Best Practices: Antibiotics and Neurotransmitter Testing

By Heather Hydzik ND | February 17, 2021

Many providers are not aware that in order to get the most accurate neurotransmitter (NT) results, certain medications are best avoided. Antibiotics in particular can impact the accuracy of results because of their capacity to temporarily alter neurotransmitter levels and impact the gut microbiome, which is responsible for a portion of neurotransmitter production.

While the research is sparse on the effects of antibiotics on neurotransmitters, there are some known mechanisms of action. Some antibiotics that are able to cross the blood brain barrier can impact GABA levels in two ways: 1) they have the capacity to competitively inhibit the binding of GABA to GABA-A receptors and 2) antibiotics can eliminate strains of bacteria that are GABA producers. Some antibiotics have monoamine oxidase (MAO) inhibition effects, which can lead to excess breakdown of monoamine neurotransmitters like serotonin and dopamine. Sulfamethoxazole and sulfonamide drugs disrupt the enzyme sepiapterin reductase, which is involved in the biosynthesis of tetrahydrobiopterin (BH4), a cofactor necessary for the production of serotonin and dopamine. This leads to depletion of these neurotransmitters, as well as those that are derived from them (norepinephrine, epinephrine, and melatonin). Knowing this, it becomes apparent that testing neurotransmitter levels during a temporary course of antibiotic treatment will not provide the most accurate information about a patient’s endogenous neurotransmitter levels.

Specific data on neurotransmitter levels after the discontinuation of antibiotics does not appear to be available at this time. Some antibiotics such as metronidazole, have been associated in rare cases with CNS side effects such as psychosis, which may be due to MAO inhibition. This adverse effect usually resolves within 14 days after discontinuation. Most other CNS side effects (e.g. seizures, personality changes) which may signal neurotransmitter imbalance, also have been shown to resolve soon after discontinuation.

To determine how long it takes for an antibiotic to be completely eliminated from the body, this formula can be used: 5.5 x elimination half-life (in hours). For example, doxycycline has a maximum elimination half-life of 22 hours, so it would take 121 hours (5.5 x 22) or around 5 days before the medication is completely eliminated from the body. Other antibiotic elimination times can be calculated in the same way by looking up the half-life and using this formula. Imbalance in the gut flora was shown to generally resolve within 4 weeks after 3 individuals completed a course of ciprofloxacin, however certain strains still had not recovered by 6 months post-treatment, one example being V3_Clostridiales_refOTU_23. However, it is not necessary to delay neurotransmitter testing until the very last microbial strains return to normal levels as it can be beneficial to see how the recent medication has impacted the balance of neurotransmitters.

To achieve the most accurate neurotransmitter results following antibiotic use, it is suggested to complete the course of antibiotics as prescribed, then wait at least two weeks before sample collection to allow time for the medication to be eliminated and for neurotransmitters to return to endogenous levels.

References

Dethlefsen L, Huse S, Sogin ML, Relman DA. The pervasive effects of an antibiotic on the human gut microbiota, as revealed by deep 16S rRNA sequencing. PLoS Biol. 2008;6(11):e280. doi:10.1371/journal.pbio.0060280

Dethlefsen L, Relman DA. Incomplete recovery and individualized responses of the human distal gut microbiota to repeated antibiotic perturbation. Proc Natl Acad Sci U S A. 2011;108 Suppl 1(Suppl 1):4554-4561. doi:10.1073/pnas.1000087107

Antibiotic side effects explained. 26 September 2013. https://nccr-chembio.ch/news/antibiotic-side-effects-explained/ Accessed 10 Feb 2021.

Grill, Marie F, and Rama K Maganti. “Neurotoxic Effects Associated with Antibiotic Use: Management Considerations.” British Journal of Clinical Pharmacology 72, no. 3 (September 2011): 381–93.

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