The μ-opioid receptor gene A118G polymorphism is associated with insecure attachment in children with disruptive mood regulation disorder and their mothers

Abstract

Background: The A118G single nucleotide polymorphism (SNP) of the μ-opioid receptor gene, with high expression of the A allele and low expression of the G allele, has been associated with emotional/behavioral dysregulation and depressive disorders and is recognized as a mediator of affiliative behavior. No study has thus far investigated this SNP in school-age children with disruptive mood regulation disorder (DMDD). This study compared a sample of healthy children and their mothers with a sample of children with DMDD and their mothers, evaluating whether insecure attachment and psychopathological symptoms are associated with A allele- or G allele-carrying mothers and children and whether caregiving capacities are associated with A allele- or G allele-carrying mothers.

Methods: For evaluation of their psychopathological symptoms and attachment styles, mothers filled out the CBCL/6-18, the SCL-90-R, and the ECR. To evaluate the types of relationship children were experiencing with their mothers, children filled out the ECR-revised child version and the PBI. Genotypic analyses were conducted on DNA samples obtained by buccal swabbing from children and mothers.

Results: An insecure attachment style was more frequent in mothers and children carrying the G allele (G/G + A/G genotypes). In the clinical sample, G allele-carrying children scored higher than homozygous A/A ones on the subscales of Withdrawal and Conduct Problems. G-carrying mothers showed higher interpersonal sensitivity, depression, hostility, and paranoid ideation and provided less care than A/A mothers.

Conclusions: This study offers new insights into the associations between the A118G SNP of the μ-opioid receptor gene and emotional/behavioral functioning, attachment style in children, and psychopathology and caregiving ability in mothers.

Keywords: A118G; OPRM1; attachment style; disruptive mood regulation disorder; infant dyad; maternal care; mother; psychopathology.

Figure 1

Infant and their mother genotype frequencies were in Hardy–Weinberg equilibrium: mothers 75% A/A and 25% G (A/G, G/G) and infants 72% A/A and 28% G (A/G, G/G) (a). The percentage of A/A homozygous infants (b) and mothers (c) with secure a secure attachment was higher than A/A homozygous infants and mothers with insecure attachment. On the contrary, the percentage of infants and mothers carrying G allele and with insecure attachment was higher than infants and mothers with the same genotype but with secure attachment (b, c)

Figure 2

The percentage of healthy A/A homozygous infants with secure attachment was higher than healthy infants with the same genotype but with insecure attachment (a), while the percentage of healthy G‐carrier infants with secure attachment was lower than healthy infants with the same genotype but with insecure attachment (b). The percentage of clinical A/A homozygous infants with insecure attachment increased compared with the healthy infants carrying the same genotype, while no changes in the attachment style distribution were detectable within the G‐carrier groups (a, b)

Figure 3

The percentage of healthy infant A/A homozygous mothers with secure attachment was higher than mothers of healthy infants with the same genotype but with insecure attachment (a). On the contrary, the percentage of healthy infant G‐carrier mothers with secure attachment was lower than healthy infant mothers with the same genotype but with insecure attachment (a). The percentage of clinical infant A/A homozygous mothers with insecure attachment increased compared with the healthy infant mothers carrying the same genotype (a, b). In parallel, the percentage of G‐carrier mothers was increased in the clinical context (a, b). Within this last group, the number of mothers with insecure attachment was also increased (b)

Figure 4

Clinical G‐carrier infants showed higher levels of CBCL‐Social Withdrawal (a) and Conduct Problems (b) compared to clinical A/A homozygous infants. *p < .05

Figure 5

Clinical infant G‐carrier mothers showed higher levels of SCL90/R‐Interpersonal sensitivity (a), Depression (b), Hostility (c), Paranoid ideation (d), and Global Severity Index (e) compared to A/A homozygous mothers of clinical infants. *p < .05, **p < .01, ***p < .001

Figure 6

G‐carrier mothers showed lower levels of PBI‐maternal Care (a) compared to A/A homozygous mothers. A/A homozygous mothers of clinical infants showed higher levels of PBI‐maternal overprotection (b) compared to A/A homozygous mothers of healthy infants. *p < .05, and ***p < .001