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. Author manuscript; available in PMC: 2019 May 1.
Published in final edited form as: Drug Alcohol Depend. 2018 Mar 10;186:154–158. doi: 10.1016/j.drugalcdep.2018.01.021

Does exposure to parental substance use disorders increase offspring risk for a substance use disorder? A longitudinal follow-up study into young adulthood

Amy M Yule 1,2, Timothy E Wilens 1,2, MaryKate Martelon 1, Lindsay Rosenthal 1, Joseph Biederman 1,2
PMCID: PMC5876721  NIHMSID: NIHMS950614  PMID: 29573650

Abstract

Objective

The main aim of this study was to examine the risk of exposure to parental substance use disorders (SUD; alcohol or drug abuse or dependence) on the risk for SUD in offspring with and without attention deficit hyperactivity disorder (ADHD) followed into young adult years.

Methods

Subjects were derived from two longitudinal case-control studies of probands of both sexes, 6 to 17 years, with and without DSM-III-R ADHD and their parents. Probands were followed for ten years into young adulthood. Probands with a parental history of non-nicotine SUD were included in this analysis. Exposure to SUD was determined by active non-nicotine parental SUD while the parent was living with their child after birth. Cox proportional hazard models were used to calculate the risk of non-nicotine SUD in offspring.

Results

171 of the 404 probands reassessed at ten-year follow up had a family history of parental SUD. 102 probands were exposed to active parental SUD. The average age of our sample was 22.2 ± 3.5 years old. Exposure to maternal but not paternal SUD increased offspring risk for an alcohol use disorder in young adulthood independently of ADHD status (OR: 2.7; 95% CI: 1.1, 6.9; p=0.04).

Conclusion

Exposure to maternal SUD increases the risk for an alcohol use disorder in offspring ten years later in young adult years irrespective of ADHD status.

Keywords: substance use disorder, familial association, exposure, attention deficit hyperactivity disorder

1. Introduction

A growing literature supports a strong bidirectional association between attention deficit hyperactivity disorder (ADHD) and substance use disorders (SUD). The available literature clearly documents that individuals with ADHD are at increased risk for SUD (Lee et al., 2011) and individuals with SUD are at increased risk for ADHD (van Emmerik-van Oortmerssen et al., 2012).

A recent familial risk analysis of youth with and without ADHD of both sexes followed into young adulthood provides strong evidence supporting a familial influence for the risk for SUD in ADHD youth (Yule et al., 2017). While these findings support the hypothesis that genetic influences are operant in mediating the risk for SUD in ADHD, this risk could also be driven by environmental influences, such as exposure to a parent with an active SUD (Newlin et al., 2000). Indeed, previous research has shown that exposure to parental substance use through parental modeling of substance use increases the risk for substance use in offspring (Arria et al., 2012; Chassin et al., 1996; Coffelt et al., 2006; Ennett et al., 2008; Gil et al., 2002; Ohannessian et al., 2004; Li et al., 2002; Shorey et al., 2013; Yu, 2003).

We previously reported on the impact of exposure to parental SUD in samples with and without ADHD followed into adolescence (Biederman et al., 2000; Yule et al., 2013) and found that exposure to parental SUD predicted SUD in the offspring. These studies also found that the timing of exposure during adolescent years was particularly impactful (Biederman et al., 2000; Yule et al., 2013). However, since follow up was limited to adolescent years, a longer follow up period is needed to evaluate the full extent of the environmental risk as the sample transitions into young adult years, a period of peak risk for developing SUD (Compton et al., 2007; Hingson et al., 2006).

Further understanding of whether exposure to parental SUD is a risk factor for SUD in young adults with and without ADHD has important implications, given the substantial morbidity and mortality associated with SUD (Whiteford et al., 2015). If exposure to parental SUD is a moderator in the relationship between ADHD and SUD, this knowledge can support the development of appropriate intervention strategies to mitigate this problem. Parents with active SUD may be motivated to change their substance use if they know that their behavior puts their children at higher risk to develop a SUD. This knowledge would also support clinical and public health efforts to screen for SUD in parents of ADHD youth, which could help decrease later development of SUD in their children.

