-0804) as well as ALF funding from Region Skåne.

Metrics & Citations

Metrics

Citations

Export Citations

If you have the appropriate software installed, you can download article citation data to the citation manager of your choice. Simply select your manager software from the list below and click Download.

For more information or tips please see 'Downloading to a citation manager' in the Help menu.

Format
Citation style
Style
Copy to clipboard

View Options

View options

PDF/EPUB

View PDF/EPUB

Login options

Already a subscriber? Access your subscription through your login credentials or your institution for full access to this article.

Personal login Institutional Login Open Athens login
Purchase Options

Purchase this article to access the full text.

PPV Articles - American Journal of Psychiatry

PPV Articles - American Journal of Psychiatry

Not a subscriber?

Subscribe Now / Learn More

PsychiatryOnline subscription options offer access to the DSM-5-TR® library, books, journals, CME, and patient resources. This all-in-one virtual library provides psychiatrists and mental health professionals with key resources for diagnosis, treatment, research, and professional development.

Need more help? PsychiatryOnline Customer Service may be reached by emailing [email protected] or by calling 800-368-5777 (in the U.S.) or 703-907-7322 (outside the U.S.).

Media

Figures

Other

Tables

Share

Share

Share article link

Share