An East Asian–specific variant on aldehyde dehydrogenase 2 ( ALDH2 rs671, G>A) is the major genetic determinant of alcohol consumption. We performed an rs671 genotype-stratified genome-wide association study meta-analysis of alcohol consumption in 175,672 Japanese individuals to explore gene-gene interactions with rs671 behind drinking behavior. The analysis identified three genome-wide significant loci ( GCKR , KLB , and ADH1B ) in wild-type homozygotes and six ( GCKR , ADH1B , ALDH1B1 , ALDH1A1 , ALDH2 , and GOT2 ) in heterozygotes, with five showing genome-wide significant interaction with rs671. Genetic correlation analyses revealed ancestry-specific genetic architecture in heterozygotes. Of the discovered loci, four ( GCKR , ADH1B , ALDH1A1 , and ALDH2 ) were suggested to interact with rs671 in the risk of esophageal cancer, a representative alcohol-related disease. Our results identify the genotype-specific genetic architecture of alcohol consumption and reveal its potential impact on alcohol-related disease risk.

Background: Seaweed has a high potential for nourishing the future planet. However, besides being beneficial, it also contains adverse components; this poses the question whether consumption of seaweed foods overall contributes beneficially or detrimentally to human health, and hence if their consumption should be promoted or restricted.Methods: This study evaluated the impact of substituting regular foods with seaweed foods in the diet, both in terms of nutritional quality (via iodine and sodium) and food safety (via arsenic, cadmium, lead, and mercury). Food consumption data from the Netherlands and Portugal (adults aged >18 years) were used, in which 10% of the amounts of pasta, bacon, and lettuce consumed were replaced by seaweed-derived products made from kelp (Saccharina latissima). Using Monte Carlo Risk Assessment software (MCRA), long-term nutrient intake and exposure to contaminants were assessed. The results obtained for the Netherlands and Portugal were compared with data from Japan, a country that has a high natural consumption of seaweed.Results: This low-tier risk-benefit study reveals that an increased seaweed consumption (as assessed by the 10% replacement with seaweed products) has no consequences in terms of intake of sodium and exposure to cadmium, lead, and mercury, and the associated (absence of) adverse health aspects. The alternative scenario almost doubled the mean iodine intake in the Netherlands (to 300 μg/day) and Portugal (to 208 μg/day) and increased the average exposure to arsenic levels in the Netherlands (to 1.02 μg/kg bw/day) and Portugal (to 1.67 μg/kg bw/day).Conclusion: The intake of iodine and exposure to arsenic in the Netherland and Portugal were certainly higher due to the modeled increase of seaweed foods. If seaweed consumption increases close to the 10% substitution, the public health consequences thereof may trigger further research.

Branched-chain amino acids (BCAA) are essential amino acids, and emerging evidence suggests that BCAAs may mediate pathways related to cancer progression, possibly due to their involvement in insulin metabolism. We investigated the association between dietary intake of BCAAs with colorectal cancer risk in three prospective cohorts: the Nurses' Health Study I [(NHS), number of participants (n) at baseline = 77,017], NHS II (n = 92,984), and the Health Professionals Follow-up Study [(HPFS) n = 47,255]. Validated food frequency questionnaires were administered every 4 years and follow-up questionnaires on lifestyle biennially. Hazard ratios (HR) and 95% confidence intervals (CI) were calculated using Cox proportional hazards regression models. Pooled HRs were obtained using random effect models. After up to 28 years of follow-up, 1,660 cases were observed in NHS, 306 in NHS II, and 1,343 in HPFS. In multivariable adjusted models, we observed a weak inverse association between BCAA intake and colorectal cancer [highest vs. lowest quintile, pooled HR including all three cohorts (95% CI): 0.89 (0.80–1.00), P_trend = 0.06, HR per standard deviation (SD) increment 0.95 (0.92–0.99)]. However, after including dairy calcium to the models, BCAA intake was no longer associated with risk of colorectal cancer [HR 0.96 (0.85–1.08), P_trend = 0.50, HR per SD increment 0.97 (0.93–1.01)]. We did not find evidence that higher dietary BCAA intake is associated with higher risk of colorectal cancer. As this is the first prospective study to examine the association between BCAA intake and colorectal cancer, our findings warrant investigation in other cohorts.