Chronic Antibiotic Use, Gut Microbiota Dysbiosis, and Increased Risk of Colorectal Cancer: An Emerging Threat

ABSTRACT

Background and Aims

The gut microbiota plays a vital role in host health by regulating metabolic processes, immune function, and epithelial barrier functions. Chronic use of antibiotics can alter this environment and introduce gut dysbiosis, which is defined as an alteration of microbial communities characterized by a loss of beneficial microbes and overgrowth of pathogenic microbes. Gut dysbiosis is increasingly associated with the development and progression of colorectal cancer (CRC). We explored the relationship between long‐term antibiotic exposure, gut microbiota dysbiosis, and CRC risk, as well as strategies for preventing and restoring gut microbiomes.

Methods

Relevant information was extracted from published articles available in PubMed, Scopus, and Google Scholar. The keywords “Gut,” “Dysbiosis,” “Antibiotic,” “Colorectal,” and “Microbiota” were used to search for relevant information.

Results

Studies have demonstrated that chronic antibiotic exposure significantly reduces microbial diversity, particularly by decreasing beneficial species (e.g., Lactobacillus, Bifidobacterium, and Faecalibacterium), while favoring pathogenic species (e.g., Klebsiella pneumoniae and Enterococcus faecium). Antibiotic‐induced dysbiosis reduces the production of microbial metabolites, including short‐chain fatty acids, which are essential for supporting epithelial integrity and immune homeostasis. Prior antibiotic use is associated with a 13% increased risk of CRC, with antibiotic‐induced microbiota alterations lasting for months to years. Several factors, including diet, pollution, and over‐the‐counter access to antibiotics in low‐and middle‐income countries, may contribute to an increased risk of dysbiosis and CRC. Additionally, interventions such as dietary fiber, probiotic supplementation, fecal microbiota transplantation, next‐generation probiotics, and phage therapy may be potential strategies to restore the microbiome and achieve gut health.

Conclusion

Substantial use of antibiotics may alter the gut microbiota and increase the risk of CRC. To mitigate this risk, it is essential to practice prudent antibiotic use and adopt dietary, probiotic, and microbiome‐restoring practices to support the health of the gut microbiome.

1. Introduction

The human gut microbiota is composed of trillions of bacteria, viruses, fungi, and other microorganisms residing together in a complex ecosystem [1, 2]. These microorganisms are essential for a wide range of physiological functions, including nutrient metabolism, pathogenesis, immune system regulation, and maintenance of the gut barrier [3, 4]. The hallmark of a healthy gut microbiome is its high diversity, meaning that a wide variety of microbial species coexist in the gut, contributing to homeostasis [5].

However, antibiotics are indiscriminate and do not separate pathogenic bacteria from beneficial bacteria [6]. Therefore, the use of antibiotics is widespread and often done indiscriminately, with notable changes to the gut microbiota, which is defined as dysbiosis [6]. Dysbiosis is characterized by a decrease in microbial diversity in favor of pathogenic microorganisms against beneficial bacteria [7]. As the implications of these changes to the microbiome accumulate, they may adversely affect gut health, impair the immune function, and increase the risk of chronic diseases, including inflammatory conditions and cancer [8, 9, 10].

In recent years, there has been increasing awareness that chronic antibiotic use not only disrupts the microbial balance but also has long‐lasting effects that go beyond infection management. These effects significantly affect colorectal carcinogenesis, as ongoing dysbiosis can lead to inflammation, production of genotoxic metabolites, and immune system imbalance. Therefore, this review aims to explain how extended antibiotic use alters the gut microbiota, increases the risk of colorectal cancer (CRC), and emphasizes preventive and restorative strategies, including dietary, probiotic, and microbiome‐targeted approaches, to maintain gut health and reduce the disease burden.

2. Methods

For this review, we examined multiple databases, PubMed, Scopus, and Google Scholar, using various relevant terms. The terms included “Gut,” “Dysbiosis,” “Antibiotic,” “Colorectal,” and “Microbiota.” This effort did not involve any data collection or analysis but focused on reviewing and comparing the findings from several notable scientific studies related to these terms.

3. Chronic Use of Antibiotics and the Development of Gut Dysbiosis

The administration of antibiotics, particularly broad‐spectrum antibiotics, can lead to long‐lasting alterations in the composition of gut microbes. Antibiotics such as clindamycin, fluoroquinolones, and flucloxacillin significantly diminish microbial diversity and upset the delicate balance of beneficial and harmful bacteria [11]. Such reductions in diversity can last for months or even years after the discontinuation of antibiotics.

