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The relationship between the expression of microRNAs (miRNAs) in blood and a variety of diseases has been investigated. MiRNA-based liquid biopsy has attracted much attention, and cancer-specific miRNAs have been reported. However, the results of analyses of the expression of these miRNAs vary among studies. The reproduction of results regarding miRNA expression levels could be difficult if there are differences in the data acquisition process. Previous studies have shown that the anticoagulant type used during plasma preparation and sample storage conditions could contribute to differences in measured miRNA levels. Thus, the impact of these preanalytical conditions on comprehensive miRNA expression profiles was examined. First, the miRNA expression profiles of samples obtained from healthy volunteers were analyzed using next-generation sequencing. Based on an analysis of the library concentration, human genome identification rate, ratio of unique sequences and expression profiles, the optimal preanalytical conditions for obtaining highly reproducible miRNA expression profiles were established. The optimal preanalytical conditions were as follows: ethylenediaminetetraacetic acid (EDTA) as the anticoagulant, whole-blood storage at room temperature within 6 hours, and plasma storage at 4°C or -20°C within 30 days. Next, plasma samples were collected from 60 cancer patients (3 facilities × 20 patients/facility), and miRNA expression profiles were analyzed. There were no significant differences in measurements except in the expression of erythrocyte-derived hsa-miR-451a. However, the variation in hsa-miR-451a levels was smaller among facilities than among individuals. This finding suggests that samples obtained from the same facility could show significantly different degrees of hemolysis across individuals. We found that the standardization of anticoagulant use and storage conditions contributed to reducing the variation in sample quality across facilities. The findings from this study could be useful in developing protocols for collecting samples from multiple facilities for cancer screening tests.

Although their functional outcomes remain largely unknown, single nucleotide polymorphisms (SNPs) in the fat mass and obesity-associated gene (FTO) may interact with adipokines, especially leptin and adiponectin, to modify the risk of colorectal cancer. We conducted a prospective study of 375 colorectal cancer cases and 750 matched controls to examine the effects of SNPs in the FTO, either alone or in interaction with pre-diagnostic plasma adipokine levels. Using a conditional logistic regression model, we obtained odds ratios (ORs) and their 95% confidence intervals (CIs) of colorectal cancer. Seven SNPs in strong linkage disequilibrium demonstrated a similarly positive association with colorectal cancer, and most evidently for rs1558902, rs8050136, rs3751812, and rs9939609 (Ptrend = 0.02). Of interest, we observed a statistically significant interaction of rs8050136 with plasma total adiponectin levels (Pinteraction = 0.03). Compared to non-carriers in the lowest quintile of plasma total adiponectin, A allele carriers in the same quintile showed a considerably elevated risk of colorectal cancer, with a body mass index-adjusted OR of 2.54 (95% CI, 1.36-4.75). This investigation of the interaction between SNPs in the FTO and pre-diagnostic plasma adipokine levels has revealed the importance of both genetic and hormonal factors associated with adiposity in colorectal carcinogenesis.

PurposeWe examined the association between meat intake and mortality due to all-cause and major causes of death using a population-based cohort study in Japan.Methods87,507 Japanese aged between 45 and 74 years old at 5-year follow-up study were followed for 14.0 years on average. Associations between meat intake and mortality risk were assessed using a Cox proportional hazards model.ResultsA heavy intake of total meat was associated with a higher risk of all-cause mortality relative to the lowest quartile intake in men (Q4: HR,1.18; 95%CIs, 1.06-1.31). A higher intake of total meat was associated with a lower risk of stroke mortality in women (Q2: HR, 0.70; 95%CIs, 0.51-0.94, Q3: HR, 0.68; 95%CIs, 0.50-0.95, Q4: HR, 0.66; 95%CIs, 0.44-0.99). A heavy intake of red meat was also associated with all-cause mortality (Q4: HR, 1.13; 95%CIs, 1.02-1.26) and heart disease mortality (Q4: HR, 1.51; 95%CIs, 1.11-2.06) in men but not in women. Heavy intake of chicken was inversely associated with cancer mortality in men.ConclusionsHeavy intakes of total and red meat were associated with an increase in all-cause and heart disease mortality in men, while total meat intake was associated with a lower risk of stroke mortality in women.

