Abstract
Goals:
We aim to describe weight loss outcomes of patients with celiac disease (CeD) taking antiobesity medications (AOMs) and compare it to weight loss outcomes of patients without CeD taking AOMs.
Background:
Increasing rates of obesity and obesity-associated comorbidities have been previously reported in patients CeD on a gluten-free diet. The effectiveness of AOMs in this population has not been previously described.
Methods:
In our retrospective cohort study, we matched 39 patients with treated CeD to 78 patients without CeD based on sex and AOM. We assessed weight loss outcomes at 3, 6, and 12 months after starting the AOM in both cohorts and analyzed if there was a differential response when comparing by type of AOM (injectable GLP-1 receptor agonists vs. oral non-GLP-1 AOMs).
Results:
Both cohorts had similar baseline demographic and anthropometric characteristics. At 12 months, the CeD cohort had a non-significantly inferior total body weight loss percentage (TBWL%) compared to the cohort without CeD (6.5% vs. 9.5, p=0.13). The CeD cohort had a similar proportion of patients achieving a TBWL% of ≥5% than the cohort without CeD (72.7% vs. 72.1%, p=1.00). No significant difference was observed when comparing weight loss outcomes of injectables (GLP-1 receptor agonists) to oral AOMs. The proportion of patients reporting side effects was similar for both groups, regardless of type of AOM.
Conclusion:
Patients with CeD taking AOMs had similar weight loss outcomes to patients without CeD. Hence, AOMs can be a safe and effective therapy for weight management in patients with CeD.
Keywords: Antiobesity Medications, Celiac Disease, Obesity, Gluten-Free Diet
Introduction
Celiac disease (CeD) is a systemic autoimmune disease, in which gluten ingestion leads to small intestinal enteropathy in genetically susceptible individuals [1]. Previous reports have indicated that the global prevalence of CeD ranges from 0.7 to 1.4% [2]. The incidence of CeD has been steadily increasing globally, only partly due to an increase in diagnostic testing and awareness of the disease [3].
Repetitive immune-mediated mucosal damage results in impaired nutrient absorption, often manifesting as chronic diarrhea, weight loss, growth failure, and reduced bone mineral density [1]. However, it has been widely recognized that a significant proportion of patients within this population have overweight/obesity [4]. The reported prevalence of overweight and obesity in patients with CeD has been significantly variable due to differences in study designs [5]. A retrospective cohort study showed that 44% of patients with CeD being treated in a community setting and 35% in a tertiary referral center had overweight or obesity [6]. A recent study in the US employing an electronic health record database reported that 45% of patients with CeD had a body mass index (BMI) >30 kg/m2, with a higher proportion among White females [7]. This is similar to the national prevalence of obesity in 2021 (41.9%) [8]. Consequently, an increased risk for developing obesity-associated comorbidities has been reported for patients with CeD, especially for those on gluten-free diet (GFD) [9]. One cohort study reported that one-third of newly treated patients gain weight after going gluten free for 6 months [10]. A case-control study reported that over one-third of patients with CeD compliant to GFD had nonalcoholic fatty liver disease [11]. Also, previous reports have suggested that patients with CeD have a higher risk of adverse cardiovascular outcomes [12].
The mechanisms underlying the relationship between CeD and increased adiposity have not been widely studied. It has been hypothesized that recovery of mucosal absorptive functions after gluten avoidance and the composition of GFD by itself might play a role in energy imbalance, leading to obesity [13]. A study reported that gluten-free products had a higher content of protein, total and saturated fats, than their gluten-containing counterparts [14]. A meta-analysis examining the effect of GFD on BMI revealed that in spite of having a lower BMI than controls at baseline, patients with CeD had a significant increase in their BMI after starting GFD as compared to controls at last follow-up, and that about 9% of the population changed to a higher BMI category after starting GFD [15].
