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Variation in the oxytocin receptor gene moderates the protective effects of a family-based prevention program on telomere length.

Smearman EL, Yu T, Brody GH - Brain Behav (2016)

Bottom Line: Parent-child relationships with high conflict and low warmth and support are associated with later adverse behavioral and physiological child outcomes.Subsequent analyses suggest that these findings may be mediated through chronic anger, whereby GG individuals exposed to nonsupportive parenting and randomized to the control condition had a greater increase in chronic anger by study follow-up, compared to those in the intervention, and this change associated with greater telomere shortening.These findings highlight the importance of individual differences and potential role of genetic status in moderating the relationship between environmental contexts and biological outcomes.

View Article: PubMed Central - PubMed

Affiliation: Behavioral Sciences and Health EducationRollins School of Public HealthEmory University1518 Clifton Road NortheastAtlantaGeorgia30322; Center for Translational and Social NeuroscienceEmory UniversityAtlantaGeorgia30322.

ABSTRACT

Introduction: Parent-child relationships with high conflict and low warmth and support are associated with later adverse behavioral and physiological child outcomes. These outcomes include shorter telomere lengths, the repetitive sequences at the ends of chromosomes that have been utilized as a biomarker for chronic stress. Our research group furthered this by exploring telomere length outcomes following a family-based prevention program and identified reduced telomere shortening 5 years post intervention among those originally exposed to nonsupportive parenting and randomized to the intervention condition. However, not all individuals respond equally, and a growing literature suggests genetic sensitivity to one's environment, with variations in the oxytocin receptor gene (OXTR) potentially influencing this sensitivity.

Methods: We utilized data from African American youths (mean age 17) randomized to intervention (n = 100) or control condition (n = 91) with baseline assessments of genetic status and nonsupportive parenting, and 5-year follow-up assessments of telomere length.

Results: We found a significant three-way interaction between nonsupportive parenting, intervention condition, and OXTR rs53576 genotype. OXTR GG individuals, who are suggested to be more sensitive to their social environment, exhibited significantly more variability, evidencing the shortest telomeres when exposed to nonsupportive parenting and randomized to the control condition, and similar telomere lengths to non at-risk groups when randomized to the intervention. In contrast, those with the A allele showed no statistical difference in telomere lengths across parental and intervention conditions. Subsequent analyses suggest that these findings may be mediated through chronic anger, whereby GG individuals exposed to nonsupportive parenting and randomized to the control condition had a greater increase in chronic anger by study follow-up, compared to those in the intervention, and this change associated with greater telomere shortening.

Conclusions: These findings highlight the importance of individual differences and potential role of genetic status in moderating the relationship between environmental contexts and biological outcomes.

No MeSH data available.


Related in: MedlinePlus

Nonsupportive parenting and telomere length outcomes by intervention and genotype status. Significant study interactions are depicted using simple slopes procedures for ± 1 standard deviation of nonsupportive parenting. Graphs display the association between nonsupportive parenting and telomere length outcomes across 5 years by a. intervention condition and b. intervention condition and OXTR rs53576 genotype. **P < 0.001. Rs53576 A+ allele, Control: n = 31; slope = 0.041; telomere length: Mean = −0.09, SD = 0.67, Range = −1.15 to −1.47. Rs53576 GG allele, Control: n = 60; slope = −0.107**; telomere length: Mean = −0.25, SD = 0.84, Range = −3.11 to 1.89. Rs53576 A+ allele, AIM: n = 38; slope = −0.027; telomere length: Mean = 0.04; SD = 0.72, Range = −1.58 to −0.04. Rs53576 GG allele, AIM: n = 62; slope = 0.033; telomere length: Mean = −0.03; SD = 0.74; Range = −2.16 to 1.58.
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brb3423-fig-0001: Nonsupportive parenting and telomere length outcomes by intervention and genotype status. Significant study interactions are depicted using simple slopes procedures for ± 1 standard deviation of nonsupportive parenting. Graphs display the association between nonsupportive parenting and telomere length outcomes across 5 years by a. intervention condition and b. intervention condition and OXTR rs53576 genotype. **P < 0.001. Rs53576 A+ allele, Control: n = 31; slope = 0.041; telomere length: Mean = −0.09, SD = 0.67, Range = −1.15 to −1.47. Rs53576 GG allele, Control: n = 60; slope = −0.107**; telomere length: Mean = −0.25, SD = 0.84, Range = −3.11 to 1.89. Rs53576 A+ allele, AIM: n = 38; slope = −0.027; telomere length: Mean = 0.04; SD = 0.72, Range = −1.58 to −0.04. Rs53576 GG allele, AIM: n = 62; slope = 0.033; telomere length: Mean = −0.03; SD = 0.74; Range = −2.16 to 1.58.

Mentions: While the direct association between nonsupportive parenting and telomere outcomes was only significant at P = 0.07 (Table 2, Model 1; β = −0.131), an interaction emerged when taking intervention condition into account. Replicating previous findings, exposure to nonsupportive parenting at age 17 forecasted shorter telomere length at age 22, but this association was attenuated for those who participated in the AIM intervention (Table 2, Model 2; β = 0.223, P < 0.05). Among those exposed to high levels of nonsupportive parenting, only those randomized to the control condition evidenced significantly shorter telomeres at age 22 (Fig. 1A, simple slope = −0.072, P < 0.01), whereas those randomized to the intervention evidenced similar telomere lengths to those with more supportive, non at‐risk parenting scores at baseline (Fig. 1A, simple slope = 0.006, P = ns).


