Sleep and Risk of Peptic Ulcer Disease: a cross-sectional study

doi:10.21203/rs.3.rs-5216763/v1

Download PDF

Article

Sleep and Risk of Peptic Ulcer Disease: a cross-sectional study

https://doi.org/10.21203/rs.3.rs-5216763/v1

This work is licensed under a CC BY 4.0 License

You are reading this latest preprint version

BACKGROUND & AIMS：The association between sleep duration and gastrointestinal disorders has been investigated extensively, but the specific link with peptic ulcer disease (PUD), including gastric ulcer (GU) and duodenal ulcer (DU), has not been thoroughly examined. Our objective was to assess the relationship between sleep duration and the occurrence of PUD, GU, and DU.

METHODS: We undertook a cross-sectional analysis involving 4,860 individuals from the Wuwei cohort. Participants' daily sleep duration was assessed by inquiring about the number of hours slept per day. Odds ratios and 95% confidence intervals were calculated using binary logistic regression.

RESULTS: In age- and sex-adjusted logistic regression analyses, those who slept > 9h were less likely to develop GU compared to those who slept 7-9h. (OR = 0.67, 95% CI= 0.55-0.80) , but had an increased risk of developing DU (OR = 1.39, 95% CI=1.10-1.77).This result remains significant in Model 2.

CONCLUSIONS: Prolonged sleep associated with gastric ulcer and duodenal ulcer disease

Sleep

Peptic Ulcer Disease

duodenal ulcer

Despite the declining incidence of peptic ulcer disease (PUD) and its complications attributed to the discovery of potent acid suppressants and the eradication of Helicobacter pylori infection, PUD continues to be prevalent in clinical settings and significantly impacts the healthcare system.Gastric ulcers and duodenal ulcers are frequently encountered peptic diseases in clinical practice.According to a systematic review including data from the USA, UK, and Europe, peptic ulcer disease affects 1–2 individuals per 1000 annually.^1,2A time trend study involving 12,612 patients from Asia demonstrated a similar incidence and a declining trend.³Earlier research indicates that 90% of duodenal ulcers and 70% of gastric ulcers are linked to Helicobacter pylori infection.^4,5However, recent studies have demonstrated that NSAID use, smoking, alcohol consumption, dietary factors, lifestyle habits, and sleep patterns all contribute to the risk of developing peptic ulcers.⁶

Sleep is fundamental to human life, and the duration of nighttime sleep significantly impacts both physical and mental well-beingPrevious research indicates that the duration of nighttime sleep is linked to a higher risk of obesity, diabetes, metabolic syndrome, inflammatory bowel disease, and hypertension.^7–10Moreover, an increasing body of clinical evidence suggests that the duration and quality of sleep can affect gastrointestinal health. For example, during deep sleep, protective mechanisms against peptic ulcer disease are activated, leading to increased gastric mucosal blood flow, gastric bicarbonate secretion, and melatonin secretion. Additionally, gastric acid secretion in the gastric lumen decreases, while it increases in the duodenum, among other effects.^11–13Research conducted in Korea revealed that women who slept for 9 hours or more had a significantly lower likelihood of experiencing peptic ulcer disease (PUD) compared to those who slept for 7 hours. In men, there was a tendency for longer sleep duration (≥ 9 hours) to be associated with a reduced risk of PUD.¹⁴

To our knowledge, no studies have investigated the influence of nighttime sleep duration on the development of gastric and duodenal ulcers separately.This cross-sectional study aimed to explore the association between self-reported nighttime sleep duration and the prevalence of gastric and duodenal ulcers in a population from Wuwei, Northwest China.