Research indicates that broad‐spectrum antibiotics, which affect a wide array of bacteria, have the greatest long‐lasting alterations in the gut microbiota, causing a loss of beneficial bacteria, such as Lactobacillus, Bifidobacterium, and Faecalibacterium [12], and an increase in the growth of opportunistic pathogens, such as Klebsiella pneumoniae and Enterococcus faecium [13], as well as bacteria linked to infections or diseases, such as Clostridium difficile [14]. Additionally, dysbiosis associated with the alteration of microbial flora creates a microenvironment conducive to chronic inflammation, dysregulated immune responses, and cancer.

Studies have demonstrated that individuals who have taken antibiotics within the last year show the most significant decrease in the composition and diversity of gut microbes [15, 16]. However, those who had consumed antibiotics several years prior still demonstrated significant differences in microbial composition. This suggests that the consequences of antibiotic use may last for years, evolving the microbiota to an altered state that is more susceptible to disease, including more severe forms of CRC.

4. Antibiotic‐Induced Dysbiosis and Risk of CRC

There is an increasing amount of data demonstrating positive associations between dysbiosis of gut microbes and the risk of developing cancer [17, 18]. A disturbed microbiome contributes to CRC in multiple aspects, such as chronic inflammation, genotoxin production, and immune system changes. Emerging evidence suggests that some specific bacterial species, such as Fusobacterium nucleatum and Bacteroides fragilis, directly contribute to CRC [19, 20].

Inflammation is one of the primary mechanisms by which dysbiosis may contribute to CRC. In a healthy gut, beneficial bacteria contribute to the integrity of the gut lining and the immune response. Conversely, the pathogenic bacteria associated with dysbiosis can disrupt this balance. For instance, F. nucleatum, which is found in the gut microbiome of patients with CRC, produces virulence factors that permit it to bind to epithelial cells in the colon, allowing it to promote local inflammation and evade immune recognition [21, 22, 23]. It is well established that chronic inflammation is a driver of carcinogenesis; thus, the dysbiotic chronic inflammatory state can cause cellular injury, DNA mutations, and eventually tumorigenesis.

Another mechanism contributing to CRC is microbial production of genotoxins or toxins that damage genetic integrity and increase the risk of cancer [24, 25]. Certain bacteria can be involved in dysbiosis, such as B. fragilis, which produces toxins that damage DNA in colon cells and promote cancer initiation [26, 27]. Furthermore, dysbiosis can change the gut environment through the production of metabolites that promote or inhibit local inflammation and the risk of cancer [8, 10].

Broad‐spectrum antibiotics have been shown to increase the risk [28]. The most pronounced effects are associated with antibiotics that exert long‐lasting effects on gut diversity, such as beta‐lactams, which can lead to drastic reorganization of microbial communities and enhance the risk of CRC [29]. The association between chronic antibiotic use and CRC risk necessitates caution and limits around the prescription of antibiotics, especially for prolonged periods of use, particularly among certain populations, such as the elderly and young.

5. Long‐Term Effects of Antibiotics on Gut Microbiota

The long‐term effects of the chronic use of antibiotics extend beyond the challenges that individuals face in the immediate aftermath of taking an antibiotic. Several studies have shown that gut dysbiosis induced by chronic antibiotic use may persist for years following the end of antibiotic treatment, as some changes in microbial composition may persist for several years [30, 31]. This type of antibiotic‐induced dysbiosis establishes a sustained state of dysbiosis (or microbial imbalance), which can have long‐term health implications, namely, a heightened risk of CRC.

The long‐term consequences of chronic antibiotic use have specific implications for antibiotic use in early life. The gut microbiome is still developing throughout the first year of life, and exposure to antibiotics during this period of significant development can lead to long‐term changes in the immune function and/or microbial composition. The same early life developmental consequences of antibiotics are observed as long‐term impacts on alterations in gut microbiota and increased susceptibility to chronic diseases such as CRC. The larger disease implications of these consequences are what make coercive stewardship particularly important when weighing the benefits of antibiotics versus the risks, especially among young children.

