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Asthma is related to various cardiovascular risk. Whether a history of asthma from childhood contributes to arterial stiffness in adulthood, a noninvasive surrogate for cardiovascular events, is unknown. Prospective analyses were performed among 1746 Bogalusa Heart Study participants aged 20 to 51 years with data on self-report asthma collected since childhood. Aorta-femoral pulse wave velocity (af-PWV, m/s) was repeatedly assessed among adults ≥aged 18 years. Generalized linear mixed models and generalized linear models were fitted for the repeated measurements of af-PWV and its changes between the last and the first measurements, respectively. After a median follow-up of 11.1 years, participants with a history of asthma from childhood had a higher af-PWV (6.78 versus 6.13; P=0.048) and a greater increase in af-PWV (8.99 versus 2.95; P=0.043) than those without asthma, adjusted for age, sex, race, smoking status, heart rate, body mass index, systolic blood pressure, lipids, and glycemia. In addition, we found significant interactions of asthma with body mass index and systolic blood pressure on af-PWV and its changes (P for interaction <0.01). The associations of asthma with af-PWV and its changes appeared to be stronger among participants who were overweight and obese (body mass index ≥25 kg/m2) or with prehypertension and hypertension (systolic blood pressure ≥120 mm Hg) compared with those with a normal body mass index or systolic blood pressure. Our findings indicate that a history of asthma from childhood is associated with higher af-PWV and greater increases in af-PWV, and such associations are stronger among young adults who are overweight or with elevated blood pressure. [ABSTRACT FROM AUTHOR]

Objective: Adiposity and the gut microbiota are both related to the risk of type 2 diabetes. We aimed to comprehensively examine how changes induced by a weight-loss diet intervention in gut microbiota-related metabolites, such as trimethylamine N-oxide (TMAO) and its precursors (choline and l-carnitine), were associated with improvements in adiposity and regional fat deposition.Research Design and Methods: This study included 510 overweight and obese individuals who were randomly assigned one of four diets varying in macronutrient intake. We examined associations of 6-month changes in blood metabolites (TMAO, choline, and l-carnitine) with improvements in body weight (BW), waist circumference (WC), body fat composition, fat distribution, and resting energy expenditure (REE).Results: Individuals with a greater reduction of choline (P < 0.0001) and l-carnitine (P < 0.01) rather than TMAO showed significant losses of BW and WC at 6 months. The reduction of choline was significantly predictive of decreases in body fat composition, fat distribution, and REE. Results of sensitivity analysis showed that the baseline diabetes risk status, such as the presence of hyperglycemia (31% of the total participants) and fasting glucose levels, did not modify the associations. Early changes in choline and l-carnitine were significantly predictive of weight loss over 2 years (P < 0.05 for all). Individuals with increases in choline or l-carnitine were 2.35-times (95% CI 1.38, 4.00) or 1.77-times (1.06, 2.95) more likely to fail to lose weight (-5% or more loss) at 2 years.Conclusions: Overweight and obese individuals who showed decreases in circulating choline or l-carnitine levels achieved greater improvements of adiposity and energy metabolism by eating a low-calorie weight-loss diet, suggesting that such metabolites are predictive of individuals' response to the treatment. Further investigations are necessary to confirm our findings, particularly in a population with prediabetes that is more representative of the U.S. population with obesity. [ABSTRACT FROM AUTHOR]

Background: Coffee consumption has been associated with glucose metabolism and risk of type 2 diabetes. Objective: We examined whether the genetic variation determining habitual coffee consumption affected glycemic changes in response to weight-loss dietary intervention. Design: A genetic risk score (GRS) was calculated based on 8 habitual coffee consumption-associated single nucleotide polymorphisms. We used general linear models to test changes in glycemic traits in groups randomly assigned to high- and low-fat diets according to tertiles of the GRS. Results: We observed significant interactions between the GRS and low compared with high dietary fat intake on 6-mo changes in fasting insulin and homeostasis model assessment of insulin resistance (HOMA-IR) (P-interaction = 0.023 and 0.022, respectively), adjusting for age, sex, race, physical activity, smoking, alcohol, seasonal variation, and baseline values of the respective outcomes. Participants with a higher GRS of habitual coffee consumption showed a greater reduction in fasting insulin and a marginally greater decrease in HOMA-IR in the low-fat diet intervention group. Conclusions: Our data suggest that participants with genetically determined high coffee consumption may benefit more by eating a low-fat diet in improving fasting insulin and HOMA-IR in a short term. This trial was registered at clinicaltrials.gov as NCT00072995 and NCT03258203. [ABSTRACT FROM AUTHOR]

