We have previously shown that juvenile bipolar disorder (BPD) is a risk for substance use disorders (SUD). Here we examine the expression of both disorders in families of youth with BPD to evaluate the familial risk mechanism.
We studied 108 adolescent BPD probands with 187 parents (34 with SUD and 58 parents) and 96 control probands with 177 parents with structured interviews. We compared the prevalence of BPD and SUD with Cox proportional hazards models with time to onset of BPD or SUD as the dependent variable and proband diagnosis (Control, BPD, or BPD+SUD) as the independent variable.
The parents of the proband youth with BPD (without SUD) and BPD+SUD were more likely to develop BPD than the parents of control subjects [omnibus test chi2=10.18, p=.006]; we found no differences between the two bipolar groups. Parents of proband youth with BPD and with BPD+SUD were more likely than relatives of control subjects to develop SUD [omnibus test chi2=14.69, p<.001]; however, we found no differences between the parents of the two proband bipolar groups. Within the parents of proband youth with BPD+SUD, we found higher risk of SUD in parents with BPD than in those without BPD [chi2=8.39, p=.004], although the frequency of BPD was low in this group of parents.
Bipolar disorder and SUD are prevalent in the first-degree relatives of adolescents with BPD. Adults with BPD were more likely to manifest SUD with preliminary evidence of BPD and SUD cosegregation.
"Second, given the familial association between AUDs and BD (Wilens et al, 2007), our exclusion of participants with AUDS, or with family histories of AUDs, may mean that some aspects of the psychopathology associated with the BPP were underestimated. Moreover, findings from some experimental studies of the LLR have been inconsistent (Peterson et al, 1996; Conrod et al, 1997; King et al, 2002, 2011; Newlin and Renton, 2010), with some evidence that it is heightened, rather than reduced, subjective responses to alcohol that are associated with increased risk for AUDs (Thomas et al, 2004). "
[Show abstract][Hide abstract] ABSTRACT: Elevated lifetime prevalence rates of alcohol use disorders (AUDs) are a feature of bipolar disorder (BD). Individuals at-risk for AUDs exhibit blunted subjective responses to alcohol (low levels of response), which may represent a biomarker for AUDs. Thus, individuals at-risk for BD may exhibit low responses to alcohol. Participants were 20 unmedicated adult males who reported high rates of hypomanic experiences (bipolar phenotype participants; BPPs), aged 18 to 21 years, and 20 healthy controls matched on age, gender, IQ, BMI, and weekly alcohol intake. Subjective and pharmacokinetic responses to acute alcohol (0.8 g/kg) vs placebo administration were collected in a randomized, double-blind, cross-over, placebo-controlled, within-subjects design. BPP participants reported significantly lower subjective intoxication effects ('feel high': F=14.2, p=0.001; 'feel effects': F=8.1, p=0.008) across time, but did not differ in their pharmacokinetic, stimulant, or sedative responses. Paradoxically, however, the BPP participants reported significantly higher expectations of the positive effects of alcohol than controls. Our results suggest that unmedicated young males with previous hypomanic experiences exhibit diminished subjective responses to alcohol. These blunted alcohol responses are not attributable to differences in weekly alcohol intake, pharmacokinetic effects (eg, absorption rates), or familial risk of AUDs. These observations suggest that the dampened intoxication may contribute to the increased rates of alcohol misuse in young people at-risk for BD, and suggest possible shared etiological factors in the development of AUDs and BD.
Neuropsychopharmacology: official publication of the American College of Neuropsychopharmacology 04/2012; 37(8):1808-15. DOI:10.1038/npp.2012.45 · 7.05 Impact Factor
"However, despite their clear contributions, the existing family studies of pediatric bipolar disorder suffer from several methodological limitations. Three studies relied on family history methods rather than directly interviewing relatives and half of the available studies examined only parents or adult relatives (Brotman et al., 2007, Findling et al., 2001, Kutcher and Marton, 1991, Neuman et al., 1997, Strober et al., 1988, Wilens et al., 2007). Of the four studies utilizing DSM-IV criteria, two (Brotman et al., 2007, Geller et al., 2006) restricted recruitment of probands to children meeting a " narrow " phenotype (Leibenluft et al., 2003) excluding other children who may have otherwise fully met DSM-IV bipolar-I disorder. "
[Show abstract][Hide abstract] ABSTRACT: To estimate the spectrum of familial risk for psychopathology in first-degree relatives of children with unabridged DSM-IV bipolar-I disorder (BP-I).
We conducted a blinded, controlled family study using structured diagnostic interviews of 157 children with BP-I probands (n=487 first-degree relatives), 162 attention deficit hyperactivity disorder (ADHD) (without BP-I) probands (n=511 first-degree relatives), and 136 healthy control (without ADHD or BP-I) probands (n=411 first-degree relatives).
The morbid risk (MR) of BP-I disorder in relatives of BP-I probands (MR=0.18) was increased 4-fold [95% confidence interval (CI) 2.3-6.9, p<0.001] over the risk to relatives of control probands (MR=0.05) and 3.5-fold (95% CI 2.1-5.8, p<0.001) over the risk to relatives of ADHD probands (MR=0.06). In addition, relatives of children with BP-I disorder had high rates of psychosis, major depression, multiple anxiety disorders, substance use disorders, ADHD and antisocial disorders compared with relatives of control probands. Only the effect for antisocial disorders lost significance after accounted for by the corresponding diagnosis in the proband. Familial rates of ADHD did not differ between ADHD and BP-I probands.
Our results document an increased familial risk for BP-I disorder in relatives of pediatric probands with DSM-IV BP-I. Relatives of probands with BP-I were also at increased risk for other psychiatric disorders frequently associated with pediatric BP-I. These results support the validity of the diagnosis of BP-I in children as defined by DSM-IV. More work is needed to better understand the nature of the association between these disorders in probands and relatives.
Psychological Medicine 11/2009; 40(7):1079-88. DOI:10.1017/S0033291709991437 · 5.94 Impact Factor
"Second, in most prior research investigators have not separated the effects of the child's mental illness from the possible effects of a preexisting mental illness in the parent. It is well documented that first-degree relatives of persons with bipolar disorder suffer from high rates of their own mental health problems, in particular anxiety and major depression (Joyce et al., 2004; Wilens et al., 2007). Thus, elevations in parental mental health symptoms might be a precursor to or a consequence of the child's mental illness (or both), depending on when the parent's mental health problems first occurred. "
[Show abstract][Hide abstract] ABSTRACT: This study extends prior research on family caregiving in mental illness by investigating late-life parenting of adult children with bipolar disorder using a randomly selected community-based sample. The health and mental health, psychological well-being, marriage, work-life, and social resources of 145 parents of adult children with bipolar disorder were examined when parents were in their mid-60s. Stratified random sampling procedures were used to select a comparison group whose children did not have disabilities. Results indicate that parents of adult children with bipolar disorder had a more compromised profile of health and mental health, and experienced more difficulties in marriage and work-life than comparison parents. Furthermore, parents of adult children with bipolar disorder who were diagnosed with mental illness before the onset of their child's symptoms were more vulnerable on multiple dimensions of mental health, psychological well-being, and work-life than parents without a preexisting mental illness.
The Journal of nervous and mental disease 06/2009; 197(5):298-304. DOI:10.1097/NMD.0b013e3181a206cc · 1.69 Impact Factor
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