BACKGROUND/AIMS:Cancer-related activation of cytokine networks are central aspects of tumor development. The goal of the study was to examine the possibility of plasma cytokines for the screening of colorectal cancer (CRC). METHODS:We carried out a multicenter, hospital-based case-control study in 66 adult Japanese patients with CRC and 87 healthy adult Japanese. A multiplex bead array immunoassay was used to examine 27 different plasma cytokines. Their association with the presence of CRC was evaluated by logistic regression analysis after adjusting for potential confounding factors. RESULTS:Thirteen plasma cytokines were notably associated with the presence of CRC (p< 0.05). Receiver operating characteristic analysis revealed that the combinatorial assessment of some of these plasma cytokines showed "good" capability for discriminating between CRC patients and control subjects (area under the curve (AUC): 0.819 for the combination of IL-9, Eotaxin, G-CSF, and TNF-α; 0.832 for the combination of IL-4, IL-8, Eotaxin, IP-10, and TNF-α). Individual cytokine assessments presented lower AUCs (0.657-0.755) than the combinatorial cytokine assessments. CONCLUSIONS:The levels of several plasma cytokines varied significantly between CRC patients and control subjects, suggesting the possibility of differentially expressed plasma cytokines as potential biomarkers for detecting the presence of CRC. Our results should be validated in other populations.

Genome-wide association studies (GWAS) have identified greater than 30 variants associated with ovarian cancer, but most of these variants were investigated in European populations. Here, we integrated GWAS and subsequent functional analyses to identify the genetic variants with potential regulatory effects. We conducted GWAS for ovarian cancer using 681 Japanese cases and 17,492 controls and found that rs137672 on 22q13.1 exhibited a strong association with a P-value of 1.05 × 10(-7) and an odds ratio of 0.573 with a 95% confidence interval of 0.466-0.703. In addition, three previously reported SNPs, i.e., rs10088218, rs9870207 and rs1400482, were validated in the Japanese population (P < 0.05) with the same risk allele as noted in previous studies. Functional studies including regulatory feature analysis and electrophoretic mobility shift assay (EMSA) revealed two regulatory SNPs in 22q13.1, rs2072872 and rs6509, that affect the binding affinity to some nuclear proteins in ovarian cancer cells. The plausible regulatory proteins whose motifs could be affected by the allele changes of these two SNPs were also proposed. Moreover, the protective G allele of rs6509 was associated with a decreased SYNGR1 expression level in normal ovarian tissues. Our findings elucidated the regulatory variants in 22q13.1 that are associated with ovarian cancer risk.

Adult height is determined by both genetic characteristics and environmental factors in early life. Although previous studies have suggested that adult height is associated with risk of mortality, comprehensive associations between height and all-cause and cause-specific mortality in the Japanese population are unclear. We aimed to evaluate the associations between adult height and all-cause and cause-specific mortality among Japanese men and women in a prospective cohort study. We investigated 107,794 participants (50,755 men and 57,039 women) aged 40 to 69 years who responded to the baseline questionnaire in the Japan Public Health Center-based Prospective Study. Participants were classified by quartile of adult height obtained from a self-reported questionnaire in men (

Adult height and sitting height may reflect genetic and environmental factors, including early life nutrition, physical and social environments. Previous studies have reported divergent associations for height and chronic disease mortality, with positive associations observed for cancer mortality but inverse associations for circulatory disease mortality. Sitting height might be more strongly associated with insulin resistance; however, data on sitting height and mortality is sparse. Using the European Prospective Investigation into Cancer and Nutrition study, a prospective cohort of 409,748 individuals, we examined adult height and sitting height in relation to all-cause and cause-specific mortality. Height was measured in the majority of participants; sitting height was measured in ~253,000 participants. During an average of 12.5 years of follow-up, 29,810 deaths (11,931 from cancer and 7,346 from circulatory disease) were identified. Hazard ratios (HR) with 95% confidence intervals (CI) for death were calculated using multivariable Cox regression within quintiles of height. Height was positively associated with cancer mortality (men: HRQ5 vs. Q1 = 1.11, 95%CI = 1.00-1.24; women: HRQ5 vs. Q1 = 1.17, 95%CI = 1.07-1.28). In contrast, height was inversely associated with circulatory disease mortality (men: HRQ5 vs. Q1 = 0.63, 95%CI = 0.56-0.71; women: HRQ5 vs. Q1 = 0.81, 95%CI = 0.70-0.93). Although sitting height was not associated with cancer mortality, it was inversely associated with circulatory disease (men: HRQ5 vs. Q1 = 0.64, 95%CI = 0.55-0.75; women: HRQ5 vs. Q1 = 0.60, 95%CI = 0.49-0.74) and respiratory disease mortality (men: HRQ5 vs. Q1 = 0.45, 95%CI = 0.28-0.71; women: HRQ5 vs. Q1 = 0.60, 95%CI = 0.40-0.89). We observed opposing effects of height on cancer and circulatory disease mortality. Sitting height was inversely associated with circulatory disease and respiratory disease mortality.