The main aim of this study was to re-examine the risk of exposure to parental SUD (alcohol or drug abuse or dependence) on the risk for SUD in offspring with and without ADHD followed into young adult years during the peak age of risk to develop a SUD. To this end, we used data from longitudinal studies of psychiatrically and pediatrically referred youth of both sexes with and without ADHD at ten-year follow-up attending to the moderating effects of sex of the parent and offspring. Based on the literature, we hypothesized that exposure to parental SUD will increase the risk for SUD in young adult offspring and that the risk will be larger in offspring with ADHD. To the best of our knowledge, this study is the most comprehensive examination of the risk of exposure to SUD in older ADHD youth.

2. Methods

2.1 Subjects

Detailed study methodology has been previously described (Biederman et al., 2006; Biederman et al., 2010). Briefly, subjects were derived from two identically designed, longitudinal, case-control family studies of ADHD. These studies recruited male and female probands aged 6 to 17 years with DSM-III-R ADHD (N=140 boys, N=140 girls) and without ADHD (i.e., Controls, N=120 boys, N=122 girls) from pediatric and psychiatric clinics. These groups had 552 parents and 472 parents, respectively. Potential subjects were excluded if they had been adopted, their nuclear family was not available for study, if they had major sensorimotor handicaps, psychosis, autism, inadequate command of the English language, or a Full Scale IQ less than 80. ADHD subjects met full DSM-III-R diagnostic criteria for ADHD at the time of the clinic referral and were subsequently reassessed for DSM-IV criteria. Parents and adult offspring provided written informed consent to participate, and parents provided consent for offspring under the age of 18. Children and adolescents provided written assent to participate. The human research committee approved the initial assessments as well as all aspects of the follow up of this study. The current sample includes data collected from subjects 10 years after their initial assessment.

2.2 Assessment procedures

Lifetime psychiatric assessments in parents were completed at baseline only using the Structured Clinical Interview for the DSM-IV (SCID; First et al., 1997; Spitzer et al., 1990) (supplemented with modules from the Schedule for Affective Disorder and Schizophrenia for Children (K-SADS-E; Orvaschel, 1994) to assess childhood diagnoses. Probands were assessed at baseline and at the 10 year follow up with the K-SADS-E for subjects younger than 18 years of age and the SCID for subjects 18 years of age and older. All diagnostic assessments were conducted by raters with Bachelor’s or Master’s degrees in psychology, who had been extensively trained and supervised by the senior investigators. Raters were blind to the ascertainment of the families. Direct interviews were conducted with subjects older than 12 years of age and indirect interviews were conducted with their mothers (i.e., mothers complete the structured interview about their offspring). We combined data from direct and indirect interviews by considering a diagnostic criterion positive if it was endorsed in either interview.

Board-certified child and adult psychiatrists and psychologists who were blind to the subject’s ADHD status, referral source, and all other data resolved diagnostic uncertainties. To assess the reliability of our overall diagnostic procedures, we computed kappa coefficients of agreement by having experienced, blinded, board-certified child and adult psychiatrists diagnose subjects from audiotaped interviews made by the assessment staff. Based on 500 assessments from interviews of children and adults, the median kappa coefficient was 0.98. The kappa coefficient for ADHD was 0.88 and for SUD was 1.0. Interviewers assessed the degree of impairment on daily functioning associated with each disorder that subjects endorsed on a three-level ordinal scale: minimal, moderate, or severe. For SUD, we made the diagnoses only when associated with at least moderate impairment. Socioeconomic status (SES) was measured using the 5-point Hollingshead scale (Hollingshead, 1975).

2.3 Statistical analysis

We stratified our sample into two groups: probands with a parental history of non-nicotine SUD with and without exposure to their parent’s SUD. Exposure was defined as active non-nicotine substance use meeting criteria for abuse or dependence to alcohol or drugs while the parent was living with their child, after birth.

We compared demographic characteristics between probands with a parental history of SUD who were exposed or not exposed to active parental SUD using the Student’s T test for continuous outcomes, the Wilcoxon Rank Sum test for socioeconomic status (SES), and the Pearson χ2 tests for binary outcomes.

We used the Kaplan-Meier cumulative failure function to calculate survival curves and cumulative lifetime risk of non-nicotine SUD in offspring. Cox proportional hazard models were used to calculate the risk of non-nicotine SUD in offspring. We first looked at the effect that maternal use and paternal use may have separately had on offspring SUD. We subsequently looked at the effect of exposure to either parent’s SUD on offspring SUD. We examined whether the timing of the exposure was related to offspring SUD using a multivariate logistic regression model (all time periods were included in the model). For this analysis, we used the age of the offspring at baseline in addition to the onset and offset of the parent’s substance use to determine the time period in which the offspring were exposed.