Study population

This cross-sectional study utilized data from the Wuwei cohort, a population-based gastric cancer cohort situated in the Wuwei Municipality of Gansu Province, China. Notably, this region exhibits some of the highest incidence and mortality rates of gastric cancer in the country. As depicted in Fig. 1, a total of 23,346 participants aged 35–70 years were selected using a cluster sampling method between March 2013 and April 2016, with 21,345 of them undergoing gastroscopies. From this cohort, 4,860 participants were chosen, including 1,003 peptic ulcer patients and 3,857 non-peptic ulcer patients, based on their completion of a sleep information questionnaire. After excluding individuals diagnosed with gastric cancer, salami ulcer, leiomyoma, obstruction, or gastric stump cancer, as well as those lacking anthropometric measurements or serum biochemical parameters, the study included 617 patients with gastric ulcers and 375 patients with duodenal ulcers. Patients with ulcers or bleeding of unclear etiology were not excluded. Written informed consent was obtained from all participants in the Wuwei cohort, who also underwent general physical and epidemiological examinations before enrollment. Furthermore, each participant underwent gastroscopy. The study received approval from the ethics committee of The First Hospital of Lanzhou University (approval number: LDYYLL2012001), and written informed consent was obtained from all participants prior to enrollment, adhering to the principles of the Declaration of Helsinki.

Measurement of sleep duration

Sleep time is defined as the average actual daily sleep time over the past 1 month, excluding time spent in bed but not asleep and other time spent in bed while awake. It excludes time spent in bed but not asleep and time spent in bed in other waking states. In this study, reference was made to In this study, we refer to the 2015 recommendations of the American Sleep Association on sleep duration¹⁵, which classified sleep duration as "≤7 hours (hours, h)", "7 ~ 9h" and "≥9h". Two questions were asked: “What time do you usually fall asleep at night?” and “What time do you wake up in the morning?”

Assessment of covariates

All participants responded to a questionnaire regarding their basic information, namely, their sex, race, address, marital status, education, and family income; personal medical history of hypertension; family medical history of gastric cancer; and behavioral factors, namely, their diet, smoking status, and alcohol intake.Trained staff members collected anthropometric measurements and serum biochemical parameters in accordance with standard procedures. The participants were asked to remove their shoes for height measurement to the nearest 0.1 cm. Weight was measured to the nearest 0.1 kg with the participants in clothing; the weight of their clothing, which was estimated on the basis of the season in which their measurements were collected, was deducted. WC and hip circumference were measured to the nearest 0.1 cm with a soft measuring tape. Blood chemistry tests were performed after the participants had fasted overnight.

Assessment of PUD

Trained hospital staff members conducted esophagogastroduodenoscopy (EGD) to confirm PUD after the participants had fasted overnight. A peptic ulcer was defined as a mucosal break ≥ 3 mm in diameter.

Data analysis.

Data were analysed using SPSS 26.0 for Windows (SPSS Inc., Chicago, IL, USA). To compare the baseline characteristics of our study sample, we assessed categorical variables as proportions (%) and continuous variables as means ± standard deviations (SD) or as medians (interquartile ranges). We compared the continuous variables were through two sample Student’s t tests or Wilcoxon rank sum tests, and we compared the categorical variables through chi-square tests.We employed binary logistic regression to analyze the associations between nighttime sleep duration with PUD in a crude analysis and ORs (with 95% CIs). We performed further analyses after adjusting for confounding factors, including age, sex, smoking, drinking, hot food diet, diet fast, H. pylori status,BMI,WC, blood pressure.

Characteristics of study subjects

Our study comprised 4,859 individuals, with 2,039 (42.0%) being male and 2,820 (58.0%) female. The characteristics of the study population stratified by both sleep duration and nap duration are presented in Table 1. The prevalence of peptic ulcer disease (PUD) was 62.1% among participants categorized by sleep duration. Significant differences (p < 0.05) were observed between genders, education levels, income brackets, waist circumference measurements, presence of gastric and duodenal ulcers, preference for hot food, and fast food consumption (defined as eating within < 8 minutes per bowl). Additionally, alcohol consumption and marital status were significantly associated with sleep duration. Individuals sleeping for more than 9 hours were more likely to be older, obese, and to have peptic ulcers and H. pylori infection compared to those with shorter sleep durations.

