Purpose:The impact of diet on the body acid-base balance may be related to the risk of various chronic diseases. Despite emerging evidence on the relationships between the dietary acid load and all-cause and cause-specific mortalities, further information is needed. This prospective cohort study examined the relationships between the dietary acid load and all-cause and cause-specific mortalities in a large Japanese population. Methods: The data of 74,360 subjects (aged 35-69 years in the baseline survey) in the Japan Multi-Institutional Collaborative Cohort Study were analyzed. The dietary acid load was estimated using the net endogenous acid production (NEAP) score. Cox proportional hazards regression analyses were performed to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) for all-cause and cause-specific mortalities according to the quartiles of the energy-adjusted NEAP score after adjustments for potential confounders. Sex-stratified analyses were also conducted. Results: During a mean follow-up of 11.6 years, 3,761 deaths (2,467 male and 1,294 female subjects) were identified. A higher NEAP score was associated with higher all-cause mortality (HR 1.16, 95% CI 1.04-1.28) and cerebrovascular disease mortality (HR 1.69, 95% CI 1.08-2.65). Sex-stratified analyses showed that the NEAP score was associated with all-cause and cause-specific mortalities, including cerebrovascular disease mortality (HR 2.32, 95% CI 1.23 - 4.40), in male subjects, but not in female subjects. Conclusion: The present results suggest that the dietary acid load is associated with a higher risk of all-cause and cause-specific mortalities, including cerebrovascular death, in Japanese male adults.
This report of a working group established by the Japan Diabetes Society proposes a new classification and diagnostic criteria for insulin resistance syndrome. Insulin resistance syndrome is defined as a condition characterized by severe attenuation of insulin action due to functional impairment of the insulin receptor or its downstream signaling molecules. This syndrome is classified into two types: genetic insulin resistance syndrome, caused by gene abnormalities, and type B insulin resistance syndrome, caused by autoantibodies to the insulin receptor. Genetic insulin resistance syndrome includes type A insulin resistance as well as Donohue and Rabson-Mendenhall syndromes, all of which are caused by abnormalities of the insulin receptor gene; conditions such as SHORT syndrome caused by abnormalities of PIK3R1, which encodes a regulatory subunit of phosphatidylinositol 3-kinase; conditions caused by abnormalities of AKT2, TBC1D4, or PRKCE; and conditions in which a causative gene has not yet been identified. Type B insulin resistance syndrome is characterized by severe impairment of insulin action due to the presence of insulin receptor autoantibodies. Cases in which hypoglycemia alone is induced by autoantibodies that stimulate insulin receptor were not included in Type B insulin resistance syndrome.
