The development and validation of a digital food-frequency questionnaire to assess habitual diet: The PREDICT Food Frequency Questionnaire.

Malnutrition constitutes a global public health challenge characterized by a dual burden: overnutrition including being overweight and obesity is increasingly prevalent in high- and middle-income countries undergoing nutritional transition, while undernutrition and micronutrient deficiency continue to disproportionately affect populations in low-income settings (, ). These two phenotypically distinct forms of malnutrition are not mutually exclusive; resource-constrained environments frequently exhibit both simultaneously, reflecting the epidemiological complexity of contemporary food systems (). Selected sub-Saharan African settings exemplify this co-occurrence: approximately 216 million children experience stunting or undernutrition in this region yet rising overweight and obesity rates driven by dietary transition are simultaneously documented across urban populations (). However, this dual burden is by no means confined to sub-Saharan Africa; analogous patterns have been reported across South and Southeast Asia, Latin America, Eastern Europe, and among indigenous and economically transitioning communities globally (). It is therefore essential to situate the malnutrition–T2DM relationship within a genuinely global framework, drawing on evidence from multiple income settings and geographic regions. Food insecurity constitutes a proximate structural driver of undernutrition across multiple low- and middle-income settings, arising from land degradation, climate vulnerability, fragile agricultural systems, and resource scarcity (). In sub-Saharan Africa particularly, these structural determinants interact with rapid urbanization and dietary transition to simultaneously sustain undernutrition while accelerating overnutrition, a dynamic that exemplifies the dual-burden pattern central to this review. Across the life course, the nutritional drivers and consequences of malnutrition vary substantially. In children and adolescents, undernutrition is characterized by stunting, wasting, and inadequate micronutrient intake, which impairs immune function, growth, and metabolic programming, with long-term consequences for cardiometabolic health that persist into adulthood (). In older adults, disease-related malnutrition arising from reduced dietary intake, malabsorption, and sarcopenia further disrupts protein and energy homeostasis, promotes hormonal dysregulation, and heightens susceptibility to chronic disease (, ). These age-dependent nutritional vulnerabilities are not geographically specific; they characterize populations across low-, middle-, and high-income settings, emphasizing the necessity of globally applicable evidence on malnutrition’s relationship with T2DM. Two mechanistically distinct pathways link malnutrition to susceptibility for type 2 diabetes mellitus (T2DM), and these must be considered separately to avoid conceptual conflation. The undernutrition pathway operates through developmental metabolic programming: early-life nutritional deprivation — whether , during infancy, or in childhood — has been associated with impaired pancreatic beta-cell development and reduced functional beta-cell mass, diminished insulin secretory capacity, and dysregulation of the hypothalamic–pituitary–adrenal axis (). These effects, consistent with the Developmental Origins of Health and Disease (DOHaD) framework, may predispose individuals to T2DM decades after the period of undernutrition has been resolved, a phenomenon referred to as metabolic programming [Barker, 1995]. Evidence from famine studies supports this pathway: Sun et al. (), included in this review, demonstrated that female participants with fetal-period famine exposure had significantly elevated adjusted odds of hyperglycemia in adulthood (aOR=1.57, 95% CI: 1.25–1.98), with risk increasing monotonically for earlier exposure windows (). Furthermore, the International Diabetes Federation’s 2025 classification recognizes Type 5 Diabetes — formerly termed malnutrition-related diabetes mellitus (MRDM) as a distinct clinical entity characterized by chronic undernutrition, beta-cell dysfunction in the absence of autoimmunity, and early-onset insulin-requiring diabetes in lean individuals in resource-limited settings. This classification reinforces the biological plausibility of a distinct undernutrition-driven pathway to insulin insufficiency, separate from classical T2DM pathophysiology. By contrast, the overnutrition pathway proceeds through insulin resistance: chronic positive energy balance promotes adipose tissue expansion, particularly visceral adiposity, which in turn drives systemic inflammation, dysregulated adipokine secretion, ectopic lipid deposition in insulin-sensitive tissues, and progressive impairment of insulin signaling (). This cascade constitutes the principal pathophysiological mechanism linking obesity to T2DM in most included studies from high- and middle-income settings. The methodological separation of these two pathways is critical t