A very valid and extremely pertinent point has been raised in this article considering the tremendous implications of Gestational Diabetes Mellitus (GDM) on the health of the mother and the child, consequently the whole family.
GDM has been implicated as a considerable pre-natal risk factor for neurodevelopmental disorders like Attention Deficit Hyperactivity disorder (ADHD) and ASD (Autism Spectrum Disorder). Approximately 1 in 110 children has ASD, and the cumulative incidence of this disorder seems to be on the rise. Children with ASD have language and cognitive delays which can also be seen in other developmental delays that occur in 1 in 83 children.
Pregnancy-related exposures have been the centre of a significant amount of epidemiological research on likely risk factors for autism. Although many studies support the hypothesis that obstetrical complications may increase the risk of autism. It is possible that the increasing maternal and paternal age at birth and rate of gestational diabetes may be contributing factors to the rising prevalence of autism (1).
Several studies including meta-analysis, involving women with diabetes found correlations between gestational measures of maternal lipid and glucose metabolism and poorer performance of the offspring on standardized IQ and motor development tests. Dionne et al reported significant expressive language impairments in young children born to mothers with gestational diabetes (GDM) compared with children of women without diabetes (2).
Krakowiak et al observed that diabetes, hypertension, and obesity were more common among mothers of children with ASD and developmental delays compared with controls. Diabetes, in particular, was associated with statistically significantly greater deficits in expressive language among children with ASD. In the study they also observed that in children without ASD, metabolic conditions like GDM, hypertension and obesity were collectively associated with impairments in visual reception, motor skills, and receptive and expressive language, as well as adaptive communication and socialization(3).
Insulin resistance and chronic inflammation in type 2 diabetes (T2D) and other conditions like obesity and hypertension have been well recognized. During GDM there may be prolonged foetal exposure to elevated glucose levels resulting in chronic foetal hyper-insulinemia, which in turn sets off the foetus to increase oxygen consumption and metabolism, inducing chronic intrauterine tissue hypoxia.
Further foetal responses to this state may result in foetal iron deficiency. Cumulative effect of both feotal hypoxia and iron deficiency can greatly affect neurodevelopment in humans, as well as alterations in myelination, cortical connectivity and aberrations in hippocampal neurons(3).
Åberg and Westbom reported that children of pre pregnancy Diabetes Mellitus women and to a lesser degree children of GDM women had a statistically significant increase in hospitalizations, evident at least up to 10 years of age more so in those with neurodevelopmental disorders.
Hence GDM, a serious risk factors for women's and children's physical and mental health, needs to be tackled with strict robust collective measures by all medical specialities and other agencies to prevent the adverse effects on women and the future health development and quality of life of the unborn children.
1 Neurodevelopment outcome at early school age of children born to mothers with gestational diabetes. Arch Dis Child Foetal Neonatal Ed. Jul 1999; 81(1): F10–F14.
2 Prenatal risk factors for autism: comprehensive meta-analysis. Hannah Gardener, Donna Spiegelman and Stephen L. Buka.The British Journal of Psychiatry (2009) 195, 7–14. doi: 10.1192/bjp.bp.108.051672
3 Maternal Metabolic Conditions and Risk for Autism and Other Neurodevelopmental Disorders .Pediatrics 2012;129;e1121;Paula Krakowiak, Cheryl K. Walker, Andrew A. Bremer, Alice S. Baker, Sally
4 Association between maternal pre-existing or gestational diabetes and health problems in children. A Åberg and L Westbom. 2 JAN 2007 DOI: 10.1111/j.1651-227.2001.tb02799.
Competing interests: No competing interests