Increased Risk Of Type Research Articles

Do early onset and pack-years of smoking increase risk of type II diabetes?

BackgroundType II diabetes is not only major public health problem but also heavy fiscal burden to each nation’s health care system around the world. This study aimed to investigate the effect of early onset and pack-years of smoking on type II diabetes risk.MethodsWe used the most recent cross-sectional National Health and Nutrition Examination Survey set of South Korea (2010) and the United States (2009–2010). Participants who were diagnosed with diabetes after age 20 were included (South Korea: n = 7273, 44% male; U.S.: n = 3271, 52% male). Cox proportional models, stratified by sex and country, were used to estimate hazard ratios.Results7.1% of South Korean men, 5.5% of South Korean women, 15.5% of U.S. men, and 12.4% of U.S. women had type II diabetes; 40% of South Korean men, 34% of U.S. men, and 21% of U.S. women began smoking before age 20 (57%, 49%, 36% of those who had type II diabetes, respectively). Type II diabetic participants were older and married; have a higher BMI, low income, and less education; lack moderate physical activity, smoked more and earlier compared to those without type II diabetes. Differences in risk factors including life-style behaviors and SES were found in both diabetic and non-diabetic populations. Men who began smoking before age 16 had a higher type II diabetes risk than who never smoked (South Korea: hazard ratio [HR] 2.46, 95% confidence interval [CI] 1.04–5.79; U.S.: HR 1.64, 95% CI 1.01–2.67), as did U.S. men who began smoking between 16 and 20 years (HR 1.58, 95% CI 1.05–2.37). Smoking pack-years were also associated with type II diabetes in U.S. men (HR 1.07, 95% CI 1.01–1.12). In women population, however, associations were not found.ConclusionsEarly onset of smoking increases type II diabetic risk among men in South Korea and the U.S., and type II diabetic risk increases with higher pack-years in U.S. men, however, no associations were found in women population. Underage tobacco policy and education programs are strongly needed in both countries.

Hypercholesterolemia and Metabolic Syndrome: Mischievous Partners

Elevations of two lipoproteins contribute to atherogenic hypercholesterolemia: low density lipoprotein (LDL) and very low density lipoprotein (VLDL). Their atherogenic potential is identified by their cholesterol (C) content. Together they constitute non-HDL-C. In populations and individuals having very low levels of non-HDL-C, atherosclerotic cardiovascular disease (ASCVD) is rare. In persons with severe elevations of non-HDL-C, these lipoproteins can initiate atherogenesis and precipitate ASCVD in the absence of other risk factors. The importance of non-HDL-C for development of ASCVD is dramatically shown by the reduction in risk accompanying cholesterol-lowering therapy. This does not negate the importance of other risk factors. The most common aggregation of these risk factors occurs in a condition called the metabolic syndrome. The prevalence of the metabolic syndrome increases in parallel with the increasing obesity in the population. This condition is characterized by abdominal obesity, insulin resistance and increased risk for type 2 diabetes, elevations in triglycerides, reduction in HDL, elevations in blood pressure, and prothrombotic and proinflammatory states. Epidemiological studies shown that the presence of the metabolic syndrome doubles the risk for ASCVD and carries a 5-fold increase in risk for type 2 diabetes. Most of the metabolic syndrome can be attributed to lifestyle factors, notably, over nutrition and decreased physical activity. Future advances on prevention of ASCVD will depend on new approaches to controlling hypercholesterolemia and to reducing the prevalence of the metabolic syndrome.

Obstructive sleep apnea is associated with impaired glucose metabolism in Han Chinese subjects.