6. Scientific and Research Enhancements

Antibiotics are known to cause a significant loss of gut microbial diversity, which may also increase the risk of CRC. Broad‐spectrum antibiotics can affect the abundance of 30% of the bacteria in the gut community, resulting in rapid and significant decreases in taxonomic richness, diversity, and evenness [32]. Antibiotics can also change the gut microbiota for extended periods, even for months and years [32]. In particular, one study found that patients who had received antibiotics as much as 15 years before being diagnosed were more likely to develop CRC [OR = 1.90, 95% CI, 1.61–2.19, p < 0.001] [33]. Another study reported that individuals who had used antibiotics had a 13% greater risk of colorectal tumor development than individuals who had never used antibiotics [OR = 1.13, 95% CI, 1.04–1.22, p < 0.01] [34].

Beneficial bacteria, such as Roseburia intestinalis, are thought to be critical members of the gut microbiota that support gut homeostasis and inhibit CRC [35]. Other studies reported that levels of Akkermansia muciniphila were lower in CRC patients and associated with progressive cancer development [36], while others stated that Akkermansia might have a protective role against CRC but also have an association with tumor growth [37]. As a probiotic, probiotic formulations of A. muciniphila could be a novel approach for the treatment or management of metabolic and inflammatory‐related diseases because of its ability to reduce and modulate mucin in the gut [37].

Gut microbiota‐derived metabolites can modulate the responses of immune cells, including T cells, B cells, dendritic cells, and macrophages [38]. Increasing evidence suggests that even metabolites derived from dietary fiber (DF) produced by commensal bacteria play essential roles in modulating immune balance in health and disease. Short‐chain fatty acids (SCFAs) such as acetate, propionate, and butyrate are primary DF metabolites. They are produced by specialized commensal microorganisms that have the capacity to digest DF to produce simple saccharides and metabolize saccharides to SCFAs [39]. SCFAs act on various cells to modulate important biological processes, including host metabolism, intestinal function, and the immune system [39]. SCFAs contribute to the maintenance of the epithelial barrier function as well as intestinal homeostasis. However, it has been suggested in recent work that SCFAs impact therapeutics against cancer as well as immunomodulate both anti‐tumor immune responses and inflammation‐related side effects [40].

7. Antibiotic Stewardship Focus

Prolonged disruption of gut microbiota has been associated with antibiotic use and the risk of developing CRC. The World Health Organization (WHO) and the Centers for Disease Control and Prevention (CDC) encourage prescribers to use antibiotics only when appropriate and to use narrow‐spectrum antibiotics when possible as part of antibiotic stewardship and combating the antibiotic resistance crisis. Narrow‐spectrum antibiotics (such as penicillin V) are usually less disruptive to the gut microbiota than broad‐spectrum antibiotics, as the former are likely to only target specific bacterial species and spare beneficial microbes. Clindamycin is a broad‐spectrum antibiotic that is effective against numerous species of bacteria (including Gram‐positive organisms and anaerobic bacteria). Studies have demonstrated that clindamycin can have devastating consequences for the gut microbiome, leading to the overgrowth of pathogenic bacteria such as C. difficile and prolonged effects on the gut microbiota ecosystem, with reduced gut microbiota signatures lasting nearly 2 years after a short‐term course of antibiotics [41, 42]. Many beta‐lactam antibiotics (such as amoxicillin‐clavulanate), which are broad‐spectrum antibiotics, are widely known to have significant effects on the gut microbiota [43]. Fluoroquinolone antibiotics are broad‐spectrum antibiotics capable of potent activity against many bacterial species, including Gram‐negative bacteria [44]. The use of herbal antimicrobials (e.g., berberine, garlic extract, curcumin) and immunomodulatory options (e.g., vitamin D, beta‐glucans, probiotics) as alternatives to antibiotics may aid in preserving gut microbes and help minimize the long‐term effects of antibiotic‐induced dysbiosis and the risk of CRC.

An overview of several antibiotics, their classes, and their effects on the gut microbiota is shown in Table 1.

Table 1.

Impact of antibiotics on gut microbiota.

