Diet-driven cardiometabolic dysfunction as a potential amplifier of antimicrobial resistance: mechanistic evidence, gut resistome ecology, and dual-action nutraceutical interventions
6 affiliations
- 1Department of Microbiology, School of Life Sciences, Federal University of Technology Akure, Akure, Nigeria
- 2Department of Biochemistry, School of Life Sciences, Federal University of Technology Akure, Akure, Nigeria
- 3Teddy Bioscience Laboratory, Ilara-Mokin, Nigeria
- 4Department of Microbiology, Adekunle Ajasin University, Akungba-Akoko, Nigeria
- 5Food Science and Agricultural Chemistry, School of Environmental and Agricultural Sciences, McGill University, Montreal, QC, Canada
- 6Department of Food Science and Technology, School of Agriculture and Agricultural Technology, Federal University of Technology Akure, Akure, Nigeria
Abstract
Over the last 30 years, two population-scale health crises have emerged as the epidemic of diet-related cardiometabolic disease (obesity, type 2 diabetes, hypertension, and cardiovascular disease) and the spread of antimicrobial resistance (AMR) as a major cause of death globally. Typically, they are investigated and controlled independently of each other. AMR may be amplified by diet-induced cardiometabolic dysfunction, which is not a parallel but an upstream, under-recognized burden. We describe four convergent pathways that might contribute to the increased risk of resistance. Impaired host immunity leading to recurrent, difficult-to-treat infection and repeated antibiotic exposure; obesity-associated pharmacokinetic changes leading to subtherapeutic antibiotic concentrations in the system; diet-induced gut dysbiosis that increases the reservoir of antibiotic-resistance genes (the gut resistome); and a bidirectional loop in which cumulative antibiotic exposure itself seems to increase cardiovascular risk. We then placed functional foods, nutraceuticals, and specific bioactive compounds as dual-action levers that act on the metabolic driver and, for a subset of molecules, directly on bacterial fitness, virulence, or the resistome. The clearest single-molecule example is developed in the form of berberine, which provides metabolic correction through the AMPK pathway, while simultaneously providing FtsZ-targeting and efflux-modulating antibacterial activity. We propose a testable framework, the metabolic–AMR augmentation loop, and highlight the gaps in evidence for longitudinal and interventional studies. If this framework proves to be robust, then diet-induced metabolic dysfunction correction could become a viable AMR-mitigation strategy on its own and one not currently employed in existing stewardship programs.
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BibTeX
@article{bayode2026dietdriven,
title = {{Diet-driven cardiometabolic dysfunction as a potential amplifier of antimicrobial resistance: mechanistic evidence, gut resistome ecology, and dual-action nutraceutical interventions}},
author = {Michael Tosin Bayode and Bashirat Akinbami and Christianah Titilayo Oladele and Ayomide Faith Okiti and Esther Oluwadarasimi Oyedeji},
journal = {Frontiers in Public Health},
year = {2026},
month = oct,
doi = {10.3389/fpubh.2026.1977386},
url = {https://doi.org/10.3389/fpubh.2026.1977386},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Diet-driven cardiometabolic dysfunction as a potential amplifier of antimicrobial resistance: mechanistic evidence, gut resistome ecology, and dual-action nutraceutical interventions
AU - Michael Tosin Bayode
AU - Bashirat Akinbami
AU - Christianah Titilayo Oladele
AU - Ayomide Faith Okiti
AU - Esther Oluwadarasimi Oyedeji
PY - 2026
DA - 2026/10/12
JO - Frontiers in Public Health
DO - 10.3389/fpubh.2026.1977386
UR - https://doi.org/10.3389/fpubh.2026.1977386
AB - Over the last 30 years, two population-scale health crises have emerged as the epidemic of diet-related cardiometabolic disease (obesity, type 2 diabetes, hypertension, and cardiovascular disease) and the spread of antimicrobial resistance (AMR) as a major cause of death globally. Typically, they are investigated and controlled independently of each other. AMR may be amplified by diet-induced cardiometabolic dysfunction, which is not a parallel but an upstream, under-recognized burden. We describe four convergent pathways that might contribute to the increased risk of resistance. Impaired host immunity leading to recurrent, difficult-to-treat infection and repeated antibiotic exposure; obesity-associated pharmacokinetic changes leading to subtherapeutic antibiotic concentrations in the system; diet-induced gut dysbiosis that increases the reservoir of antibiotic-resistance genes (the gut resistome); and a bidirectional loop in which cumulative antibiotic exposure itself seems to increase cardiovascular risk. We then placed functional foods, nutraceuticals, and specific bioactive compounds as dual-action levers that act on the metabolic driver and, for a subset of molecules, directly on bacterial fitness, virulence, or the resistome. The clearest single-molecule example is developed in the form of berberine, which provides metabolic correction through the AMPK pathway, while simultaneously providing FtsZ-targeting and efflux-modulating antibacterial activity. We propose a testable framework, the metabolic–AMR augmentation loop, and highlight the gaps in evidence for longitudinal and interventional studies. If this framework proves to be robust, then diet-induced metabolic dysfunction correction could become a viable AMR-mitigation strategy on its own and one not currently employed in existing stewardship programs.
SN - 2296-2565
ER -