How Microplastics May Disrupt the Human Gut Microbiome: What the Research Shows

Table of Contents

• Key Points
• Background: Why This Research Matters
• How the Research Was Conducted
• Key Findings: Changes in Gut Bacterial Composition
• Key Findings: Changes in Microbial Diversity
• Key Findings: Disruption of Metabolic Functions
• How Plastic Properties Influence Gut Effects
• Clinical Implications for Patients
• Limitations of the Research
• Recommendations and Next Steps
• Frequently Asked Questions
• Source Information

Key Points

• A review of 12 studies found that microplastics such as polyethylene, polystyrene, and PET can disrupt gut bacteria by reducing beneficial species and increasing harmful ones.
• Microplastic exposure impaired short-chain fatty acid production, which can weaken the intestinal barrier and promote inflammation.
• These gut changes were linked to intestinal diseases, metabolic syndrome, and chronic inflammation, with damage depending on plastic type, size, and concentration.
• The review included only 12 studies, mostly from a few countries, and could not determine safe exposure levels for microplastics.
• Patients can reduce exposure by avoiding plastic food containers, not heating food in plastic, choosing fresh foods, and supporting policies that reduce plastic pollution.

Background: Why This Research Matters

Global plastic waste production remains a critical environmental problem. Microplastics (MPs), which are plastic particles less than 5 millimeters in diameter, are now found throughout ecosystems worldwide. Nanoplastics (NPs) are even smaller particles, typically ranging from 1 to 100 nanometers in diameter, and they may form when microplastics break down further.

Both microplastics and nanoplastics are present in air, water, soil, household products, and food. This means that human exposure is unavoidable. People are exposed through three main routes: ingestion (eating and drinking), inhalation (breathing), and dermal contact (skin contact).

Researchers have already detected microplastics and nanoplastics in human tissues, including the lungs, placenta, feces, and blood. These findings raise urgent concerns about potential effects on human health. This widespread exposure has been associated with an increased risk of several acute and chronic health conditions. These conditions include inflammatory bowel disease (IBD), infertility, diabetes, and neurodegenerative disorders.

Among the known exposure routes, food consumption is considered the primary source of microplastics. Contamination in drinking water systems is also widespread. Because people drink large volumes of water daily, and because both tap water and bottled water contain microplastics, drinking water represents a critical and unavoidable pathway for chronic microplastic exposure.

Once ingested, microplastics can be absorbed through the gastrointestinal (GI) tract. They can disrupt gut microbiota by altering dietary habits, microbial metabolism, and immune responses.

The human microbiome is a diverse community of microorganisms that live in different parts of the body. These sites include the skin, oral cavity, reproductive system, and gut. The gut microbiome has drawn the most scientific attention because of its critical role in health and disease.

The gut microbiome plays a crucial role in human physiology. It regulates immune responses, metabolism, and intestinal integrity. Disruptions in microbial composition, also known as dysbiosis, have been linked to intestinal barrier dysfunction and metabolic disorders.

One essential role of the gut microbiome is the fermentation of dietary components. This process produces key metabolites such as short-chain fatty acids (SCFAs) and aryl hydrocarbon receptor (AhR) ligands. These metabolites are known to support intestinal barrier integrity and modulate immune responses. They provide evidence for the microbiome's influence on gastrointestinal and systemic health.

Ingested microplastics could interact with the intestinal environment before excretion. This interaction could potentially cause toxic effects on the gut. While several studies have reported detecting microplastics in human feces, a critical gap remains in synthesizing and analyzing how microplastics affect human microbiota composition, diversity, and function specifically in humans.

Existing reviews have largely centered on environmental contamination or findings from animal models. They have not addressed human-relevant microbiome alterations. Studies in mammals and aquatic organisms have consistently demonstrated that microplastics such as polystyrene (PS), polyethylene (PE), polyvinyl chloride (PVC), and polyethylene terephthalate (PET) accumulate in the intestinal tract. This accumulation leads to conditions such as IBD, irritable bowel syndrome (IBS), and colitis.

Polystyrene microplastics have also been shown to disrupt gut microbial composition and induce hepatic lipid metabolism disorders in mice. This suggests gut-level toxicity. Segment-specific intestinal damage, especially in the colon, has been linked to reduced microbiota diversity and impaired nutrient metabolism.