To examine the impact of ADHD and sex on the associations between parental SUD exposure and offspring SUD, we examined the ADHD-by-exposure and the sex-by-exposure interaction terms. At any point, if either interaction term was significant, we estimated the effect of exposure to parental SUD separately by ADHD/sex. If either interaction was not significant, we removed it from the analyses and reran the model adjusting for ADHD and sex. All tests were two-tailed, and our alpha level was set at 0.05 for all analyses. We calculated all statistics using STATA, version 12.0. Data are expressed as mean ± standard deviation (SD) unless otherwise specified.

3. Results

As previously described, (Biederman et al., 2010; Biederman et al., 2012) with very few exceptions, there were no significant differences between those who were lost-to-follow-up and those who remained in the study on age, race, global assessment of functioning score, familial intactness, or psychiatric outcomes. There was a significant difference in SES in both ADHD and control probands in those who were lost-to-follow-up and had lower SES than those successfully reassessed (Biederman et al., 2011). The final sample, reassessed at ten-year follow-up, included 404 probands (ADHD: 112 boys and 96 girls; Control: 105 boys and 91 girls). Among their 800 parents, there were 404 mothers (age at baseline ± SD: 40.9 ± 5.4 years) and 396 fathers (43.3 ± 6.1 years). Twenty-seven percent of parents (N=214) had a SUD: 22% (N=174) with an alcohol use disorder, 13% (N=106) with a drug use disorder, and 8% (N=66) had both an alcohol and drug use disorder. The sample for this analysis included the 171 probands who had a family history of parental SUD (maternal SUD and/or paternal SUD).

As shown in Table 1, at the ten-year follow-up, the average age of our sample was 22.2 ± 3.5 years old. Offspring exposed to parental SUD had a lower SES and were older (both p values <0.05) than those unexposed (Table 1). There were no other meaningful differences in socio demographic characteristics (Table 1) in sex, race, or lifetime ADHD status between offspring with a family history of parental SUD who were exposed and unexposed to parental SUD. Among offspring with a family history of parental SUD 45% (N=77) had any SUD, 38% (N=65) had an alcohol use disorder, 29% (N=49) had a drug use disorder, and 22% (N=37) had both an alcohol and drug use disorder.

Table 1.

Clinical Demographics in Offspring Unexposed and Exposed1 to Parental substance use disorders (SUD, Alcohol and/or Drug Use Disorders) at 10 year follow up (N=171)

Unexposed to Parental SUD
(N=69)		 Exposed to Parental SUD
(N=102)
Age [age range], y 21.1 ± 3.2 [16–29] 22.6 ± 3.5 [16–31] t=−2.8, p=0.005
SES2 1.8 ± 0.9 2.2 ± 1.1 z=−2.0, p=0.04
N (%) N (%)
Sex (% male) 28 (41) 53 (52) χ2(1)=2.1, p=0.14
Race (% Caucasian) 68 (99) 98 (96) χ2(1)=4.2, p=0.24
Lifetime ADHD3 49 (71) 62 (61) χ2(1)=1.9, p=0.17
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1

=Exposure defined as active parental non-nicotine SUD while the parent was living with their child, after birth

2

=SES denotes Socioeconomic Status

3

=ADHD denotes Attention Deficit/Hyperactivity Disorder

3.1 Effect of proband sex on SUD outcomes

No meaningful sex-by-exposure status interaction terms were identified, indicating that the associations between parental SUD exposure and offspring SUD did not differ based on offspring sex (all p values ≥0.05). However, in general, male sex was a significant predictor of offspring SUD. For example, boys (grown up) were 1.8 times more likely to develop any SUD (95% Confidence Interval (CI): 1.2, 2.6; p=0.006), 1.9 times more likely to develop an alcohol use disorder (95% CI: 1.2, 2.8; p=0.003), and 1.7 times more likely to develop a drug use disorder (95% CI: 1.1, 2.7; p=0.02) compared to girls (grown up).

3.2 Effect of ADHD on SUD outcomes

No meaningful ADHD-by-exposure status interaction terms were identified, indicating the associations between parental SUD exposure and offspring SUD did not differ based on offspring ADHD status (all p values ≥0.05). ADHD was a significant predictor of offspring SUD irrespective of exposure. For example, ADHD probands were 2 times more likely (95% CI: 1.4, 3.1; p=0.001) to develop any SUD, 1.9 times more likely (95% CI: 1.2, 2.9; p=0.003) to develop an alcohol use disorder, and 4.0 times more likely (95% CI: 2.3, 6.8; p<0.001) to develop a drug use disorder compared to control probands.

