Emi Ushigome

Aims: Smoking cessation may transiently increase diabetes risk through weight gain, but its temporal trajectory remains unclear. We evaluated the long‐term effect of smoking cessation on incident diabetes. Materials and Methods: We conducted a target trial emulation using a sequential‐cohort design with repeated annual enrollment. Using annual health checkup data of Japanese employees from 2008 to 2022, we newly enrolled, at each annual assessment, and started follow‐up individuals aged 40 years or older who were currently smoking and free of diabetes. Inverse probability weighting was used to adjust for baseline confounding in every sequential cohort. We estimated cumulative risks for quit‐smoking and persistent‐smoking groups, and their differences and ratios. Results: From 52 880 unique participants, a total of 331 701 participants were followed‐up in the sequential cohorts, with a mean (standard deviation) age of 49.1 (5.7) years, and 25 749 developed diabetes. The risk ratio (95% confidence interval) for diabetes in the quit‐smoking group relative to the persistent‐smoking group was 1.15 (1.07–1.24) at 3 years and 0.95 (0.85–1.06) at 15 years. Per‐protocol analyses showed a similar pattern. Conclusions: Smoking cessation was associated with a short‐term increase in diabetes risk, but this excess risk diminished over time, and no long‐term increase in risk was observed. These findings support sustained smoking cessation as metabolically beneficial in the long term.

Objective: Annual health screening provides repeated measurements of body mass index (BMI) and waist‐based indices, but the implications of short‐term changes in general and central adiposity for cardiometabolic risk remain unclear. We examined whether 1‐year changes in BMI and waist‐to‐height ratio (WHtR) were associated with subsequent cardiometabolic outcomes and cardiovascular–kidney–metabolic (CKM) syndrome progression. Methods: We analysed longitudinal health examination data from 144 394 Japanese employees aged 40–74 years between 2008 and 2023. One‐year changes in BMI and WHtR were calculated from two consecutive annual examinations, and outcomes were assessed during the following year. Outcomes included incident hypertension, dyslipidemia, hyperuricemia, diabetes, major adverse cardiovascular events, all‐cause mortality, and CKM stage progression. Pooled logistic regression with natural cubic splines was used to assess nonlinear associations, with analyses stratified by baseline BMI or WHtR quartiles. Results: Increases in BMI and WHtR were consistently associated with higher risks of hypertension, dyslipidemia, hyperuricemia, and early CKM stage progression across baseline body size categories. For diabetes, increases in BMI and WHtR were associated with higher risk, whereas decreases were also associated with higher risk among leaner individuals. Associations with major adverse cardiovascular events were generally U‐shaped. BMI loss was associated with higher mortality odds, although estimates were imprecise and potentially affected by reverse causation. Conclusions: One‐year changes in BMI and WHtR were associated with subsequent cardiometabolic risk and CKM stage progression. Anthropometric changes, particularly weight loss, may serve as signals for further assessment rather than causal determinants of risk.

Aims: To evaluate the effects of probiotics Bifidobacterium bifidum G9‐1 (BBG9‐1) on gastrointestinal symptoms in patients with Type 2 diabetes mellitus (T2DM) with diarrhoea or constipation. Materials and Methods: In a 12‐week open‐label randomised controlled trial, 100 participants were randomized 1:1 to a control or BBG9‐1 group, with 12 mg of Bifidobacterium administered daily. The primary endpoint was the change in total Gastrointestinal Symptom Rating Scale (GSRS) score (range: 1–7) in the full analysis set (BBG9‐1: n = 43; control: n = 51). Results: BBG9‐1 intake significantly improved the GSRS total score (from 2.22 ± 0.67 to 1.83 ± 0.62) compared with control (from 2.08 ± 0.67 to 2.06 ± 0.63; between‐group difference, −0.34 [95% CI: −0.55 to −0.14; p = 0.001]). Subgroup analyses indicated greater GSRS total score improvement in women, participants with constipation, aged ≥ 65 years, and BMI < 25 kg/m ² . Among the GSRS subscales, BBG9‐1 showed a significantly greater mean reduction in constipation scores than control (−0.79 ± 1.38 vs. −0.13 ± 1.04; p = 0.013). Although the mean change in diarrhoea scores did not differ significantly (−0.42 ± 1.14 vs. −0.06 ± 1.08; p = 0.14), the follow‐up diarrhoea score was significantly lower with BBG9‐1 (2.04 ± 1.00 vs. 2.58 ± 1.44; p = 0.049). Through gut microbiota analysis, the relative abundance of genera Phocaeicola increased significantly in the BBG9‐1 group (from 15.98 ± 13.75 to 19.56% ± 14.79% vs. from 18.14 ± 14.17 to 18.21 ± 13.58, p = 0.042). Assessment of faecal short‐chain fatty acids (SCFAs) revealed no significant changes associated with BBG9‐1 administration. The incidence of adverse effects were similar between the groups. Conclusions: BBG9‐1 administration significantly improved gastrointestinal symptoms in patients with T2DM. Trial Registration: Japan Registry of Clinical Trials (jRCTs051220127)