Increasingly, evidence from population, clinic-based and laboratory studies supports an independent association between obstructive sleep apnea syndrome (OSAS) and an increased risk of type 2 diabetes; however, this observation has yet to be replicated in China and the potential mechanisms that link these two conditions are not clear. A total of 179 Han Chinese subjects were enrolled in this study. All subjects underwent polysomnography, the oral glucose tolerance-insulin releasing test (OGTT-IRT) and serum HbA(1)c measurement. Indexes including homeostasis model assessment-IR (HOMA-IR), Matsuda index, HOMA-β, early phase insulinogenic index (ΔI(30)/ΔG(30)), AUC-I(180) and oral disposition index (DIo) were calculated for the assessment of insulin resistance and pancreatic β-cell function. Based on OGTT, 25.4%, 44.6% and 54.5% subjects were diagnosed having glucose metabolic disorders respectively in control, mild to moderate and severe OSAS groups (P < 0.05). Serum HbA(1)c levels were highest in subjects with severe OSAS (P < 0.05). In contrast, compared with normal subjects, HOMA-β, ΔI(30)/Δ(G30) and DIO were lower in severe OSAS group (P < 0.05). In stepwise multiple linear regressions, 0-min glucose and HbA(1)c were positively correlated with the percentage of total sleep time below an oxyhemoglobin saturation of 90% (T90) (Beta = 0.215 and 0.368, P < 0.05); 30-min and 60-min glucose was negatively correlated with the lowest SpOO(2) (LSpO(2)) (Beta = -0.214 and -0.241, P < 0.05). HOMA-β and DI(O) were negatively correlated with T90 (Beta = -0.153 and -0.169, P < 0.05) while body mass index (BMI) was the only determinant of HOMA-IR and Matsuda index. OSAS is associated with impairment in glucose tolerance and pancreatic β-cell function in Han Chinese subjects while insulin sensitivity is mainly determined by obesity.

Assessment and Treatment of Cardiometabolic Risk in Adults at Risk for or with Type 2 Diabetes Mellitus

Cardiometabolic risk (CMR) refers to the collective consideration of traditional and emerging risk factors that amplify the potential of developing atherogenic cardiovascular disease, as well as the emergence of type 2 diabetes mellitus. Cumulative data suggest that the metabolic syndrome confers a 5-fold increase in risk for type 2 diabetes mellitus and also increases the cardiovascular risk calculated by conventional algorithms by an additional 1.5- to 2.0-fold. This article is a summary of the recently published position article on cardiometabolic risk by the nationally represented inter-disciplinary Cardiometabolic Risk Working Group (Can J Cardiol. 2011;27:e1–e33). The objective of this article is to review what the emerging risk factors are, how to determine if individuals at risk for or with type 2 diabetes mellitus have elevated CMR and the steps that should be taken to optimally manage and reduce CMR in these patients.

Cardiovascular Benefits and Diabetes Risks of Statin Therapy in Primary Prevention: An Analysis From the JUPITER Trial