Whether change in physical activity over time modifies the genetic susceptibility to long-term weight gain is unknown. We calculated a BMI-genetic risk score (GRS) based on 77 BMI-associated single nucleotide polymorphisms (SNPs) and a body fat percentage (BF%)-GRS based on 12 BF%-associated SNPs in 9,390 women from the Nurses' Health Study (NHS) and 5,291 men from the Health Professionals Follow-Up Study (HPFS). We analyzed the interactions between each GRS and change in physical activity on BMI/body weight change within five 4-year intervals from 1986 to 2006 using multivariable generalized linear models with repeated-measures analyses. Both the BMI-GRS and the BF%-GRS were associated with long-term increases in BMI/weight, and change in physical activity consistently interacted with the BF%-GRS on BMI change in the NHS (P for interaction = 0.025) and HPFS (P for interaction = 0.001). In the combined cohorts, 4-year BMI change per 10-risk allele increment was -0.02 kg/m2 among participants with greatest increase in physical activity and 0.24 kg/m2 among those with greatest decrease in physical activity (P for interaction < 0.001), corresponding to 0.01 kg versus 0.63 kg weight changes every 4 years (P for interaction = 0.001). Similar but marginal interactions were observed for the BMI-GRS (P for interaction = 0.045). Our data indicate that the genetic susceptibility to weight gain may be diminished by increasing physical activity. [ABSTRACT FROM AUTHOR]

Salivary and pancreatic amylases (encoded by AMY1 and AMY2 genes, respectively) are responsible for digesting starchy foods. AMY1 and AMY2 show copy number variations that affect differences in amylase amount and activity, and AMY1 copies have been associated with adiposity. We investigated whether genetic variants determining amylase gene copies are associated with 2-year changes in adiposity among 692 overweight and obese individuals who were randomly assigned to diets varying in macronutrient content. We found that changes in body weight (BW) and waist circumference (WC) were significantly different according to the AMY1-AMY2 rs11185098 genotype. Individuals carrying the A allele (indicating higher amylase amount and activity) showed a greater reduction in BW and WC at 6, 12, 18, and 24 months than those without the A allele (P < 0.05 for all). The association was stronger for long-term changes compared with short-term changes of these outcomes. The genetic effects on these outcomes did not significantly differ across diet groups. In conclusion, the genetic variant determining starch metabolism influences the response to weight-loss dietary intervention. Overweight and obese individuals carrying the AMY1-AMY2 rs11185098 genotype associated with higher amylase activity may have greater loss of adiposity during low-calorie diet interventions. [ABSTRACT FROM AUTHOR]

Background: Previous studies have indicated that the cardioprotective effects of long-chain (LC) n-3 (ω-3) polyunsaturated fatty acids (PUFAs) may vary across various ethnic populations. Emerging evidence has suggested that the gene-environment interaction may partly explain such variations. Proprotein convertase subtilisin/kexin type 9 (PCSK9) was shown to have a mutually regulating relation with LC n-3 PUFAs and also to reduce the risk of cardiovascular diseases (CVDs). Therefore, we hypothesized that certain PCSK9 genetic variants may modify the association between LC n-3 PUFA intake and CVD risk. Objective: We determined whether a PCSK9 variant (rs11206510), which has been identified for early onset myocardial infarction (MI), modified the association of LC n-3 PUFAs with nonfatal MI risk in Costa Rican Hispanics. Design: We analyzed cross-sectional data from 1932 case subjects with a first nonfatal MI and 2055 population-based control subjects who were living in Costa Rica to examine potential gene-environment interactions. Two-sided P values <0.05 were considered significant. Results: We observed a significant interaction between the PCSK9 rs11206510 genotype and LC n-3 PUFA intake on nonfatal MI risk (P-interaction = 0.012). The OR of nonfatal MI was 0.84 (95% CI: 0.72, 0.98) per 0.1% increase in total energy intake from LC n-3 PUFAs in protective-allele (C-allele) carriers, whereas the corresponding OR (95% CI) in non-C-allele carriers was 1.02 (95% CI: 0.95, 1.10). Similar results were observed when we examined the association between docosahexaenoic acid, which is one type of LC n-3 PUFA, and nonfatal MI risk (P-interaction = 0.003). Conclusion: LC n-3 PUFA intake is associated with a lower risk of nonfatal MI in C-allele carriers of PCSK9 rs11206510 (n = 799) but not in non-C-allele carriers (n = 3188). [ABSTRACT FROM AUTHOR]

Zinc transporter 8 genetic variant SLC30A8 has been associated with postpartum risk of type 2 diabetes among women with gestational diabetes mellitus (GDM). Gestational weight gain is one of the strongest risk factors for postpartum hyperglycemia. We assessed the interaction between type 2 diabetes-associated SLC30A8 rs13266634 and gestational weight gain on 1-5 years of postpartum glycemic changes in 1,071 women with prior GDM in a longitudinal study. Compared with gestation of 26-30 weeks, postpartum levels of fasting glucose, oral glucose tolerance test 2-h glucose, and hemoglobin A1c (HbA1c) increased across rs13266634 TT, CT, and CC genotypes in women with excessive gestational weight gain, whereas opposite genetic associations were found in women with inadequate or adequate gestational weight gain. Postpartum changes in fasting glucose per additional copy of the C allele were 20.18, 20.04, and 0.12 mmol/L in women with inadequate, adequate, and excessive gestational weight gain, respectively (P for interaction = 0.002). We also found similar interactions for changes in 2-h glucose and HbA1c (P for interaction = 0.003 and 0.005, respectively). Our data indicate that gestational weight gain may modify SLC30A8 variant on long-term glycemic changes, highlighting the importance of gestational weight control in the prevention of postpartum hyperglycemia in women with GDM. [ABSTRACT FROM AUTHOR]

