Bio
Dr. Lee is a gastroenterologist at Stanford University who specializes in pancreas disease. Her clinical focus is on the care of patients with pancreatic disorders such as acute pancreatitis, chronic pancreatitis, pancreas cysts, pancreatic insufficiency, and screening for pancreas cancer in high-risk individuals. Dr. Lee conducts clinical research in early detection of pancreatic cancer, including the investigation of risk factors for pancreatic cancer and biomarkers to detect early cancer.
Clinical Focus
- Gastroenterology
- Pancreas
- Acute Pancreatitis
- Chronic Pancreatitis
- Pancreatic Cysts
- Exocrine Pancreatic Insufficiency
- Early Detection of Pancreatic Cancer
Boards, Advisory Committees, Professional Organizations
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Member, American College of Gastroenterology (2020 - Present)
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Member, American Gastroenterological Association (2020 - Present)
Professional Education
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Board Certification: American Board of Internal Medicine, Gastroenterology (2023)
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Master of Public Health, Harvard T. H. Chan School of Public Health, MPH (2023)
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Fellowship, Brigham and Women's Hospital/Harvard Medical School, Gastroenterology and Hepatology (2023)
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Board Certification: American Board of Internal Medicine, Internal Medicine (2020)
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Residency, University of Southern California, Internal Medicine (2020)
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Medical Education, Rush University Medical College, MD (2017)
Current Research and Scholarly Interests
Dr. Lee's research focuses on the early detection of pancreatic cancer, including the investigation of risk factors for pancreatic cancer and biomarkers to detect early cancer.
All Publications
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Cancer Diagnoses After Recent Weight Loss.
JAMA
2024; 331 (4): 318-328
Abstract
Weight loss is common in primary care. Among individuals with recent weight loss, the rates of cancer during the subsequent 12 months are unclear compared with those without recent weight loss.To determine the rates of subsequent cancer diagnoses over 12 months among health professionals with weight loss during the prior 2 years compared with those without recent weight loss.Prospective cohort analysis of females aged 40 years or older from the Nurses' Health Study who were followed up from June 1978 until June 30, 2016, and males aged 40 years or older from the Health Professionals Follow-Up Study who were followed up from January 1988 until January 31, 2016.Recent weight change was calculated from the participant weights that were reported biennially. The intentionality of weight loss was categorized as high if both physical activity and diet quality increased, medium if only 1 increased, and low if neither increased.Rates of cancer diagnosis during the 12 months after weight loss.Among 157 474 participants (median age, 62 years [IQR, 54-70 years]; 111 912 were female [71.1%]; there were 2631 participants [1.7%] who self-identified as Asian, Native American, or Native Hawaiian; 2678 Black participants [1.7%]; and 149 903 White participants [95.2%]) and during 1.64 million person-years of follow-up, 15 809 incident cancer cases were identified (incident rate, 964 cases/100 000 person-years). During the 12 months after reported weight change, there were 1362 cancer cases/100 000 person-years among all participants with recent weight loss of greater than 10.0% of body weight compared with 869 cancer cases/100 000 person-years among those without recent weight loss (between-group difference, 493 cases/100 000 person-years [95% CI, 391-594 cases/100 000 person-years]; P < .001). Among participants categorized with low intentionality for weight loss, there were 2687 cancer cases/100 000 person-years for those with weight loss of greater than 10.0% of body weight compared with 1220 cancer cases/100 000 person-years for those without recent weight loss (between-group difference, 1467 cases/100 000 person-years [95% CI, 799-2135 cases/100 000 person-years]; P < .001). Cancer of the upper gastrointestinal tract (cancer of the esophagus, stomach, liver, biliary tract, or pancreas) was particularly common among participants with recent weight loss; there were 173 cancer cases/100 000 person-years for those with weight loss of greater than 10.0% of body weight compared with 36 cancer cases/100 000 person-years for those without recent weight loss (between-group difference, 137 cases/100 000 person-years [95% CI, 101-172 cases/100 000 person-years]; P < .001).Health professionals with weight loss within the prior 2 years had a significantly higher risk of cancer during the subsequent 12 months compared with those without recent weight loss. Cancer of the upper gastrointestinal tract was particularly common among participants with recent weight loss compared with those without recent weight loss.
