Study reveals a link between obesity and chronic diarrhea


Obesity affects approximately 40 percent of Americans, according to the Centers for Disease Control and Prevention (CDC).

While obesity is known to be associated with increased risk of other health conditions – such as heart disease, diabetes, and gastrointestinal diseases – less is known about the relationship between obesity and abnormal bowel habits.

In the most comprehensive analysis of the relationship between Body Mass Index (BMI) and bowel habits to date, published today in Alimentary Pharmacology & Therapeutics, a team of physician-researchers at Beth Israel Deaconess Medical Center (BIDMC) found a strong association between obesity and chronic diarrhea independent of an individual’s dietary, lifestyle, psychological factors or medical conditions.

The findings could have important implications for how physicians might approach and treat symptoms of diarrhea in patients with obesity.

“While several previous studies have pointed to an association between obesity and bowel habits, all lacked data on whether dietary or other factors drive the connection,” said corresponding author Sarah Ballou, PhD, a health psychologist in the Division of Gastroenterology, Hepatology, and Nutrition at BIDMC.

“Our research confirms a positive association between obesity and chronic diarrhea and reveals for the first time that this relationship is not driven by confounding factors such as diet or physical activity level.”

Using the 2009-2010 National Health and Nutrition Examination Survey (NHANES) – a program of studies administered by the CDC designed to assess the health and nutritional status of adults and children in the United States – Ballou and colleagues analyzed the bowel health questionnaire responses of 5,126 patients over the age of 20 years who did not report a history of irritable bowel syndrome, celiac disease or colon cancer.

The team compared the reported bowel habits of patients who had a BMI associated with being underweight, normal weight, overweight, obese and severely obese.

After controlling for dietary, physical activity, diabetes, laxative use, and demographic factors, the team found that respondents who were obese or severely obese were 60 percent more likely to have experienced chronic diarrhea compared to those with normal bowel habits or constipation.

After controlling for dietary, physical activity, diabetes, laxative use, and demographic factors, the team found that respondents who were obese or severely obese were 60 percent more likely to have experienced chronic diarrhea compared to those with normal bowel habits or constipation.

While the study reveals the association is not driven by compounding factors the team controlled for, questions still remain about what underlying causes may explain why obese individuals would be more likely than non-obese individuals to have diarrhea.

One possible explanation may be related to the link between obesity and chronic low-grade inflammation, which may contribute to diarrhea.

Future research clarifying this relationship and determining how obesity triggers inflammation could serve as a base for how physicians approach treating abnormal bowel habits with this patient population.

“The treatment of obesity and obesity-related medical conditions requires multidisciplinary management,” said senior author Anthony Lembo, MD, a gastroenterologist in the Division of Gastroenterology, Hepatology, and Nutrition at BIDMC.

“Clinicians should be aware of the relationship between obesity and diarrhea, especially considering the potential negative impacts altered bowel habits can have on quality of life.”

In addition to Ballou and Lembo, co-authors include Prashant Singh, Vikram Rangan, Johanna Iturrino and Judy Nee, all of the Department of Medicine at BIDMC.

Funding: This work was supported by the National Institutes of Health (T32DK007760).

Obesity usually is associated with morbidity related to diabetes mellitus and cardiovascular diseases. However, there are many gastrointestinal and hepatic diseases for which obesity is the direct cause (eg, nonalcoholic fatty liver diseases [NAFLDs]) or is a significant risk factor such as in reflux esophagitis and gallstones. When obesity is a risk factor, it may interact with other pathogenetic mechanisms and result in earlier presentation of disease or more complicated disease.

The gastrointestinal tract plays a key role in obesity through its contributions to satiation and satiety, production of gut hormones that influence appetite (such as ghrelin, cholecystokinin, and peptide YY), incretins (eg, glucagon-like peptide-1) that impact postprandial glycemia, absorption of nutrients that ultimately determine the positive energy balance that results in obesity, changes in bile acids and the microbiome, and the metabolic products of microbial digestion of nutrients (short-chain fatty acids) that modify some of the metabolic factors that are associated with obesity.