Conclusion: The cardiovascular mortality benefits of statin therapy exceed the potential diabetes hazard induced by statins. Summary: Recent trial data and meta-analysis have suggested that statins confer an increase risk for development of diabetes (Ridker PM, et al, N Engl J Med 2008;359:2195-207; and Sattar N, et al, Lancet 2010;375:735-42). Recognition of the increased risk of diabetes with statin therapy has lead to questions on the balance of benefit and risk of statin drugs for primary prevention. The authors, therefore, analyzed data from participants from the JUPITER trial to address the balance of vascular benefits and diabetes hazards with statin use. In the JUPITER trial, 17,603 men and women without previous cardiovascular disease were randomly assigned to rosuvastatin (20 mg/d) or placebo and were monitored for 5 years for the primary end point of myocardial infarction, stroke, admission to the hospital for unstable angina, arterial revascularization, or cardiovascular death. Prespecified secondary end points of the trial included venous thromboembolism, incident of physician-reported diabetes, and all-cause mortality. With respect to diabetes development, patients were stratified on the basis of having none or at least one of the major four risk factors for developing diabetes: metabolic syndrome, impaired fasting glucose, body mass index ≥30 kg/m2, or glycated hemoglobin A1c >6%. There were 11,508 trial participants with one or more major diabetes risk factors. In individuals with one or more diabetes risk factors, statin allocation was associated with a 39% reduction in the primary end point (hazard ratio [HR], 0.61, 95% confidence interval [CI], 0.47-0.79, P = .0001), a 36% reduction in venous thromboembolism (HR, 0.64; 95% CI, 0.39-1.06; P = .08), a 17% reduction in total mortality (HR, 0.83; 95% CI, 0.64-1.0; P = .15), and a 28% increase in diabetes (HR, 1.28; 95% CI, 1.07-1.54, P = .01). For those with diabetes risk factors, 134 vascular events or deaths were avoided for every 54 new cases of diabetes diagnosed. For trial participants with no major diabetes risk factors, statin allocation was associated with a 52% reduction in the primary end point (HR, 0.48; 95% CI, 0.33-0.68; P = .001), a 53% reduction in venous thromboembolism (HR, 0.47; 95% CI, 0.21-1.03; P = .05), a 22% reduction in total mortality (HR, 0.78l; 95% CI, 0.59-1.03; P = .08), and no increase in diabetes (HR, 0.99; 95% CI, 0.45-2.21; P = .99). In patients without diabetes risk factors, 86 vascular events were avoided, with no new cases of diabetes diagnosed. In the 486 participants in the trial who developed diabetes in the follow-up (270 on rosuvastatin vs 216 on placebo; HR, 1.25, 95% CI, 1.05-1.49; P = .01), the point estimate of cardiovascular risk reduction associated with statin therapy (HR, 0.63; 95% CI, 0.25-1.06) was consistent with that for the trial as a whole (HR, 0.56; 95% CI, 0.46-0.69). Compared with placebo, statin accelerated the average time to diagnosis of diabetes by 5.4 weeks (83.3 [standard deviation, 47.8] weeks on rosuvastatin vs 89.7 [50.4] weeks on placebo). Comment: Three meta-analyses were published between 2009 and 2011 indicating an increase risk of type 2 diabetes in patients taking a statin medication. In addition, intensive-dose statin therapy appeared to be associated with higher risk than lower-dose therapy (Preiss D, et al, JAMA 2011;305:2556-64). This prompted the Food and Drug Administration to recommend safety label changes to statin drugs (http://www.FDA.gov/drugs/drugsaftey/ucm293101.htm). This report, while confirming the increased risk of diabetes in patients on statin medications, suggests that in the setting of primary prevention, even in the face of risk factors for development of diabetes, the use of statin medications has a favorable overall effect on mortality and cardiovascular events, despite an increased risk of diabetes. The authors believe the data provide reassurance for patients and physicians with regard to lipid-lowering agents as adjuncts to smoking sensation, exercise, and diet in the prevention of major cardiovascular events.

Predictive value of serum uric acid on type 2 diabetes mellitus

To evaluate the predictive value of uric acid (UA) on type 2 diabetes mellitus (DM). 711 subjects aged 45 - 60 years old with normal fasting blood glucose (FBG) were studied in 1992. The subjects were divided into 2 groups according to their 1992 UA data in the normal UA group and in the hyperuricemia (HUA) group. We analyzed the prevalence of DM-2 in 2007 according to data on UA in 1992. Relative risk (RR) of the cohort was calculated under χ(2) test and logistic regression analysis. FBG and the prevalence rate of DM in 2007 in the HUA group were statistically higher than those in the normal group. The relative risk (RR) of HUA to DM was 3.749 (P = 0.000), with 95% Confidence interval (CI) as 2.387 - 5.890. Data from the logistic regression analysis, after adjusting for other risk factors, the RR of UA to DM was 1.426 (P = 0.003), with 95%CI as 1.173 - 1.705. The abnormal UA was closely related to glucose metabolism disorder while hyperuricemia appeared to be associated with increased risk of type 2 DM.

Association between mannose-binding-lectin gene and type 2 diabetic patients in Chinese population living in the northern areas of China