Given the increased risk for obesity-associated comorbidities in the CeD population, patients may benefit from multiple weight management modalities, including lifestyle interventions, bariatric procedures, and more recently, antiobesity medications (AOMs) [16]. At this time, the FDA has approved the following drugs for long-term weight management, available in oral (orlistat, phentermine-topiramate, bupropion-naltrexone) or subcutaneous injection formulations (liraglutide, setmelanotide, and semaglutide). Notably, repetitive mucosal intestinal damage in CeD could lead to impaired drug absorption of oral medications [17], which could potentially impact weight loss outcomes of oral AOMs. Newer AOMs targeting the glucagon-like peptide 1 (GLP-1) receptor lead to weight loss by inducing a delay in gastric emptying and reducing food intake through central and peripheral satiety mechanisms [18]. In this study, we intend to explore weight loss outcomes of patients with CeD and overweight/obesity taking different AOMs and compare them to outcomes in a matched population without CeD taking AOMs.
Methods
Study design, eligibility criteria and data collection
This is a retrospective matched cohort study of adult participants with CeD and overweight/obesity taking AOMs. The Mayo Clinic Institutional Review Board approved the study and waived the need for informed consent due to its minimal-risk nature. We conducted a search in the electronic medical records to identify patients with a diagnosis of CeD with a subsequent prescription for an antiobesity medication. We chart reviewed 81 electronic medical records for inclusion/exclusion. We included patients with a diagnosis of CeD, with overweight/obesity (BMI≥27 kg/m2) at baseline (start date of AOM), and that were prescribed an AOM at any dose. We excluded those with a duration of AOM treatment of less than 3 months, that started taking an AOM before being diagnosed with CeD, with no weight data at baseline or follow-ups, or with active malignancy or pregnancy (Figure S1). Then, we selected a cohort of patients without CeD taking AOMs from our previously existing database, that were matched by sex and AOM (phentermine, phentermine-topiramate, liraglutide, low-dose semaglutide, high-dose semaglutide), on a 2:1 ratio to the group with CeD.
We extracted data on demographic and baseline anthropometric characteristics, data on AOM use and obesity-associated comorbidities for all included patients. We also collected weights at 3,6, and 12 months from the start of the AOM. For patients with CeD, we collected data on the date of diagnosis, self-reported adherence to GFD, and TTG IgA levels at time of initial diagnosis and upon AOM start, if available. We assessed for the presence of side effects on clinic encounter notes and patient communications. We followed the Strengthening the Reporting of Observational Studies in Epidemiology (STROBE) reporting guideline (Supplementary material).
Endpoints
Our primary endpoint was the total body weight loss percentage (TBWL%) at 12 months in patients with or without CeD taking different AOMs. Secondary endpoints included the TBWL% at 3 and 6 months and the proportion of patients in each group achieving a categorical TBWL% of ≥5%, ≥10%, and ≥15% at 12 months. We also compared weight loss outcomes of glucose-like peptide 1 (GLP-1) receptor agonists (semaglutide and liraglutide) and other AOMs (phentermine and phentermine-topiramate) in patients with or without CeD. For patients with CeD, we compared weight loss response with different AOMs (GLP-1 receptor agonists vs non-GLP-1 AOMs).
Statistical Analysis
Baseline characteristics and percentual chance in body weight at 3, 6 and 12 months had a normal distribution, and are presented as mean (SD), or N (%), as appropriate. We assessed the primary endpoint with an independent t test. For other endpoints, continuous data were analyzed using an independent t test, and categorical data were analyzed with a Fisher’s exact test. Missing weight data at different follow-ups were not replaced, and the analyses were done with the available data at each timepoint. A 2-tailed p-value <0.05 was considered statistically significant. We conducted all analyses on JMP (Version 16.2.0, SAS Institute Inc., Cary, NC).
Results
We included 39 patients with CeD (CeD+AOM group) and matched to 78 patients without CeD (AOM group) taking AOMs. In our cohort, 89.7% of the patients were female, and the mean age for patients with CeD was 49.8 (13.8), while the mean age for the group without CeD was 50.8 (11.2). In addition, 38 patients (97.4%) in the CeD+AOM group, and 75 patients (96.1%) in the AOM group self-reported as White. The mean BMI was 38.5 (7.7) kg/m2 for the CeD+AOM group and 37.7 (8.0) kg/m2 for the AOM group. Baseline clinical and anthropometric characteristics were similar among groups (Table 1).