Few empirical studies have been conducted to identify modifiable factors that may affect cognitive impairment in Japanese individuals. The present study aimed to clarify whether body mass and lifestyle are associated with cognitive impairment in Japanese middle-aged and elderly individuals.Subjects were 1814 community-dwelling individuals aged 44-79 years, all of whom were participants of the Murakami Cohort Study baseline survey conducted in 2011-2013. Cognitive function was assessed using the Mini-Mental State Examination (MMSE) in 2014-2016, and cognitive impairment, the outcome measure, was defined as an MMSE score

Previous studies have suggested associations of family composition with morbidity and mortality; however, the evidence of associations with risk of stroke is limited. We sought to examine the impact of changes in the household composition on risk of stroke and its types in Japanese population. Cox proportional hazard modelling was used to assess the risk of incident stroke and stroke types within a cohort of 77,001 Japanese men and women aged 45-74 years who experienced addition and/or loss of family members [spouse, child(ren), parent(s) and others] to their households over a five years interval (between 1990-1993 and 1995-1998). During 1,043,446 person-years of the follow-up for 35,247 men and 41,758 women, a total of 3,858 cases of incident stroke (1485 hemorrhagic and 2373 ischemic) were documented. When compared with a stable family composition, losing at least one family member was associated with 11-15% increased risk of stroke in women and men; hazard ratios (95% confidence interval) were 1.11 (1.01-1.22) and 1.15 (1.05-1.26), respectively. The increased risk was associated with the loss of a spouse, and was evident for ischemic stroke in men and hemorrhagic stroke in women. The addition of any family members to the household was not associated with risk of stroke in men, whereas the addition of a parent (s) to the household was associated with increased risk in women: 1.49 (1.09-2.28). When the loss of a spouse was accompanied by the addition of other family members to the household, the increased risk of stroke disappeared in men: 1.18 (0.85-1.63), but exacerbated in women: 1.58 (1.19-2.10). In conclusion, men who have lost family members, specifically a spouse have higher risk of ischemic stroke, and women who gained family members; specifically a parent (s) had the higher risk of hemorrhagic stroke than those with a stable family composition.

OBJECTIVE:A meta-analysis showed an inverse association of a prudent/healthy dietary pattern with all-cause mortality and no association of a western/unhealthy dietary pattern. However, the association of distinctive dietary patterns of Japanese population with mortality remains unclear. We prospectively investigated the association between dietary patterns and all-cause, cancer, and cardiovascular disease mortality among Japanese adults. METHODS:Participants were 36,737 men and 44,983 women aged 45-74 years who participated in the second survey of the Japan Public Health Center-based Prospective Study (1995-1998) and who had no history of serious disease. Dietary patterns were derived from principal component analysis of the consumption of 134 food and beverage items ascertained by a food frequency questionnaire. Hazard ratios of death from the second survey to December 2012 were estimated using cox proportional hazard regression analysis. RESULTS:A prudent dietary pattern, which was characterized by high intake of vegetables, fruit, soy products, potatoes, seaweed, mushrooms, and fish, was significantly associated with decreased risk of all-cause and cardiovascular disease mortality. The multivariable-adjusted hazard ratios (95% confidence intervals) of all-cause and cardiovascular disease mortality for the highest versus lowest quartile of the prudent dietary pattern score were 0.82 (0.77 to 0.86) and 0.72 (0.64 to 0.79), respectively (P for trend