View details for DOI 10.1001/jama.2023.25869
View details for PubMedID 38261044
View details for PubMedCentralID PMC10807298
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A Shift Toward Early Oral Feeding in Acute Pancreatitis.
Pancreas
2023
Abstract
The 2018 American Gastroenterological Association (AGA) guidelines strongly recommended early oral feeding as tolerated in patients with acute pancreatitis (AP). We compare early oral feeding rates in AP patients hospitalized in the periods before (2013-2016, Period A) and after (2019-2020, Period B) publication of the AGA guidelines, hypothesizing increased adherence in Period B.We performed a retrospective cohort study of AP patients presenting to the emergency department during each period. Early oral feeding was defined as diet initiation within the first 48 hours of presentation.The cohort included 276 AP cases in period A and 104 in period B. A higher percentage of patients were offered early oral feeding during period B as compared to period A (70.2% vs. 43.5%). Similarly, more patients in period B were started on solid diet as compared to period A (34.6% vs. 20.3%). On multivariable regression analysis, the independent predictors of delayed oral feeding included early opioid analgesics use (OR 0.37), presence of pancreatic necrosis (OR 0.14), and organ failure (OR 0.33).More AP patients were initiated on early oral feeding in the period following the publication of the AGA guidelines. Opioid analgesics use, pancreatic necrosis, and organ failure were associated with delayed oral feeding.
View details for DOI 10.1097/MPA.0000000000002280
View details for PubMedID 38019610
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Sex-specific associations between adiponectin and leptin signaling and pancreatic cancer survival.
Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology
2023
Abstract
BACKGROUND: Circulating adiponectin and leptin have been associated with risk of pancreatic cancer. However, the relationship between long-term exposure to these adipokines in the prediagnostic period with patient survival has not been investigated.METHODS: Adipokine levels were measured in prospectively collected samples from 472 pancreatic cancer patients. Due to sex-specific differences in adipokine levels, associations were evaluated separately for men and women. In a subset of 415 patients, we genotyped 23 nucleotide polymorphisms (SNPs) in adiponectin receptor genes (ADIPOR1, ADIPOR2) and 30 SNPs in the leptin receptor gene (LEPR).RESULTS: Adiponectin levels were inversely associated with survival in women (HR=1.47, 95% CI: 1.03-2.11, comparing top to bottom quartile) but not in men (HR=0.93, 95% CI: 0.54-1.59). The SNPs rs10753929 and rs1418445 in ADIPOR1 were associated with survival in the combined population (per minor allele HR=0.66, 95% CI: 0.51-0.84, and HR=1.33, 95% CI: 1.12-1.58, respectively). Among SNPs in LEPR, rs12025906, rs3790431, and rs17127601 were associated with survival in the combined population [HRs (95% CI) of 1.54 (1.25-1.90), 0.72 (0.59-0.88), and 0.70 (0.56-0.89), respectively], while rs11585329 was associated with survival in men only (HR=0.39, 95% CI: 0.23-0.66) (P-interaction=0.0002).CONCLUSIONS: High levels of adiponectin in the prediagnostic period were associated with shorter survival among women, but not among men with pancreatic cancer. Several polymorphisms in ADIPOR1 and LEPR are associated with patient survival.IMPACT: Our findings reveal the association between adipokine signaling and pancreatic cancer survival and demonstrate the importance of examining obesity-associated pathways in relation to pancreatic cancer in a sex-specific manner.
View details for DOI 10.1158/1055-9965.EPI-23-0505
View details for PubMedID 37555827
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Adipose tissue and skeletal muscle wasting precede clinical diagnosis of pancreatic cancer.
Nature communications
2023; 14 (1): 4317
Abstract
Patients with pancreatic cancer commonly develop weight loss and muscle wasting. Whether adipose tissue and skeletal muscle losses begin before diagnosis and the potential utility of such losses for earlier cancer detection are not well understood. We quantify skeletal muscle and adipose tissue areas from computed tomography (CT) imaging obtained 2 months to 5 years before cancer diagnosis in 714 pancreatic cancer cases and 1748 matched controls. Adipose tissue loss is identified up to 6 months, and skeletal muscle wasting is identified up to 18 months before the clinical diagnosis of pancreatic cancer and is not present in the matched control population. Tissue losses are of similar magnitude in cases diagnosed with localized compared with metastatic disease and are not correlated with at-diagnosis circulating levels of CA19-9. Skeletal muscle wasting occurs in the 1-2 years before pancreatic cancer diagnosis and may signal an upcoming diagnosis of pancreatic cancer.