Table 1

Baseline characteristics of the study subjects by sleep duration and napping
		Sleep durtion		P
	<7	7–9	>9
n	419	1634	2806
Age	47.7 ± 6.4	47.8 ± 6.7	48.2 ± 7.3	0.066
Woman(%)	222(53.0%)	912(55.8%)	1686(60.1%)	0.002
Married	401(95.7%)	1597(97.7%)	2701(96.3%)	0.011
Smoking	140(33.5%)	527(32.3%)	846(30.2%)	0.187
Drinking	43(10.3%)	107(6.5%)	254(9.1%)	0.004
Education
Uneducated	39(9.3%)	169(10.3%)	495(17.6%)	0.000
Primary school	134(32.0%)	628(38.4%)	1024(36.5%)	0.000
Middle/high school	243(58.0%)	825(50.5%)	1281(45.7%)	0.000
University	3(0.7%)	12(0.7%)	6(0.2%)	0.000
Income	2.0(1.0,3.0)	1.95(1.0,3.0)	2.0(1.0,3.0)	0.000
Systolic BP (mmHg)	120.6 ± 12.5	120.5 ± 14.4	121.1 ± 14.4	0.384
Diastolic BP (mmHg)	76.0 ± 8.5	76.4 ± 9.7	76.8 ± 9.8	0.282
BMI				0.153
< 18.5	11(2.6%)	41(2.5%)	57(2.0%)
18.5 to < 24.0	232(55.4%)	905(55.4%)	1472(52.5%)
24.0 to < 28.0	140(33.4%)	578(35.4%)	1082(38.6%)
≥ 28.0	36(8.6%)	110(6.7%)	195(6.9%)
WC (cm, male)				0.001
< 70	2(1.0%)	32(4.4%)	21(1.9%)
70 to < 85	87(44.2%)	340(47.1%)	487(43.5%)
85 to < 90	50(25.4%)	192(26.6%)	276(24.6%)
90 to < 95	20(10.2%)	59(8.2%)	121(10.8%)
≥ 95	38(19.3%)	99(13.7%)	215(19.2%)
WC (cm, female)				0.027
< 65	3(1.4%)	17(1.9%)	22(1.3%)
65 to < 80	97(43.7%)	433(47.5%)	715(42.4%)
80 to < 85	54(24.3%)	202(22.1%)	344(20.4%)
85 to < 90	46(20.7%)	171(18.8%)	387(23.0%)
≥ 90	22(9.9%)	89(9.8%)	218(12.9%)
PUD	85(20.3%)	360(22.0%)	556(19.8%)	0.209
GU	64(15.3%)	248(15.2%)	305(10.9%)	0.000
DU	21(5.0%)	108(6.6%)	246(8.8%)	0.003
Helicobacter pylori status (%)	225(53.8%)	866(53.4%)	1409(50.3%)	0.088
Hot Food	246(58.7%)	935(57.2%)	1805(64.3%)	0.000
Fast eat time	138(32.9%)	348(21.3%)	660(23.5%)	0.000

Associations between sleep duration, napping and PUD

Table 2 displays the associations between sleep duration and peptic ulcer disease (PUD) after adjusting for multiple risk factors. In age- and sex-adjusted logistic regression analyses, individuals sleeping more than 9 hours were less likely to develop gastric ulcers (GU) compared to those sleeping 7–9 hours (OR = 0.67, 95% CI = 0.55–0.80), but had an increased risk of developing duodenal ulcers (DU) (OR = 1.39, 95% CI = 1.10–1.77). When additional factors such as smoking, alcohol consumption, diet preferences (hot food and fast food), H. pylori infection, body mass index (BMI), abdominal circumference, and blood pressure were included for full adjustment in logistic regression models, the results remained largely unchanged. However, none of the models demonstrated a statistically significant relationship between sleep duration and PUD.