Table 1.
Demographic, anthropometric, and clinical characteristics at baseline
| Characteristics | Celiac disease + AOM N=39 | AOM N=78 | p value |
|---|---|---|---|
| Demographic | |||
| Age, years (SD) | 49.8 (13.8) | 50.8 (11.2) | 0.69 |
| Sex, females (%) | 35 (89.7) | 70 (89.7) | 1.00 |
| Race, White (%) | 38 (97.4) | 75 (96.1) | 1.00 |
| Anthropometric | |||
| Weight, kg (SD) | 105.3 (24.6) | 109.6 (25.1) | 0.37 |
| Body mass index, kg/m2 (SD) | 38.5 (7.7) | 37.7 (8.0) | 0.59 |
| Overweight, N (%) | 5 (12.8) | 4 (5.1) | 0.16 |
| Obesity Class 1, N (%) | 12 (30.8) | 22 (28.2) | 0.83 |
| Obesity Class 2, N (%) | 9 (23.1) | 28 (35.9) | 0.21 |
| Obesity Class 3, N (%) | 13 (33.3) | 24 (30.8) | 0.83 |
| Height, m (SD) | 1.67 (0.08) | 1.68 (0.08) | 0.35 |
| Comorbidities, N (%) | |||
| Type 2 diabetes | 14 (35.90) | 32 (41.0) | 0.69 |
| Dyslipidemia | 19 (48.7) | 42 (53.9) | 0.70 |
| Hypertension | 16 (41.0) | 35 (44.9) | 0.84 |
| GERD | 16 (41.0) | 27 (34.6) | 0.55 |
| NAFLD | 4 (10.3) | 12 (15.38) | 0.57 |
| OSA | 12 (30.8) | 26 (33.3) | 0.84 |
| AOM usage, N (%) | |||
| Semaglutide | 18 (46.2) | 36 (43.6) | 1.00 |
| Low dose | 16 (88.9) | 32 (88.9) | 1.00 |
| High dose | 2 (11.1) | 4 (11.1) | 1.00 |
| Phentermine | 11 (28.2) | 22 (28.2) | 1.00 |
| Phentermine + Topiramate | 7 (18.0) | 14 (18.0) | 1.00 |
| Liraglutide (high dose) | 3 (7.7) | 6 (7.7) | 1.00 |
AOM indicates antiobesity medication; GERD, Gastroesophageal reflux disorder; NAFLD, non-alcoholic fatty liver disease; OSA, obstructive sleep apnea.
Dyslipidemia was the most frequent obesity-associated comorbidity in both groups (53.9% in the CeD+AOM group vs. 48.7% in the AOM group), followed by hypertension. Over a third of the patients in our cohorts had type 2 diabetes (35.9% in the CeD+AOM group vs. 41.0% in the AOM group). All comorbidities were evenly distributed among both groups.
Semaglutide was the most frequently used AOM in both groups (46.2%), followed by phentermine (28.2%), phentermine-topiramate (18.0%) and liraglutide (7.7%). For patients taking semaglutide, both cohorts had the same proportion of patients taking low dose (less than 1.7 mg/weekly) or high dose (1.7 mg/weekly or more) injectable semaglutide, 88.9% and 11.1%, respectively. For liraglutide, all patients were taking a dose of 3 mg. No other AOM was prescribed in our cohort of patients with CeD.
Among the CeD cohort, patients had a mean age of 41.5 at diagnosis, with a mean time from diagnosis to start of AOM of 8.9 years. As well, 84.2% self-reported following a strict GFD (Table 2).
Table 2.
Celiac disease characteristics
| Characteristics | Celiac disease N=39 |
|---|---|
| Age at diagnosis, years (SD) | 40.9 (14.4) |
| Time from diagnosis to start of AOM, years (SD) | 8.9 (6.8) |
| TTG IgA at time of diagnosis, U/mL (SD) (N=24) | 23.6 (34.7) |
| TTG IgA ≤4 U/mL, N (%) | 9 (37.5) |
| TTG IgA >4 U/mL, N (%) | 15 (62.5) |
| TTG IgA during AOM treatment period, U/mL (SD) (N=24) | 6.0 (20.1) |
| TTG IgA ≤4 U/mL, N (%) | 21 (87.5) |
| TTG IgA >4 U/mL, N (%) | 3 (12.5) |
| Self-reported strict GFD, N (%) | 32 (82.0) |
AOM indicates antiobesity medication; GFD, gluten-free diet; IgA, immunoglobulin A; TTG, tissue transglutaminase.
