Iron Deficiency and Obesity Interrelationships

Summary

Iron deficiency and obesity represent two of the most pervasive nutritional challenges of the twenty‐first century, yet their coexistence often goes unrecognised. Although obesity is associated with excessive energy stores, chronic low‐grade inflammation in adipose tissue drives increased production of the iron‐regulatory hormone hepcidin. Elevated hepcidin inhibits duodenal iron absorption and blocks iron release from macrophages, leading to functional and absolute iron deficiency despite adequate or even excessive dietary intake. At the same time, expanded blood volume and hemodilution in obesity can confound standard biomarkers, masking true iron stores. The resulting iron deficiency may exacerbate fatigue, impair cognitive and immune function, and perpetuate a cycle of reduced physical activity. Conversely, some data suggest that alterations in iron metabolism may influence adipocyte function and systemic energy homeostasis, hinting at a bidirectional relationship. Globally, these interconnections carry practical implications: screening programmes must adjust interpretation of ferritin and transferrin indices in populations with high adiposity, and tailored supplementation strategies may be required to overcome hepcidin‐mediated barriers to iron uptake. A clear understanding of these mechanisms is essential for effective public‐health policies and personalised clinical interventions.

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Iron Deficiency and Obesity Interrelationships publication trend

The graph below shows the total number of articles in iron deficiency and obesity interrelationships across all publications each year (not limited to Nature Index journals).

Technical terms

Ferritin: An intracellular protein that stores iron and releases it in a controlled manner; serum ferritin concentration reflects body iron stores but may be elevated by inflammation.

Hepcidin: A peptide hormone produced by the liver that regulates iron absorption and distribution by binding to the iron exporter ferroportin, leading to its internalisation and degradation.

Transferrin saturation: The proportion of the iron-binding protein transferrin that is occupied by iron; a marker of circulating bioavailable iron.

Divalent metal transporter 1 (DMT1): A membrane protein expressed in the duodenal enterocyte that mediates uptake of divalent metal ions, including dietary ferrous iron.

Body mass index (BMI): A measure of body fat based on weight in kilograms divided by height in metres squared; widely used to categorise underweight, normal weight, overweight and obesity.

Mendelian randomisation: A genetic epidemiology method that uses inherited genetic variants as proxies for modifiable exposures to infer causal relationships between risk factors and health outcomes.

References

  1. Overnutrition is a risk factor for iron, but not for zinc or vitamin A deficiency in children and young people: a systematic review and meta-analysis. BMJ Global Health (2024).
  2. Effect of diet-induced weight loss on iron status and its markers among young women with overweight/obesity and iron deficiency anemia: a randomized controlled trial. Frontiers in Nutrition (2023).
  3. Iron status and obesity-related traits: A two-sample bidirectional Mendelian randomization study. Frontiers in Endocrinology (2023).
  4. Greater blood volume and Hb mass in obese women quantified by the carbon monoxide-rebreathing method affects interpretation of iron biomarkers and iron requirements. International Journal of Obesity (2018).
  5. Iron Metabolism in Obesity and Metabolic Syndrome. International Journal of Molecular Sciences (2020).

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