To investigate whether the mannose-binding-lectin 2 (MBL2) gene was associated with type 2 diabetes in the populations living the northern part of China. The study involved 318 type 2 diabetic patients and 448 normoglycemic controls. The variances of rs1800450, rs1800451 and rs11003125 were determined by the Multiplex SNaPshot method. Fasting blood-glucose, triglyceride and total cholesterol were also measured. All of these results were analyzed by logistic regression method. Linkage disequilibrium and Haplotype measures were computed in all samples using Haploview. There seemed no mutation on rs1800451 while the rs1800450 and rs11003125 polymorphism was consistent with Hardy-Weinberg expectations in both the case and the control groups. Genotypes and allele frequencies of rs1800450 as well as rs11003125 were observed (P = 0.006, P = 0.003) and (P = 0.010, P = 0.004), respectively. Data from logistic regression analysis revealed that factors as overweight, abdominal obesity, hypercholesterolemia, GG genotype frequencies of Exon1 rs1800450 polymorphism as well as (GC + CC) genotype frequencies of rs11003125 polymorphism in MBL2 conferred increased risks for type 2 diabetes. Haplotype analyses of the two SNPs (rs1800450, rs11003125) revealed similar effects as compared with the single SNP associations. Only haplotype constructed from GC alleles conferred increased trends for type 2 diabetes (OR = 2.21, 95%CI: 1.47 - 3.33, P = 0.000). Our result suggested that the Exon1 rs1800450 polymorphism and promoter region rs11003125 polymorphism in MBL2 gene were both associated with type 2 diabetes in the Chinese population living in the northern areas of China. The G allele of rs1800450 and C allele of rs11003125 might be the risk factors of type 2 diabetes.

SIRT1 is associated with a decrease in acute insulin secretion and a sex specific increase in risk for type 2 diabetes in Pima Indians

Genetic variation in SIRT1 affects obesity-related phenotypes in several populations. The purpose of this study was to determine whether variation in SIRT1 affects susceptibility to obesity or type 2 diabetes in Pima Indians, a population with very high prevalence and incidence rates of these diseases. Genotypic data from single nucleotide polymorphisms (SNPs) identified by sequencing regions of SIRT1 combined with SNPs in/near SIRT1 from a prior genome-wide association study determined that 4 tag SNPs (rs7895833, rs10509291, rs7896005, and rs4746720) could capture information across this gene and its adjacent 5′ region. The tag SNPs were genotyped in a population-based sample of 3501 Pima Indians (44% had diabetes, 58% female) for association with type 2 diabetes and BMI. Metabolic trait data and adipose biopsies were available on a subset of these subjects. Two tag SNPs, rs10509291 and rs7896005, were nominally associated with type 2 diabetes (P=0.01, OR=1.25 95%CI 1.05–1.48, and P=0.02, OR=1.17 95%CI 1.02–1.34, respectively; additive P values adjusted for age, sex, birth year, and family membership), but not BMI (adjusted P values 0.52 and 0.45, respectively). Among metabolically characterized subjects with normal glucose tolerance (N=243), those carrying the diabetes risk allele (T) for rs10509291 and (G) for rs7896005 had a reduced acute insulin response (AIR) to an intravenous glucose bolus (adjusted P=0.045 and 0.035, respectively). SIRT1 expression in adipose biopsies was negatively correlated with BMI (adjusted P=0.00001). We conclude that variation in SIRT1 is nominally associated with reduced AIR and increased risk for type 2 diabetes. SIRT1 expression in adipose is correlated with BMI, but it remains unknown whether this is a cause or consequence of obesity.

Variation in the PTEN-induced putative kinase 1 gene associated with the increase risk of type 2 diabetes in northern Chinese

Variation in the PTEN-induced putative kinase 1 gene associated with the increase risk of type 2 diabetes in northern Chinese

Preventing Type 1 Diabetes

Several studies have suggested that early exposure to complex dietary proteins might be associated with increased risk for type 1 diabetes, perhaps by

Does the relative risk for type 1 diabetes conferred by HLA-DQ, INS, and PTPN22 polymorphisms vary with maternal age, birth weight, or cesarean section?

Maternal age at birth, birth weight, and cesarean section has been associated with a weak but significant increase in risk of type 1 diabetes. The objective was to assess whether the relative risk for type 1 diabetes conferred by established susceptibility loci human leukocyte antigen (HLA)-DQ, INS, and PTPN22 differed depending on these perinatal factors. We employed a case-control study with 456 cases of type 1 diabetes diagnosed before 15 yr of age and 1377 population-based control children. HLA genotypes were divided into high to moderate risk (DQ8/DQ2, DQ8/DQ8, DQ8/X, DQ2/DQ2) vs. all other genotypes. Case-only analysis using logistic regression was used to test for significant interaction. There was no significant difference in the relative risks conferred by HLA-DQ, INS, or PTPN22 by maternal age, birth weight, or mode of delivery, except the relative risk conferred by PTPN22 which was 2.11 [95% confidence interval (CI): 1.64-2.72] for those born vaginally and 0.99 (95% CI: 0.50-1.99) for those born by cesarean section [p(interaction) = 0.028]. The relative risks conferred by the three established susceptibility genes investigated here were independent of the perinatal factors, apart from a possible interaction between PTPN22 and mode of delivery.

