Study protocol of brief intervention using gene polymorphism information for excessive drinking among Japanese college students and adults aged 20-30 years: a randomized controlled trial.

BACKGROUND: The alcohol-metabolizing enzyme aldehyde dehydrogenase 2 (ALDH2) is a carcinogenic acetaldehyde-degrading enzyme, and its low activity is a genetic constitution peculiar to East Asians. People with low alcohol dehydrogenase 1B activity (ADH1B*1/*1 genotype) have a high risk of developing head and neck cancer and alcoholism. The study aims to evaluate the effectiveness of brief interventions for excessive drinking among college students and adults in their 20s, including information on five constitutions that combine the ALDH2 and ADH1B genotypes. METHODS: Participants comprised university students and staff aged 20-30 years who had consumed ≥40 g (males) or ≥20 g (females) of pure alcohol; they were classified into intervention and control groups using a simple randomization method. Participants anonymously filled out questionnaires linked to identification numbers and recorded the drinking days and amounts on the drinking calendar. The intervention group will then be tested for genotype testing using saliva (5 types of combinations of ALDH2 and ADH1B enzyme activities); the result report will arrive approximately 1 month later. We will conduct a 30-min face-to-face or online intervention. The control group will be merely given the conventional materials, and genetic testing will be performed voluntarily after 6 months (end of study). The intervention group will undergo questionnaire surveys 1 month after the intervention and 3 and 6 months after baseline. Questionnaire surveys will be conducted 1, 3, and 6 months after baseline for the control group. The average amount of drinking before and after the intervention, attribute/baseline data between the two groups, and time-series data were compared using various analysis tools. For interventions, we engaged in dialog based on intervention materials that added genotyping content to the existing materials, result reports, baseline data, and drinking calendar records. Participants' ingenuity is respected to support their drinking behavior and goal setting. DISCUSSION: Individual information on the genetic makeup of alcohol-metabolizing enzymes provided during the intervention is more personal and objective than general health information, especially in Japan, where the ALDH2 low activity rate is high. This information may be useful for health care and precautionary measures. TRIAL REGISTRATION: R000050379, UMIN000044148, Registered on June 1, 2021. Scientific Title: Examination of simple intervention using genetic polymorphism information for excessive drinking.

Supplementation with Fermented Barley Extract Prevents Mammary Epithelial Cell Invasion in an Early Breast Cancer Model.

Diet-based prevention of malignant transformation contributes to the maintenance of quality of life by avoiding a battle against cancer. Invasion is one of the features of malignant breast cancer, and the prevention of invasion may reduce breast cancer malignancy. A recently established early breast cancer model system showed mammary ductal dysplasia with invasion in mice. This study utilized the model system and investigated the effect of fermented barley extract (FBE), a food material. The elastic fiber layer is the outermost layer of the mammary duct. A reduction in the elastic fiber layer was observed in the mammary glands of the model system, whereas supplementation with 8% FBE containing water prevented this reduction. Moreover, we found that FBE supplementation prevented mammary epithelial cell invasion. Based on our findings, FBE might be a candidate material for a diet-based prevention of early breast cancer invasion.

Fermented barley extract supplementation maintained antioxidative defense suppressing lipopolysaccharide-induced inflammatory liver injury in rats.

Utilizing phytochemicals in treating inflammation is becoming a viable alternative to pharmacological treatment. We have reported that fermented barley extract (FBE) effectively suppresses oxidative stress in chronically ethanol-fed rats. Here we report that FBE suppressed acute increases in oxidative stress as a response to lipopolysaccharide (LPS)-induced inflammation. Rats supplemented with FBE for 10 d showed decreases in plasma interleukin (IL)-1ß, IL-6, and tumor necrosis factor-α by 25%, 34%, and 35% respectively after LPS challenge. Liver damage was significantly suppressed, as marked by a 44% decrease in plasma alanine aminotransferase. FBE supplementation sustained liver anti-oxidative enzymes, catalase, glutathione peroxidase, and superoxide dismutase, at transcriptional and enzymatic levels, thus suppressing oxidative stress markers such as plasma nitric oxide and 8-hydroxy-2'-deoxyguanosine, by 42% and 23% respectively. We concluded that active compounds in FBE effectively inhibited the propagation of inflammation by suppressing oxidative stress.