Effect of exposure to maternal diabetes during pregnancy on offspring’s brain cortical thickness and neurocognitive functioning

ABSTRACT

Little is known about the long-term effects of maternal diabetes during pregnancy (DP), either gestational diabetes or preexisting diabetes (type 1 or type 2), on offspring’s brain morphometry and neurocognitive functioning (NCF). This study examined the effect of prenatal exposure to maternal DP on the brain structure and NCF in children between 9 and 10 years of age. This study used cross-sectional neuroimaging and NCF data from the baseline wave of the Adolescent Brain and Cognitive Development® study. Exposure to maternal DP was assigned from the developmental history questionnaire. Differences in the brain cortical thickness (CTh) and five cognitive abilities (executive function, working and episodic memory, processing speed, and language abilities) were examined in diabetes-exposed and diabetes-unexposed children. Linear mixed effect models and generalized linear models were used to adjust for the effect of confounding variables. A total of 9,967 children (718 diabetes-exposed and 9249 unexposed) were included in the analysis. Diabetes-exposed children had lower whole-brain CTh [mean: exposed vs unexposed = 2.725 mm vs 2.732 mm; difference (95%CI): −0.007 mm (−0.013, −0.001)] compared to unexposed children after adjusting for confounding variables. Diabetes-exposed children had lower CTh in most part of the occipital lobe of both hemispheres, right postcentral gyrus, and left superior parietal cortex. Diabetes-exposed children also had lower scores in processing speed task [mean difference (95%CI): −1.7 (−2.8, −0.6)] and total cognition [mean difference (95%CI): −0.6 (−1.2, −0.02)]. Diabetes-exposed children have reduced CTh and NCF during preadolescence, which might have implications for psychomotor development during later life. Prospective studies are needed to confirm our findings.

KEYWORDS:

• Gestational diabetes
• cortical thickness
• neurocognition
• preadolescent

Acknowledgments

Data used in the preparation of this article were obtained from the Adolescent Brain Cognitive Development (ABCD) Study (https://abcdstudy.org), held in the NIMH Data Archive (NDA). This is a multisite, longitudinal study designed to recruit more than 10,000 children aged 9-10 and follow them over 10 years into early adulthood. The ABCD Study® was supported by the National Institutes of Health and additional federal partners under award numbers U01DA041048, U01DA050989, U01DA051016, U01DA041022, U01DA051018, U01DA051037, U01DA050987, U01DA041174, U01DA041106, U01DA041117, U01DA041028, U01DA041134, U01DA050988, U01DA051039, U01DA041156, U01DA041025, U01DA041120, U01DA051038, U01DA041148, U01DA041093, U01DA041089, U24DA041123, and U24DA041147. A full list of supporters is available at https://abcdstudy.org/federal-partners.html. A listing of participating sites and a complete listing of the study investigators can be found at https://abcdstudy.org/consortium_members/. ABCD consortium investigators designed and implemented the study and/or provided data but did not necessarily participate in the analysis or writing of this report. This manuscript reflects the views of the authors and may not reflect the opinions or views of the NIH or ABCD consortium investigators. The ABCD data repository grows and changes over time. The ABCD data used in this report came from http://dx.doi.org/10.15154/1519007.

Disclosure statement

No potential conflict of interest was reported by the author(s).

Supplementary material

Supplemental data for this article can be accessed at https://doi.org/10.1080/09297049.2022.2103105

Additional information

Funding

The author(s) reported that there is no funding associated with the work featured in this article.