Antibiotic	Class	Microbiota impact
Trimethoprim‐sulfamethoxazole	Sulfonamide	Impacts both Gram‐positive and Gram‐negative bacteria [45] Affect the abundance, diversity, and composition of gut microbiota [46]
Cephalexin	Beta‐lactam	Changes in gut flora [47]
Azithromycin	Macrolide	Decreases gut bacterial diversity [48]
Metronidazole	Nitroimidazole	Alters microbiota with an increase in bifidobacteria and enterobacteria [49]
Vancomycin	Glycopeptide	Reduces fecal microbial diversity with a decrease of Gram‐positive bacteria and an increase of Gram‐negative bacteria [50]
Amoxicillin	Beta‐lactam	Promotes the growth of proteobacteria such as Escherichia coli, and decreases the abundance of beneficial organisms [51]
Clindamycin	lincosamide	Markedly reduces the diversity of the intestinal microbiota [52]
Ciprofloxacin	Fluoroquinolone	Reduces the diversity of the intestinal microbiota [53] Increases the Firmicutes to Bacteroidetes ratio [54]

8. Microbiome Restoration Techniques

Chronic antibiotic exposure correlates with an increased incidence of CRC, primarily through alterations in the gut microbiome and subsequent dysbiosis. Multiple strategies, including diet, diet‐derived microbiota therapies, and new development therapies, will be explored to mitigate this chronic disease state and improve health. Dietary interventions include resistant starch and polyphenol‐rich foods, both of which promote the growth of beneficial bacteria [55, 56]. Additionally, DF, as prebiotics, can be digested and fermented by beneficial gut bacteria and used to produce SCFAs, including butyrate (Figure 1).

Figure 1.

Intestinal microbiota produce SCFAs from dietary fiber fermentation, which are absorbed by colonocytes through MCT1, SMCT1, and passive diffusion, and converted into ATP for energy. Created with Biorender.com.

Butyrate, an SCFA produced primarily in the colon, is critical for colonic cell health, acts as the primary energy source for colon cells, and may play a role in cancer prevention [57, 58]. Probiotics can play an important role in mitigating dysbiosis by improving the microbial balance to inhibit pathogens such as Clostridioides difficile [59]. Prebiotics also promote the growth and metabolism of beneficial gut bacteria, such as Lactobacilli and Bifidobacteria, while suppressing pathogens [60]. Fecal microbiota transplantation (FMT) is a significant and effective means of restoring beneficial diversity and limiting systemic inflammation in patients with chronic dysbiosis. FMT involves the transplantation of fecal material from a healthy donor to a recipient, with the goal of restoring balance to the gut microbiome and improving health. FMT is now recommended in guidelines for the prevention of multiple recurrent C. difficile infection after two recurrences, with treatment and cure rates approaching 90% [61]. Next‐generation probiotics (NGPs) are a novel group of probiotic bacteria that are actively being studied and developed for future use as probiotics [62]. NGPs are a diversified and developed group of probiotics that extend beyond traditional strains (Lactobacillus and Bifidobacterium). Studies have focused on their claimed benefits and therapeutic applications for health. The development of NGPs employs genetics and engineering through potential metabolic activity or designs NGPs to contain engineered probiotics that offer usability to promote a specific health outcome or disease treatment, such as inflammatory bowel disease and metabolic disorders. Engineered probiotics have the potential to activate or suppress immune responses specific to their target, which promotes health and potentially diseased states, while also protecting against particular pathogens.

Probiotics, including engineered pore‐forming varieties, have gained popularity and are beginning to play a role in influencing and protecting the gut microbiome and overall health. Upon entry into the gut, pore‐forming probiotics form endospores that are durable and persistent in the harsh digestive environment (stomach acid, bile salts, and enzymes), before individually germinating in the intestine, where they can come into contact with their target environment, exerting active benefits.

In addition to lifestyle modifications, phage therapy can mitigate antibiotic‐induced dysbiosis. Engaging in healthy lifestyle choices can positively impact gut health and restore microbiome balance. Exercise has been shown to support diverse and balanced gut microbiota, and managing lifestyle stressors can help prevent dysbiosis due to chronic stress and stress‐induced microbial changes [63, 64]. Avoiding unnecessary antibiotic treatment and ensuring that antibiotics are prescribed responsibly can reduce the long‐term effects of antibiotics on gut health. Phage therapy is an emerging therapeutic intervention for modulating bacteria using bacteriophages to kill specific bacterial pathogens, and is a clinically promising alternative to antibiotics [65, 66]. Phage therapy is specific to pathogenic bacterial strains and does not cause broad disruption of the microbiome; therefore, it could play an essential role in the prevention of dysbiosis and CRC caused by antibiotic use [67, 68].