3.3 Risk associated with exposure to parental SUD

We found evidence that maternal but not paternal exposure to SUD was associated with increased risk for SUD in offspring (Table 2). We found no significant evidence overall that parental exposure to SUD increased the risk for SUD in offspring exposed (Table 2). Further, adding SES and ADHD to the models did not alter the results.

Table 2.

Prevalence of Offspring SUD (Alcohol and/or Drug Use Disorders) among Offspring Unexposed and Exposed to Parental SUD (Alcohol and/or Drug Use Disorders) (N=171)

Unexposed with Maternal SUD History
(N=37)		 Exposed with Maternal SUD History
(N=26)		 Odds Ratio, 95% Confidence Interval, p-value
Offspring Disorder N (%) N (%)
Any SUD 9 (24) 14 (54) 0.7 (0.3, 1.7), p=0.4
 Alcohol Use Disorders 7 (19) 13 (50) 2.7 (1.1, 6.9), p=0.04
 Drug Use Disorders 6 (16) 7 (27) 1.7 (0.6, 5.1), p=0.3
Unexposed with Paternal SUD History
(N=62) 		Exposed with Paternal SUD History
(N=91)
Offspring Disorder N (%) N (%)
Any SUD 33 (53) 39 (43) 0.6 (0.4, 1.0), p=0.07
 Alcohol Use Disorders 26 (42) 35 (38) 0.8 (0.5, 1.3), p=0.3
 Drug Use Disorders 21 (34) 25 (27) 0.8 (0.4, 1.4), p=0.4
Unexposed with Parental SUD History
(N=69) 		Exposed with Parental SUD History
(N=102)
Offspring Disorder N (%) N (%)
Any SUD 32 (46) 45 (44) 0.7 (0.4, 1.1), p=0.2
 Alcohol Use Disorders 25 (36) 40 (39) 0.99 (0.6, 1.6), p=1.0
 Drug Use Disorders 21 (30) 28 (27) 0.9 (0.5, 1.6), p=0.7
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3.4 Exposure to one parent vs. two parents with SUD

We also examined whether the risk of SUD in the offspring differed based on whether the offspring was exposed to one parent’s or both parents’ SUD. Among all exposed offspring (N=102), 85% (N=87) were exposed by one parent and 15% (N=15) were exposed by both parents. Among offspring exposed by one parent, 43% (N=37) developed any SUD, and among offspring exposed by both parents, 53% (N=8) developed any SUD (OR: 0.8; 95% CI: 0.4, 1.8; p=0.7).

3.5 Timing of exposure to parental SUD

To evaluate whether there are critical periods during development in which offspring are at particular risk from parental SUD, we examined whether exposure to parental SUD occurred during the pre-adolescent (≤12) or adolescent (>12) years. Among all probands at baseline evaluation who were exposed and who had reached the age of 12 (N=51)), 63% (N=32) were exposed during their pre-adolescent years and 37% (N=19) were exposed during their pre-adolescent and/or adolescent years. We found no significant differences in the risk of any SUD, alcohol use disorder, and drug use disorder between those who were exposed during their pre-adolescent years and those exposed in their adolescent years (OR:1.7; 95% CI: 0.5, 5.5; p=0.36; OR:1.0; 95% CI: 0.3, 3.2; p=1.0; OR: 1.4; 95% CI: 0.4, 4.5; p=0.6, respectively).

4. Discussion

The results of this analysis, based on ten-year follow-up of a large sample of male and female probands with and without ADHD, showed a modest effect for exposure to maternal SUD as a risk factor for an alcohol use disorder in offspring, independent of ADHD status. While limited by information about parental SUD at baseline assessment only and limited sample sizes within subgroups, these data suggest that exposure to maternal SUD is a risk factor for SUD in young adults.

The results of this study in young adult years are consistent with our previous work in the same sample during adolescent years (Biederman et al., 2000; Yule et al., 2013). Our previous study showed that exposure to parental SUD was associated with increased offspring SUD in male probands with and without ADHD and their siblings (Biederman et al., 2000). Similar to our current findings, exposure to maternal SUD, specifically drug use disorders, was associated with an increased risk for offspring drug use disorders in female probands with and without ADHD and their siblings (Yule et al., 2013).

