Purpose: We aimed to investigate how genetic predisposition to drinking and gastric cancer (GC) modifies the association between alcohol consumption and GC risk in the Korean population. Materials and Methods: Polygenic risk scores for GC (PRS-GC) and alcohol consumption (PRS-Alcohol) were formulated using genome-wide association results from BioBank Japan. Validation was performed using Korean cohorts (SNUBH-GENIE cohort), incorporating 8,846 controls and 531 patients with GC. Subsequently, these PRSs were applied to an independent Korean cohort of 67,771 participants, including 313 patients with GC during the follow-up for 14 years (KoGES cohort). Results: In KoGES cohort, the influence of alcohol consumption on GC risk was significantly altered by the PRS-GC and exhibited a synergistic interaction effect. PRS-Alcohol itself shows a negative correlation with GC risk. However, when actual alcohol consumption significantly exceeded genetically predicted levels, the risk of alcohol-related GC was notably increased (adjusted hazard ratio, 1.32; 95% confidence interval, 1.01 to 1.72). Heavy drinkers in the high–PRS-GC/low–PRS-Alcohol group had a 2.16 times higher risk of GC than non-to-light drinkers, which was prominent in males. Conclusion Korean drinkers with higher PRS-GC who consume alcohol more than genetically predicted levels are susceptible to GC. PRS-GC and PRS-Alcohol may be beneficial for assessing the impact of alcohol consumption on GC risk in Koreans.

Background: and Purpose The Karolinska Sleepiness Scale (KSS) is widely used for assessing current level of sleepiness, but it has not been validated in South Korea. This study aimed to validate the KSS using the Stanford Sleepiness Scale (SSS), polysomnography (PSG), and electroencephalography (EEG). Methods: The sample consisted of 27 adult participants in this study aged 40.5±7.7 years (mean±standard deviation) and included 22 males. They completed questionnaires and underwent EEG recording and overnight PSG. The KSS was completed from 18:00 to 24:00 every 2 hours and following PSG (at 07:00). KSS scores changed over time and in particular increased with the time since waking, with the score peaking at 24:00. Results: Convergent validity of the KSS was verified by performing a Spearman correlation analysis between the KSS and SSS (r=0.742, p<0.01). Concurrent validity of the KSS was verified by performing a Spearman correlation analysis between the KSS administered before sleep and the sleep onset latency measured using PSG (r=-0.456, p<0.05). Alpha waves were measured 5 minutes before administering the KSS, and the KSS scores were compared with these alpha waves. There were no significant correlations observed between the KSS scores and alpha waves measured in the left occipital area (O1), left frontal area (F3), or left central area (C3). In addition, Spearman correlation analyses of the difference between KSS scores and alpha waves measured at O1, F3, and C3 produced no significant results. Conclusions This study verified the convergent validity and concurrent validity of the KSS, and confirmed the capabilities of this scale in assessing sleepiness changes over time.