To examine associations between work-family conflict and self-rated health among Japanese workers and to determine whether the associations differed by household income. Data was derived from the Japan Public Health Center-based Prospective Study for the Next Generation in Saku area in 2011-2012 (7,663 men and 7,070 women). Multivariate odds ratios (ORs) and 95% confidence intervals (CIs) for poor self-rated health by work-family conflict consisting of two dimensions (work-to-family and family-to-work conflicts) were calculated by gender and household income. Multivariate ORs of high work-to-family and family-to-work conflicts for poor self-rated health were 2.46 (95% CI; 2.04-2.97) for men and 3.54 (95% CI; 2.92-4.30) for women, with reference to the low work-to-family and family-to-work conflicts (p-value for gender interaction = 0.02). Subgroup analysis indicated that health effects of work-family conflict were likely to be more evident in the low income group only among women. Work-family conflict was associated with poor self-rated health among middle-aged Japanese men and women; its health impact was relatively stronger among women, and particularly economically disadvantaged women.

IntroductionSex hormones have been implicated in the etiology of a number of diseases. To better understand disease etiology and the mechanisms of disease-risk factor associations, this analysis aimed to investigate the associations of anthropometric, sociodemographic and behavioural factors with a range of circulating sex hormones and sex hormone-binding globulin.MethodsStatistical analyses of individual participant data from 12,330 male controls aged 25-85 years from 25 studies involved in the Endogenous Hormones Nutritional Biomarkers and Prostate Cancer Collaborative Group. Analysis of variance was used to estimate geometric means adjusted for study and relevant covariates.ResultsOlder age was associated with higher concentrations of sex hormone-binding globulin and dihydrotestosterone and lower concentrations of dehydroepiandrosterone sulfate, free testosterone, androstenedione, androstanediol glucuronide and free estradiol. Higher body mass index was associated with higher concentrations of free estradiol, androstanediol glucuronide, estradiol and estrone and lower concentrations of dihydrotestosterone, testosterone, sex hormone-binding globulin, free testosterone, androstenedione and dehydroepiandrosterone sulfate. Taller height was associated with lower concentrations of androstenedione, testosterone, free testosterone and sex hormone-binding globulin and higher concentrations of androstanediol glucuronide. Current smoking was associated with higher concentrations of androstenedione, sex hormone-binding globulin and testosterone. Alcohol consumption was associated with higher concentrations of dehydroepiandrosterone sulfate, androstenedione and androstanediol glucuronide. East Asians had lower concentrations of androstanediol glucuronide and African Americans had higher concentrations of estrogens. Education and marital status were modestly associated with a small number of hormones.ConclusionCirculating sex hormones in men are strongly associated with age and body mass index, and to a lesser extent with smoking status and alcohol consumption.

Differences in DNA collection protocols may be a potential confounder in epigenome-wide association studies (EWAS) using a large number of blood specimens from multiple biobanks and/or cohorts. Here we show that pre-analytical procedures involved in DNA collection can induce systematic bias in the DNA methylation profiles of blood cells that can be adjusted by cell-type composition variables. In Experiment 1, whole blood from 16 volunteers was collected to examine the effect of a 24 h storage period at 4°C on DNA methylation profiles as measured using the Infinium HumanMethylation450 BeadChip array. Our statistical analysis showed that the P-value distribution of more than 450,000 CpG sites was similar to the theoretical distribution (in quantile-quantile plot, λ = 1.03) when comparing two control replicates, which was remarkably deviated from the theoretical distribution (λ = 1.50) when comparing control and storage conditions. We then considered cell-type composition as a possible cause of the observed bias in DNA methylation profiles and found that the bias associated with the cold storage condition was largely decreased (λ adjusted = 1.14) by taking into account a cell-type composition variable. As such, we compared four respective sample collection protocols used in large-scale Japanese biobanks or cohorts as well as two control replicates. Systematic biases in DNA methylation profiles were observed between control and three of four protocols without adjustment of cell-type composition (λ = 1.12-1.45) and no remarkable biases were seen after adjusting for cell-type composition in all four protocols (λ adjusted = 1.00-1.17). These results revealed important implications for comparing DNA methylation profiles between blood specimens from different sources and may lead to discovery of disease-associated DNA methylation markers and the development of DNA methylation profile-based predictive risk models.