View details for DOI 10.1038/s41467-023-40024-3
View details for PubMedID 37463915
View details for PubMedCentralID PMC10354105
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Drug-induced acute pancreatitis due to medications used for inflammatory bowel disease: A VigiBase pharmacovigilance database study.
Pancreatology : official journal of the International Association of Pancreatology (IAP) ... [et al.]
2023
Abstract
BACKGROUND: Nearly all medications used for inflammatory bowel disease (IBD) have been reported as causes of acute pancreatitis (AP), with the thiopurines being among the most frequently described. However, with the development of newer medications, thiopurine monotherapy has largely been replaced by newer immunosuppressive drugs. There are few data on the association between AP and biologic/small molecule agents.METHODS: VigiBase, the World Health Organization's Global Individual Case Safety Report database, was used to assess the association between AP and common IBD medications. A case/non-case disproportionality analysis was performed and disproportionality signals were reported as a reporting odds ratio (ROR) with 95% confidence intervals (CIs).RESULTS: A total of 4,223 AP episodes were identified for common IBD medications. Azathioprine (ROR 19.18, 95% CI 18.21-20.20), 6-mercaptopurine (ROR 13.30, 95% CI 11.73-15.07), and 5-aminosalicylic acid (ROR 17.44, 95% CI 16.24-18.72) all had strong associations with AP, while the biologic/small molecule agents showed weaker or no disproportionality. The association with AP was much higher for thiopurines when used for Crohn's disease (ROR 34.61, 95% CI 30.95-38.70) compared to ulcerative colitis (ROR 8.94, 95% CI 7.47-10.71) or rheumatologic conditions (ROR 18.87, 95% CI 14.72-24.19).CONCLUSIONS: We report the largest real-world database study investigating the association between common IBD medications and AP. Among commonly used IBD medications including biologic/small molecule agents, only thiopurines and 5-aminosalicylic acid are strongly associated with AP. The association between thiopurines and AP is much stronger when the drug is used for Crohn's disease compared to ulcerative colitis and rheumatologic conditions.
View details for DOI 10.1016/j.pan.2023.06.003
View details for PubMedID 37302896
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Pancreatic cancer is associated with medication changes prior to clinical diagnosis
NATURE COMMUNICATIONS
2023; 14 (1): 2437
Abstract
Patients with pancreatic ductal adenocarcinoma (PDAC) commonly develop symptoms and signs in the 1-2 years before diagnosis that can result in changes to medications. We investigate recent medication changes and PDAC diagnosis in Nurses' Health Study (NHS; females) and Health Professionals Follow-up Study (HPFS; males), including up to 148,973 U.S. participants followed for 2,994,057 person-years and 991 incident PDAC cases. Here we show recent initiation of antidiabetic (NHS) or anticoagulant (NHS, HFS) medications and cessation of antihypertensive medications (NHS, HPFS) are associated with pancreatic cancer diagnosis in the next 2 years. Two-year PDAC risk increases as number of relevant medication changes increases (P-trend <1 × 10-5), with participants who recently start antidiabetic and stop antihypertensive medications having multivariable-adjusted hazard ratio of 4.86 (95%CI, 1.74-13.6). These changes are not associated with diagnosis of other digestive system cancers. Recent medication changes should be considered as candidate features in multi-factor risk models for PDAC, though they are not causally implicated in development of PDAC.
View details for DOI 10.1038/s41467-023-38088-2
View details for Web of Science ID 000983415900008
View details for PubMedID 37117188
View details for PubMedCentralID PMC10147931
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Helicobacter pylori Seropositivity, ABO Blood Type, and Pancreatic Cancer Risk From 5 Prospective Cohorts.