Most of these topics are addressed elsewhere in this issue of Gastroenterology. Therefore, this article focuses on the gastrointestinal and hepatobiliary complications of obesity in adults (Figure 1); a separate article addresses the complications of pediatric obesity. Table 1 summarizes the quantified risks (odds ratios [ORs] and relative risks [RRs]) of gastrointestinal complications of obesity in adults.

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Figure 1
Gastrointestinal and hepatic morbidity associated with obesity.

Small Intestine

The small intestine is the site of digestion and absorption of most nutrients. In the past, it was thought that the small intestine played a passive role, simply absorbing the excess calories ingested by obese people.

Bile acids play a critically important role in the absorption of fats; the role of bile acids in metabolic regulation52 or as potential therapeutic approaches for obesity and metabolic syndrome53 are beyond the scope of this article; however, there is no evidence that bile acid synthesis or enterohepatic circulation is altered by obesity.

On the other hand, there is evidence that the small intestine is able to adapt its absorptive functions for the 3 macronutrient classes, as follows:

(1) lipid absorption capacity adapts to the fat content of the diet, especially through the coordinated induction of lipid binding proteins, which are involved in the intestinal absorption of long-chain fatty acids as well as their uptake, trafficking, and re-assembly into chylomicrons54;

(2) energy intake from infusion of intraduodenal whey protein hydrolysate tended to be higher in obese nondiabetic men than in lean controls55; and (

3) in morbid obesity, glucose absorption in the proximal intestine is accelerated and this is related to increased sodium-glucose linked transporter-1 (SGLT-1) expression.

The increased glucose absorption in the proximal gut may predispose to obesity and type 2 diabetes.56

Although alterations in the physiology of the small intestine may allow greater absorption capacity,54 it is likely that small-bowel absorption adapts to the over-consumption of calories associated with obesity, leading to more rapid absorption without an increase in energy absorption.


The prevalence of diarrhea in obese people is higher compared with normal-weight controls.57 A population-based survey study of 2660 people showed that the prevalence of diarrhea in obese individuals was 30% compared with 17% in normal-weight controls (OR, 2.7; 95% CI, 1.1–6.8).38 Similar studies have been replicated in Australia and New Zealand.58,59 In an epidemiologic study of more than 35,000 persons in France, functional diarrhea was associated with BMI in females (OR, 1.05; 1.03–1.07), but not in males.60

Among 1001 Swedes, diarrhea (OR, 2.2; 95% CI, 1.38– 3.46), stool urgency (OR, 1.60; 95% CI, 1.04–2.47), and nocturnal urgency (OR, 2.57; 95% CI, 1.33–4.98) were more prevalent in obese people than in lean controls, adjusting for age, sex, and education.61

The higher prevalence of diarrhea could be attributed to several potential mechanisms associated with obesity: changes in bile acids resulting in bile acid diarrhea,62 accelerated colonic transit,63 increased mucosal permeability, 64,65 or intestinal inflammation as evidenced by increased levels of fecal calprotectin.66 These interesting studies require replication. Medications used by obese individuals, such as metformin for type 2 diabetes mellitus or polycystic ovary syndrome, also may cause diarrhea.67

Celiac Disease

Celiac disease is an immune response to gluten in genetically susceptible people and it mainly affects the small intestine. The typical presentation includes weight loss, diarrhea, and malabsorption. Paradoxically, the recognition and prevalence of celiac disease in the obese population is increasing. In patients with newly diagnosed celiac disease, the prevalence of obesity varies from 39% to 44%.68,69 Obese adult or pediatric patients with celiac disease are more likely to gain more weight on a gluten-free diet.68,70,71

Inflammatory Bowel Diseases

Crohn’s disease or ulcerative colitis are autoimmune disorders that mainly target the small bowel and colon, respectively.


