Nutrition, thyroid function, and tuberculosis: exploring the endocrine-immune axis.
- 1Department of Biomedical Sciences, College of Osteopathic Medicine of the Pacific, Western University of Health Sciences, Pomona, CA, United States.
Abstract
Tuberculosis (TB) remains a major global health challenge, with undernutrition recognized as one of the most significant modifiable risk factors influencing disease susceptibility and clinical outcomes. Emerging evidence suggests that nutritional status may also affect TB risk indirectly through its impact on thyroid function and immune regulation. This review examines the current evidence linking nutrition, thyroid dysfunction, and susceptibility to Mycobacterium tuberculosis (M. tuberculosis), with particular emphasis on the biological mechanisms that connect these factors. Essential micronutrients, including iodine, selenium, iron, zinc, and vitamin D, are critical for thyroid hormone synthesis, metabolism, antioxidant defense, and immune function. Deficiencies in these nutrients can impair thyroid physiology, disrupt endocrine homeostasis, and alter innate and adaptive immune responses that are essential for controlling M. tuberculosis infection. Thyroid hormones regulate macrophage activation, T-cell differentiation, cytokine production, immunometabolism, and oxidative stress, suggesting that thyroid dysfunction may compromise host resistance to TB. Conversely, chronic TB infection and antitubercular therapy may further disrupt thyroid function, creating a bidirectional relationship between these conditions. Collectively, the available evidence supports a conceptual framework in which nutritional deficiencies contribute to thyroid dysfunction, thyroid dysfunction impairs antimicrobial immunity, and TB further exacerbates nutritional and endocrine disturbances, establishing a self-perpetuating cycle that may increase disease susceptibility and worsen clinical outcomes. Although direct clinical evidence linking thyroid disorders with TB risk remains limited, the convergence of nutritional, endocrine, and immunological pathways provides a strong biological rationale for further investigation. Future prospective studies are needed to determine whether nutritional optimization, targeted micronutrient supplementation, and early identification and management of thyroid dysfunction can improve immune competence, reduce TB susceptibility, and enhance treatment outcomes in high-risk populations.
Related
- Early nutrition modulates transcriptomic responses to endocrine-active compounds in neonatal porcine uterine explants
- Endocrine complications of COVID-19: diabetes, musculoskeletal, thyroid, pituitary, adrenal, and gonadal disorders.
- Editorial: Exploring socio-cultural factors in human nutrition: the importance of multidimensional approaches
- Does the aging skeletal muscle maintain its endocrine function?
- Coupling characteristics of endocrine regulation and system function under massage interventions.
BibTeX
@article{khachatourian2026nutrition,
title = {{Nutrition, thyroid function, and tuberculosis: exploring the endocrine-immune axis.}},
author = {Nooneh Khachatourian and Rubina Takhmazian and Vishwanath Venketaraman},
journal = {Frontiers in tuberculosis},
year = {2026},
month = oct,
doi = {10.3389/ftubr.2026.1945832},
url = {https://europepmc.org/article/MED/42923651},
note = {CC BY},
}
RIS
TY - JOUR
TI - Nutrition, thyroid function, and tuberculosis: exploring the endocrine-immune axis.
AU - Nooneh Khachatourian
AU - Rubina Takhmazian
AU - Vishwanath Venketaraman
PY - 2026
DA - 2026/10/08
JO - Frontiers in tuberculosis
DO - 10.3389/ftubr.2026.1945832
UR - https://europepmc.org/article/MED/42923651
AB - Tuberculosis (TB) remains a major global health challenge, with undernutrition recognized as one of the most significant modifiable risk factors influencing disease susceptibility and clinical outcomes. Emerging evidence suggests that nutritional status may also affect TB risk indirectly through its impact on thyroid function and immune regulation. This review examines the current evidence linking nutrition, thyroid dysfunction, and susceptibility to Mycobacterium tuberculosis (M. tuberculosis), with particular emphasis on the biological mechanisms that connect these factors. Essential micronutrients, including iodine, selenium, iron, zinc, and vitamin D, are critical for thyroid hormone synthesis, metabolism, antioxidant defense, and immune function. Deficiencies in these nutrients can impair thyroid physiology, disrupt endocrine homeostasis, and alter innate and adaptive immune responses that are essential for controlling M. tuberculosis infection. Thyroid hormones regulate macrophage activation, T-cell differentiation, cytokine production, immunometabolism, and oxidative stress, suggesting that thyroid dysfunction may compromise host resistance to TB. Conversely, chronic TB infection and antitubercular therapy may further disrupt thyroid function, creating a bidirectional relationship between these conditions. Collectively, the available evidence supports a conceptual framework in which nutritional deficiencies contribute to thyroid dysfunction, thyroid dysfunction impairs antimicrobial immunity, and TB further exacerbates nutritional and endocrine disturbances, establishing a self-perpetuating cycle that may increase disease susceptibility and worsen clinical outcomes. Although direct clinical evidence linking thyroid disorders with TB risk remains limited, the convergence of nutritional, endocrine, and immunological pathways provides a strong biological rationale for further investigation. Future prospective studies are needed to determine whether nutritional optimization, targeted micronutrient supplementation, and early identification and management of thyroid dysfunction can improve immune competence, reduce TB susceptibility, and enhance treatment outcomes in high-risk populations.
SN - 2813-7868
ER -