ABSTRACT
Substance use and psychopathology symptoms increase in adolescence. One key risk factor for these is high parent stress. Mindfulness interventions reduce stress in adults and may be useful to reduce parent stress and prevent substance use (SU) and psychopathology in adolescents. This study tested the feasibility and effects of a mindfulness intervention for parents on adolescent SU and psychopathology symptoms. Ninety-six mothers of 11-17 year olds were randomly assigned to a mindfulness intervention for parents (the Parenting Mindfully [PM] intervention) or a brief parent education [PE] control group. At pre-intervention, post-intervention, 6-month follow-up, and 1-year follow-up, adolescents reported on SU and mothers and adolescents reported on adolescent externalizing and internalizing symptoms. Primary intent to treat analyses found that the PM intervention prevented increases in adolescent SU over time, relative to the PE control group. The PM intervention also prevented increases in mother-reported externalizing symptoms over time relative to the PE control group. However, PM did not have a significant effect on internalizing symptoms. PM had an indirect effect on adolescent-reported externalizing symptoms through greater mother mindfulness levels at post-intervention, suggesting mother mindfulness as a potential intervention mechanism. Notably, while mothers reported high satisfaction with PM, intervention attendance was low (31% of mothers attended zero sessions). Secondary analyses with mothers who attended > = 50% of the interventions (n = 48) found significant PM effects on externalizing symptoms, but not SU. Overall, findings support mindfulness training for parents as a promising intervention and future studies should work to promote accessibility for stressed parents.Clinical Trials Identifier: NCT02038231; Date of Registration: January 13, 2014.
Subject(s)
Mindfulness , Substance-Related Disorders , Adolescent , Adult , Female , Humans , Mothers , Parenting , ParentsABSTRACT
BACKGROUND: The gene encoding phosphatidylinositol-4-phosphate 5-kinase (PIP5K1C) has been recently implicated in pain regulation. Interestingly, a recent cross-tissue and cross-phenotypic epigenetic analysis identified the same gene in alcohol use disorder (AUD). Given the high comorbidity between AUD and chronic pain, we hypothesized that genetic variation in PIP5K1C might contribute to susceptibility to AUD. METHODS: We conducted a case-control association study of genetic variants in PIP5K1C. Association analyses of 16 common PIP5K1C single nucleotide polymorphisms (SNPs) were conducted in cases and controls of African (427 cases and 137 controls) and European ancestry (488 cases and 324 controls) using standard methods. In addition, given the prominent role of the opioid system in pain signaling, we investigated the effects of acute alcohol exposure on PIP5K1C expression in humanized transgenic mice for the µ-opioid receptor that included the OPRM1 A118G polymorphism, a widely used mouse model to study analgesic response to opioids in pain. PIP5K1C expression was measured in the thalamus and basolateral amygdala (BLA) in mice after short-term administration (single 2 g/kg dose) of alcohol or saline using immunohistochemistry and analyzed by 2-way analysis of variance. RESULTS: In the case-control association study using an NIAAA discovery sample, 8 SNPs in PIP5K1C were significantly associated with AUD in the African ancestry (AA) group (p < 0.05 after correction; rs4807493, rs10405681, rs2074957, rs10432303, rs8109485, rs1476592, rs10419980, and rs4432372). However, a replication analysis using an independent sample (N = 3,801) found no significant associations after correction for multiple testing. In the humanized transgenic mouse model with the OPRM1 polymorphism, PIP5K1C expression was significantly different between alcohol and saline-treated mice, regardless of genotype, in both the thalamus (p < 0.05) and BLA (p < 0.01). CONCLUSIONS: Our discovery sample shows that genetic variants in PIP5K1C are associated with AUD in the AA group, and acute alcohol exposure leads to up-regulation of PIP5K1C, potentially explaining a mechanism underlying the increased risk for chronic pain conditions in individuals with AUD.