Fetal Alcohol Spectrum Disorder: Risk for Diabetes and Congenital Heart Defects

Jenny Salmon

doi:10.18314/idcd.v1i1.1080

Abstract

Excessive use of alcohol can be a cause for many disease and injury conditions. These include amongst many others, myocardial infarction, diabetes mellitus, atrial fibrillation, nonischaemic cardiomyopathy, fetal alcohol spectrum disorder (FASD), congenital heart defects (CHD) and liver cirrhosis. Even low levels of prenatal alcohol ethanol) exposure, such as in a single dose, can produce birth defects termed fetal alcohol syndrome (FAS) which is the highest marker on the spectrum. Diabetes is regarded as a major cause of cardiovascular disease whilst prenatal alcohol exposure (PAE) can range from no observable adverse effects to mortality. CHD are stated to be the most prevalent cause of mortality in individuals with FASD. The dimension of the problems is still greatest in the Western world although it is stated to be the leading cause of mental retardation in North America. FASD is a neurodevelopmental disability which can be occasioned when a pregnant woman consumes alcohol. The diagnostic criteria for FASD includes growth impairment, abnormal facial features and neurocognitive impairments. The most frequently reported abnormal facial features in FASD are thin upper lip, indistinct or smooth philtrum and short palpebral fissure length. Other features are microganthia, low set ears, ptosis, absent or indistinct philtral ridge, epicanthal folds, cleft palate, flat nasal bridge and midface hypoplasia. The neurocognitive features commonly reported in FASD are microcephaly, intellectual disability, attention-deficit hyperactivity disorder (ADHD) and behavioural impairments. Central nervous system (CNS) injury is also seen and is debilitating. Structural abnormalities of the CNS can include microcephaly, agenesis/absence of the corpus callosum and multiple severe brain malformations. This review article seeks to address the association of FASD with diabetes and CHD.

Highlights

The range of structural abnormalities and functional deficits caused by prenatal alcohol exposure (PAE) are referred to as fetal alcohol spectrum disorder (FASD)
The limitations of this study indicated that the nomenclature for diagnosis had been modified over the past 35 years for cases included in the review, that there is no widely accepted threshold for exposure that is necessary or sufficient to cause FASD and it is likely that many deaths occur in people with undiagnosed FASD or where a past diagnosis is not available at the time of the death [20]
Many previous studies have focused on the neurodevelopmental symptoms of FASD, but comparatively few have investigated cardiac birth defects and diabetes associated with PAE

Summary

Introduction

The range of structural abnormalities and functional deficits caused by PAE are referred to as FASD. One clinical marker for an adverse intrauterine environment is low birth weight, a result of decreased fetal growth, which has been associated with characteristics of the metabolic syndrome including impaired glucose tolerance, insulin resistance and type-2 diabetes in adult life [14]. Unlike the adult, this fetal hypoglycaemia is associated with decreased hepatic glycogen stores and not decreased gluconeogenesis, as gluconeogenesis does not occur during fetal life for either rats or humans [14] This is said to be the first study to explore the effect of chronic low-moderate PAE on glucose homeostasis in rats. PAE is routinely accompanied by high rates of maternal smoking, poor diet, other substance abuse and multiple other adverse factors which increase the risk for a broad range of adverse outcomes in exposed pregnancies including CHD [4]. Clinical trials have already demonstrated that ethanol exposure can have direct vascular effects, including basal vasoconstriction and potentiation of vasodilation [31]

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Conclusion