Our findings show an association between exposure to active maternal SUD and offspring risk for an alcohol use disorder are consistent with findings in the literature that suggest exposure to maternal SUD is particularly influential in increasing risk for SUD onset in adolescence and young adulthood (Coffelt et al., 2006; Ohannessian et al., 2004). Although the reasons why exposure to maternal and not paternal modeling of substance use increases offspring risk for SUD remain unclear, we can posit possible explanations. The literature suggests that women are more likely than men to have more severe psychiatric, medical, and occupational consequences associated with their SUD (Hernandez-Avila et al., 2004) that may preferentially influence the ultimate impact of exposure to maternal SUD compared to paternal SUD on offspring SUD. It is also possible that exposure to maternal SUD during pregnancy preferentially primes offspring to be at increased risk for SUD when exposed later in development. More research is needed to clarify parental and offspring sex relationships and the mediators within those relationships that increase risk for SUD in the offspring, including in utero exposure to substances.

The absence of an association between the timing of exposure to parental SUD and offspring risk for development of a SUD in young adulthood is dissimilar to our previous findings. We previously found an association between exposure to parental SUD during adolescence and the risk for developing a SUD in late adolescence (Biederman et al., 2000; Yule et al., 2013). These discrepant results may be related to timing. It is possible that offspring with early onset SUD were more influenced by parental use patterns relative to older offspring. More longitudinal research is needed to evaluate the impact of exposure to parental SUD during different developmental periods to determine if there are critical periods for exposure to parental SUD related to offspring risk for SUD.

Our finding that exposure to parental SUD was independent of ADHD status is noteworthy. Previous research on the familial association between ADHD and SUD showed a strong familial relationship between ADHD and SUD (Yule, 2017). If an environmental familial influence accounted for the association between ADHD and SUD, one would have expected young adults with ADHD exposed to parental SUD to have a higher prevalence of SUD when compared to young adults without ADHD who were exposed to parental SUD. Since this was not the case, it suggests that genetic influences remain the most potent driver of the risk for SUD in ADHD youth.

Our findings should be viewed in light of their substantial methodological limitations. Exposure to parental substance use is heterogeneous. We relied on carefully performed, structured interviews to formally assess for parental diagnosis of abuse and dependence and onset/offset of symptoms to quantify exposure to parental SUD. While the diagnosis of abuse and dependence signifies functional difficulty, there are other variables not quantified by this definition that may affect the impact of exposure to parental SUD, such as the substance used, the nature of the relationship between the parent and offspring, and family functioning. We also did not assess for nicotine abuse or dependence in parents or offspring. Additionally, since parents were only interviewed at baseline, we were unable to assess exposure to parental SUD after the initial assessment. Substance use was assessed in parents and offspring using subjective measures rather than objective measures, which could have resulted in an underestimation of SUD in the study. We have previously shown that clinical data is more sensitive for the screening of SUD than urine toxicology testing (Gignac et al., 2005). Additionally, the number of offspring with family history of SUD who were exposed to parental SUD was small, limiting our power to assess parent and offspring sex differences based on exposure and contributed to significant variance in our analysis. Our findings are associative in nature and do not infer causality.

Despite these limitations, our work suggests that exposure to maternal SUD has modest effects in moderating the risk for SUD in offspring relative to strong genetic influences. Taken together with our previously reported familial risk analysis, our findings suggest children with ADHD, particularly those with a family history of SUD, should be carefully monitored for SUD.

Highlights.

  • Examined impact of exposure to parental substance use disorder (SUD) on offspring.

  • Exposure to maternal SUD increased offspring risk for an alcohol use disorder.

  • No association existed between exposure to paternal SUD and offspring risk.

  • Exposure risk was independent of attention deficit hyperactivity disorder.

Acknowledgments

Role of Funding Source

The data used in the current analysis was collected with support from the NIH awards R01 HD036317 and R01 MH050657 to Dr. Biederman. The data analysis and manuscript preparation was supported by a pilot research award from the American Academy of Child and Adolescent Psychiatry funded by Eli Lilley, LLC; the Massachusetts General Hospital Louis V. Gerstner III Research Scholar Award, and 5K12DA000357-17. None of these funding sources were involved in study design, data collection, analysis and interpretation of the data, in writing the report, or in the decision to submit the article for publication.