Clinical and translational gastroenterology
2023; 14 (5): e00573
Abstract
BACKGROUND: Helicobacter pylori infection may be a risk factor for pancreatic cancer, particularly infection by strains without the cytotoxin-associated gene A (CagA) virulence factor. Non-O blood type is a known risk factor for pancreatic cancer, and H. pylori gastric colonization occurs largely from bacterial adhesins binding to blood group antigens on gastric mucosa.METHODS: We included 485 pancreatic cancer cases and 1,122 matched controls from 5 U.S. prospective cohorts. Prediagnostic plasma samples were assessed for H. pylori and CagA antibody titers. Conditional logistic regression was used to estimate odds ratios (ORs) and 95% confidence intervals (CIs) for pancreatic cancer. ABO blood type was assessed using genetic polymorphisms at the ABO gene locus or self-report.RESULTS: Compared with H. pylori -seronegative participants, those who were seropositive did not demonstrate an increased risk of pancreatic cancer (OR 0.83, 95% CI 0.65-1.06). This lack of association was similar among CagA-seropositive (OR 0.75, 95% CI 0.53-1.04) and -seronegative (OR 0.89, 95% CI 0.65-1.20) participants. The association was also similar when stratified by time between blood collection and cancer diagnosis ( P -interaction = 0.80). Consistent with previous studies, non-O blood type was associated with increased pancreatic cancer risk, but this increase in risk was similar regardless of H. pylori seropositivity ( P -interaction = 0.51).DISCUSSION: In this nested case-control study, history of H. pylori infection as determined by H. pylori antibody serology was not associated with pancreatic cancer risk, regardless of CagA virulence factor status. The elevated risk associated with non-O blood type was consistent in those with or without H. pylori seropositivity.
View details for DOI 10.14309/ctg.0000000000000573
View details for PubMedID 36854058
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Undiagnosed Exocrine Pancreatic Insufficiency in Diarrhea-Predominant Irritable Bowel Syndrome.
Digestive diseases and sciences
2022; 67 (12): 5364-5365
View details for DOI 10.1007/s10620-022-07574-w
View details for PubMedID 35705731
View details for PubMedCentralID 5656454
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The age-dependent association of risk factors with pancreatic cancer
ANNALS OF ONCOLOGY
2022; 33 (7): 693-701
Abstract
Pancreatic cancer presents as advanced disease in >80% of patients; yet, appropriate ages to consider prevention and early detection strategies are poorly defined. We investigated age-specific associations and attributable risks of pancreatic cancer for established modifiable and non-modifiable risk factors.We included 167 483 participants from two prospective US cohort studies with 1190 incident cases of pancreatic cancer during >30 years of follow-up; 5107 pancreatic cancer cases and 8845 control participants of European ancestry from a completed multicenter genome-wide association study (GWAS); and 248 893 pancreatic cancer cases documented in the US Surveillance, Epidemiology, and End Results (SEER) Program. Across different age categories, we investigated cigarette smoking, obesity, diabetes, height, and non-O blood group in the prospective cohorts; weighted polygenic risk score of 22 previously identified single nucleotide polymorphisms in the GWAS; and male sex and black race in the SEER Program.In the prospective cohorts, all five risk factors were more strongly associated with pancreatic cancer risk among younger participants, with associations attenuated among those aged >70 years. The hazard ratios comparing participants with three to five risk factors with those with no risk factors were 9.24 [95% confidence interval (CI) 4.11-20.77] among those aged ≤60 years, 3.00 (95% CI 1.85-4.86) among those aged 61-70 years, and 1.46 (95% CI 1.10-1.94) among those aged >70 years (Pheterogeneity = 3×10-5). These factors together were related to 65.6%, 49.7%, and 17.2% of incident pancreatic cancers in these age groups, respectively. In the GWAS and the SEER Program, the associations with the polygenic risk score, male sex, and black race were all stronger among younger individuals (Pheterogeneity ≤0.01).Established risk factors are more strongly associated with earlier-onset pancreatic cancer, emphasizing the importance of age at initiation for cancer prevention and control programs targeting this highly lethal malignancy.