Table 2

OR for PUD by sleep duration
	PUD		GU		DU
	Model 1	Model 2	Model 1	Model 2	Model 1	Model 2
Sleep duration < 7	0.88(0.67–1.16)	0.91(0.69–1.21)	1.00(0.74–1.36)	1.06(0.77–1.45)	0.73(0.45–1.19)	0.75(0.46–1.22)
7–9	Ref	Ref	Ref	Ref	Ref	Ref
> 9	0.88(0.78–1.08)	0.92(0.78–1.08)	0.67 (0.55–0.80)	0.71(0.59–0.86)	1.40(1.10–1.78)	1.39(1.09–1.77)
Model 1: adjusted age sex
Model 2: adjusted for variables in model 1, plus smoking, drinking, hot food diet, diet fast, H. pylori status,BMI, blood pressure

Length of Sleep duration and PUD Stratified by BMI

We examined the association between sleep duration and peptic ulcer disease (PUD) based on BMI categories,and summarized in Table 3.Among individuals with a BMI less than 24, those sleeping more than 9 hours were less likely to have PUD (OR = 0.78, 95% CI = 0.63–0.96). After adjusting for covariates in model 2, this association remained significant, although slightly attenuated (OR = 0.82, 95% CI = 0.65–1.02). Additionally, individuals with a BMI less than 24 who slept more than 9 hours were less likely to have gastric ulcers (GU) (OR = 0.54, 95% CI = 0.42–0.69) but more likely to have duodenal ulcers (DU) (OR = 1.51, 95% CI = 1.08–2.10). These associations remained statistically significant after adjustment for covariates in model 2.

Table 3

OR of PUD by sleep duration stratified by BMI
	PUD		GU		DU
BMI < 24
Sleep duration	Model 1	Model 2	Model 1	Model 2	Model 1	Model 2
< 7	0.93(0.65–1.34)	0.95(0.65–1.39)	1.04(0.70–1.55)	1.07(0.71–1.62)	0.76(0.39–1.48)	0.79(0.40–1.56)
7–9	ref	ref	ref	ref	ref	ref
> 9	0.78(0.63–0.96)	0.82(0.66–1.02)	0.54(0.42–0.69)	0.58(0.44–0.75)	1.51(1.08–2.10)	1.52(1.09–2.14)
BMI 24–28
< 7	0.93(0.59–1.49)	0.99(0.61–1.58)	1.09(0.64–1.84)	1.16(0.67–1.98)	0.75(0.34–1.64)	0.76(0.35–1.68)
7–9	ref	ref	ref	ref	ref	ref
> 9	0.95(0.74–1.23)	1.00(0.77–1.30)	0.80(0.58–1.08)	0.83(0.61–1.14)	1.29(0.88–1.89)	1.29(0.88–1.90)
BMI ≥ 28
< 7	0.50(0.17–1.44)	0.53(0.18–1.57)	0.55(0.15–2.08)	0.67(0.17–2.62)	0.59(0.12–2.82)	0.50(0.10–2.53)
7–9	ref	ref	ref	ref	ref	ref
> 9	1.16(0.66–2.02)	1.29(0.72–2.29)	1.22(0.62–2.41)	1.41(0.69–2.86)	1.13(0.51–2.54)	1.13(0.51–2.59)

A study from South Korea indicated that longer sleep duration could potentially prevent peptic ulcer disease (PUD) in women, although this association was not significant in men. ¹⁴ Additionally, a prospective cohort study conducted in China suggested that older adults with poor sleep quality might face a heightened risk of PUD compared to those with good sleep quality. However, increased or continued social engagement could potentially modify this association, offering protection against PUD recurrence for older adults with poor sleep quality. ¹⁶

Our study did not identify a significant relationship between sleep duration and PUD. However, we found evidence suggesting that longer sleep duration may serve as a protective factor for gastric ulcers (GU), contrasting with excessive sleep duration, which could potentially increase the risk of duodenal ulcers (DU). Individuals who engaged in daytime napping were more likely to develop GU, while longer daytime naps appeared to be protective for patients with DU. Notably, the association between sleep duration, nap duration, and PUD was not significant. Even after adjusting for BMI and age, our findings remained largely unchanged. Particularly among individuals with a normal BMI, longer sleep duration was associated with a reduced likelihood of developing GU.

While numerous epidemiological studies have established an association between nocturnal sleep and peptic disease, few have delved into the underlying mechanisms. Thus, further research is warranted to elucidate the pathways linking sleep patterns and peptic ulcers.

