21/01/2026
The link between antibiotics, nutrition, and thoughts is physiological.
Antibiotics do not act only on “harmful” bacteria; they profoundly alter the gut microbiome, and the gut is a major neuroendocrine organ. Approximately 90% of serotonin is produced in the gut, along with precursors for dopamine, GABA, and acetylcholine. When the microbiome is disrupted, the synthesis and regulation of these neurotransmitters are altered, which directly affects mental state, clarity of thinking, anxiety, irritability, confusion, or the sensation commonly described as “brain fog”.
Source (gut serotonin and gut–brain axis):
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6469458/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4367209/
Broad-spectrum antibiotics reduce bacterial diversity, including species involved in the production of short-chain fatty acids, which are essential for maintaining the integrity of the intestinal barrier and regulating systemic inflammation. Chronic low-grade inflammation is a well-established mechanism that affects brain function and is associated with depression, anxiety, and cognitive changes. This connection is well documented in psychoneuroimmunology research.
Source (microbiome, inflammation, brain function):
https://pmc.ncbi.nlm.nih.gov/articles/PMC5641835/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5542322/
Another key mechanism is impaired absorption of B-complex vitamins. Antibiotics can reduce intestinal bacteria that synthesize vitamins such as B1, B6, B9, and B12, or they can damage the intestinal lining, decreasing the absorption of these nutrients from food. B vitamins are essential cofactors in neurotransmitter synthesis and neuronal energy metabolism. Deficiencies may manifest as mental fatigue, difficulty concentrating, repetitive thoughts, irritability, or depressive symptoms.
Source (B vitamins, microbiome, cognition):
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4772032/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5793267/
Antibiotics can also influence the gut–brain axis by increasing intestinal permeability. When the intestinal barrier is compromised, bacterial fragments can enter the bloodstream and trigger inflammatory responses that affect the brain. This can alter the function of the HPA axis (hypothalamic–pituitary–adrenal axis), increasing cortisol levels and promoting states of hypervigilance, anxiety, or mental exhaustion.
Source (intestinal permeability, inflammation, HPA axis):
https://www.frontiersin.org/articles/10.3389/fncel.2018.00403/full
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7213601/
There is also direct evidence that antibiotic use is associated with changes in mood and cognition. Observational studies have shown an association between repeated antibiotic use and an increased risk of depression and anxiety, particularly with frequent or long-term use. This is not a simple one-cause relationship, but the result of multiple interacting biological mechanisms.
Source (antibiotics and depression/anxiety):
https://jamanetwork.com/journals/jamapsychiatry/fullarticle/2521958
It is important to clarify what happens at the level of thoughts. Antibiotics do not “create” negative thoughts in a psychological sense, but they can modify the biological substrate on which thoughts arise. When neurotransmitters are dysregulated, inflammation is elevated, and neuronal energy is reduced, the brain tends to shift toward more rigid, repetitive, anxious, or depressive thought patterns. This is often perceived as “purely psychological,” when in reality a metabolic and neurochemical imbalance is present.
Source (neuroinflammation and cognition):
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6595548/
The data-based conclusion is this: antibiotics can influence thinking indirectly through changes in the microbiome, vitamin absorption, inflammation, and the stress axis. This does not invalidate emotional or experiential factors, but it explains why, in some individuals, noticeable mental changes appear during or after antibiotic treatment, even in the absence of a clear psychological trigger.
Source (integrative overview):
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6170050/