View details for DOI 10.1016/j.annonc.2022.03.276
View details for Web of Science ID 000814934800005
View details for PubMedID 35398288
View details for PubMedCentralID PMC9233063
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Comprehensive meta-analysis of randomized controlled trials of Lactated Ringer's versus Normal Saline for acute pancreatitis
PANCREATOLOGY
2021; 21 (8): 1405-1410
Abstract
Fluid resuscitation is the keystone of treatment for acute pancreatitis. Though clinical guidelines and expert opinions agree on large volume resuscitation, debate remains on the optimal fluid type. The most commonly used fluids are Lactated Ringer's (LR) and Normal Saline (NS), but the studies published to date comparing LR vs NS yield conflicting results. We aimed to identify and quantitatively synthesize existing high quality data of the topic of fluid type or acute pancreatitis resuscitation.In collaboration with the study team, an information specialist performed a comprehensive literature review to identify reports addressing type of fluid resuscitation. Studies were screened using the Covidence system by two independent reviewers in order to identify Randomized controlled trials comparing LR versus NS. The main outcome was the development of moderately severe or severe pancreatitis and additional outcomes included local complications, ICU admission, and length of stay. Pooled odds ratios were estimated using the random effects model and standardized mean difference to compare continuous variables.We reviewed 7964 abstracts and 57 full text documents. Four randomized controlled trials were identified and included in our meta-analyses. There were a total of 122 patients resuscitated with LR versus 126 with NS. Patients resuscitated with LR were less likely to develop moderately severe/severe pancreatitis (OR 0.49; 95 % CI 0.25-0.97). There was no difference in development of SIRS at 24 or 48 h or development of organ failure between the two groups. Patients resuscitated with LR were less likely to require ICU admission (OR 0.33; 95 % CI 0.13-0.81) and local complications (OR 0.42; 95 % CI 0.2-0.88). While there was a trend towards shorter hospitalizations for LR (SMD -0.18, 99 % CI -0.44-0.07), it was not statistically significant.Resuscitation with LR reduces the development of moderately severe-severe pancreatitis relative to NS. Nevertheless, no difference in SIRS development or organ failure underscores the need for further studies to verify this finding and define its mechanism.
View details for DOI 10.1016/j.pan.2021.07.003
View details for Web of Science ID 000757476100001
View details for PubMedID 34332907
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ASGE guideline on the management of cholangitis
GASTROINTESTINAL ENDOSCOPY
2021; 94 (2): 207-+
Abstract
Cholangitis is a GI emergency requiring prompt recognition and treatment. The purpose of this document from the American Society for Gastrointestinal Endoscopy's (ASGE) Standards of Practice Committee is to provide an evidence-based approach for management of cholangitis. This document addresses the modality of drainage (endoscopic vs percutaneous), timing of intervention (<48 hours vs >48 hours), and extent of initial intervention (comprehensive therapy vs decompression alone). Grading of Recommendations, Assessment, Development, and Evaluation methodology was used to formulate recommendations on these topics. The ASGE suggests endoscopic rather than percutaneous drainage and biliary decompression within 48 hours. Additionally, the panel suggests that sphincterotomy and stone removal be combined with drainage rather than decompression alone, unless patients are too unstable to tolerate more extensive endoscopic treatment.
