Systems biology insights into the molecular drivers of childhood stunting and implications for intervention

TL;DR

This paper reviews how systems biology helps understand the molecular causes of childhood stunting and suggests ways to develop better interventions.

Contribution

The paper provides new insights into molecular pathways linked to stunting and highlights potential biomarkers for targeted interventions.

Findings

Disrupted mTOR signaling and tryptophan-kynurenine pathways are linked to stunting.

One-carbon metabolism and chronic inflammation contribute to stunting mechanisms.

Gut microbiome dysbiosis and environmental enteric dysfunction are key factors.

Abstract

Childhood stunting is a condition resulting from chronic malnutrition affecting millions globally, with lasting consequences for growth, cognition, and productivity. This review explores the molecular mechanisms underlying stunting, focusing on evidence obtained from systems biology to uncover biochemical pathways and potential biomarkers for early detection and targeted interventions. Key findings highlight the role of disrupted pathways such as the mechanistic target of rapamycin (mTOR) signaling, the tryptophan-kynurenine pathway, one-carbon metabolism, and chronic inflammation associated with environmental enteric dysfunction and dysbiosis of the gut microbiome. These insights emphasize the multifactorial nature of stunting, influenced by nutrition, infections, socioeconomic and maternal factors. Integrating systems biology to support public health strategies may provide avenues for precision nutrition-driven interventions that address specific deficiencies and systemic biochemical disturbances.

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