Epidemiological and experimental evidence suggest that vitamin D is protective against the risk of colorectal cancer. Polymorphisms in the gene encoding vitamin D receptor (VDR), which mediates most of the known cellular effects of vitamin D, have been suggested to alter this association. Here, using a tag SNP approach, we comprehensively evaluated the role of common genetic variants in VDR and their interaction with plasma vitamin D levels in relation to colorectal cancer risk in Japanese populations. A total of 356 colorectal cancer cases and 709 matched control subjects were selected from the participants of the Japan Public Health Center-based Prospective Cohort Study. Among these subjects, 29 VDR single nucleotide polymorphisms (SNPs) were selected and genotyped, and plasma vitamin D concentrations were measured. Conditional logistic regression models were used to estimate odds ratios (ORs) and 95% confidence intervals (CIs) of colorectal cancer, with adjustment for potential confounding factors. Among the results, eight VDR SNPs, namely rs2254210, rs1540339, rs2107301, rs11168267, rs11574113, rs731236, rs3847987 and rs11574143, the latter 5 of which were located in the 3' region, were nominally associated with the risk of colorectal cancer (P = 0.01-0.048). Furthermore, of the above 5 3' region SNPs, the inverse associations for 3 SNPs (rs11574113, rs3847987 and rs11574143) appeared to be evident only in those with high plasma vitamin D concentration. However, neither of these direct and suggestive interaction analysis associations was significant after multiple testing adjustment. Overall, the findings of this study provide only limited support for an association between common genetic variations in VDR and colorectal cancer risk in the Japanese population.

Heterocyclic aromatic amines formed in cooked meat may be an underlying mechanism for the red meat-colorectal cancer (CRC) association. These compounds require bioactivaction by N-acetyltransferase 2 (NAT2). An interaction effect between red meat consumption and NAT2 in increasing CRC risk has been inconsistently reported in whites. We investigated this interaction in two populations in which the high-activity rapid NAT2 phenotype is 10- and 2-fold more common than in whites. We meta-analyzed four studies of Japanese (2,217 cases, 3,788 controls) and three studies of African Americans (527 cases, 4,527 controls). NAT2 phenotype was inferred from an optimized seven-SNP genotyping panel. Processed and total red meat intakes were associated with an increased CRC risk in Japanese and in both ethnic groups combined (P's ≤ 0.002). We observed an interaction between processed meat intake and NAT2 in Japanese (P = 0.04), African Americans (P = 0.02), and in both groups combined (P = 0.006). The association of processed meat with CRC was strongest among individuals with the rapid NAT2 phenotype (combined analysis, OR for highest vs. lowest quartile: 1.62, 95% CI: 1.28-2.05; Ptrend = 8.0×10-5), intermediate among those with the intermediate NAT2 phenotype (1.29, 95% CI: 1.05-1.59; Ptrend = 0.05) and null among those with the slow phenotype (Ptrend = 0.45). A similar interaction was found for NAT2 and total red meat (Pinteraction = 0.03). Our findings support a role for NAT2 in modifying the association between red meat consumption and CRC in Japanese and African Americans.

Evidence is sparse and contradictory regarding the association between low-carbohydrate diet score and type 2 diabetes risk, and no prospective study examined the association among Asians, who consume greater amount of carbohydrate. We prospectively investigated the association of low-carbohydrate diet score with type 2 diabetes risk.Participants were 27,799 men and 36,875 women aged 45-75 years who participated in the second survey of the Japan Public Health Center-Based Prospective Study and who had no history of diabetes. Dietary intake was ascertained by using a validated food-frequency questionnaire, and low-carbohydrate diet score was calculated from total carbohydrate, fat, and protein intake. The scores for high animal protein and fat or for high plant protein and fat were also calculated. Odds ratios of self-reported, physician-diagnosed type 2 diabetes over 5-year were estimated by using logistic regression.During the 5-year period, 1191 new cases of type 2 diabetes were self-reported. Low-carbohydrate diet score for high total protein and fat was significantly associated with a decreased risk of type 2 diabetes in women (P for trend

