Psychiatric epidemiologists have long observed that married adults have fewer mental health problems as compared to unmarried age-peers (1). There are two broad categories of explanation for the positive association between marital status and health: social selection and social causation (2). Social selection describes processes in which healthier individuals are more likely to marry and stay married. Social causation refers to processes in which marriage improves health. Randomized experiments testing marriage effects are not ethical. Cross-sectional studies cannot disentangle selection from causation (3). Instead, researchers have turned to prospective cohort studies that follow individuals from before marriage, into their married lives. The prospective longitudinal design can account for pre-marriage health differences and test if getting married is associated with health improvement or slower health decline as compared to remaining unmarried. Prospective studies find clear evidence for social selection, but they also find evidence for social causation (4; 5); people who marry are healthier than peers who remain unmarried, but after accounting for these differences, marriage benefits health. However, there are few prospective data to address association of marriage with psychiatric disorders. Because individual disorders affect only small portions of the population, cohort studies typically lack power for such analysis. National registers, which record official data on entire populations, provide an alternative.
Start and end dates of marriages are legal records. In countries with national health systems, disorder diagnosis and treatment are also recorded. Linked register analysis can examine whether individuals who get and stay married are less likely to “register” indications of disorder as compared to individuals who do not marry or who get divorced. In this issue of the Journal, Kendler and colleagues analyze register data from Sweden to test whether divorce increases risk for alcohol use disorder (AUD) (6).
The authors constructed histories of divorce, remarriage, and AUD in people born 1960–1990, married from 1990 onward, with no AUD history prior to marriage (N=942,366). Swedish Hospital Discharge, Outpatient Care, Primary Health Care, Prescribed Drug, Crime, and Suspicion Registers were linked to evaluate AUD incidence through 2011. Over 20 years of follow-up, 16% of men and 17% of women were divorced. AUD registration, determined from ICD codes, records of disulfiram, acamprosate, or naltrexone prescription, or conviction or suspicion of at least two alcohol-related crimes, was recorded in 1.1% of men and 0.5% of women. Survival analysis tested if divorce increased risk for AUD relative to remaining married. Record linkages with Census data, the Multi-Generation Register, and the Swedish Twin Register were used for covariate-adjusted and co-relative comparison analyses to address confounds.
Divorce predicted six- to seven-fold increase in risk for first AUD registration relative to individuals of the same age and sex who stayed married. This association was not accounted for by measures of prior deviant behavior, family history of AUD, or parental education. The association was significantly reduced among individuals married to spouses with AUD histories.
AUD risk among divorced persons increased in the years leading up to divorce, peaked in the divorce year, and remained elevated for over a decade in those who remained un-married. For those who remarried, AUD risk declined substantially. These findings are consistent with AUD as a cause of divorce and barrier to remarriage, i.e., reverse-causation. However, parallel analysis of widowhood, which is less likely to be caused by AUD, showed similar results. The pre-divorce increase in AUD risk may reflect other causes of divorce, e.g., marital discord (7).
Genetic factors explained some of the divorce-AUD association. Analyses comparing divorced individuals to still-married siblings and cousins estimated that about half of the six-fold increase in AUD risk associated with divorce was attributable to genetic causes, about the same result reported in a biometric analysis published by these authors (8). Individuals with prior deviant behavior and/or a family history of AUD were more likely to develop an AUD following divorce as compared to same-aged peers without these risk factors. Whether this heterogeneity reflects gene-environment interaction or synergies among non-genetic risks was not examined in this study.
Results are broadly consistent with a previous register study by the same authors testing protective effects of marriage on AUD (9). As in this study, estimated effects were large, even after adjusting for potential confounders and re-estimating associations within families. Also in parallel, the effect of marriage on alcohol-related problems was largest for individuals with a family history of AUD. Taken together, results suggest marriage and divorce are clinically significant factors in the development of AUD. Moreover, while social selection contributes to the association between marriage/divorce and AUD, a portion of marriage/divorce-associated AUD risk may reflect social causation.
We highlight two considerations in interpreting findings. First, register analysis may fail to observe some AUD cases. For example, past-year prevalence rates of DSM-5 AUD among married and divorced/widowed/separated individuals in the National Epidemiologic Survey on Alcohol and Related Conditions-III (NESARC-III) were about 10% (10), compared with the approximately 1% observed in this sample. Milder cases that do not result in treatment seeking or criminal behavior may go under-observed, as will cases occurring in individuals who face barriers to treatment. The Swedish health system provides free access to care; but other barriers may exist, e.g., stigma (11). Second, many individuals in the cohorts studied by Kendler and colleagues never married, and those who did tended to marry in their late twenties or early thirties (12). Although patterns of AUD involvement vary across countries, AUD typically onsets prior to the age of marriage in this Swedish sample (10; 13). Kendler and colleagues’ analysis may be most informative for understanding the minority of alcohol problems with later onset.