Generation, validation and humanisation of a novel insulin resistant cell model

Insulin resistance is a characteristic of type 2 diabetes and is a major independent risk factor for progression to the disease. In particular, insulin resistance associates with increased body fat and almost certainly contributes to the dramatic increase in risk of type 2 diabetes associated with obesity. Therefore, in order to design truly effective insulin sensitising agents, targeted at the mechanism of disease development, we aimed to generate an obesity-related insulin resistant cell model. Rat hepatoma cells were grown in the presence of serum isolated from obese rodents or obese human volunteers, and the insulin sensitivity of the cells monitored over time by measuring a well-characterised insulin regulated gene promoter. Higher insulin concentrations were required to fully repress the gene in the cells grown in obese rodent serum compared with those grown in serum from lean rodents (almost a 10-fold shift in insulin sensitivity). This was reversed by restoration of normal growth medium, while the insulin resistance was prevented by pioglitazone or metformin. Meanwhile, growth of cells in serum collected from obese human volunteers with diabetes also reduced the insulin sensitivity of the rat cells. No clinical marker predicted the degree of insulin resistance that was generated by the human serum. We have developed a novel insulin resistant cell model for the study of the molecular development of obesity-linked insulin resistance, screen for compounds to overcome obesity-related insulin resistance and potentially search for novel serum biomarkers of insulin resistance.

Birthweight and the risk of childhood-onset type 1 diabetes: a meta-analysis of observational studies using individual patient data

We investigated whether children who are heavier at birth have an increased risk of type 1 diabetes. Relevant studies published before February 2009 were identified from literature searches using MEDLINE, Web of Science and EMBASE. Authors of all studies containing relevant data were contacted and asked to provide individual patient data or conduct pre-specified analyses. Risk estimates of type 1 diabetes by category of birthweight were calculated for each study, before and after adjustment for potential confounders.Meta-analysis techniques were then used to derive combined ORs and investigate heterogeneity between studies. Data were available for 29 predominantly European studies (five cohort, 24 case-control studies), including 12,807 cases of type 1 diabetes. Overall, studies consistently demonstrated that children with birthweight from 3.5 to 4 kg had an increased risk of diabetes of 6% (OR 1.06 [95% CI 1.01-1.11]; p=0.02) and children with birthweight over 4 kg had an increased risk of 10% (OR 1.10 [95% CI 1.04-1.19]; p=0.003), compared with children weighing 3.0 to 3.5 kg at birth. This corresponded to a linear increase in diabetes risk of 3% per 500 g increase in birthweight (OR 1.03 [95% CI 1.00-1.06]; p=0.03). Adjustments for potential confounders such as gestational age, maternal age, birth order, Caesarean section, breastfeeding and maternal diabetes had little effect on these findings. Children who are heavier at birth have a significant and consistent, but relatively small increase in risk of type 1 diabetes.

Preventing type 2 diabetes: public health implications for women with a history of gestational diabetes mellitus

There is now strong evidence that lifestyle modification can prevent or delay the development of type 2 diabetes mellitus in high-risk individuals. Women with gestational diabetes mellitus are at increased risk for type 2 diabetes and so are candidates for prevention programs. We review literature on type 2 diabetes risk in women with gestational diabetes, examine current recommendations for postpartum and long-term follow-up, and summarize findings from a 2007 expert-panel meeting. We found data to support that women with gestational diabetes have an increase in risk of type 2 diabetes comparable in magnitude with that of individuals with impaired glucose tolerance and/or impaired fasting glucose and that prevention interventions likely are effective in this population. Current recommendations from leading organizations on follow-up of women after delivery are conflicting and compliance is poor. Clinicians and public health workers face numerous challenges in developing intervention strategies for this population. Translation research will be critical in addressing this important public health issue.