Background: Type 2 diabetes (T2D) has been linked to impairments in skeletal muscle performance, encompassing reductions in both muscle strength and muscle quality. While malnutrition is a known modifiable factor contributing to muscle quality deterioration, its specific relationship with the Geriatric Nutritional Risk Index (GNRI) in T2D remains underexplored. Using data from 743 participants in the KAMOGAWA-A cohort, this cross-sectional study evaluated the association between muscle quality and GNRI in individuals with type 2 diabetes. Methods: Muscle quality was defined as handgrip strength divided by arm lean mass. GNRI was calculated using serum albumin and body mass index. Multiple linear regression models were used to assess associations between GNRI and muscle quality. To account for BMI-related dependency in muscle quality measurements, we derived BMI-adjusted GNRI residuals and performed the same regression analysis to evaluate the stability of the observed relationship beyond BMI-induced confounding. Results: In the overall population, GNRI was inversely associated with muscle quality (β = −0.17, p < 0.001). Conversely, residual GNRI demonstrated a significant positive association with muscle quality (β = 0.13, p < 0.001), especially among men, individuals under 65 years of age, and across all BMI categories. Stratified analyses suggested that the strength and direction of associations varied by age, sex, and glycemic control status. Conclusions: The GNRI showed an inverse correlation with muscle quality, whereas residual GNRI showed a consistent positive relationship. These findings suggest that improving nutritional status may support muscle function in T2D, but BMI confounds the interpretation of GNRI in this context.

Aim: This study aimed to investigate how sarcopenia and nutritional risk influence all-cause mortality among older individuals with type 2 diabetes mellitus. Methods: In view of the presence of sarcopenia, defined according to the Asian Working Group for Sarcopenia (AWGS) criteria, and nutritional risk, as determined by the Geriatric Nutritional Risk Index (GNRI), a total of 396 participants were divided into four distinct groups (group 1: no nutritional risk and no sarcopenia, n = 306; group 2: nutritional risk and no sarcopenia, n = 32; group 3: no nutritional risk and sarcopenia, n = 36; and group 4: nutritional risk and sarcopenia, n = 22). Mortality risk was assessed through time-to-event analysis using Cox regression. Results: Throughout the 86-month median follow-up, 31 participants died. Compared to group 1, hazard ratios (HRs) for mortality of groups 2, 3, and 4 were 9.08 (95% confidence interval (95% CI), 2.44–33.8), 9.08 (95% CI: 2.44–33.8), and 14.0 (95% CI: 4.62–42.4), respectively. The risk of death was significantly higher in groups 2, 3, and 4 compared to group 1. Additionally, group 4 had a significantly higher risk of death than group 3. However, no significant difference in mortality risk was observed between groups 3 and 4 when compared to group 2. Conclusions: Coexistence of nutritional risk and sarcopenia was linked to an increased risk of mortality across older individuals with type 2 diabetes mellitus. There was no significant difference in mortality between individuals presenting or not presenting with sarcopenia within the nutritional risk group; therefore, greater attention should be directed toward malnutrition.

Background: This study aimed to investigate the effects of oral semaglutide on the changes in food preference of Japanese patients with type 2 diabetes. Methods: This retrospective multicenter study included 75 patients with type 2 diabetes who received oral semaglutide. The primary outcome was the change in the score of brief-type self-administered diet history questionnaire (BDHQ) score 3 months after the initiation of oral semaglutide treatment. The secondary outcome was the change in the Control of Eating Questionnaire (CoEQ), HbA1c, and body mass index (BMI) after 3 months. Results: The median age, BMI, and HbA1c of the 23 participants were 64.0 years, 26.9 kg/m², and 7.6% (59 mmol/mol). The BDHQ results showed total energy was significantly reduced. Among the individual nutrients, carbohydrates most decreased. The CoEQ results particularly showed declines in cravings for something sweet, chocolate or chocolate flavored foods, and starchy foods, satisfaction at meals, frequency and intensity of food craving, difficulty of resisting the craving for food, and frequency of eating in response to cravings for food were significantly lower after 3 months. The mean HbA1c and BMI significantly decreased. Conclusions: In Japanese patients with type 2 diabetes, oral semaglutide treatment decreased total energy intake and changed food preferences.