According to new research, a baby born to a mother with gestational diabetes mellitus, diabetes that is brought about by pregnancy, and who is poor appears to be at far greater risk for eventually developing childhood attention deficit hyperactivity disorder (ADHD) — 14 times greater than children exposed to neither.
Researchers led by Yoko Nomura, M.D., Ph.D., of Queens College, City University of New York, were interested to see whether there was any association between gestational diabetes mellitus (GDM) along with low socioeconomic status, and a child’s risk for developing ADHD or another neurodevelopmental problem.
So researchers compared offspring of mothers with and without GDM in an economically diverse sample of 212 parents of either “at risk” children or “typically developing” children. The children were between 3 and 4 years of age at the time of the study, and comparisons were done using an ADHD rating scale.
“At-risk” children had at least six inattention or six hyperactive and impulsive symptoms as rated by parents, teachers, or both (in keeping with the diagnostic criteria for ADHD). “Typically developing” children had fewer than three symptoms in each domain.
“The prevalence of gestational diabetes mellitus has been rising for over 20 years, particularly among ethnic minorities and individuals with low socioeconomic status (SES), as have lifestyle changes that heighten risk including greater consumption of saturated fats, sugar, and processed foods, and sedentary working environments,” said Joel Nigg, Ph.D., of Oregon Health and Science University, Portland, writing in an accompanying editorial. “Most of the relevant environmental risks are presumed to occur very early in development.”
The average inattention score at the start of the study for offspring exposed to mother’s GDM was significantly higher than for offspring unexposed, but there was no difference in hyperactivity/impulsivity scores between the two groups.
Children in low SES families, compared to high SES families, had greater inattention and hyperactivity/impulsivity scores.
The results showed no difference in the risk for ADHD at baseline, but a two-fold increased risk at age 6 years among children exposed to GDM compared with children who were not exposed. There was also a two-fold increased risk for ADHD at baseline and at age 6 years among children in low SES families.
“Gestational diabetes mellitus (GDM) typically develops in the second and third trimesters and is defined as glucose intolerance with onset or first recognition during pregnancy,” the authors write in the article.
Children exposed to both gestational diabetes mellitus and low SES showed compromised neurobehavioral functioning, including lower IQ, poorer language abilities and diminished behavioral and emotional functioning.
When examining the relationship of both GDM and SES exposure on outcomes, the authors found a 14-fold increased risk of developing ADHD among children exposed to both GDM and low SES. Conversely, children exposed to maternal GDM alone or low SES alone had no significant increased risk for ADHD.
“This study demonstrates that children of mothers with GDM raised in lower SES households are at far greater risk for developing ADHD and showing signs of suboptimal neurocognitive and behavioral development,” the authors conclude.
“Since ADHD is a disorder with high heritability, efforts to prevent exposure to environmental risks through patient education may help to reduce the nongenetic modifiable risk for ADHD and other developmental problems.”
“If causal, and if able to be understood pathophysiologically, such environmental effects on ADHD are of ‘game-changing’ importance because they open the door to eventually preventing that portion of cases of ADHD caused by early insult to the nervous system,” said Nigg.
“If a specific environmental causal influence can be demonstrated, even if effective in a subset of children, and its biological mechanisms elucidated, then a powerful model will be created for how ADHD can develop,” Nigg concluded.
“That discovery will be a crucial stepping-stone toward parsing multiple causal routes to what may be a final common pathway of the ADHD phenotype.”
The new research is published in the Online First edition of the journal Archives of Pediatrics & Adolescent Medicine.