The pathogenesis of peptic ulcers primarily involves an imbalance between the protective mechanisms of the gastroduodenal mucosa and the aggressiveness of gastric acid and pepsin. In gastric ulcers (GU), diminished mucosal barrier function stands out as a key factor, whereas duodenal ulcers (DU) typically arise from elevated gastric acid secretion.

Our analysis suggests that the varied correlations between sleep duration and duodenal ulcers (DU) and gastric ulcers (GU) in our study may stem from differences in their respective pathogenic mechanisms. In Western countries, the primary causes of gastric ulcers are often the use of NSAIDs or infection with H. pylori.¹⁷As the prevalence of H. pylori infection declines in the West, NSAID and aspirin use increasingly contribute to gastric ulcers. NSAIDs induce gastric ulcers primarily by inhibiting COX-1 synthesis, leading to reduced prostaglandin E secretion, which normally supports mucosal regeneration and repair.^18,19Our findings indicate that longer sleep duration at night may serve as a protective factor against GU. One explanation for this observation is the increase in gastric mucosal blood flow, gastric mucus production, and melatonin secretion during sleep, coupled with a decrease in gastric acid secretion.^20–22Partial sleep deprivation in animal studies has been shown to elevate gastric acid secretion, suppress mucosal blood flow, and induce gastric lesions. Research has shown that spontaneous gastric alkalinization occurs at night, coinciding with sleep and being interrupted by waking, further reducing the invasive potential of the gastric mucosa and facilitating its repair.^23–25 Additionally, gastric acid secretion decreases during deep sleep, particularly during the rapid eye movement (REM) phase.²⁶²⁷Another contributing factor may be melatonin secretion. Normally, melatonin levels begin to rise 1 to 2 hours before bedtime, peak between 2 to 4 a.m., and decline thereafter. Melatonin acts as a potent stimulant for bicarbonate secretion, aiding in neutralizing gastric acid and promoting gastric mucosal repair. Furthermore, research in the United States has revealed that the gastric mucosa secretes trefoil factor family (TFF) proteins, which form a protective mucus layer on the gastric mucosal surface, shielding it from damage and alkalizing gastric acid. Experimental data indicate that TFF protein secretion during sleep is significantly higher compared to daytime secretion.²⁸

The available studies suggest that melatonin may play a role in the pathogenesis of duodenal ulcers, particularly in exacerbating their condition. This could be attributed to excessive sleep and a significant increase in melatonin production during the day, disrupting biorhythms. The mismatch of biorhythms may contribute to the development of duodenal ulcers. ²⁹Additionally, it has been observed that duodenal ulcers are associated with hormone secretion. The release of growth hormone is closely linked to slow-wave sleep, with growth hormone (G.H.) and adrenocorticotropic hormone (A.C.T.H.) exhibiting circadian rhythms, peaking in their blood concentrations around 1:30 a.m. and 9:00 a.m., respectively. Nocturnal gastric acid measurements indicate that peak gastric acid secretion also occurs during these times. The sleep phase follows an ultradian rhythm in a 90-110-minute cycle. ³⁰. During the initial sleep cycle, the release of G.H. is closely tied to slow-wave sleep and adapts promptly to changes in sleep patterns by releasing it at the new time of slow-wave sleep. If the normal adult sleep cycle is prolonged beyond 9 hours, the release of secretin is relatively impaired due to increased duodenal acidity, reducing the duodenum's buffering capacity and heightening the ulcerogenic effect of hydrochloric acid (HCl).³¹ It is believed that growth inhibitor suppression in the hypothalamus is the mechanism by which G.H. release is linked to slow-wave sleep, possibly mediated by activation of the serotonin pathway in the brain. Simultaneous inhibition of intestinal growth inhibitor leads to increased gastric production of HCl.

However, there are several limitations to this study. Firstly, the study cohort only obtained cross-sectional data related to the population, without follow-up data, thus preventing the establishment of a clear causal relationship. Future follow-up studies are planned to conduct further in-depth analysis and research. Secondly, the study only covered the Wuwei City area in Gansu Province, limiting the generalizability of the findings to the wider population. Finally, due to time constraints and specific operational challenges, the study primarily focused on epidemiological research and did not monitor and analyze objective physiological and biochemical indices related to sleep in the cohort population. If feasible, future efforts will involve collecting relevant data and expanding the study's depth.

