Evidence map›Paper›PMID 42177305›Full record

ArticleTheory in biosciences = Theorie in den Biowissenschaften2026

Humans as an extended phenotype of their microbiota.

Michael Bordonaro

Abstract read
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In one paragraph

Article in Theory in biosciences = Theorie in den Biowissenschaften, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

1 author.

Michael BordonaroDepartment of Medical Education, Geisinger College of Health Sciences, 525 Pine Street, Scranton, PA, 18509, USA. mbordonaro1@geisinger.edu.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The human gastrointestinal system is colonized by microbiota, consisting of more than 100 trillion cells, which is essential for gastrointestinal development, nutrient absorption, and immune system function. Disruption of the microbiota has been linked to obesity, metabolic syndromes, inflammatory bowel disorders, and cancer. The microbiota has also been linked to nervous system development, and animal studies have suggested that the gut microbiota influences behavior of the host, with significant effects on host fitness. We hypothesize that at least some of these effects on host behavior, in part mediated by factors produced by the microbiota, have adaptive value for the microorganisms. There is evolutionary evidence of host-symbiont co-evolution; the microbiota may have evolved mechanisms to alter host behavior to enhance the fitness of the microbial species living within the host. In this sense, host behavior is an extended phenotype of its microbiota. Therefore, human behavior can also be interpreted as being an extended phenotype of the microbiota, which is a fundamental conclusion of this work. Analyzing the evolutionary tradeoffs with respect to the microbiota and its relationship with the host can inform optimized approaches to enhance host fitness. Such approaches can take advantage of the fitness "needs" of the microbiota as a tool to improve host health and well-being, thus decreasing human morbidity and mortality. We discuss methods for testing this hypothesis and consider its implications.

Indexed as

Gastrointestinal MicrobiomeMicrobiotaAnimalsBiological EvolutionGastrointestinal TractHumansPhenotypeSymbiosisBehaviorEvolutionExtended phenotypeMicrobiotaTransmission

Identifiers

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.