Exposure to microplastics worsened colitis in animal studies. It led to shorter colon length, increased inflammation, and reduced mucus secretion. These changes increase the risk of colorectal cancer. Microplastics have been increasingly suggested as potential environmental drivers of rising early-onset colorectal cancer rates.

Despite this growing concern, no study to date has analyzed how specific types of microplastics affect the human gut microbiome. There is also a lack of synthesized evidence on the biological mechanisms by which microplastics influence microbial communities.

This systematic review aims to examine the effects of microplastics on the human gut microbiome. It focuses on changes in microbial composition at the phylum, family, and genus levels, along with alterations in microbial diversity and richness. The review also looks into how microplastics disrupt microbial functions and metabolic pathways. It highlights the health implications of microplastic-induced dysbiosis and identifies consistent microbial patterns. Furthermore, the review assesses how microplastic-specific properties such as size, shape, and polymer type influence microbiome responses.

How the Research Was Conducted

This systematic review was conducted in adherence to the guidelines outlined in the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) framework. PRISMA offers a structured and transparent approach to identifying, selecting, and synthesizing relevant research. This approach ensures the reliability and generalizability of the findings.

The literature search was conducted in July 2024 using two major scientific databases: Scopus and PubMed. The search string used was "(microplastic OR nanoplastic) AND (human) AND (microbiome* OR microbiota* OR microbiomic*)." This search was designed to identify relevant studies. The search pertained to the impact of micro- and nano-plastics on the human gut microbiome. No publication date restrictions were imposed, thereby ensuring the inclusion of all pertinent publications.

The initial search resulted in a total of 320 records. Of these, 235 came from Scopus and 85 came from PubMed. The records covered studies published between 2021 and May 2024.

Predefined inclusion and exclusion criteria were applied to ensure an unbiased screening process. To focus on original data and findings, only primary research articles were included. This excluded secondary publications such as reviews and book chapters. This step avoided duplication of findings that were potentially already identified in those secondary publications.

Second, the language of publication was restricted to English. This restriction mitigated language barriers and potential bias associated with translation. Finally, all studies included had to directly address the impact of microplastics and nanoplastics on the human gut microbiome. Studies outside the scope of this specific human health concern, or those using animal models, were excluded.

To expedite the screening process and ensure efficiency, initial filtering was conducted within each database using built-in filters. These filters eliminated non-primary research and non-English studies. Following this initial filter, the search results from both databases were exported to EndNote 21, a reference management software, to identify and remove duplicate entries.

Next, titles and abstracts were screened against the predefined inclusion and exclusion criteria. This ensured that only English-language primary research studies investigating the effects of microplastics and nanoplastics on the human gut microbiome were advanced for full-text evaluation. A total of 18 studies met these criteria and were retrieved for full-text evaluation.

A full-text review of these 18 studies resulted in the exclusion of 6 additional studies. These excluded studies were either review articles or utilized animal models.

In the selection process, human cohort studies were prioritized due to their higher external validity and direct relevance. In vitro and in silico models were included only when they offered mechanistic insights that complemented findings of human studies.

The quality of observational studies was evaluated using the Risk Of Bias In Non-randomized Studies of Interventions (ROBINS-I) tool. Formal risk-of-bias assessments were not applied to in vitro or in silico studies. However, their methodological limitations were acknowledged and considered during the synthesis and interpretation of results.

Ultimately, this selection process yielded 12 high-quality studies for inclusion in this systematic review. These comprised cross-sectional observational studies (n = 5) and in vitro simulated digestion models using human-derived samples (n = 7).

Given the involvement of human participants or their biological materials, ethical approvals and informed consent were reported in most studies (n = 8). Two studies stated that ethical approval was not required under their national regulations for sample use (n = 2). Two studies (n = 2) did not provide information regarding ethical oversight.

The final included studies that met the inclusion criteria, particularly those focusing on human subjects or using human-derived samples, were geographically limited. Most studies originated from a small number of countries. These included China (n = 7), followed by Spain (n = 2), France (n = 2), and Indonesia (n = 1). This reflects the narrow geographic distribution of current human-relevant research on microplastic-microbiome interactions.

China's prominence in microplastic research is closely tied to its status as a major plastics producer and its central role in global plastic waste management. Studies frequently report high microplastic levels in China's inland waters, particularly in densely populated and industrialized regions. This likely drives the volume of research output in this area.

Key Findings: Changes in Gut Bacterial Composition

At the phylum level, gut bacterial composition varies across intestinal compartments. Microbiome analysis from fecal samples, conducted using simulated in vitro gastrointestinal models, showed distinct increases and decreases in specific phyla.