Clinically, results affirm importance of AUD screening among patients going through divorce, particularly those with prior conduct problems or family AUD history. Results also highlight opportunities for prevention (14). Providing psychoeducation regarding association between divorce and AUD, early AUD indicators, and healthy drinking practices to individuals experiencing marital distress or divorce may help reduce alcohol-related problems. Findings do not suggest clinicians should encourage patients to remain married to prevent AUD. However, to the degree spouses are protective, intervention to promote positive marital dynamics may prove an effective strategy for prevention. Couples interventions exist for treatment of AUDs after they have onset (15). Intervening earlier may help prevent AUDs.
Future research is needed to identify mechanisms by which marriage reduces AUD risk. Fostering of protective features of marriage within existing marital or other social relationships (16) could offer a universal approach to AUD prevention. One mechanism highlighted by Kendler and colleagues is monitoring. AUD-related psychological processes influenced by social relationships also deserve consideration. Genetic analysis of heterogeneity in divorce-related AUD risk may inform understanding of etiology and guide intervention. Recent genome-wide association studies of AUD suggest progress toward identifying molecular genetic risks (17). Follow-up using gene-environment interaction designs within very-large genetic databases, such UK Biobank (18), or genetically-informed studies of spouses, such as the US Health and Retirement Study (19), should be a priority.
Kendler and colleagues’ analysis, employing multiple complementary methodologies within a large registry dataset, provides evidence that divorce increases risk for alcohol use disorder. Results can inform clinical and public health efforts toward prevention and guide research into social and genetic etiology of AUD.
Acknowledgments
DWB acknowledges support from US National Institute on Aging grants R01AG032282, P30AG028716, and P30AG034424, and from the Jacobs Foundation. LSR received support from AA023419.
References
- 1.Malzberg B. Marital status in relation to the prevalence of mental disease. Psychiatr. Q. 1936;10:245–261. [Google Scholar]
- 2.Kiecolt-Glaser JK, Newton TL. Marriage and health: his and hers. Psychol. Bull. 2001;127:472–503. doi: 10.1037/0033-2909.127.4.472. [DOI] [PubMed] [Google Scholar]
- 3.Goldman N. Marriage selection and mortality patterns: Inferences and fallacies. Demography. 1993;30:189–208. [PubMed] [Google Scholar]
- 4.House JS, Landis KR, Umberson D. Social relationships and health. Science. 1988;241:540–545. doi: 10.1126/science.3399889. [DOI] [PubMed] [Google Scholar]
- 5.Smith KP, Christakis NA. Social networks and health. Annu Rev Sociol. 2008;34:405–429. [Google Scholar]
- 6.Kendler KS, Lönn SL, Salvatore J, Sundquist J, Sundquist K. Divorce and the Onset of Alcohol Use Disorder: A Swedish Population-Based Longitudinal Cohort and Co-Relative Study. Am. J. Psychiatry. 2017 doi: 10.1176/appi.ajp.2016.16050589. appi.ajp.2016.16050589. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 7.Whisman MA, Uebelacker LA, Bruce ML. Longitudinal association between marital dissatisfaction and alcohol use disorders in a community sample. J. Fam. Psychol. JFP J. Div. Fam. Psychol. Am. Psychol. Assoc. Div. 43. 2006;20:164–167. doi: 10.1037/0893-3200.20.1.164. [DOI] [PubMed] [Google Scholar]
- 8.Salvatore JE, Larsson Lönn S, Sundquist J, Lichtenstein P, Sundquist K, Kendler KS. Alcohol use disorder and divorce: evidence for a genetic correlation in a population-based Swedish sample. Addict. Abingdon Engl. 2016 doi: 10.1111/add.13719. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 9.Kendler KS, Lönn SL, Salvatore J, Sundquist J, Sundquist K. Effect of Marriage on Risk for Onset of Alcohol Use Disorder: A Longitudinal and Co-Relative Analysis in a Swedish National Sample. Am. J. Psychiatry. 2016;173:911–918. doi: 10.1176/appi.ajp.2016.15111373. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 10.Grant BF, Goldstein RB, Saha TD, Chou SP, Jung J, Zhang H, Pickering RP, Ruan WJ, Smith SM, Huang B, Hasin DS. Epidemiology of DSM-5 Alcohol Use Disorder: Results From the National Epidemiologic Survey on Alcohol and Related Conditions III. JAMA Psychiatry. 