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METABOLIC, SEASONAL, AND DIAGNOSTIC DETERMINANTS OF GESTATIONAL DIABETES MELLITUS: AN INTEGRATIVE ANALYSIS OF MATERNAL ADIPOSITY, SCREENING PARADIGMS, AND DEVELOPMENTAL ORIGINS OF HEALTH

4 Sorbonne University, France

Abstract

 

Gestational diabetes mellitus (GDM) has emerged as one of the most significant metabolic disorders of pregnancy, with profound implications for maternal, fetal, and long-term population health. Its increasing global prevalence reflects the convergence of multiple biological, environmental, and healthcare system factors, including rising maternal adiposity, altered dietary patterns, seasonal variation in insulin sensitivity, and evolving diagnostic criteria. Drawing strictly upon the scientific literature provided, this article offers an integrative and theoretically grounded analysis of GDM as a multifactorial disorder embedded within both immediate pregnancy physiology and the broader developmental origins of health and disease paradigm.

The aim of this work is not merely to summarize previous findings, but to synthesize them into a unified conceptual framework that explains how metabolic vulnerability, adipose tissue dysfunction, placental endocrinology, and screening practices interact to shape both the detection and consequences of GDM. Evidence from large cohort studies and systematic reviews demonstrates that pre-pregnancy body mass index and gestational weight gain are dominant predictors of GDM risk and severity (Torloni et al., 2009; Chen et al., 2018; De Souza et al., 2015). These metabolic states influence insulin resistance through adipocyte hypertrophy, inflammatory signaling, and altered lipid metabolism, mechanisms that are amplified during pregnancy by placental hormones such as placental lactogen (Parsons et al., 1992; Plows et al., 2018; Svensson et al., 2015).

At the same time, gestational diabetes cannot be understood purely through body composition. Seasonal variation in diagnosis rates, observed consistently in Sweden, Taiwan, and Southern Europe, reveals that ambient temperature, physical activity, and perhaps circadian and vitamin D–related mechanisms modulate glucose tolerance during pregnancy (Katsarou et al., 2016; Wang et al., 2020; Chiefari et al., 2017). These findings challenge the assumption that GDM is a static metabolic state and instead position it as a dynamic condition sensitive to environmental and temporal contexts.

Diagnostic and screening strategies further complicate the epidemiology of GDM. The adoption of the International Association of the Diabetes and Pregnancy Study Groups (IADPSG) criteria and the World Health Organization guidelines has dramatically increased the number of women diagnosed, raising debates about cost-effectiveness, clinical benefit, and potential overmedicalization (Benhalima et al., 2013; Werner et al., 2012; Aubry et al., 2021). Yet large randomized trials confirm that treatment of even mild GDM significantly reduces rates of macrosomia, shoulder dystocia, and hypertensive complications (Landon et al., 2009; Horvath et al., 2010).

This article also situates GDM within the fetal programming framework, emphasizing how intrauterine hyperglycemia imprints long-term metabolic risk on offspring through mechanisms of altered organ development, epigenetic modification, and dysregulated adipogenesis (Godfrey et al., 2001; Hoffman et al., 2017). The association between maternal hyperglycemia, fetal overgrowth, and future obesity and type 2 diabetes thus becomes a central public health concern, linking pregnancy care to the prevention of chronic disease across generations.

Through an in-depth analysis of recurrence patterns, biomarker research, assisted reproductive technologies, and evolving diagnostic thresholds, this study demonstrates that GDM is not a discrete clinical entity but a spectrum of dysglycemia shaped by biological susceptibility and healthcare systems. By integrating metabolic, environmental, and policy-level evidence, this article argues for a more nuanced, individualized, and prevention-oriented approach to gestational diabetes that recognizes its roots in maternal adiposity, its modulation by seasonality, and its lifelong consequences for mothers and children alike.

Keywords

References

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