Polyethylene terephthalate (PET) was associated with shifts in bacterial communities. These shifts included increases in phyla such as Firmicutes, Synergistetes, and Desulfobacterota. PET exposure also led to reductions in Proteobacteria and Bacteroidetes in all compartments. These compartments included the ascending colon (AC), descending colon (DC), and transverse colon (TC).

Exposure to a mixture of microplastics was associated with an increase in Actinobacteria and a decrease in Bacteroidetes. Notably, in humans, Firmicutes and Bacteroidetes are the main constituents of the gut microbiome.

An increased proportion of various phyla could alter microbial ecosystems by consuming hydrogen and influencing metabolic pathways. This could potentially be implicated in inflammation and childhood nutrition.

At the genus level, several specific changes were observed across the reviewed studies:

• Polylactic acid (PLA) and polyvinyl chloride (PVC) microplastics disrupted microbial community structure. Beneficial genera such as Bifidobacterium, Faecalibacterium, and Prevotella were suppressed. Pathogenic species such as Escherichia-Shigella were enriched.
• PLA microplastics caused greater metabolic disruption while PVC microplastics caused stronger dysbiosis.
• Polyethylene (PE) microplastics promoted pathogenic taxa including Enterobacteriaceae, Desulfovibrionaceae, and Christensenellaceae. PE microplastics also reduced beneficial taxa including Akkermansia and Rikenellaceae.
• In a study of 60 postgraduate students in China, no significant species-level changes were observed. However, Bacteroidetes decreased and Actinobacteria increased at the phylum level.
• In a study of 22 healthy adults in Indonesia, no significant difference in microbiome composition, diversity, or genus abundance was found between groups with and without microplastic contamination.
• In a study of 18 mother-infant pairs in Shanghai, China, increased alpha diversity was observed. Positive correlations were found between polyamide (PA) and polyurethane (PU) and Escherichia-Shigella and Enterococcus. Positive correlations were also found between polystyrene (PS), PET, and PVC and Rikenellaceae.
• In a study of 40 healthy participants in China, high exposure to microplastics increased Bifidobacterium, Streptococcus, and Fusobacterium. High exposure decreased Dorea, Ruminococcus torques group, Muribaculaceae, and Coprococcus.
• In a study of 32 healthy adults in China, PET microplastics reduced short-chain fatty acid levels, including acetate, butyrate, and total SCFAs.
• In a study of 10 healthy volunteers in China, PE microplastics slightly increased Bacteroidetes.

In a study of 52 adult participants in Spain, PET microplastics decreased Bacteroidetes, Parabacteroides, and Alistipes across all compartments. Increases in pro-inflammatory genera were observed. These included Escherichia/Shigella, Cloacibacillus, Bilophila, Eisenbergiella, Megasphaera, and Oscillibacter.

PET microplastics caused shifts in phyla. Firmicutes, Desulfobacterota, and Synergistetes increased. Bacteroidetes decreased. These shifts occurred particularly in the CT and DC compartments.

Key Findings: Changes in Microbial Diversity

Microplastic exposure significantly reduced alpha diversity in the post-exposure group in one study of 60 postgraduate students in China. Alpha diversity is a measure of how many different types of bacteria are present in a sample. Beta diversity changes were also observed, indicating delayed dysbiosis. No significant species-level changes were observed in the post-exposure group.

In a study of 18 mother-infant pairs in Shanghai, China, increased alpha diversity was observed in meconium samples. Meconium is the first stool passed by a newborn. Particle size (100-150 micrometers) was positively correlated with Rikenellaceae and negatively correlated with alpha diversity in meconium.

In a study of 22 healthy adults in Indonesia, no significant difference in microbiome composition, diversity, or genus abundance was found between groups with and without microplastic contamination.

In a study of 40 healthy participants in China, high exposure to microplastics was associated with changes in specific bacterial groups. Bifidobacterium, Streptococcus, and Fusobacterium increased. Dorea, Ruminococcus torques group, Muribaculaceae, and Coprococcus decreased.

Key Findings: Disruption of Metabolic Functions

Microplastics impaired short-chain fatty acid (SCFA) production in multiple studies. SCFAs are key metabolites that support intestinal health. Reduced SCFA production can weaken the intestinal barrier and promote inflammation.