BACKGROUND: Despite evidence that neighbourhood conditions affect residents' health, no prospective studies of the association between neighbourhood socio-demographic factors and all-cause mortality have been conducted in non-Western societies. Thus, we examined the effects of areal deprivation and population density on all-cause mortality in Japan. METHODS: We employed census and survival data from the Japan Public Health Center-based Prospective Study, Cohort I (n = 37,455), consisting of middle-aged residents (40 to 59 years at the baseline in 1990) living in four public health centre districts. Data spanned between 1990 and 2010. A multilevel parametric proportional-hazard regression model was applied to estimate the hazard ratios (HRs) of all-cause mortality by two census-based areal variables--areal deprivation index and population density--as well as individualistic variables such as socioeconomic status and various risk factors. RESULTS: We found that areal deprivation and population density had moderate associations with all-cause mortality at the neighbourhood level based on the survival data with 21 years of follow-ups. Even when controlling for individualistic socio-economic status and behavioural factors, the HRs of the two areal factors (using quartile categorical variables) significantly predicted mortality. Further, this analysis indicated an interaction effect of the two factors: areal deprivation prominently affects the health of residents in neighbourhoods with high population density. CONCLUSIONS: We confirmed that neighbourhood socio-demographic factors are significant predictors of all-cause death in Japanese non-metropolitan settings. Although further study is needed to clarify the cause-effect relationship of this association, the present findings suggest that health promotion policies should consider health disparities between neighbourhoods and possibly direct interventions towards reducing mortality in densely populated and highly deprived neighbourhoods.

In many developed countries, socioeconomic status is associated with cancer incidence and survival. However, research in Japan is sparse. We examined the association between neighborhood deprivation based on the Japanese Deprivation Index and the risk of incidence, mortality and survival from total and major cancers in the Japan Public Health Center-based Prospective Study.86,112 participants were followed through the end of 2009. A total of 10,416 incident cases and 5,510 deaths from cancer were identified among 1,348,437 person-years of follow-up (mean follow-up: 15.7 years). The Japanese deprivation index was used to access neighborhood deprivation. Hazard ratios and 95% confidence intervals were calculated by Cox regression analysis.We found no associations between neighborhood deprivation index and the incidence of total and major cancers. In some cancer risks or deaths, however, we found positive or inverse associations with a higher deprivation index, such as a decreased risk of colorectal cancer incidence and an increased risk of liver cancer incidence and deaths in women.Although some positive or inverse associations were detected for specific sites, the neighborhood deprivation index has no substantial overall association with the risk of incidence, mortality and survival from cancer in the Japanese population.

BackgroundThe definition of incident type 2 diabetes varies across studies; hence, the actual incidence of type 2 diabetes in Japan is unclear. Here, we reviewed the various definitions of incident type 2 diabetes used in previous epidemiologic studies and estimated the diabetes incidence rate in Japan.MethodsWe searched for related literature in the MEDLINE, EMBASE, and Ichushi databases through September 2012. Two reviewers selected studies that evaluated incident type 2 diabetes in the Japanese population.ResultsFrom 1824 relevant articles, we included 33 studies with 386,803 participants. The follow-up period ranged from 2.3 to 14 years and the studies were initiated between 1980 and 2003. The random-effects model indicated that the pooled incidence rate of diabetes was 8.8 (95% confidence interval, 7.4-10.4) per 1000 person-years. We observed a high degree of heterogeneity in the results (I(2) = 99.2%; p < 0.001), with incidence rates ranging from 2.3 to 52.6 per 1000 person-years. Three studies based their definition of incident type 2 diabetes on self-reports only, 10 on laboratory data only, and 20 on self-reports and laboratory data. Compared with studies defining diabetes using laboratory data (n = 30; pooled incidence rate = 9.6; 95% confidence interval = 8.3-11.1), studies based on self-reports alone tended to show a lower incidence rate (n = 3; pooled incidence rate = 4.0; 95% confidence interval = 3.2-5.0; p for interaction < 0.001). However, stratified analyses could not entirely explain the heterogeneity in the results.ConclusionsOur systematic review and meta-analysis indicated the presence of a high degree of heterogeneity, which suggests that there is a considerable amount of uncertainty regarding the incidence of type 2 diabetes in Japan. They also suggested that laboratory data may be important for the accurate estimation of the incidence of type 2 diabetes.

