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Habitual Coffee Intake Shapes the Gut Microbiome and Modifies Host Physiology and Cognition

ABSTRACT:

Coffee influences multiple physiological processes, including gut function, stress, cognition, and the microbiome. However, the mechanisms underlying these effects remain poorly understood. In this study, we examined coffee’s impact on the microbiota–gut–brain axis—a bidirectional communication pathway between the gut microbiome and the brain—and assessed whether these effects occur independently of caffeine in healthy participants. Significant group differences emerged in faecal microbiome composition, with coffee drinkers showing increased relative abundance of Cryptobacterium and Eggerthella species, alongside reduced levels of the metabolite’s indole-3-propionic acid, indole-3-carboxyaldehyde, and the neurotransmitter γ-aminobutyric acid. Behaviourally, coffee drinkers exhibited greater impulsivity and emotional reactivity, whereas non-coffee drinkers demonstrated better memory performance. Some alterations in the faecal metabolome were reversible following coffee abstinence, and reintroduction triggered acute microbiome changes independent of caffeine. An integrated model identified nine key metabolites—including theophylline, caffeine, and selected phenolic acids—strongly linked to microbial species and cognitive measures. These findings reveal previously unrecognised effects of coffee on the microbiota–gut–brain axis, suggesting that microbiome profiles could potentially predict coffee consumption patterns and highlighting a close association between coffee intake and gut microbial composition.

INSTRUMENT(S): Liquid Chromatography MS - negative - reverse-phase, Liquid Chromatography MS - positive - reverse-phase

PROVIDER: MTBLS13494 | MetaboLights | 2026-04-07

REPOSITORIES: MetaboLights

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			Action	DRS
	a_MTBLS13494_LC-MS_negative_reverse-phase_metabolite_profiling-1.txt	Txt
	a_MTBLS13494_LC-MS_negative_reverse-phase_metabolite_profiling.txt	Txt
	a_MTBLS13494_LC-MS_positive_reverse-phase_metabolite_profiling-1.txt	Txt
	a_MTBLS13494_LC-MS_positive_reverse-phase_metabolite_profiling.txt	Txt
	i_Investigation.txt	Txt

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Project description:Background: Cadmium (Cd) is a heavy metal recognized as a neurotoxicant. However, the mechanisms underlying its neurotoxicity remain poorly understood. The gut-brain axis, a bidirectional communication pathway between the central nervous system and the gut microbiome, has been linked to various neurological disorders. Because the gut microbiome is a known target of Cd, it is important to investigate whether the gut-brain axis mechanistically contributes to the Cd-induced neurotoxicity. Objective: In our initial exploration of the role of the gut-brain axis in modulating Cd neurotoxicity on cognition, we investigated whether Cd exposure induces gut dysbiosis before the onset of cognitive deficits and explored the potential link between gut microbiome alterations and Cd-induced cognitive deficits. Methods: Adult male mice were exposed to 3 mg/L Cd via drinking water for nine weeks. Behavioral assessments were conducted throughout the exposure period to evaluate cognitive function. Fresh fecal pellets were collected weekly to monitor gut microbiome composition. The effects of Cd on the hippocampus and intestine were analyzed using transcriptomics and mass spectrometry (MS)-based metabolomics. Results: Cd exposure resulted in hippocampus-dependent learning and memory deficits, first observed at four weeks into exposure. RNA sequencing of the hippocampus at the terminal time point revealed reduced expression of genes involved in cognition and neuroinflammation in Cd exposed mice. Metagenomic shotgun sequencing showed that Cd-induced gut dysbiosis preceded the onset of cognitive impairments, with specific bacterial species associated with Cd-induced cognitive deficits, confirmed by using the cor.test function (Spearman correlation, p < 0.1) in R. Furthermore, Cd exposure compromised intestinal barrier integrity, increased inflammatory cytokines levels, and altered the levels of neuroactive microbial metabolites in mice, which may be linked to Cd-induced gut dysbiosis Conclusion: Our study is the first to show that Cd exposure triggers gut microbial shifts before the onset of cognitive deficits, accompanied by increased intestinal permeability and elevated proinflammatory biomarkers in both the intestine and brain at the terminal time point. These findings suggest a potential critical role of gut-brain axis in modulating Cd neurotoxicity and underscore the need for future research to elucidate the mechanistic involvement of gut microbiome as a potential target for mitigating Cd-induced cognitive decline.

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Habitual Coffee Intake Shapes the Gut Microbiome and Modifies Host Physiology and Cognition

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