In a study of 32 healthy adults in China, PET microplastics reduced SCFA levels, including acetate, butyrate, and total SCFAs. Functional pathway analysis showed increased energy metabolism and amino acid metabolism. Decreased lipid metabolism, carbohydrate metabolism, xenobiotic metabolism, and immune-related pathways were also observed.

In a study of 10 healthy volunteers in China, PE microplastics inhibited benzo[a]pyrene (BaP) metabolism and lipopolysaccharide (LPS) synthesis. LPS is a component of certain bacterial cell walls that can trigger inflammation.

In a study of 52 adult participants in Spain, PET microplastics altered metabolic activity. Acetate increased while propionate and butyrate decreased. Butyrate is a key SCFA that supports colon health. The potential for AhR activity was reduced. AhR is a receptor that helps regulate immune responses and intestinal barrier function.

In a study of 6 healthy volunteers in China, PLA microplastics enriched the steroid degradation pathway and induced xenobiotic metabolism. Xenobiotic metabolism refers to how the body processes foreign substances. PLA microplastics also affected the FOXN1 gene and the SIGMAR1 gene.

In a study of 4 healthy adults in France, PE microplastics did not significantly impact SCFA activity. However, PE microplastics did reduce AhR activity.

In a study of 4 healthy adults in France, PE microplastics promoted Desulfovibrionaceae and Christensenellaceae. PE microplastics reduced beneficial taxa including Akkermansia and Rikenellaceae.

In a study of 10 healthy volunteers in China, PE microplastics slightly increased Bacteroidetes. The arrows in the original table indicate increased and decreased abundance or levels, respectively.

How Plastic Properties Influence Gut Effects

The extent of microbiome disruption is influenced by microplastic-specific properties. These properties include the type of plastic, the size of the particles, and the concentration of exposure.

Different types of plastic had different effects. Polylactic acid (PLA) microplastics caused greater metabolic disruption. Polyvinyl chloride (PVC) microplastics caused stronger dysbiosis. Polyethylene terephthalate (PET) microplastics caused shifts in bacterial communities across all colon compartments.

Particle size also mattered. In a study of 18 mother-infant pairs in Shanghai, China, particle size (100-150 micrometers) was positively correlated with Rikenellaceae and negatively correlated with alpha diversity in meconium. In another study, microplastics with a particle size of 20-500 micrometers were detected in fecal samples.

Concentration of exposure also influenced effects. In a study of 40 healthy participants in China, high exposure to microplastics was associated with changes in specific bacterial groups. The high-exposure group worked in a plastic factory. The low-exposure group lived within 1 kilometer of Huainan Xiuai Park in Chengdu, China.

In a study of 60 postgraduate students in China, the exposure group had a detected concentration of 24.650 items per gram. The control group had a detected concentration of 19.645 items per gram. The post-exposure group had a detected concentration of 9.805 items per gram. The particle size was 20-500 micrometers.

In a study of 22 healthy adults in Indonesia, microplastics detected included high-density polyethylene (HDPE), polypropylene (PP), and polystyrene (PS). No significant difference in microbiome composition, diversity, or genus abundance was found between groups with and without microplastic contamination.

In a study of 18 mother-infant pairs in Shanghai, China, microplastics detected included polyamide (PA), polyurethane (PU), PET, PS, PVC, and polyethylene (PE). The particle size was 20-500 micrometers.

In a study of 40 healthy participants in China, microplastics detected included rayon (RY), polyethylene (PE), polyethylene terephthalate (PET), and polyacrylonitrile (PAN). The particle size was 20-500 micrometers.

In a study of 52 adult participants in Spain, microplastics detected included PET. The particle size was 160 plus or minus 110 micrometers.

In a study of 10 healthy volunteers in China, microplastics detected included PE. The particle size was 30-140 micrometers.

In a study of 6 healthy volunteers in China, microplastics detected included PLA. The particle size was approximately 5 millimeters.

In a study of 4 healthy adults in France, microplastics detected included PE. The particle size was 1-10 micrometers. The dose was 12 milligrams per gram.

Clinical Implications for Patients

The findings of this systematic review suggest that microplastics are emerging environmental risk factors with tangible implications for human health. Exposure to microplastics induces gut dysbiosis. This dysbiosis is marked by a loss of beneficial genera and enrichment of pathogenic species.

Microplastics also impair short-chain fatty acid production. They alter metabolic functions and modulate immune pathways. These changes contribute to intestinal diseases, metabolic syndrome, and chronic inflammation.