9. Early‐Life Microbiota Development

The gut microbiota undergoes critical early establishment, with implications for long‐term health and the risk of disease. Both maternal and environmental factors contribute to the newborn microbiome, with the maternal microbiota serving as one of the first exposures to microbial seeding at birth. Infants delivered through vaginal delivery are exposed to both the maternal vaginal and fecal microbiota. This is an essential process in which microbial colonization of the infant gut begins with species such as Lactobacillus, Prevotella, and Bacteroides [69]. Alternatively, infants born by cesarean section encounter a distinctly different bacterial environment with mostly skin‐associated bacteria such as Staphylococcus, Corynebacterium, and Propionibacterium [69]. This difference in early exposure to microbes may ultimately result in delayed colonization of the infant gut by beneficial microbes, typically acquired through vaginal delivery. Breastfeeding is also supportive of a healthy infant gut microbiome due to beneficial bacteria and prebiotic compounds that are found in human breast milk [70]. For example, human milk oligosaccharides are prebiotics that stimulate beneficial bacteria, such as Bifidobacteria and Lactobacilli, in the infant's gut [71]. Immunoglobulins (IgA), as well as other bioactive components found in breast milk, contribute to the development of the immune system and protection against infections [72]. In the infant gut, Bifidobacteria are essential for maintenance of the mucosal barrier, as well as for the modulation of immunological and inflammatory responses to pathogens [73]. The combination of probiotic and prebiotic components of human breast milk provides breastfed infants with a more stable and relatively uniform gut microbiome in comparison to formula feeding [73].

Gut microbiome development occurs rapidly during the first few years of life, which is a critical period for immune system maturation. Antibiotic exposure in early infancy disrupts the balance of the gut microbiome, resulting in antibiotic‐associated dysbiosis or a loss of microbial diversity, and possibly the emergence of antibiotic‐resistant strains. Alterations in the gut microbiome and immune system during infancy have been linked to dysbiosis‐associated immune‐related and metabolic disorders later in life. Dysbiosis‐associated changes in the gut microbiota that persist for up to 2 years after antibiotic exposure and the development of obesity, allergic reactions, and asthma are some of the long‐term consequences of early‐life antibiotic exposure [30]. Gut dysbiosis has also been implicated in a range of diseases, including irritable bowel disease, obesity, allergic disorders, type 1 diabetes, and autism [74]. The major forms of irritable bowel disease are Crohn's disease and ulcerative colitis, both characterized by chronic relapsing intestinal mucosal inflammation and distinct gut microbiome signatures [74].

10. Cancer‐Specific Pathways

Recent evidence has shown that microbial dysbiosis, which is defined as an imbalance in the gut microbial population, is an important contributor to the progression of CRC. Specific bacteria, especially enterotoxigenic B. fragilis, can produce toxins that interfere with Wnt/β‐catenin and STAT3 signaling, causing inflammation and tumor growth [75, 76]. Exposure to B. fragilis toxin causes the MAPK and NF‐κB pathways, which stimulate the release of proinflammatory cytokines, such as IL‐8 and TNF‐α [76]. Colibactin, produced primarily by certain strains of Escherichia coli belonging to the B2 phylogenetic group, directly cross‐links DNA in both mammalian and bacterial cells and can induce colon cancer in a human host [77]. Colibactin has been reported to disrupt p53 SUMOylation, induce double‐strand breaks, generate DNA adducts, and induce mutations [78]. In addition to SCFAs and phenolic acids, which aid in the fight against cancer and ammonia, there are also harmful metabolites such as polyamines, hydrogen sulfide (H₂S), and secondary bile acids (BAs) that make cancer worse and more aggressive [79]. Secondary bile acids, such as deoxycholic acid (DCA), induce oxidative DNA damage after prolonged exposure to high concentrations, resulting from nitro‐DCA and oxidation, which can lead to apoptosis or DNA damage [80]. Long‐term high DCA concentrations cause DNA damage in cells, resulting in mutations and naturally selected mutated cells, which can lead to the production of cancer cells. To develop microbiome‐informed approaches to diagnose or treat CRC, these multiphasic modes of interactions between the microbiome and tumors need to be differentiated based on their context.

11. Global and Environmental Aspects

The composition and diversity of the gut microbiota vary markedly from region to region due to the complex interplay of diet, lifestyle, and medicine, especially antibiotic use. Individuals living rurally tend to follow a diet high in complex carbohydrates and low in animal fat, which influences the abundance of SCFA‐producing bacteria such as Faecalibacterium prausnitzii and Roseburia spp. [35, 81]. A high‐fiber dietary regimen has been shown to positively affect microbiome alpha diversity and SCFA‐producing bacteria in the human gut [82]. In contrast, the Western diet is high in saturated fats and refined sugars and has been reported to be associated with dysbiosis and increased inflammation [83]. Animal‐based proteins, specifically red meat and dairy, can cause an increase in the abundance of bile‐tolerant anaerobes such as Bacteroides, Alistipes, and Bilophila [84].