Amy Yule, MD: Dr. Amy Yule received grant support from the American Academy of Child and Adolescent Psychiatry Pilot Research Award for Junior Faculty supported by Lilly USA, LLC in 2012. She received grant support from the Massachusetts General Hospital Louis V. Gerstner III Research Scholar Award from 2014 to 2016. Dr. Yule is currently receiving funding through the American Academy of Child and Adolescent Psychiatry Physician Scientist Program in Substance Abuse 5K12DA000357-17. She is a consultant to Phoenix House (clinical service). Timothy Wilens, MD: Dr. Timothy Wilens receives or has received grant support from the following sources: NIH(NIDA). Dr. Wilens is or has been a consultant for: Alcobra, Neurovance/Otsuka, and Ironshore. He has published books: Straight Talk About Psychiatric Medications for Kids (Guilford Press); and co/edited books ADHD in Adults and Children (Cambridge University Press), Massachusetts General Hospital Comprehensive Clinical Psychiatry (Elsevier) and Massachusetts General Hospital Psychopharmacology and Neurotherapeutics (Elsevier). Dr. Wilens is co/owner of a copyrighted diagnostic questionnaire (Before School Functioning Questionnaire) and he has a licensing agreement with Ironshore (BSFQ Questionnaire). Dr. Wilens is Chief, Division of Child and Adolescent Psychiatry and (Co) Director of the Center for Addiction Medicine at Massachusetts General Hospital. He serves as a clinical consultant to the US National Football League (ERM Associates), U.S. Minor/Major League Baseball; Phoenix House and Bay Cove Human Services.

Joseph Biederman, MD: Dr. Joseph Biederman is currently receiving research support from the following sources: the American Academy of Child and Adolescent Psychiatry (AACAP), The Department of Defense, Food and Drug Administration, Headspace, Lundbeck, Neurocentria Inc., NIDA, PamLab, Pfizer, Shire Pharmaceuticals Inc., Sunovion, and NIH.

Dr. Biederman has a financial interest in Avekshan LLC, a company that develops treatments for attention deficit hyperactivity disorder (ADHD). His interests were reviewed and are managed by Massachusetts General Hospital and Partners HealthCare in accordance with their conflict of interest policies. Dr. Biederman’s program has received departmental royalties from a copyrighted rating scale used for ADHD diagnoses, paid by Ingenix, Prophase, Shire, Bracket Global, Sunovion, and Theravance; these royalties were paid to the Department of Psychiatry at MGH. In 2017, Dr. Biederman is a consultant for Akili, Guidepoint, and Medgenics. He is on the scientific advisory board for Alcobra and Shire. He received honoraria from the MGH Psychiatry Academy for tuition-funded CME courses. Through MGH corporate licensing, he has a US Patent (#14/027,676) for a non-stimulant treatment for ADHD, and a patent pending (#61/233,686) on a method to prevent stimulant abuse. In 2016, Dr. Biederman received honoraria from the MGH Psychiatry Academy for tuition-funded CME courses, and from Alcobra and APSARD. He was on the scientific advisory board for Arbor Pharmaceuticals. He was a consultant for Akili and Medgenics. He received research support from Merck and SPRITES. In 2015, Dr. Biederman received honoraria from the MGH Psychiatry Academy for tuition-funded CME courses, and from Avekshan. He received research support from Ironshore, Magceutics Inc., and Vaya Pharma/Enzymotec. In 2014, Dr. Biederman received honoraria from the MGH Psychiatry Academy for tuition-funded CME courses. He received research support from AACAP, Alcobra, Forest Research Institute, and Shire Pharmaceuticals Inc.

Footnotes

Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.

Contributors: Authors Amy Yule, MD, Timothy Wilens, MD, and Joseph Biederman, MD designed the study and generated hypotheses for this manuscript. Lindsay Rosenthal, BS, managed the literature searches and summaries of previous work. Author MaryKate Martelon, MPH undertook the statistical analyses. Authors Amy Yule, MD, and MaryKate Martelon, MPH wrote the first draft of the manuscript. Timothy Wilens, MD, Joseph Biederman, MD, and Lindsay Rosenthal, BS edited and provided revisions to the initial draft. All authors contributed to and have approved the final manuscript.

Conflict of Interest

MaryKate Martelon, MPH and Lindsay Rosenthal, BS: The authors report no conflict of interest.

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