The disruption of the gut microbiome by microplastics could have several health consequences for patients:

• Reduced levels of beneficial bacteria such as Bifidobacterium, Faecalibacterium, and Akkermansia. These bacteria help maintain intestinal health and reduce inflammation.
• Increased levels of harmful bacteria such as Escherichia-Shigella and Enterobacteriaceae. These bacteria can cause infections and trigger inflammation.
• Decreased production of short-chain fatty acids such as butyrate. Butyrate is a key energy source for colon cells and helps maintain the intestinal barrier.
• Increased intestinal permeability, sometimes called leaky gut. This allows bacteria and toxins to pass through the intestinal wall into the bloodstream.
• Chronic inflammation that could contribute to inflammatory bowel disease (IBD), irritable bowel syndrome (IBS), and colorectal cancer.
• Metabolic disruption that could contribute to metabolic syndrome and diabetes.

The review also found that microplastics can modulate immune pathways. The aryl hydrocarbon receptor (AhR) is a receptor that helps regulate immune responses and intestinal barrier function. Reduced AhR activity was observed in several studies. This reduction could impair the body's ability to maintain a healthy intestinal barrier and control inflammation.

Microplastics have been increasingly suggested as potential environmental drivers of rising early-onset colorectal cancer rates. The review found that exposure to microplastics worsened colitis in animal studies. This worsening led to shorter colon length, increased inflammation, and reduced mucus secretion. These changes increase the risk of colorectal cancer.

The review also found that microplastics can alter xenobiotic metabolism. Xenobiotic metabolism refers to how the body processes foreign substances, including drugs and environmental toxins. Disruption of this process could affect how the body handles medications and other chemicals.

Limitations of the Research

The review identified several limitations in the current research on microplastics and the human gut microbiome. These limitations affect how confidently the findings can be applied to patient care.

First, direct evidence of microplastics' impact on human health remains lacking. Numerous studies have shown harmful effects in tissue cultures and animal models. However, translating these findings to humans requires more human-relevant research.

Second, the included studies were geographically limited. Most studies originated from a small number of countries. These included China (n = 7), Spain (n = 2), France (n = 2), and Indonesia (n = 1). This narrow geographic distribution limits the generalizability of the findings to other populations.

Third, the studies used different methodologies. Some studies used fecal samples analyzed in in vitro models designed to mimic the human gastrointestinal system. A smaller number of studies focused on meconium samples. This variation in methodology makes it difficult to compare results across studies.

Fourth, formal risk-of-bias assessments were not applied to in vitro or in silico studies. Their methodological limitations were acknowledged and considered during the synthesis and interpretation of results. However, the lack of formal assessment limits the strength of conclusions that can be drawn from these studies.

Fifth, the review included only 12 studies. This small number of studies limits the robustness of the conclusions. More research is needed to confirm the findings and to understand the long-term health effects of microplastic exposure.

Sixth, the studies used different types of microplastics at different concentrations and particle sizes. This variation makes it difficult to determine which specific properties of microplastics are most harmful.

Seventh, the review could not determine safe exposure levels for microplastics. The studies did not provide enough data to establish a threshold below which microplastics do not affect the gut microbiome.

Recommendations and Next Steps

The review authors emphasize the importance of additional research to address gaps in existing studies. They provide a critical foundation for future risk assessment and targeted research to better understand microplastics' impact on human health.

To fully understand the health concerns associated with microplastics long-term, human-relevant studies with standardized methodologies are urgently needed. These studies should define safe exposure levels and guide policies aimed at reducing microplastic-related health risks.

Based on the findings, patients can take several practical steps to reduce their exposure to microplastics:

1. Reduce consumption of food and water from plastic containers. Microplastics are present in both tap water and bottled water.
2. Avoid heating food in plastic containers. Heat can cause plastics to break down and release more particles.
3. Choose fresh foods over highly processed foods. Highly processed foods may contain more microplastics from packaging and processing.
4. Support policies that reduce plastic pollution. Reducing plastic waste at the source is the most effective way to reduce human exposure.
5. Stay informed about ongoing research. As new studies emerge, recommendations for reducing exposure may change.

The review authors also call for standardized methodologies in future research. Standardized methods would allow researchers to compare results across studies and to draw more robust conclusions. They also call for studies that define safe exposure levels. Safe exposure levels would help guide policies aimed at reducing microplastic-related health risks.

