Could diabetes be damaging your digestive system?

June 3, 2026

Healthcaretoday, Assunta Hospital, Diabetes, hyperglycemia, insulin resistance, GI complications, Type 1 Diabetes, Type 2 diabetes, Dr Jeeta Muthumanikam, Diabetic autonomic neuropathy, Gastroesophageal reflux disease, GERD, Esophageal candidiasis,

Diabetes can significantly affect digestive health, particularly when diabetic autonomic neuropathy develops. Damage to the autonomic nervous system may disrupt gastrointestinal motility, leading to symptoms such as bloating, constipation, diarrhea, and discomfort.

Diabetes mellitus (DM) is a chronic metabolic disease characterized by elevated blood glucose levels (hyperglycemia) resulting from insulin deficiency and/or insulin resistance. Gastrointestinal complications such as diarrhea, constipation, and dyspepsia are commonly associated with diabetes. The first step in managing these gastrointestinal symptoms is to stabilize blood sugar levels.

The major types of diabetes mellitus are Type 1 diabetes mellitus, which results from autoimmune destruction of pancreatic beta cells leading to absolute insulin deficiency, and Type 2 diabetes mellitus, which is characterized by a combination of insulin resistance and impaired insulin secretion. Type 2 diabetes mellitus accounts for more than 90% of adult diabetes cases.

“Most patients have Type 2 diabetes. Nowadays, most cases are related to insulin resistance because there is insulin in the bloodstream, but it does not function effectively. The cells cannot take up glucose properly because of receptor-related problems. Type 1 diabetes is usually due to an autoimmune condition that develops early in life. Most of these patients require insulin from childhood, adolescence, or their teenage years,” explains Dr Jeeta Muthumanikam (pix below), Consultant Gastroenterologist & Hepatologist, during Assunta Hospital’s GP Symposium, Diabetes 360: A Multidisciplinary Approach for GPs.

Glucosensors in the gastrointestinal tract
There are specialized cells throughout the gastrointestinal tract that detect fluctuations in glucose levels. These cells release hormones such as glucagon-like peptide-1 (GLP-1), which help regulate blood sugar by controlling glucose absorption. They also communicate through neuronal pathways, particularly the autonomic nervous system, which regulates gastrointestinal motility.

The purpose of these glucose sensors is to regulate glucose metabolism and maintain glycemic homeostasis.

Gastrointestinal involvement in diabetes
Diabetes commonly affects the gastrointestinal tract. Gastrointestinal complications become more significant in the presence of diabetic autonomic neuropathy (DAN) because the autonomic nervous system is involved in regulating digestive function.

Chronic hyperglycemia affects the gastrointestinal tract in two major ways. First, it impairs gastrointestinal motility, causing movement through the digestive tract to become either too slow or too rapid. This can result in symptoms such as diarrhea, constipation, abdominal pain, and bloating. Second, it alters secretion and absorption processes, affecting the movement of fluids within the gastrointestinal tract.

These changes can affect the esophagus, stomach, small intestine, colon, and liver.

Diabetic gastroenteropathy
Diabetic gastroenteropathy is a collective term used to describe gastrointestinal complications caused by diabetes. Common manifestations include dysphagia, gastroparesis, gastroesophageal reflux disease (GERD), diarrhea, constipation, and fecal incontinence.

Esophageal complications in diabetes mellitus
Esophageal complications are common in patients with longstanding or poorly controlled diabetes because esophageal motility becomes impaired. The contractions, peristalsis, and propulsion of food through the esophagus are affected.

Patients with uncontrolled diabetes often complain that food feels stuck halfway down the esophagus or experience painful swallowing. These symptoms are primarily caused by diabetic autonomic neuropathy and may affect up to 50% of people with diabetes.

Normally, food moves through coordinated peristaltic contractions beginning at the upper esophageal sphincter and progressing toward the stomach. In diabetes, this coordination may be disrupted, causing food to become lodged in the esophagus. Some patients may vomit or find that food does not pass easily into the stomach.

This condition is known as esophageal hypomotility and is associated with delayed food transit and reduced lower esophageal sphincter (LES) tone. When LES tone is reduced, stomach contents can reflux back into the esophagus.