A novel report indicated that, while antibiotic consumption in high‐income countries showed a modest increase, the defined daily doses per 1,000 inhabitants per day decreased by 4%, and there was no correlation with the gross domestic product per capita [85]. Additionally, this report suggested that the antibiotic consumption rate in low‐ and middle‐income countries has been converging toward (and in some countries surpassing) high‐income country levels [85]. On the other hand, low‐ and middle‐income countries may encounter the dual burden of insufficient medical advice coupled with over‐the‐counter antibiotic accessibility, creating imbalances in bacteria.

Environmental factors also powerfully shape gut microbial composition and CRC risk. The microbiomes of urban areas show reduced diversity, a higher ratio of Firmicutes/Bacteroidetes, and increased prevalence of Coprococcus and Parasutterella [86]. In contrast to urban populations, rural populations have a greater level of microbial diversity and abundance of Ligilactobacillus, Sutterella, and Paraprevotella [86]. Pollution, especially microplastics, can also physically irritate the intestinal lining, with the sharp edges of microplastics creating micro‐abrasions of the gut barrier [87]. Microplastics have been shown to accumulate within the gastrointestinal tract, disrupt gut microbiome homeostasis, and ultimately cause dysbiosis (i.e., an imbalance between beneficial and non‐beneficial bacteria) [87]. In addition, artificial sweeteners, emulsifiers, preservatives, and food additives can alter the delicate balance of the gut microbial ecosystem, and as such, microbial diversity is reduced, inflammation may increase, gut permeability may increase, and dysbiosis may occur [88]. These regional and environmental characteristics highlight the importance of a globally contextualized understanding of microbiome health.

12. Public Health and Education

Chronic antibiotic exposure, gut dysbiosis, and an elevated risk of developing CRC can be approached through public health initiatives and educational interventions. Public education campaigns can improve microbiome literacy and be integrated into the school curriculum, community health, and outreach programs. Microbiome testing can become a routine preventive care provision through molecular sequencing technologies, which could enable early screening of the microbiome to assess the risk of developing CRC and create individualized plans to reduce this risk. Additionally, promoting antibiotic stewardship programs at the policy level for inpatient and community settings may decrease inappropriate antibiotic prescriptions and lessen the downstream effects of altering gut health and cancer risk. These recommendations may create systematic changes focused on gut health and microbiome‐mediated diseases, including, but not limited to, CRC.

13. Conclusion

Increasing evidence associated with chronic antibiotic use, gut dysbiosis, and an increased risk of CRC should prompt a more thoughtful approach to prescribing antibiotics. Although antibiotics are necessary to treat bacterial infections, their long‐term consequences on gut health should be carefully considered, especially for prolonged treatment and among high‐risk populations.

There are many strategies to mitigate the impact of antibiotic‐induced dysbiosis through dietary interventions, probiotics, FMT, and lifestyle changes that will help reverse gut dysbiosis, thereby reducing the risk of developing CRC. Importantly, developing a deeper understanding of the gut microbiome and its relationship to chronic disease can help advance the health of people and mitigate the risks of developing cancer.

As our understanding of the microbiome grows, we should be aware of the need for healthcare providers, researchers, and the public to collaborate to spread awareness of gut health. If we promote careful antibiotic stewardship and institute gut‐health‐promoting behaviors, we can greatly reduce the long‐term risks of dysbiosis and CRC, ultimately enhancing public health globally.

Author Contributions

Md Mohiuddin: conceptualization, writing – review and editing, resources.

Funding

The author received no specific funding for this work.

Ethics Statement

The author has nothing to report.

Conflicts of Interest

The author declares no conflicts of interest.

Transparency Statement

The lead author, Md Mohiuddin, affirms that this manuscript is an honest, accurate, and transparent account of the study being reported; that no important aspects of the study have been omitted; and that any discrepancies from the study as planned (and, if relevant, registered) have been explained.

Mohiuddin M., “Chronic Antibiotic Use, Gut Microbiota Dysbiosis, and Increased Risk of Colorectal Cancer: An Emerging Threat,” Health Science Reports 9 (2026): e71866. 10.1002/hsr2.71866.

Data Availability Statement

The author confirms that the data supporting the findings of this study are available within the article.