Weight loss outcomes
The CeD cohort had a similar mean total body weight loss percent when compared to patients without CeD at 3 (4.53% vs. 4.40%, p=0.90) and 6 (6.41% vs. 6.54%, p=0.93) months (Table 3). There was a trend towards inferior TBWL% in the CeD+AOM group at 12 months (6.47% vs. 9.47, p=0.13) as compared to the AOM group, however, it was not significant (Figure 1).
Table 3.
Weight loss outcomes
| Characteristics | Celiac disease + AOM | AOM | p value |
|---|---|---|---|
| Total Body Weight Loss percentage (SD) | |||
| 3 months (N=26; 65) | 4.53 (4.4) | 4.40 (3.7) | 0.90 |
| 6 months (N= 18; 59) | 6.41 (6.9) | 6.54 (5.0) | 0.93 |
| 12 months (N=11; 43) | 6.47 (5.1) | 9.47 (7.4) | 0.13 |
| Categorical Total Body Weight Loss % at 12 months, N (%) | |||
| ≥5% (N=11; 43) | 8 (72.7) | 31 (72.1) | 1.00 |
| ≥10% (N=11; 43) | 4 (36.4) | 14 (32.6) | 0.49 |
| ≥15% (N=11; 43) | 0 (0.0) | 8 (18.6) | 0.18 |
AOM indicates antiobesity medication.
Figure 1.
Total body weight loss percentage (TBWL%) for Celiac + AOM and AOM groups at 3, 6, and 12 months. Whiskers in plot represent standard error of the mean. CeD: celiac disease, AOM: antiobesity medication, ns: not significant
At 12 months, 11 patients with and 43 without CeD had available weight data. The CeD+AOM group had a similar proportion of patients achieving a TBWL% of ≥5% (72.7% vs. 72.1%, p=1.00) and ≥10% (36.4% vs. 32.6%, p=0.49) when compared to patients in the AOM group, respectively (Figure 2). No patients with CeD achieved a TBWL≥15%, while 8 (18.6%) patients without CeD did (p=0.18).
Figure 2.
Categorical total body weight loss percentage (TBWL%) for Celiac + AOM and AOM groups at 12 months. CeD: celiac disease, AOM: antiobesity medication, ns: not significant.
Weight loss outcomes per AOM type and celiac disease status
At 12 months, we had weight data for 5 patients with CeD and 31 patients without CeD taking subcutaneous injectable GLP-1 receptor agonists. Patients without CeD had a mean TBWL% of 8.4% (7.3%), while patients in the CeD cohort had a TBWL% of 4.6% (6.9%). The proportion of patients achieving a total body weight loss of at least 5% at 12 months was similar in patients with (60%) or without (64.5%) CeD.
In our cohort, we had weight data at 12 months for 6 patients with and 12 patients without CeD taking either phentermine or phentermine-topiramate. Patients with CeD had a mean TBWL% of 8.0% (2.8%), while patients without CeD had a mean TBWL% of 12.3% (7.1%). In addition, 5 patients (83.3%) with and 11 patients (91.7%) without CeD lost at least 5% of total body weight loss with an oral AOM. Weight loss outcomes for individual AOMs in patients with or without CeD are reported in Table S1.
Side effect profile per AOM type
The proportions of patients with or without CeD experiencing side effects after taking AOMs were similar (30.8% vs. 28.2%) (Table 4). For patients taking injectable GLP-1 receptor agonists, there was a similar proportion of patients with or without CeD experiencing side effects (33.3% vs. 35.7%, p=1.00), and most side effects were gastrointestinal symptoms for both groups. In addition, the proportion of patients with CeD (27.8%) and controls (19.4%) that reported side effects with oral AOMs were similar (p=0.51), with non-gastrointestinal symptoms being more frequent.