In a case-control study, there was a U-shaped association between BMI and Crohn’s disease. Patients who are underweight or overweight were more likely to have Crohn’s disease.72 These findings were not reproduced in a European cohort, which showed no association between obesity and IBD in adults,73 and a meta-analysis of 24 studies that included 1442 adult patients with IBD disease and 2059 healthy controls showed that obesity was less prevalent in patients with Crohn’s disease (OR, −1.88; 95% CI, −2.77 to −1.00) and that there was no difference in ulcerative colitis.74 On the other hand, in children, the prevalence of obesity in IBD was similar to that in the general population, but obese children with IBD had more severe disease than normal-weight children.75 

The latter study also identified that treatment with corticosteroids may be a confounder in the interpretation of the relationship between obesity and IBD because the steroid treatment may have predisposed to the development of obesity. In addition, ethnic differences, illustrated by the observation that African Americans (OR, 1.64; 95% CI, 1.10–2.48) and those on Medicaid insurance (OR, 1.67; 95% CI, 1.19–2.34), were associated positively with overweight/obese status, and this may provide an explanation for the absence of this association in European cohorts, which likely were more ethnically homogeneous.

Mechanisms of IBD related to obesity

There are similarities in some of the pathophysiological features occurring in metabolic syndrome and IBD, including adipose tissue dysregulation, inadequate immune response, dysbiosis, and inflammation.

Thus, in metabolic syndrome and IBD, inflammation affects adipose tissue and disturbs adipokine secretion. Both Crohn’s disease and ulcerative colitis are associated with high levels of 2 adipokines (resistin and visfatin) and low levels of a third adipokine (leptin).76

 Another study showed that active Crohn’s disease was associated with significantly lower adiponectin levels compared with the control group.77 Given the contradictory data in these 2 studies, the significance of these adipokine levels still is unclear. Inflammatory disease affecting the ileocolonic mucosa also could impact the synthesis or release of incretins, which may have metabolic effects,78 and, paradoxically, increased release of glucagon-like peptide-1 has been reported to retard gastric emptying in patients with active inflammatory bowel disease.79

Treatment and Outcomes

Obesity is one of the factors associated with increased risk of surgical site infections in patients with IBD.80 In a metropolitan US population, patients with obesity and IBD were significantly less likely to receive anti–tumor necrosis factor-α treatment, undergo surgery, or experience hospitalization for their IBD than their nonobese counterparts.81 These observations require confirmation.

Another retrospective study in 1494 patients with IBD addressed the relationship between BMI and dose of medications for IBD, and reported that obesity was associated with a lower dosage (milligrams per kilogram) of purine analogs and biologics. 82 It is interesting that, although the role of obesity in IBD still is unclear, obesity does influence outcome in IBD management.

In a study of 124 patients with IBD naive to biologic therapy, who were started on infliximab, it was observed that higher body weight was associated with an earlier time to loss of response to infliximab, this was independent of the dose in patients with Crohn’s disease (adjusted hazard ratio, 3.03; P < .001) or ulcerative colitis (adjusted hazard ratio, 9.68; P = .06).83 Similar findings were reported for adalimumab in obese patients with Crohn’s disease who had a significant loss of response compared with lean controls.84

Conversely, in a cohort study of 391 patients who underwent surgery for IBD, obesity did not worsen postoperative complication rates in IBD patients.85

Media Contacts:
Chloe Meck – BIDMC
Image Source:
The image is in the public domain.

Original Research: Open access
“Obesity is associated with significantly increased risk for diarrhoea after controlling for demographic, dietary and medical factors: a cross‐sectional analysis of the 2009‐2010 National Health and Nutrition Examination Survey”. Sarah Ballou, Prashant Singh, Vikram Rangan, Johanna Iturrino, Judy Nee, Anthony Lembo.
Alimentary Pharmacology & Therapeutics doi:10.1111/apt.15500.


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