Pesticides Shown to Harm Good Gut Bacteria and Increase Belly Fat

Common chemicals used in food production, including pesticides and fungicides, among others, have been shown to compromise beneficial gut bacteria and promote belly fat, obesity, diabetes, inflammation and more!

April is Earth Month so let's turn our attention to how multiple chemicals, used along the early steps of modern food production, are increasingly shown to contribute to some of the most rapidly increasing health problems in our country: obesity, diabetes, inflammation and metabolic disease in general!

Research published earlier this year in The American Journal of Physiology-Endocrinology and Metabolism illustrated how the chemicals used in food growth and harvesting ultimately have deleterious effects on our metabolic health, and it happens through the gut!

These metabolic diseases like obesity, type 2 diabetes, and fatty liver disease have been rising steadily in recent decades. While diet and lifestyle play a significant role, this is another major contributor flying under the radar—environmental chemicals introduced through our food supply.

From the pesticides used to grow crops to chemical residues that linger in our environment, these substances don’t just pass through us unnoticed. They interact with our biology in ways that can profoundly affect our gut, immune system, and metabolism.

The Gut-Health Connection

Your gut microbiome—a bustling ecosystem of trillions of microbes—plays a central role in digestion, immunity, and even weight regulation. But this delicate balance is easily disrupted by chemical exposures.

Studies show that many environmental toxins can:

• Disturb the diversity and function of gut bacteria

• Damage the intestinal barrier, leading to increased permeability (often called “leaky gut”)

• Promote chronic, low-grade inflammation

• Disrupt metabolic and hormonal pathways

These changes set the stage for a wide range of chronic diseases, including obesity, insulin resistance, cardiovascular disease, and non-alcoholic fatty liver disease.

Chemicals That Disrupt Metabolism

Researchers have identified a variety of environmental pollutants that contribute to metabolic dysfunction by altering the microbiome and interfering with hormone and immune function. These include:

• Persistent Organic Pollutants (POPs) such as DDE (a breakdown product of DDT) and PCBs: These chemicals remain in the environment for decades and accumulate in body fat. They’re associated with increased risk of obesity and diabetes, as well as disruptions in gut microbial composition.

• Chlorpyrifos (CPFs): A widely used organophosphate pesticide that has been linked to obesity, elevated blood pressure, and metabolic disturbances. Though banned in some countries, it’s still used in many parts of the world and can linger on produce.

• Fungicides like carbendazim (CBZ), propamocarb (PM) and imazalil (IML): Often used on fruits and vegetables, these have been linked to weight gain, liver inflammation, and alterations in gut bacteria that influence glucose metabolism.

Even prenatal and early-life exposures to these chemicals can have long-term consequences. Studies show that in utero exposure to certain pesticides can predispose children to metabolic issues, including increased fat accumulation and insulin resistance later in life.

The Microbiome’s Role in Detox and Disease

Interestingly, our gut microbes don’t just suffer the consequences of toxic exposures—they also play a role in processing these chemicals. Some microbes can detoxify certain compounds, while others may convert them into more harmful substances. These microbial byproducts (known as postbiotics) can either protect us or promote inflammation, depending on which microbes dominate the gut environment.

This two-way relationship means that keeping a healthy microbiome may offer some protection against the metabolic effects of environmental chemicals!

                                                                                                                                                     *image credits

Effects on Metabolism

Chemical exposure to POPs, organophosphate pesticides, or fungicides promotes dysmetabolism in rodent models. Multiple studies demonstrate these chemicals can enhance body weight and impair blood glucose control in mice and rats. DDE exposure in rats (2 mg/kg daily for 3 weeks) increased blood lipids, insulin resistance, and blood glucose compared with controls. Two doses of 1 µmol/kg of PCB-126 two weeks apart induced hyperinsulinemia and increased intestinal and peripheral inflammation in atherosclerotic and hyperlipidemic mice (Ldlr-/- mice). Oral CPF administration of 5 mg/kg/day for 12 weeks increased body weight, adiposity, and fasting blood glucose levels, and reduced insulin sensitivity, independent of diet or changes in food consumption. In mice, CPF exposure promotes obesity by inhibiting thermogenesis in brown adipose tissue.

Fungicide exposure, specifically CBZ at 0.2–5 mg/kg for 14 days, increased body weight, adiposity, blood glucose, and serum triglyceride levels. These results demonstrate that toxicants can impair blood glucose control and promote obesity!

These toxicants also negatively impact the liver, inducing inflammation and lipid accumulation leading to hepatic steatosis, fibrosis, and oxidative stress. Exposure to CBZ in mice increased hepatic lipid accumulation, circulating proinflammatory cytokines (e.g., IL-1β, IL-6), total cholesterol, and HDL levels, along with upregulation of lipogenic gene expression in liver and adipose tissue.

PM exposure can promote atherosclerosis: wild-type C57BL/6J mice given 20 mg/L of PM in drinking water for 24 weeks exhibited decreased HDL-cholesterol, increased serum triglycerides, cholesterol, and LDL-cholesterol, and developed atherosclerotic lesions and hepatic lipid accumulation, alongside increased circulating cytokines.

Prenatal exposure to these chemicals can induce lifelong metabolic abnormalities. For example, PBDE exposure during pregnancy reduced maternal serum metabolites related to amino acid, lipid, and energy metabolism. Offspring exposed to PBDEs in utero and during lactation displayed worsened diet-induced obesity, hepatic steatosis, and impaired glucose regulation. Neonatal CPF exposure led to persistent hyperinsulinemia, hyperglycemia, and impaired hepatic insulin signaling. These compounds can promote metabolic disease across the lifespan, with associated disruptions to the intestinal microbiota.

What You Can Do

While we can't completely eliminate exposure to environmental pollutants, we can reduce their impact:

• Choose organic produce when possible to limit pesticide intake.

• Wash fruits and vegetables thoroughly to remove surface residues.

• Increase your fiber intake, especially from prebiotic sources like leafy greens, legumes, garlic, and onions—fiber feeds the good bacteria in your gut.

• Incorporate fermented foods like yogurt, kefir, kimchi, and sauerkraut to support microbiome diversity.

• Support detox pathways through antioxidant-rich foods (like berries, cruciferous vegetables, and herbs) and proper hydration.

  
  

Final Thoughts

Metabolic health isn’t just about how much we eat or how often we exercise. It’s also about what we’re exposed to—especially through our food. By understanding how environmental chemicals can disrupt the gut microbiome and drive chronic inflammation, we can take proactive steps to protect ourselves and promote long-term vitality.

Your microbiome matters—and protecting it starts with what's on your plate!

References:

1.    Barra NG, Fang H, Bhatwa A, et al. Food supply toxicants and additives alter the gut microbiota and risk of metabolic disease. Am J Physiol Endocrinol Metab. 2025;328(3):E337-E353. doi:10.1152/ajpendo.00364.2024. https://pubmed.ncbi.nlm.nih.gov/39871724/

The content and any recommendations in this article are for informational purposes only. They are not intended to replace the advice of the reader's own licensed healthcare professional or physician and are not intended to be taken as direct diagnostic or treatment directives. Any treatments described in this article may have known and unknown side effects and/or health hazards. Each reader is solely responsible for his or her own healthcare choices and decisions. The author advises the reader to discuss these ideas with a licensed naturopathic physician.