The authors note that the extent of disruption is influenced by microplastic-specific properties such as type, size, and concentration. Future research should investigate how these properties affect the gut microbiome. This research could help identify which types of plastics are most harmful and inform strategies to reduce exposure.

The authors also highlight the need for research on the biological mechanisms by which microplastics influence microbial communities. Understanding these mechanisms could lead to new treatments or preventive strategies for microplastic-induced dysbiosis.

Finally, the authors emphasize that microplastics are emerging environmental risk factors with tangible implications for human health. Reducing plastic pollution and human exposure to microplastics could have significant public health benefits.

Frequently Asked Questions

What did the research find about microplastics and gut bacteria?

A review of 12 studies found that common plastics such as polyethylene, polystyrene, and PET can disrupt gut bacteria. Exposure reduced beneficial species, increased harmful ones, and impaired production of protective short-chain fatty acids. These changes were linked to intestinal diseases, metabolic syndrome, and chronic inflammation. The extent of damage depended on the plastic's type, size, and concentration.

How are people exposed to microplastics?

People are exposed through three main routes: ingestion (eating and drinking), inhalation (breathing), and skin contact. Food consumption is considered the primary source, and drinking water is also a critical pathway because both tap and bottled water contain microplastics. Microplastics and nanoplastics are present in air, water, soil, household products, and food, making exposure unavoidable.

What health conditions have been linked to microplastic exposure?

Exposure has been associated with an increased risk of several conditions, including inflammatory bowel disease, infertility, diabetes, and neurodegenerative disorders. The review also found that microplastic-induced gut changes were linked to intestinal diseases, metabolic syndrome, and chronic inflammation. However, direct evidence of microplastics' impact on human health remains lacking, and more human-relevant research is needed.

Can microplastics cause leaky gut or inflammation?

The review found that microplastics can impair short-chain fatty acid production, which can weaken the intestinal barrier and promote inflammation. Reduced levels of beneficial bacteria and increased harmful bacteria were also observed. These changes may lead to increased intestinal permeability, sometimes called leaky gut, and chronic inflammation that could contribute to conditions like IBD, IBS, and colorectal cancer.

What are the limitations of this research?

The review included only 12 studies, mostly from a few countries, so findings may not apply to all populations. Studies used different methods, plastic types, sizes, and concentrations, making comparisons difficult. Formal risk-of-bias assessments were not applied to in vitro studies. The review could not determine safe exposure levels, and direct evidence of microplastics' impact on human health remains lacking.

What practical steps can I take to reduce microplastic exposure?

Patients can reduce consumption of food and water from plastic containers, avoid heating food in plastic containers, and choose fresh foods over highly processed foods. Supporting policies that reduce plastic pollution and staying informed about ongoing research are also recommended. These steps are based on the review's findings and aim to lower exposure to microplastics.

What does it mean if a study found no significant changes in gut microbiome?

In a study of 22 healthy adults in Indonesia, no significant difference in microbiome composition, diversity, or genus abundance was found between groups with and without microplastic contamination. This suggests that not all studies observed effects, and results can vary. The review noted that findings depend on plastic type, size, concentration, and study population.

If I have gut symptoms and I'm worried microplastics are causing dysbiosis, when should I seek a second opinion?

Microplastic exposure is linked to gut dysbiosis, reduced beneficial bacteria such as Bifidobacterium and Akkermansia, lower butyrate and other short-chain fatty acids, and increased intestinal permeability. Direct evidence in humans remains limited, the 12 reviewed studies were geographically narrow, and no safe exposure level has been established, so findings cannot be applied confidently to an individual. A second opinion can help when symptoms persist, when inflammatory bowel disease, irritable bowel syndrome, or metabolic concerns are being considered, or when the basis for a diagnosis or plan is unclear. Diagnostic Detectives Network provides independent expert second opinions.

Source Information

Original article title: Impact of microplastics on the human gut microbiome: a systematic review of microbial composition, diversity, and metabolic disruptions.

Authors: Thin ZS, Chew J, Ong TYY, Raja Ali RA, Gew LT.

Publication: BMC Gastroenterology (2025) 25:583

DOI: https://doi.org/10.1186/s12876-025-04140-2

Correspondence: Lai Ti Gew (janeg@sunway.edu.my)

Note: This patient-friendly article is based on peer-reviewed research. The original article is an open-access systematic review published under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.