ObjectiveThe aim of the present study was to test a hypothesis that a history of having a macrosomic infant (≥ 4000 g) is associated with the risk of diabetes.MethodsData on the Japan Public Health Center-based Prospective diabetes cohort were analyzed, which is a population-based cohort study on diabetes. The survey of diabetes was performed at baseline and at the 5-year follow-up. A history of having a macrosomic infant was assessed using a self-administered questionnaire. A cross-sectional analysis was performed among 12,153 women who participated in the 5-year survey of the cohort. Logistic regression was used to examine the relationship between a history of having a macrosomic infant and the presence of diabetes. A longitudinal analysis was also conducted among 7,300 women without diabetes who participated in the baseline survey. Logistic regression was used to investigate the relationship between a history of having a macrosomic infant and the incidence of diabetes between the baseline survey and the 5-year survey.ResultsIn the cross-sectional analysis, parous women with a positive history were more likely to have diabetes in relation to parous women without (OR = 1.44, 95% CI = 1.13-1.83). The longitudinal analysis showed a modest but non-significant increased risk of developing diabetes among women with a positive history (OR = 1.24, 95% CI = 0.80-1.94).ConclusionsAn increased risk of diabetes was implied among women with a history of having a macrosomic infant although the longitudinal analysis showed a non-significant increased risk.

OBJECTIVE: The effect of smoking cessation on the risk of diabetes has been reported previously. However, it is unknown whether the association is influenced by weight gain and other potential risk factors. METHODS: The Japan Public Health Center-Based Prospective Study established in 1990 for Cohort I and in 1993 for Cohort II provided data, and 25,875 men and 33,959 women were analyzed. The response rate to the baseline questionnaire was 80.9%, and 68.4% of the respondents participated both the 5- and 10-year follow-up surveys. Smoking cessation was noted during the initial five years and the development of diabetes was reported in the subsequent five years. RESULTS: An increased risk was observed among individuals who newly quit smoking compared with never smokers among men (odds ratio (OR)=1.42, 95% CI=1.03-1.94) and women (OR=2.84, CI=1.53-5.29). The risk of developing diabetes among male new quitters who gained 3 kg or more during the 5-year follow-up did not substantially differ from the risk among male never smokers with less than 3 kg of weight gain or no weight gain, while an increased risk was observed among male new quitters with less or no weight gain (OR=1.46, 95%CI 1.00-2.14). An insignificant increased risk was observed among male new quitters with a family history of diabetes compared with male never smokers with a family history of diabetes. The risk was more than twice as high for male new quitters who used to smoke 25 or more cigarettes per day compared with never smokers (OR=2.15, 95%CI: 1.34-3.47). DISCUSSION: An increased risk of diabetes was implied among individuals who quit smoking. However, the increased risk was not implied among those who gained weight over the 5-years of follow-up. Those who had major risk factors for diabetes or who smoked heavier had a higher risk.

The occurrence of diabetes has greatly increased in low- and middle-income countries, particularly in Asia, as has the prevalence of overweight and obesity; in European-derived populations, overweight and obesity are established causes of diabetes. The shape of the association of overweight and obesity with diabetes risk and its overall impact have not been adequately studied in Asia.A pooled cross-sectional analysis was conducted to evaluate the association between baseline body mass index (BMI, measured as weight in kg divided by the square of height in m) and self-reported diabetes status in over 900,000 individuals recruited in 18 cohorts from Bangladesh, China, India, Japan, Korea, Singapore and Taiwan. Logistic regression models were fitted to calculate cohort-specific odds ratios (OR) of diabetes for categories of increasing BMI, after adjustment for potential confounding factors. OR were pooled across cohorts using a random-effects meta-analysis. The sex- and age-adjusted prevalence of diabetes was 4.3% in the overall population, ranging from 0.5% to 8.2% across participating cohorts. Using the category 22.5-24.9 kg/m²) as reference, the OR for diabetes spanned from 0.58 (95% confidence interval [CI] 0.31, 0.76) for BMI lower than 15.0 kg/m² to 2.23 (95% CI 1.86, 2.67) for BMI higher than 34.9 kg/m². The positive association between BMI and diabetes prevalence was present in all cohorts and in all subgroups of the study population, although the association was stronger in individuals below age 50 at baseline (p-value of interaction