Gastroesophageal reflux disease (GERD)
People with diabetes are approximately 1.2 to 1.5 times more likely to develop GERD, largely because of autonomic neuropathy involving the vagus nerve and delayed gastric emptying (gastroparesis).

Common symptoms include heartburn, acid regurgitation, and a bitter taste in the mouth.

Complications may include peptic esophageal strictures, esophageal ulcers, and Barrett’s esophagus.

Esophageal candidiasis
Another condition affecting the esophagus is candidiasis.

“High blood sugar levels can delay the passage of food through the esophagus and into the stomach. Sometimes food may remain there for prolonged periods. When this occurs, food can undergo decomposition, creating conditions that favor fungal overgrowth. This can result in severe esophageal candidiasis,” explains Dr Jeeta.

Clinical features include painful swallowing (odynophagia), dysphagia, and retrosternal discomfort.

Acute esophageal necrosis (black esophagus)
This is a rare but serious condition commonly referred to as black esophagus. It is characterized by extensive esophageal tissue necrosis and is considered life-threatening.

It is most commonly seen in patients with diabetic ketoacidosis and severe hyperglycemic states.

This condition constitutes a medical emergency. Some patients may require surgery to remove ischemic tissue, while others may be managed conservatively if the ischemia improves with treatment.

Common symptoms of esophageal disease in diabetes include persistent heartburn, dysphagia, odynophagia, chest pain, hoarseness, and acid reflux symptoms.

Diagnostic methods
Upper gastrointestinal endoscopy is used to detect inflammation, ulcers, strictures, necrosis, and candidiasis.

Esophageal manometry involves inserting a high-resolution manometry catheter through the nose and advancing it to the gastroesophageal junction. The device measures swallowing function while the patient drinks water. This test helps identify esophageal hypomotility (reduced muscle movement) or hypermotility (excessive or uncoordinated contractions).

Management and treatment
Good glycemic control is essential. Achieving an HbA1c target of approximately 6% to 7% can help prevent the progression of neuropathy.

Dietary counseling should be individualized, followed by regular follow-up visits to assess progress. Patients are encouraged to monitor their blood glucose using a glucometer at least once before breakfast. If daily testing is not possible, testing two to three times per week may still provide useful information for adjusting medications.

Proton pump inhibitors (PPIs) and prokinetic agents are commonly prescribed for diabetic reflux disease and dysphagia. Vonoprazan and Tegoprazan are potassium-competitive acid blockers representing a newer class of acid-suppressive medications used in acid reflux treatment.

Lifestyle modifications are equally important. Smaller, more frequent meals may improve gastric emptying. Patients should avoid large meals, elevate the head of the bed during sleep, and avoid lying down immediately after eating.

Weight management is also critical. Patients should aim for a body mass index (BMI) below 25 kg/m² or achieve a weight reduction of approximately 10% to 15% if overweight or obese.

Stomach complications in diabetes mellitus
Stomach complications are commonly caused by diabetic autonomic neuropathy. Persistently elevated blood glucose levels damage the nerves that control the stomach and intestines, resulting in abnormal gastrointestinal motility and digestion.

These symptoms can significantly affect nutrition and blood glucose control.

Gastroparesis, or delayed gastric emptying, is commonly seen in diabetes. It involves delayed movement of food from the stomach into the small intestine and is primarily caused by vagus nerve damage and weakened stomach muscle contractions.

“So what happens is that the stomach should normally digest and move food into the small intestine within about four hours. In diabetes, this process may take six to twelve hours. This can cause severe regurgitation, fullness, and blood sugar fluctuations due to a mismatch between food absorption and medication action,” says Dr Jeeta.

Basic symptoms include early satiety, nausea, vomiting, bloating, abdominal discomfort, poor appetite, and unpredictable blood sugar levels.

Diabetes enteropathy
Diabetes enteropathy is a neuropathic disorder affecting the intestinal nerves. Manifestations include constipation, diarrhea (often nocturnal), fecal incontinence, or alternating constipation and diarrhea.

These symptoms can significantly reduce quality of life and increase the risk of dehydration and electrolyte imbalances.

Chronic constipation
One of the primary goals in managing constipation among people with diabetes is restoring normal intestinal function. Treatment includes dietary and lifestyle modifications.