Cardiovascular Fitness in Hong Kong Population

The WHO recommends adults to participate moderate intensity exercise on most days of the week in order to maintain health. Physical inactivity results in deterioration of aerobic and metabolic fitness, weight gain; increase risk of type 2 diabetes, cardiovascular disease and premature mortality. PURPOSE: To investigate the relationship between cardiovascular fitness and physical inactivity in a Hong Kong population. METHODS: Four hundred and seventeen (196 male and 221 female) Hong Kong Chinese (age from 20 to 64 years) participated in this study during 2003 to 2004. All subjects were community-dwelling, ambulatory and had no major medical problems. A maximal bicycle exercise test was performed to assess VO2max. Pair wise comparison Fisher's LSD test was applied as post hoc to see change of cardiovascular fitness between age groups. The result was correlated with a report which used IPAQ to investigate physical activities and exercise levels of Hong Kong population (6370 subjects) in the same period of time. International Physical Activity Questionnaire (IPAQ) was used to describe the physical activity level. RESULTS: VO2max reduced from 29.6 to 18.4 ml/kg/min (P<0.001) in the females from the younger to the older age group. The corresponding values for the males were 39.9 and 26.0 ml/kg/min (p<0.01). Of note is the very low aerobic fitness level for all young female not the least in the light of most of them having a low BMI (range 20 - 23). The lower cardiovascular fitness reflected a low level of physical activity among the females with less involvement in vigorous (5.8% vs. 12.9%) and moderate (20.3% vs. 23.8%) physical activity compared with males. The youngest groups of female showed the highest % of physical inactivity. CONCLUSIONS: An alarming number of young female in Hong Kong have very low aerobic fitness level which is not linked with overweight or obesity. People in Hong Kong especially young female are all recommended to increase their physical activity and thereby their fitness to reduce the risk of early development of chronic disease leading to premature death.

The ENPP1 K121Q Polymorphism Is Associated With Type 2 Diabetes in European Populations

Functional studies suggest that the nonsynonymous K121Q polymorphism in the ectoenzyme nucleotide pyrophosphate phosphodiesterase 1 (ENPP1) may confer susceptibility to insulin resistance; genetic evidence on its effect on type 2 diabetes, however, has been conflicting. We therefore conducted a new meta-analysis that includes novel unpublished data from the ENPP1 Consortium and recent negative findings from large association studies to address the contribution of K121Q to type 2 diabetes. After a systematic review of the literature, we evaluated the effect of ENPP1 K121Q on diabetes risk under three genetic models using a random-effects approach. Our primary analysis consisted of 30 studies comprising 15,801 case and 26,241 control subjects. Due to considerable heterogeneity and large differences in allele frequencies across populations, we limited our meta-analysis to those of self-reported European descent and, when available, included BMI as a covariate. We found a modest increase in risk of type 2 diabetes for QQ homozygotes in white populations (combined odds ratio [OR] 1.38 [95% CI 1.10-1.74], P = 0.005). There was no evidence of publication bias, but we noted significant residual heterogeneity among studies (P = 0.02). On meta-regression, 16% of the effect was accounted for by the mean BMI of control subjects. This association was stronger in studies in which control subjects were leaner but disappeared after adjustment for mean control BMI (combined OR 0.93 [95% CI 0.75-1.15], P = 0.50). The ENPP1 Q121 variant increases risk of type 2 diabetes under a recessive model of inheritance in whites, an effect that appears to be modulated by BMI.