Table 4.
Side effect profile by type of antiobesity medication
| Characteristic, N (%) | Celiac disease + AOM N=39 | AOM N=78 | p value |
|---|---|---|---|
| Any side effect | 12 (30.7) | 22 (28.2) | 0.83 |
| GI side effects* | 8 (66.7) | 12 (54.5) | 0.71 |
| Non-GI side effects¶ | 4 (33.3) | 10 (45.5) | 0.71 |
| Injectable GLP-1 receptor agonists | |||
| Any side effect | 7 (33.3) | 15 (35.7) | 1.00 |
| GI side effects | 6 (85.7) | 11 (73.3) | 1.00 |
| Non-GI side effects | 1 (14.3) | 4 (26.7) | 1.00 |
| Oral non-GLP-1 AOMs | |||
| Any side effect | 5 (27.8) | 7 (19.4) | 0.51 |
| GI side effects | 2 (40.0) | 1 (14.3) | 0.52 |
| Non-GI side effects | 3 (60.0) | 8 (85.7) | 0.52 |
Gastrointestinal symptoms included nausea/vomiting, abdominal pain, heartburn, diarrhea, and constipation.
Non-GI symptoms included dry mouth, fatigue, anxiety, insomnia, paresthesias, blurry vision and skin reaction.
AOM indicates antiobesity medication; GLP-1, glucagon-like peptide 1.
Discussion
In our study, we found that patients with CeD had similar weight loss outcomes as compared to a cohort without CeD after 12 months of treatment with AOMs. In addition, we did not find any difference when comparing patients with CeD receiving either injectable GLP-1 receptor agonists or oral AOMs.
The efficacy of different treatment modalities for obesity in patients with CeD has not been extensively studied. Bariatric surgery continues to be the most effective modality for weight loss and metabolic improvement in patients with obesity [19]. Some studies have assessed the efficacy of bariatric surgery in patients with CeD [20, 21]. A matched case-control study examined the outcomes and safety of bariatric surgery in 13 patients with CeD and 65 controls [22]. Patients with CeD had similar weight loss than the control group at all timepoints, with the highest weight loss at 12 months (TBWL% for CeD: 28.4% vs. 29.1% for controls). As well, both groups had an improvement in obesity-associated comorbidities, with a similar rate of side effects and micronutrient deficiencies after the procedure [22].
Patients with CeD had a trend towards inferior weight loss outcomes at 12 months, as compared to the group without CeD. However, this difference was not statistically significant and could be partly attributed to other factors. Patients in the AOM group were taking these medications for weight loss management, and likely received additional lifestyle interventions such as consultations with dietitians and behavioral bariatric psychologists, resulting in better weight loss outcomes. This effect was not assessed in our study and could have been different among both groups. As well, it has been previously reported that semaglutide has superior weight loss outcomes among patients without diabetes [23], however, in our study both cohorts had a similar prevalence of diabetes. A previous study examining real-world outcomes of long-term therapy with AOMs reported that patients taking phentermine-topiramate had a TBWL% of 12% at 12 months, as compared to 5.61% for liraglutide [24]. In the present study, the TBWL% for phentermine-topiramate was similar at 12 months (CeD+AOM: 7.6% vs. AOM: 10.4%), however, we found superior weight loss outcomes with liraglutide (CeD+AOM: 13.1% vs. AOM: 23.6%). These results could be partly explained by the fact that most participants in the previously mentioned study were on lower doses of liraglutide, while all patients included in our study were on doses approved for weight loss. Nonetheless, this analysis is limited by a small sample size and the vast heterogeneity in weight loss outcomes to different therapeutic modalities. Importantly, most of the patients included in our study were taking lower doses of semaglutide (doses inferior to 1.7 mg weekly). Higher doses of semaglutide (1.7 mg weekly or more) have been associated with superior weight loss outcomes in people with or without diabetes, and are approved by the FDA for chronic weight management [23, 25]. In a study assessing the effect of semaglutide in a real-world setting, semaglutide led to a mean TBWL% of 10.9% at 6 months, with 87.3% of patients achieving a TBWL% of at least 5% [26]. Differences in semaglutide doses could explain the lower-than-expected total body weight loss percentage in the group receiving semaglutide in our study.