Patients are encouraged to increase fiber intake, consume adequate fluids, and eat more vegetables and fruits.

“Excessive fiber intake can worsen bloating and gas, leading to intestinal cramps. Therefore, the recommended dietary fiber intake is 20 to 30 grams per day.”

Patients with diabetes mellitus are encouraged to engage in at least 150 minutes of moderate-intensity aerobic exercise per week, spread over at least three days. A sedentary lifestyle should be avoided, and some form of physical activity should ideally be performed every other day.

According to the Rome Criteria and recommendations from the Asian Neurogastroenterology and Motility Association, patients who do not respond adequately to bulk-forming fiber agents may require laxative therapy.

Osmotic laxatives are generally recommended first, followed by stimulant laxatives if needed. Osmotic laxatives draw water into the stool, making it softer and easier to pass.

Stimulant laxatives promote contractions of the colon muscles, facilitating bowel movements. Common examples include senna, bisacodyl, and sodium picosulfate.

Bulk-forming laxatives such as methylcellulose, bran, and psyllium husk are available over the counter. Fiber may help improve glycemic control, cholesterol levels, and body weight management.

Some studies suggest that psyllium may also reduce cardiovascular risk in people with Type 2 diabetes.

Diabetes and diarrhea
Diabetic diarrhea most commonly affects individuals with poorly controlled diabetes and generalized neuropathy.

Bacterial overgrowth and pancreatic exocrine insufficiency have both been proposed as contributing factors, although no single cause has been consistently identified.

Treatment depends on the underlying cause and may include antidiarrheal medications such as loperamide, antibiotics for bacterial overgrowth, and probiotics.

Diabetes and metabolic dysfunction-associated fatty liver disease
This relationship is bidirectional. Diabetes worsens fatty liver disease, while metabolic dysfunction-associated fatty liver disease (MAFLD) worsens diabetes.

Each condition increases the risk of developing the other, creating a vicious cycle that accelerates disease progression and increases the risk of severe complications.

How diabetes causes/worsens metabolic dysfunction-associated fatty liver disease
Insulin resistance: In diabetes, cells respond poorly to insulin. This causes the pancreas to produce more insulin, signaling the liver to synthesize and store additional fat.

Rapid progression: Diabetes increases the likelihood that simple fatty liver disease will progress to inflammation, fibrosis, and advanced liver disease.

How metabolic dysfunction-associated fatty liver disease causes/worsens diabetes
Releasing toxins: A fatty liver releases inflammatory proteins and stored fats into the bloodstream.

Worsening blood sugar: These substances worsen insulin resistance, making blood sugar levels increasingly difficult to control.

Impact of diabetes on the liver
High blood sugar levels and insulin resistance promote fat accumulation within the liver (steatosis). In individuals with Type 2 diabetes, this combination significantly increases the risk of liver inflammation, fibrosis, cirrhosis, and liver cancer.

A fatty liver increases glucose production and systemic inflammation, directly contributing to insulin resistance. This significantly increases cardiovascular risk and makes blood glucose control more challenging.

Screening and diagnosis
Because Type 2 diabetes is a major metabolic driver of MAFLD, current guidelines recommend risk stratification for fatty liver disease in all adults with prediabetes or diabetes.

Blood tests are commonly used to assess liver enzymes and calculate fibrosis scores such as the FIB-4 index.

FibroScan (transient elastography) and specialized ultrasound techniques are increasingly used to evaluate liver stiffness and fat content without requiring a liver biopsy.

Management and treatment
Managing metabolic syndrome as a whole remains the cornerstone of treatment.

Weight loss of approximately 5% to 10% of body weight, a balanced diet, and regular physical activity are highly effective in reducing liver fat and improving insulin sensitivity.

Certain diabetes medications, including GLP-1 receptor agonists such as semaglutide and tirzepatide, as well as pioglitazone, may improve both glycemic control and liver inflammation.

Because cardiovascular disease remains the leading cause of death among patients with both diabetes and metabolic dysfunction-associated fatty liver disease, aggressive management of blood pressure and cholesterol is essential.

Could diabetes be damaging your digestive system?

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