The findings indicate that both extended nocturnal sleep and napping contribute to the onset of PUD within a population from northwest China. Additionally, prolonged sleep duration (> 9 hours per night) might act as a protective factor against GU development. Further prospective investigations are required to elucidate the biological pathways linking sleep duration, napping habits, and the risk of PUD.

Data availability statement

Original data supporting the conclusions of this article were kindly provided by the corresponding author, Yongning Zhou.

Ethics statement

The studies involving human participants were reviewed and approved by the Ethics Committee of The First Hospital of Lanzhou University. The patients/participants provided their written informed consent to participate in this study.

Funding

This study was supported by Health Industry Research Project of Gansu Province (GSWSKY2020-07), the Fundamental Research Funds for the Central Universities (lzujbky-2021-ct17), Natural Science Foundation of Gansu Province (21JR7RA381), Ministry of Science and Technology of the People’s Republic of China (2012GS620101).

Conflict of interest

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Cai S, Garcia RL, Masso-Gonzalez EL, Hernandez-Diaz S. Uncomplicated peptic ulcer in the UK: trends from 1997 to 2005. Aliment Pharmacol Ther. 2009;30(10):1039-48
Aro P, Storskrubb T, Ronkainen J et al. Peptic ulcer disease in a general adult population: the Kalixanda study: a random population-based study. Am J Epidemiol. 2006;163(11):1025-34
Leow AH, Lim YY, Liew WC, Goh KL. Time trends in upper gastrointestinal diseases and Helicobacter pylori infection in a multiracial Asian population--a 20-year experience over three time periods. Aliment Pharmacol Ther. 2016;43(7):831-7
Marshall BJ, McGechie DB, Rogers PA, Glancy RJ. Pyloric Campylobacter infection and gastroduodenal disease. Med J Aust. 1985;142(8):439-44
Graham DY, Klein PD, Opekun AR, Boutton TW. Effect of age on the frequency of active Campylobacter pylori infection diagnosed by the [13C]urea breath test in normal subjects and patients with peptic ulcer disease. J Infect Dis. 1988;157(4):777-80
Sverden E, Agreus L, Dunn JM, Lagergren J. Peptic ulcer disease. BMJ. 2019;367:l5495
Huang M, Yang Y, Huang Z, Yuan H, Lu Y. The association of nighttime sleep duration and daytime napping duration with hypertension in Chinese rural areas: a population-based study. J Hum Hypertens. 2021;35(10):896-902
Li W, Kondracki A, Gautam P et al. The association between sleep duration, napping, and stroke stratified by self-health status among Chinese people over 65 years old from the China health and retirement longitudinal study. Sleep Breath. 2021;25(3):1239-1246
Pyo JH, Lee H, Kim JE et al. Obesity and Risk of Peptic Ulcer Disease: A Large-Scale Health Check-Up Cohort Study. Nutrients. 2019;11(6)
Fang B, Yang S, Xu R, Chen G. Association between Poor Sleep Quality and Subsequent Peptic Ulcer Recurrence in Older Patients with Mild Cognitive Impairment: Examining the Role of Social Engagement. Sci Rep. 2019;9(1):2188
Brzozowska I, Ptak-Belowska A, Pawlik M et al. Mucosal strengthening activity of central and peripheral melatonin in the mechanism of gastric defense. J Physiol Pharmacol. 2009;60 Suppl 7:47-56
Konturek SJ, Konturek PC, Brzozowski T, Bubenik GA. Role of melatonin in upper gastrointestinal tract. J Physiol Pharmacol. 2007;58 Suppl 6:23-52
Tormey WP, Davis WG, Darragh AS. Nocturnal ulcer pain associated with slow-wave sleep. Lancet. 1978;1(8078):1340-1
