
07/10/2025
Another reason why it's so important to focus on staying well, healthy and healthy aging as your best preventative tool for enjoyable old age and life in general :)
I recently posted a study suggesting that non-antibiotic drugs may have an unexpected disruptive effect on gut flora. Now a study from Australia has generated findings suggesting that certain drugs might also contribute to the development of antimicrobial resistance (AMR). While antibiotic overuse is a primary driver, emerging evidence suggests that non-antibiotic medications (NAMs) may also play a role. The authors note that this concern is particularly relevant in residential aged care facilities (RACFs), where both NAMs and antibiotics are frequently used.
They investigated nine NAMs commonly used in RACFs, including ibuprofen, diclofenac, paracetamol (acetaminophen), furosemide, metformin, atorvastatin, tramadol, temazepam and pseudoephedrine at gut-relevant concentrations in a test tube model of ciprofloxacin-induced mutagenesis in Escherichia coli.
Findings showed that ibuprofen and paracetamol significantly increased mutation frequency and conferred high-level ciprofloxacin resistance. Whole-genome sequencing identified mutations in the regulatory genes GyrA, MarR, and AcrR, with the latter two correlated with overexpression of a key drug efflux pump (a bacterial defense mechanism). Co-exposure to two NAMs further elevated mutation rates and ciprofloxacin resistance levels. Mutants showed ≥4 fold increased resistance, not only for ciprofloxacin but also for other antibiotic classes such as β lactams, levofloxacin and minocycline. Notably, ciprofloxacin resistance rose by up to 32 fold.
The authors suggested their findings underscored the overlooked role of NAMs in driving AMR and highlighted the need to reassess polypharmacy risks in aged care settings.
The University of South Australia’s official media release (dated 26 August 2025) emphasised that common painkillers "quietly fuel one of the world’s biggest health threats: antibiotic resistance" by increasing bacterial mutations and resistance.
However, it should be noted that this work needs to be repeated, and the findings were laboratory-generated and may not reflect the real-world situation.
For more information see: https://pubmed.ncbi.nlm.nih.gov/40855113/