New Treatment Strategies for Patients with Hypertension and Insulin Resistance

The metabolic syndrome is characterized by the clustering of insulin resistance, dyslipidemia, and hypertension and is associated with increased risk of cardiovascular disease and type 2 diabetes mellitus. However, older antihypertensive agents such as thiazide diuretics and β-blockers have potentially adverse effects on glucose and lipid metabolism and may even the exacerbate the metabolic syndrome and increase risk of type 2 diabetes. Recent clinical trials have suggested that antihypertensive agents that inhibit the renin-angiotensin system may reduce risk for new-onset type 2 diabetes, but only a few of these studies were placebo controlled, and in most cases, the absolute antidiabetic effects were relatively modest. Evidence is accumulating that telmisartan, in addition to blocking the angiotensin II type 1 receptor, activates the peroxisome proliferator-activated receptor (PPAR)–γ a well-known target for treatment of the metabolic syndrome and diabetes. By contrast, other angiotensin-receptor blockers are largely devoid of activity on PPAR-γ. Telmisartan is a partial agonist of PPAR-γ and has a superior tolerability profile without causing the fluid retention and edema associated with full agonists of PPAR-γ such as pioglitazone and rosiglitazone. Recent studies have indicated that in addition to antidiabetic properties, PPAR-γ activators may also provide protection against atherosclerosis and coronary events. Thus, the ability of telmisartan both to activate PPAR-γ and to block the angiotensin receptor may provide added value not only in the treatment of the metabolic syndrome and prevention of type 2 diabetes but also in prevention and treatment of atherosclerotic cardiovascular disease.

Table of Contents

AbstractExperts Speak Out. Juvenile Firesetting Interventions: What Works for Children and Families?Bills Address National Shortage of Children's Mental Health Professionals…alarms Reduce Nighttime Bedwetting…post 9/11 Psychiatric Disorders…depression May Increase Risk of Type 2 DiabetesER Physician Expectations of Stress/Anxiety in ChildrenPower Sports Increases Antisocial Behavior in BoysSurvey: One‐in‐five Teens Abuse Prescription DrugsLet's Have an Honest Fight Against Child Sex Abuse

Weight Change and Risk of Developing Type 2 Diabetes

To examine the association between weight change and risk of type 2 diabetes and whether initial weight modifies the association. This is a prospective cohort study of 20,187 alumni from Harvard University and the University of Pennsylvania. At baseline in 1962 or 1966, men (mean age, 45.9 years) reported their weight, height, and other risk factors. They also had had their weight and height measured at university entry (mean age, 18.5 years). Participants were followed from baseline to 1998 for type 2 diabetes. During follow-up, 1223 men developed type 2 diabetes. Weight gain significantly increased the risk of this disease. The multivariate relative risks associated with BMI change from university entry to baseline of <-0.5, +/-0.5, >0.5 to 1.0, >1.0 to 1.5, >1.5 to 2.0, >2.0 to 3.0, and >3.0 kg/m(2) per decade were 0.88, 1.00 (referent), 1.29, 2.09, 2.69, 4.67, and 7.02, respectively (p for trend < 0.0001). Even among men with a low initial BMI < 21 kg/m(2), weight gain significantly increased risk; the corresponding relative risks were (no cases), 1.00 (referent), 1.00, 1.93, 2.47, 4.82, and 7.68, respectively (p for trend < 0.0001). A low initial BMI does not ameliorate the increase in risk of type 2 diabetes with weight gain. Avoidance of weight gain, even among lean individuals, is important to reduce the risk of this disease.

No association between preeclampsia or cesarean section and incidence of type 1 diabetes among children: a large, population-based cohort study.

The objective was to investigate whether selected perinatal factors, as indicators of perinatal exposures, are associated with the risk of type 1 diabetes in children. Specifically, we tested whether maternal preeclampsia, Rhesus-immunization, induced labor, cesarean section, and multiple birth were associated with incidence of type 1 diabetes. A cohort study was designed by linking records of the Medical Birth Registry and the National Childhood Diabetes Registry of Norway. Live births in the study period were followed for a maximum of 15 y and contributed 8,166,731 person-years between 1989 and 1998. Altogether, 1824 cases of type 1 diabetes diagnosed between 1989 and 1998 were identified within the cohort. There was a suggestive, but nonsignificant, increase in risk of type 1 diabetes associated with Rhesus-immunization. Maternal preeclampsia, cesarean section, and the other perinatal factors investigated in this study were not significantly associated with incidence of type 1 diabetes in the children. Previous indications that cesarean section and preeclampsia are associated with type 1 diabetes were not supported by this large study. The majority of routinely recorded perinatal factors are only weakly associated with type 1 diabetes, or not at all.