Background: Habitually skipping breakfast may promote the initiation and progression of gastrointestinal (GI) cancers, which have never been systematically explored in large-scale prospective studies. Methods: We prospectively examined the effects of breakfast frequency on the occurrence of GI cancers among 62,746 participants. The hazard ratios (HRs) and 95% confidence intervals (95% CIs) of GI cancers were calculated by Cox regression. The CAUSALMED procedure was used to perform the mediation analyses. Results: During a median follow-up of 5.61 (5.18 ~ 6.08) years, 369 incident GI cancer cases were identified. Participants who consumed 1–2 times breakfasts per week exhibited an increased risk of stomach (HR = 3.45, 95% CI: 1.06–11.20) and liver cancer (HR = 3.42, 95% CI: 1.22–9.53). Participants who did not eat breakfast had an elevated risk of esophageal (HR = 2.72, 95% CI: 1.05–7.03), colorectal (HR = 2.32, 95% CI: 1.34–4.01), liver (HR = 2.41, 95% CI: 1.23–4.71), gallbladder, and extrahepatic bile duct cancer (HR = 5.43, 95% CI: 1.34–21.93). In the mediation effect analyses, BMI, CRP, and TyG (fasting triglyceride-glucose) index did not mediate the association between breakfast frequency and the risk of GI cancer incidence (all P for mediation effect > 0.05). Conclusions: Habitually skipping breakfast was associated with a greater risk of GI cancers including esophageal, gastric, colorectal, liver, gallbladder, and extrahepatic bile duct cancer. Trial Registration: Kailuan study, ChiCTR–TNRC–11001489. Registered 24 August, 2011-Retrospectively registered, http://www.chictr.org.cn/showprojen.aspx?proj=8050

Approximately 19.3 million new cancer cases and 10 million cancer-related deaths occur worldwide each year [1]. Cancer is a complex disease that poses a substantial threat to public health, which makes understanding its characteristics and the underlying developmental mechanisms necessary [2]. Recent studies have demonstrated a close relationship between cancer, inflammation, and metabolic disorders, with […]

Background: The effect of serum L-carnitine (LC) concentrations on cancer risk remains unclear. This study aims to explore the association between serum LC and the risk of incident cancer. Methods: This is a case-control study, including 574 patients with incident cancer and 574 controls matched in a 1:1 ratio by age, sex, and residence, nested within the China H-Type Hypertension Registry Study (CHHRS). Conditional logistic regression analysis was used to assess the association of serum LC and incident cancer risk. Results: When LC was assessed as quartiles, compared with patients with low LC (Q1), patients in the highest quartile (Q4) had a 33% (OR = 0.67, 95% CI: 0.46 to 0.99), 52% (OR = 0.48, 95% CI: 0.23 to 0.99), and 39% (OR = 0.61, 95% CI: 0.38 to 0.99) decreased risk of overall, digestive system, and non-digestive system cancer in the adjusted models, respectively. In subgroup analyses, an inverse association of LC with cancer risk was observed in individuals who were overweight (obese), who never drink, who never smoke, and who were female. In the mediation analysis, serum trimethylamine-N-oxide (TMAO) concentrations did not mediate the reversed association of LC with cancer risk. Conclusions: This study showed that serum LC concentrations had a protective impact on overall, digestive system, and non-digestive system cancer risk.

Background: Baseline sleep duration is associated with cancer risk and cancer-specific mortality; however, the association between longitudinal patterns of sleep duration and these risks remains unknown. Objective: This study aimed to elucidate the association between sleep duration trajectory and cancer risk and cancer-specific mortality. Methods: The participants recruited in this study were from the Kailuan cohort, with all participants aged between 18 and 98 years and without cancer at baseline. The sleep duration of participants was continuously recorded in 2006, 2008, and 2010. Latent mixture modeling was used to identify shared sleep duration trajectories. Furthermore, the Cox proportional risk model was used to examine the association of sleep duration trajectory with cancer risk and cancer-specific mortality. Results: A total of 53,273 participants were included in the present study, of whom 40,909 (76.79%) were men and 12,364 (23.21%) were women. The average age of the participants was 49.03 (SD 11.76) years. During a median follow-up of 10.99 (IQR 10.27-11.15) years, 2705 participants developed cancers. Three sleep duration trajectories were identified: normal-stable (44,844/53,273, 84.18%), median-stable (5877/53,273, 11.03%), and decreasing low-stable (2552/53,273, 4.79%). Compared with the normal-stable group, the decreasing low-stable group had increased cancer risk (hazard ratio [HR] 1.39, 95% CI 1.16-1.65) and cancer-specific mortality (HR 1.54, 95% CI 1.18-2.06). Dividing the participants by an age cutoff of 45 years revealed an increase in cancer risk (HR 1.88, 95% CI 1.30-2.71) and cancer-specific mortality (HR 2.52, 95% CI 1.22-5.19) only in participants younger than 45 years, rather than middle-aged or older participants. Joint analysis revealed that compared with participants who had a stable sleep duration within the normal range and did not snore, those with a shortened sleep duration and snoring had the highest cancer risk (HR 2.62, 95% CI 1.46-4.70). Conclusions: Sleep duration trajectories and quality are closely associated with cancer risk and cancer-specific mortality. However, these associations differ with age and are more pronounced in individuals aged <45 years. Trial Registration: Chinese Clinical Trial Registry ChiCTR–TNRC–11001489; http://tinyurl.com/2u89hrhx

BACKGROUND Baseline sleep duration is associated with cancer risk and cancer-specific mortality; however, the association between longitudinal patterns of sleep duration and these risks remains unknown. OBJECTIVE This study aimed to elucidate the association between sleep duration trajectory and cancer risk and cancer-specific mortality. METHODS The participants recruited in this study were from the Kailuan cohort, with all participants aged between 18 and 98 years and without cancer at baseline. The sleep duration of participants was continuously recorded in 2006, 2008, and 2010. Latent mixture modeling was used to identify shared sleep duration trajectories. Furthermore, the Cox proportional risk model was used to examine the association of sleep duration trajectory with cancer risk and cancer-specific mortality. RESULTS A total of 53,273 participants were included in the present study, of whom 40,909 (76.79%) were men and 12,364 (23.21%) were women. The average age of the participants was 49.03 (SD 11.76) years. During a median follow-up of 10.99 (IQR 10.27-11.15) years, 2705 participants developed cancers. Three sleep duration trajectories were identified: normal-stable (44,844/53,273, 84.18%), median-stable (5877/53,273, 11.03%), and decreasing low-stable (2552/53,273, 4.79%). Compared with the normal-stable group, the decreasing low-stable group had increased cancer risk (hazard ratio [HR] 1.39, 95% CI 1.16-1.65) and cancer-specific mortality (HR 1.54, 95% CI 1.18-2.06). Dividing the participants by an age cutoff of 45 years revealed an increase in cancer risk (HR 1.88, 95% CI 1.30-2.71) and cancer-specific mortality (HR 2.52, 95% CI 1.22-5.19) only in participants younger than 45 years, rather than middle-aged or older participants. Joint analysis revealed that compared with participants who had a stable sleep duration within the normal range and did not snore, those with a shortened sleep duration and snoring had the highest cancer risk (HR 2.62, 95% CI 1.46-4.70). CONCLUSIONS Sleep duration trajectories and quality are closely associated with cancer risk and cancer-specific mortality. However, these associations differ with age and are more pronounced in individuals aged <45 years. CLINICALTRIAL Chinese Clinical Trial Registry ChiCTR–TNRC–11001489; http://tinyurl.com/2u89hrhx