Ko SH, Baeg MK, Ko SY, Han KD. Women Who Sleep More Have Reduced Risk of Peptic Ulcer Disease; Korean National Health and Nutrition Examination Survey (2008-2009). Sci Rep. 2016;6:36925
Hirshkowitz M, Whiton K, Albert SM et al. National Sleep Foundation's sleep time duration recommendations: methodology and results summary. Sleep Health. 2015;1(1):40-43
Fang B, Yang S, Xu R, Chen G. Association between Poor Sleep Quality and Subsequent Peptic Ulcer Recurrence in Older Patients with Mild Cognitive Impairment: Examining the Role of Social Engagement. Sci Rep. 2019;9(1):2188
Warren JR, Marshall B. Unidentified curved bacilli on gastric epithelium in active chronic gastritis. Lancet. 1983;1(8336):1273-5
Gisbert JP, Gonzalez L, de Pedro A et al. Helicobacter pylori and bleeding duodenal ulcer: prevalence of the infection and role of non-steroidal anti-inflammatory drugs. Scand J Gastroenterol. 2001;36(7):717-24
Weil J, Colin-Jones D, Langman M et al. Prophylactic aspirin and risk of peptic ulcer bleeding. BMJ. 1995;310(6983):827-30
Ricciotti E, FitzGerald GA. Prostaglandins and inflammation. Arterioscler Thromb Vasc Biol. 2011;31(5):986-1000
Brzozowski T, Konturek PC, Konturek SJ et al. Classic NSAID and selective cyclooxygenase (COX)-1 and COX-2 inhibitors in healing of chronic gastric ulcers. Microsc Res Tech. 2001;53(5):343-53
Takeeda M, Hayashi Y, Yamato M, Murakami M, Takeuchi K. Roles of endogenous prostaglandins and cyclooxygenase izoenzymes in mucosal defense of inflamed rat stomach. J Physiol Pharmacol. 2004;55(1 Pt 2):193-205
Brzozowska I, Ptak-Belowska A, Pawlik M et al. Mucosal strengthening activity of central and peripheral melatonin in the mechanism of gastric defense. J Physiol Pharmacol. 2009;60 Suppl 7:47-56
Konturek PC, Brzozowski T, Konturek SJ. Gut clock: implication of circadian rhythms in the gastrointestinal tract. J Physiol Pharmacol. 2011;62(2):139-50
Konturek SJ, Konturek PC, Brzozowski T, Bubenik GA. Role of melatonin in upper gastrointestinal tract. J Physiol Pharmacol. 2007;58 Suppl 6:23-52
Guo JS, Chau JF, Cho CH, Koo MW. Partial sleep deprivation compromises gastric mucosal integrity in rats. Life Sci. 2005;77(2):220-9
Guo JS, Chau JF, Cho CH, Koo MW. Partial sleep deprivation compromises gastric mucosal integrity in rats. Life Sci. 2005;77(2):220-9
Otto WR, Patel K, McKinnell I et al. Identification of blottin: a novel gastric trefoil factor family-2 binding protein. Proteomics. 2006;6(15):4235-45
Alpatov AM. [Human circadian rhythms and the work and rest regimen: the hypothesis of the "coiled spring"]. Izv Akad Nauk Ser Biol. 1993;(6):874-82
Forgacs I. Clinical gastroenterology. BMJ. 1995;310(6972):113-6
Rubin RT, Poland RE, Rubin LE, Gouin PR. The neuroendocrinology of human sleep. Life Sci. 1974;14(6):1041-52

No competing interests reported.

Download PDF

Editor invited by journal
20 Oct, 2024
Submission checks completed at journal
15 Oct, 2024
First submitted to journal
07 Oct, 2024

You are reading this latest preprint version

Sleep and Risk of Peptic Ulcer Disease: a cross-sectional study

Status:

Version 1

Abstract

Figures

Introduction

Material and Methods

Study population

Measurement of sleep duration

Assessment of covariates

Assessment of PUD

Data analysis.

Results

Characteristics of study subjects

Associations between sleep duration, napping and PUD

Length of Sleep duration and PUD Stratified by BMI

Discussion

Conclusions

Declarations

References

Additional Declarations

Status:

Version 1