Variation in the oxytocin receptor gene moderates the protective effects of a family-based prevention program on telomere length.

Smearman EL, Yu T, Brody GH - Brain Behav (2016)

Nonsupportive parenting and telomere length outcomes by intervention and genotype status. Significant study interactions are depicted using simple slopes procedures for ± 1 standard deviation of nonsupportive parenting. Graphs display the association between nonsupportive parenting and telomere length outcomes across 5 years by a. intervention condition and b. intervention condition and OXTR rs53576 genotype. **P < 0.001. Rs53576 A+ allele, Control: n = 31; slope = 0.041; telomere length: Mean = −0.09, SD = 0.67, Range = −1.15 to −1.47. Rs53576 GG allele, Control: n = 60; slope = −0.107**; telomere length: Mean = −0.25, SD = 0.84, Range = −3.11 to 1.89. Rs53576 A+ allele, AIM: n = 38; slope = −0.027; telomere length: Mean = 0.04; SD = 0.72, Range = −1.58 to −0.04. Rs53576 GG allele, AIM: n = 62; slope = 0.033; telomere length: Mean = −0.03; SD = 0.74; Range = −2.16 to 1.58.
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brb3423-fig-0001: Nonsupportive parenting and telomere length outcomes by intervention and genotype status. Significant study interactions are depicted using simple slopes procedures for ± 1 standard deviation of nonsupportive parenting. Graphs display the association between nonsupportive parenting and telomere length outcomes across 5 years by a. intervention condition and b. intervention condition and OXTR rs53576 genotype. **P < 0.001. Rs53576 A+ allele, Control: n = 31; slope = 0.041; telomere length: Mean = −0.09, SD = 0.67, Range = −1.15 to −1.47. Rs53576 GG allele, Control: n = 60; slope = −0.107**; telomere length: Mean = −0.25, SD = 0.84, Range = −3.11 to 1.89. Rs53576 A+ allele, AIM: n = 38; slope = −0.027; telomere length: Mean = 0.04; SD = 0.72, Range = −1.58 to −0.04. Rs53576 GG allele, AIM: n = 62; slope = 0.033; telomere length: Mean = −0.03; SD = 0.74; Range = −2.16 to 1.58.
Mentions: While the direct association between nonsupportive parenting and telomere outcomes was only significant at P = 0.07 (Table 2, Model 1; β = −0.131), an interaction emerged when taking intervention condition into account. Replicating previous findings, exposure to nonsupportive parenting at age 17 forecasted shorter telomere length at age 22, but this association was attenuated for those who participated in the AIM intervention (Table 2, Model 2; β = 0.223, P < 0.05). Among those exposed to high levels of nonsupportive parenting, only those randomized to the control condition evidenced significantly shorter telomeres at age 22 (Fig. 1A, simple slope = −0.072, P < 0.01), whereas those randomized to the intervention evidenced similar telomere lengths to those with more supportive, non at‐risk parenting scores at baseline (Fig. 1A, simple slope = 0.006, P = ns).

Bottom Line: Parent-child relationships with high conflict and low warmth and support are associated with later adverse behavioral and physiological child outcomes.Subsequent analyses suggest that these findings may be mediated through chronic anger, whereby GG individuals exposed to nonsupportive parenting and randomized to the control condition had a greater increase in chronic anger by study follow-up, compared to those in the intervention, and this change associated with greater telomere shortening.These findings highlight the importance of individual differences and potential role of genetic status in moderating the relationship between environmental contexts and biological outcomes.

View Article: PubMed Central - PubMed

Affiliation: Behavioral Sciences and Health EducationRollins School of Public HealthEmory University1518 Clifton Road NortheastAtlantaGeorgia30322; Center for Translational and Social NeuroscienceEmory UniversityAtlantaGeorgia30322.

ABSTRACT

Introduction: Parent-child relationships with high conflict and low warmth and support are associated with later adverse behavioral and physiological child outcomes. These outcomes include shorter telomere lengths, the repetitive sequences at the ends of chromosomes that have been utilized as a biomarker for chronic stress. Our research group furthered this by exploring telomere length outcomes following a family-based prevention program and identified reduced telomere shortening 5 years post intervention among those originally exposed to nonsupportive parenting and randomized to the intervention condition. However, not all individuals respond equally, and a growing literature suggests genetic sensitivity to one's environment, with variations in the oxytocin receptor gene (OXTR) potentially influencing this sensitivity.

Methods: We utilized data from African American youths (mean age 17) randomized to intervention (n = 100) or control condition (n = 91) with baseline assessments of genetic status and nonsupportive parenting, and 5-year follow-up assessments of telomere length.

Results: We found a significant three-way interaction between nonsupportive parenting, intervention condition, and OXTR rs53576 genotype. OXTR GG individuals, who are suggested to be more sensitive to their social environment, exhibited significantly more variability, evidencing the shortest telomeres when exposed to nonsupportive parenting and randomized to the control condition, and similar telomere lengths to non at-risk groups when randomized to the intervention. In contrast, those with the A allele showed no statistical difference in telomere lengths across parental and intervention conditions. Subsequent analyses suggest that these findings may be mediated through chronic anger, whereby GG individuals exposed to nonsupportive parenting and randomized to the control condition had a greater increase in chronic anger by study follow-up, compared to those in the intervention, and this change associated with greater telomere shortening.

Conclusions: These findings highlight the importance of individual differences and potential role of genetic status in moderating the relationship between environmental contexts and biological outcomes.

No MeSH data available.


Related in: MedlinePlus