2015;72:757–766. doi: 10.1001/jamapsychiatry.2015.0584. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 11.Keyes KM, Hatzenbuehler ML, McLaughlin KA, Link B, Olfson M, Grant BF, Hasin D. Stigma and Treatment for Alcohol Disorders in the United States. Am. J. Epidemiol. 2010;172:1364–1372. doi: 10.1093/aje/kwq304. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 12.Ohlsson-Wijk S. Sweden’s marriage revival: An analysis of the new-millennium switch from long-term decline to increasing popularity. Popul. Stud. 2011;65:183–200. doi: 10.1080/00324728.2011.574724. [DOI] [PubMed] [Google Scholar]
- 13.Hasin DS, Stinson FS, Ogburn E, Grant BF. Prevalence, correlates, disability, and comorbidity of DSM-IV alcohol abuse and dependence in the United States: results from the National Epidemiologic Survey on Alcohol and Related Conditions. Arch. Gen. Psychiatry. 2007;64:830–842. doi: 10.1001/archpsyc.64.7.830. [DOI] [PubMed] [Google Scholar]
- 14.American Psychological Association: Guidelines for prevention in psychology. Am. Psychol. 2014;69:285. doi: 10.1037/a0034569. [DOI] [PubMed] [Google Scholar]
- 15.Powers MB, Vedel E, Emmelkamp PMG. Behavioral couples therapy (BCT) for alcohol and drug use disorders: a meta-analysis. Clin. Psychol. Rev. 2008;28:952–962. doi: 10.1016/j.cpr.2008.02.002. [DOI] [PubMed] [Google Scholar]
- 16.Rosenquist JN, Murabito J, Fowler JH, Christakis NA. The spread of alcohol consumption behavior in a large social network. Ann. Intern. Med. 2010;152:426–433. W141. doi: 10.1059/0003-4819-152-7-201004060-00007. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 17.Schumann G, Liu C, O’Reilly P, Gao H, Song P, Xu B, Ruggeri B, Amin N, Jia T, Preis S, Lepe MS, Akira S, Barbieri C, Baumeister S, Cauchi S, Clarke T-K, Enroth S, Fischer K, Hällfors J, Harris SE, Hieber S, Hofer E, Hottenga J-J, Johansson Å, Joshi PK, Kaartinen N, Laitinen J, Lemaitre R, Loukola A, Luan J, Lyytikäinen L-P, Mangino M, Manichaikul A, Mbarek H, Milaneschi Y, Moayyeri A, Mukamal K, Nelson C, Nettleton J, Partinen E, Rawal R, Robino A, Rose L, Sala C, Satoh T, Schmidt R, Schraut K, Scott R, Smith AV, Starr JM, Teumer A, Trompet S, Uitterlinden AG, Venturini C, Vergnaud A-C, Verweij N, Vitart V, Vuckovic D, Wedenoja J, Yengo L, Yu B, Zhang W, Zhao JH, Boomsma DI, Chambers J, Chasman DI, Daniela T, Geus E de, Deary I, Eriksson JG, Esko T, Eulenburg V, Franco OH, Froguel P, Gieger C, Grabe HJ, Gudnason V, Gyllensten U, Harris TB, Hartikainen A-L, Heath AC, Hocking L, Hofman A, Huth C, Jarvelin M-R, Jukema JW, Kaprio J, Kooner JS, Kutalik Z, Lahti J, Langenberg C, Lehtimäki T, Liu Y, Madden PAF, Martin N, Morrison A, Penninx B, Pirastu N, Psaty B, Raitakari O, Ridker P, Rose R, Rotter JI, Samani NJ, Schmidt H, Spector TD, Stott D, Strachan D, Tzoulaki I, Harst P van der, Duijn CM van, Marques-Vidal P, Vollenweider P, Wareham NJ, Whitfield JB, Wilson J, Wolffenbuttel B, Bakalkin G, Evangelou E, Liu Y, Rice KM, Desrivières S, Kliewer SA, Mangelsdorf DJ, Müller CP, Levy D, Elliott P. KLB is associated with alcohol drinking, and its gene product β-Klotho is necessary for FGF21 regulation of alcohol preference. Proc. Natl. Acad. Sci. 2016;113:14372–14377. doi: 10.1073/pnas.1611243113. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 18.Tyrrell J, Wood AR, Ames RM, Yaghootkar H, Beaumont RN, Jones SE, Tuke MA, Ruth KS, Freathy RM, Davey Smith G, Joost S, Guessous I, Murray A, Strachan DP, Kutalik Z, Weedon MN, Frayling TM. Gene–obesogenic environment interactions in the UK Biobank study [Internet] [cited 2017 Feb 8];Int. J. Epidemiol. doi: 10.1093/ije/dyw337. Available from: https://academic.oup.com/ije/article/doi/10.1093/ije/dyw337/2886194/Gene-obesogenic-environment-interactions-in-the-UK. [DOI] [PMC free article] [PubMed]
- 19.Domingue B, Liu H, Okbay A, Belsky DW. Genetic heterogeneity in depressive symptoms following the death of a spouse: Polygenic score analysis of the US Health and Retirement Study. Am. J. Psychiatry Accepted. doi: 10.1176/appi.ajp.2017.16111209. [DOI] [PMC free article] [PubMed] [Google Scholar]