In our study, the proportion of patients experiencing side effects with AOMs were similar in the CeD and in the control population, regardless of the type of AOM. However, the estimated prevalence of side effects in both groups were significantly lower than reports from previous randomized clinical trials of the included AOMs [23, 25, 27, 28]. Due to the retrospective nature of our study, it is likely that the prevalence of side effects in both groups was underestimated, which could be partly attributed to potential underreporting of mild side effects by patients [29].
Strengths and Limitations
To our knowledge, this is the first study reporting weight loss outcomes of AOMs in patients with CeD and overweight/obesity. However, this study has multiple limitations. Despite including patients from different centers, we had a small sample size of patients with CeD taking AOMs. Most of our study population were White females, which is consistent with previous reports that this population is most frequently affected by co-existent CeD and obesity [7], however, this could limit the generalizability of our results. As previously discussed, most participants included in our study were taking low doses of semaglutide, which could explain the inferior weight loss outcomes observed with this drug in this study, however, by matching participants by semaglutide dose (low/high), we consider that we minimized the potential effect on the relationship between CeD status and weight loss outcomes. In addition, even though we were able to gather self-reported adherence to GFD during chart review, we did not have a method to assess for diet compliance. The role of adherence to GFD in weight loss outcomes of different therapeutic modalities for obesity needs to be further examined. In our study, patients had a mean time interval of 8 years from diagnosis of CeD to start of AOM. The time needed to recover mucosal absorptive functionality after starting GFD has not been clearly defined, and factors like non-compliance with GFD or inadvertent gluten ingestion might influence the process [30]. Patients with a shorter interval between diagnosis of CeD and start of an AOM might have a different response to weight management modalities, and this effect remains to be assessed. Additional studies with a larger sample size are needed to draw more robust conclusions about the effectiveness and safety of antiobesity medications in weight loss and metabolic improvement of obesity-associated comorbidities for patients with CeD and overweight/obesity. In addition, the effect of high dose semaglutide, and novel agents such as tirzepatide, a dual glucose-dependent insulinotropic polypeptide and GLP-1 receptor analogue, remains to be studied.
Conclusions
Patients with CeD have similar weight loss outcomes in response to AOM than patients without CeD. In addition, oral and injectable subcutaneous AOMs led to similar weight loss response for patients with CeD. Antiobesity medications are a safe and effective weight management intervention in patients with CeD and overweight/obesity.
Supplementary Material
Conflicts of Interest and Source of Funding:
Dr. Acosta is a stockholder in Gila Therapeutics, Phenomix Sciences; he served as a consultant for Rhythm Pharmaceuticals, General Mills, and Amgen Pharmaceuticals. Dr. Murray reports grants (to institution) from Nexpep/ImmusanT, National Institutes of Health, Immunogenix, Takeda Pharmaceutical, Allakos, ProventionBio, Oberkotter Foundation, and 9Meters, Inc.; contract (to institution) from Kanyos Bio (a wholly owned subsidiary of Anokion); and consultancy fees from Johnson and Johnson, Bristol Myers Squibb, Intrexon Corporation, Dren Bio, Neoleukin, Reistone pharma, Immunic Therapeutics, Senda Biosciences, Brightseed Bio, Chugai Pharma, Alimentiv, Equillium, Ukko, Medibeacon, Precigen, triangle insights group, Sanofi and Orbimed and has received royalties from Torax Medical and Evelo. Dr. Murray is supported by DK 133947. Dr. Bledsoe receives grant funding (to institution) from Kanyos Bio (subsidiary of Anokion).
Abbreviations:
- AOMs
Antiobesity medications
- CeD
Celiac disease
- GFD
Gluten-free diet
- GLP-1
Glucagon-like peptide 1
- TBWL
Total body weight loss
Footnotes
Writing Assistance: None.
Data Transparency Statement: Deidentified individual participant data can be shared to bona fide researchers upon request.
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