Background: There is increasing evidence that parental determinants of offspring early life development begin well before pregnancy.
There is little evidence relating to the effects of adding guidance to internet-based gambling interventions. The primary aim was to compare the effectiveness of an online self-directed cognitive-behavioural gambling program (GamblingLess) with and without therapist-delivered guidance. It was hypothesised that, compared to the unguided intervention, the guided intervention would result in superior improvements in gambling symptom severity, urges, frequency, expenditure, psychological distress, quality of life and help-seeking. A two-arm, parallel-group, randomised trial with pragmatic features and three post-baseline evaluations (8 weeks, 12 weeks, 24 months) was conducted with 206 gamblers (106 unguided; 101 guided). Participants in both conditions reported significant improvements in gambling symptom severity, urges, frequency, expenditure, and psychological distress across the evaluation period, even after using intention-to-treat analyses and controlling for other low- and high-intensity help-seeking, as well as clinically significant changes in gambling symptom severity (69% recovered/improved). The guided intervention resulted in additional improvements to urges and frequency, within-group change in quality of life, and somewhat higher rates of clinically significant change (77% cf. 61%). These findings, which support the delivery of this intervention, suggest that guidance may offer some advantages but further research is required to establish when and for whom human support adds value.
Maternal internalizing symptoms during pregnancy, specifically depression and/or anxiety, are commonly linked to negative affectivity (NA) in infant offspring. These links are commonly attributed to biological effects of the in utero environment on fetal development. However, research suggests that internalizing symptoms before and after pregnancy, as well as in fathers, may also be associated with NA in infant offspring. Such findings suggest greater complexity in transmission than can be explained by biological in utero programming alone. Further, infant NA is often treated as an homogenous construct, yet it covers a range of facets including fear, frustration, sadness, and slow recovery from distress that may each be differentially associated with parent internalizing distress. Here we aimed to (1) meta-analytically quantify associations between maternal and paternal internalizing symptoms and infant offspring NA, (2) examine how associations varied as a function of distinct phenotypic facets of NA, and (3) examine how associations varied by timing of parental symptoms (preconception, antenatal, postnatal) and infant age. Using random-effects meta-analysis, we found that maternal internalizing symptoms were positively associated with infant NA (r = 0.17 [95% CI 0.14, 0.21], 42 studies, 149 estimates). Preliminary evidence from studies of fathers likewise suggested a positive association with infant NA (r = 0.13 [95% CI 0.04, 0.22], 6 studies, 40 estimates). We observed associations with the global infant NA construct, as well as effect modification by infant NA facet (maternal r range .12 to .22; paternal r range .03 to.21). In mothers, there was no evidence of effect modification by timing of internalizing symptoms or infant age; in fathers, preliminary associations were larger for postnatal than antenatal symptoms. Further studies of preconception and paternal symptoms are now needed, and we suggest avenues for research to advance understanding of the relations between parent internalizing symptoms and infant NA.
Maternal internalizing symptoms during pregnancy, specifically depression and/or anxiety, are commonly linked to negative affectivity (NA) in infant offspring. These links are commonly attributed to biological effects of the in utero environment on fetal development. However, research suggests that internalizing symptoms before and after pregnancy, as well as in fathers, may also be associated with NA in infant offspring. Such findings suggest greater complexity in transmission than can be explained by biological in utero programming alone. Further, infant NA is often treated as an homogenous construct, yet it covers a range of facets including fear, frustration, sadness, and slow recovery from distress that may each be differentially associated with parent internalizing distress. Here we aimed to (1) meta-analytically quantify associations between maternal and paternal internalizing symptoms and infant offspring NA, (2) examine how associations varied as a function of distinct phenotypic facets of NA, and (3) examine how associations varied by timing of parental symptoms (preconception, antenatal, postnatal) and infant age. Using random-effects meta-analysis, we found that maternal internalizing symptoms were positively associated with infant NA (r = 0.17 [95% CI 0.14, 0.21], 42 studies, 149 estimates). Preliminary evidence from studies of fathers likewise suggested a positive association with infant NA (r = 0.13 [95% CI 0.04, 0.22], 6 studies, 40 estimates). We observed associations with the global infant NA construct, as well as effect modification by infant NA facet (maternal r range .12 to .22; paternal r range .03 to.21). In mothers, there was no evidence of effect modification by timing of internalizing symptoms or infant age; in fathers, preliminary associations were larger for postnatal than antenatal symptoms. Further studies of preconception and paternal symptoms are now needed, and we suggest avenues for research to advance understanding of the relations between parent internalizing symptoms and infant NA.
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