Iron2026-06

Ironing Out Possible Micronutrient Deficiencies Associated with Incretin Receptor Agonist-Based Therapies: Proposed Practical Strategies to Prevent and Manage Iron Deficiency.

Infante Marco, Ricordi Camillo, Pacifici Francesca, Pastore Donatella et al. — Nutrients

Summary

Medications known as incretin receptor agonists, used for managing type 2 diabetes and obesity, are becoming more common. This paper discusses emerging evidence suggesting a potential link between these drugs and iron deficiency. It explores possible reasons for this connection and proposes practical strategies for healthcare providers to help prevent and manage iron deficiency in patients using these treatments.

AI-generated summary — read the original

Key points

Incretin receptor agonist drugs are widely used for type 2 diabetes and obesity.
Some early evidence suggests a possible link between these medications and iron deficiency.
Potential causes include reduced food intake and changes in how the body absorbs iron.
The paper outlines practical approaches for healthcare providers to address this potential issue.

What the study looked at

**What question the study asked:** This paper explores whether medications called incretin receptor agonists, commonly prescribed for type 2 diabetes and obesity, might increase the risk of iron deficiency. It also investigates the potential biological reasons behind such a link and how to address it. **How it was studied:** This is a commentary paper that reviews and discusses existing preliminary observational evidence and scientific hypotheses. It synthesizes current understanding rather than presenting new research data from a specific study. The authors examine various factors, including changes in diet, reduced food intake, and potential impacts on iron absorption in the gut. **What it found:** The paper suggests a possible connection between incretin receptor agonist use and iron deficiency, though it notes this is currently uncommon. It identifies several potential mechanisms, such as decreased appetite leading to lower iron intake, changes in food preferences, and impaired iron absorption due to effects on the digestive system. The authors propose practical strategies for healthcare professionals to prevent and manage iron deficiency in patients on these medications, while emphasizing the need for more definitive research.

Dietary takeaway

If you are taking incretin receptor agonist medications for diabetes or weight management, it's wise to be mindful of your iron intake. Focus on consuming iron-rich foods like lean meats, beans, and fortified cereals, and discuss any new or worsening fatigue with your doctor. Remember, this is an emerging area of research, and while the paper proposes strategies, more studies are needed to fully confirm the link and optimal management.

Abstract

Over the last years, incretin receptor agonists-including glucagon-like peptide-1 (GLP-1) receptor agonists (GLP-1 RA) and the dual glucose-dependent insulinotropic polypeptide (GIP)/GLP-1 receptor agonist tirzepatide-have dramatically improved the management of type 2 diabetes, overweight and obesity. However, as the use of incretin receptor agonists continues to increase worldwide, micronutrient deficiencies-including iron deficiency-have emerged as newly recognized adverse effects of these drugs. The present article aims to discuss recent preliminary observational evidence on the potential relationship between incretin receptor agonist-based therapies and the development of iron deficiency and iron deficiency anemia (IDA), as well as the potential mechanisms by which incretin receptor agonists may affect iron homeostasis. Potential mechanisms and factors underlying the development of iron deficiency and IDA in patients treated with incretin receptor agonist-based therapies include inadequate dietary iron intake (due to incretin receptor agonist-mediated reduction in food intake and/or gastrointestinal adverse effects of incretin receptor agonists), low dietary variety, monotonous diets, and changes in food preferences, as well as impairment of intestinal iron absorption (due to delayed gastric emptying, reduced small intestinal motility and/or decreased gastric acid secretion caused by incretin receptor agonists). Moreover, vitamin B2 (riboflavin) deficiency and changes in gut microbiota composition are hypothetical mechanisms that may partly explain iron deficiency in patients treated with incretin receptor agonists, although these hypotheses require confirmation through mechanistic studies. Even though iron deficiency and IDA currently appear to be uncommon adverse effects of incretin receptor agonist-based therapies, clinicians should be aware of the possibility of their occurrence to ensure appropriate prevention and management of these nutritional complications. Nevertheless, future prospective studies are certainly needed to better establish the causal relationship between the initiation of incretin receptor agonist-based therapies and the development of iron deficiency/IDA, as well as the exact mechanisms underlying the potential development of these nutritional complications in patients treated with incretin receptor agonists. Meanwhile, the prescription of incretin receptor agonists should not be unjustifiably restricted by the possible and modest risk of iron deficiency and IDA in patients with one or more approved indications for therapeutic use of these agents. Since no established guidelines currently exist for the prevention and management of iron deficiency and IDA in patients treated with incretin receptor agonists, we herein propose practical strategies to address these possible nutritional complications of incretin receptor agonist-based therapies. These proposed strategies should only be regarded as practical clinical approaches deriving from the existing recommendations for the prevention and management of iron deficiency and IDA, although their cost-effectiveness for the prevention and management of incretin receptor agonist-associated iron deficiency/IDA should be appropriately assessed in future clinical trials.

View on PubMed →DOI: 10.3390/nu18132038