View details for DOI 10.1016/j.gie.2020.12.032
View details for Web of Science ID 000672795700001
View details for PubMedID 34023065
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Lactated Ringers vs Normal Saline Resuscitation for Mild Acute Pancreatitis: A Randomized Trial
GASTROENTEROLOGY
2021; 160 (3): 955-+
View details for DOI 10.1053/j.gastro.2020.10.044
View details for Web of Science ID 000627420700056
View details for PubMedID 33159924
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Qualitative and Quantitative Contrast-enhanced Endoscopic Ultrasound Improves Evaluation of Focal Pancreatic Lesions
CLINICAL GASTROENTEROLOGY AND HEPATOLOGY
2020; 18 (4): 917-+
Abstract
Endoscopic ultrasound (EUS) is a sensitive method to evaluate the pancreas but its diagnostic capability for several diseases is limited. We compared the diagnostic yield of unenhanced EUS with that of contrast-enhanced EUS for focal pancreas lesions and identified and tested quantitative parameters of contrast enhancement.We performed a prospective tandem-controlled trial in which 101 patients with focal pancreas lesions (48 with masses, 28 with cysts, and 25 with pancreatitis) underwent conventional EUS followed by contrast EUS using intravenous perflutren microspheres. The diagnosis at each stage was scored and compared with a standard (findings from surgical pathology analysis, cytologic, and/or 6-month clinical follow-up evaluations). Quantitative parameters were generated by time-intensity curve analysis. Solid lesions were divided into derivation and testing cohorts for a crossover validation analysis of the quantitative parameters. The primary outcome was diagnostic yield of unenhanced vs contrast EUS in analysis of focal pancreas lesions.Contrast increased the diagnostic yield of EUS from 64% (65/101 lesions accurately assessed) to 91% (92/101 lesions accurately assessed); the odds ratio [OR] was 7.8 (95% CI, 2.7-30.2) for accurate analysis of lesions by contrast-enhanced EUS relative to unenhanced EUS. The contrast increased accuracy of analysis of pancreas masses (OR, 6.0; 95% CI, 1.8-31.8), improving assessment of neuroendocrine and other (non-carcinoma) tumors. Contrast increased the diagnostic yield for pancreas cysts to 96% (27/28) compared with 71.4% (20/28) for unenhanced EUS (P = .02), due to improved differentiation of mural nodules vs debris. Time-intensity curve analysis revealed distinct patterns of relative peak enhancement (rPE) and in-slope (rIS) for different lesions following contrast injection: for adenocarcinomas, values were low rPE and low rIS; for neuroendocrine masses, values were high rPE and normal IS; and for chronic pancreatitis foci, values were normal rPE and low rIS. In the validation cohort, these parameters correctly characterized 91% of lesions and improved yield relative to unenhanced EUS (OR, 10; 95% CI, 1.4-34.0).Contrast-enhanced EUS improves the accuracy of analysis of focal pancreas lesions, compared with unenhanced EUS. Integration of practical quantitative parameters, specifically relative peak enhancement and in-slope, might increase the diagnostic accuracy of contrast EUS. ClinicalTrials.gov no: 02863770.
View details for DOI 10.1016/j.cgh.2019.08.054
View details for Web of Science ID 000520865700030
View details for PubMedID 31499247
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Chronotype, social jet lag, sleep debt and food timing in inflammatory bowel disease
SLEEP MEDICINE
2018; 52: 188-195
Abstract
The preference of the sleep/wake cycle can be grouped into categories or chronotypes. Inflammatory bowel disease (IBD) has been linked to poor sleep quality which correlates with disease severity. Social jet lag (SJL) is the difference between sleep timing on work and free days and is a marker for circadian misalignment which has been linked to increased inflammation. We investigated whether chronotype, SJL, sleep debt (SD), and food timing were associated with an IBD specific complications and a lower quality of life. Overall, 191 subjects (115 IBD subjects and 76 healthy controls (HC)) completed the Pittsburgh Sleep Quality Index (PSQI), Morningness-Eveningness Questionnaire (MEQ), Munich ChronoType Questionnaire (MCTQ), Short Inflammatory Bowel Disease Questionnaire (SIBDQ), and a structured Food Timing Questionnaire. Later chronotype (by MEQ) was associated with a worse SIBDQ (r = -0.209; P < 0.05). SJL was increased in IBD at 1.32 h ± 1.03 vs. 1.05 h ± 0.97 in HC, P < 0.05, when adjusted for age. SJL (>2 h) was present in 40% of severe/complicated Crohn's patients (fistulizing or structuring Crohn's or history of Crohn's related surgery) compared to only 16% of uncomplicated Crohn's patients (P < 0.05). Sleep debt was increased in IBD subjects compared to HC at 21.90 m ± 25.37 vs. 11.49 m ± 13.58, P < 0.05. IBD subjects with inconsistent breakfast or dinner times had lower SIBDQ scores (4.78 ± 1.28 vs. 5.49 ± 1.02, P < 0.05; 4.95 ± 0.31 vs. 5.42 ± 0.32, P < 0.05 respectively). In summary, later chronotype, and markers of circadian misalignment (social jet lag, sleep debt, and inconsistent meal timing) were associated with IBD disease specific complications and/or lower quality of life.
View details for DOI 10.1016/j.sleep.2018.08.002
View details for Web of Science ID 000450326800032
View details for PubMedID 30243610
View details for PubMedCentralID PMC8177729