BACKGROUND Pregnancy-induced hypertension (PIH) causes increased risk of maternal, fetal, and neonatal morbidity and mortality. Identification of risk factors for PIH in early life is central to the development of prevention strategies. METHODS A cohort of 703 women aged 25.5-51.3 years from the Bogalusa Heart Study were included. PIH were defined as self-reported hypertension during pregnancy and a blood pressure level <140/90 mm Hg without antihypertensive medication (n = 131) at the subsequent examinations. Body mass index (BMI), systolic and diastolic blood pressure, high- and low-density lipoprotein cholesterol, and triglycerides measured during childhood (4-17 years) were considered. General linear models were used to examine differences in childhood between those who did and those who did not develop PIH. Logistic regression models were used to estimate odds ratios for PIH associated with childhood risk factors. RESULTS Compared to women who did not develop PIH, those who developed PIH had higher BMI (20.2 vs. 19.2 kg/m2, P = 0.0002) and systolic blood pressure (104.1 vs. 103.3 mm Hg, P = 0.008) in childhood. After adjustment for other variables, childhood BMI was the only risk factor associated with PIH, with each standard deviation increase in childhood BMI being associated with an odds ratio of 1.35 (95% confidence interval: 1.08-1.68) for PIH. The odds of PIH increased significantly as childhood BMI increased from the bottom quartile to the top quartile (P for trend = 0.006). CONCLUSIONS Elevated childhood BMI is a significant risk factor for PIH in adulthood, which underscores the importance of body weight control in childhood for prevention of PIH. [ABSTRACT FROM AUTHOR]

Although obesity and insulin resistance are closely correlated, their temporal sequences in early life and influence on adult hypertension are largely unknown. This study aims to delineate the temporal relationship patterns between body mass index (BMI) and insulin in childhood and their impact on adult hypertension. The longitudinal cohort consisted of 990 adults (630 whites and 360 blacks) who had BMI and fasting insulin measured twice 5.4 years apart in childhood (mean age, 10.5 years at baseline and 15.9 years at follow-up) and blood pressure measured 14.7 years later in adulthood (mean age, 30.5 years). Cross-lagged panel and mediation analysis models were used to examine the temporal relationship between childhood BMI and insulin and its impact on adult hypertension. After adjusting for age, race, sex, and follow-up years, the cross-lagged path coefficient (β=0.33; P<0.001) from baseline BMI to follow-up insulin was significantly greater than the path coefficient (β=-0.02; P>0.05) from baseline insulin to follow-up BMI in childhood with P<0.001 for the difference in βs. Blacks and whites showed similar patterns of the temporal relationship. The path coefficient (β=0.59; P<0.001) from BMI to insulin in the hypertensive group was significantly greater than that (β=0.24; P<0.001) in normotensive group, with P<0.001 for the difference in βs between these 2 groups. The mediation effect of childhood insulin on the childhood BMI-adult hypertension association was estimated at 21.1% (P<0.001). These findings provide evidence that higher BMI levels precede hyperinsulinemia during childhood, and this 1-directional relation plays a role in the development of hypertension. [ABSTRACT FROM AUTHOR]

This study assessed the temporal relationship between elevated blood pressure (BP) and arterial stiffness in a biracial (black-white) cohort of middle-aged adults aged 32-51 years from the semirural community of Bogalusa, Louisiana. Measurements of aortic-femoral pulse wave velocity (afPWV; n = 446) and large-and small-arterial compliance (n = 381) were obtained at 2 time points between 2000 and 2010, with an average follow-up period of 7 years. A cross-lagged path analysis model was used to examine the temporal relationship of elevated BP to arterial stiffness and elasticity. The cross-lagged path coefficients did not differ significantly between blacks and whites. The path coefficient (ρ2) from baseline BP to follow-up afPWV was significantly greater than the path coefficient (ρ2 from baseline afPWV to follow-up BP(ρ2 = 0.20 vs. ρ1 = 0.07 (P= 0.048) for systolic BP; ρ2 = 0.19vs. ρ1 =0.05 (P= 0.034) for diastolic BP). The results for this 1 -directional path from baseline BP to follow-up afPWV were confirmed, although marginally significant, by using large- and small-artery elasticity measurements. These findings provide strong evidence that elevated BP precedes large-artery stiffening in middle-aged adults. Unlike the case in older adults, the large-arterial wall is not stiff enough in youth to alter BP levels during young adulthood. [ABSTRACT FROM AUTHOR]

Background/Aim: Salivary amylase, which is encoded by the salivary gene (AMY1), is responsible for digesting starchy foods into sugar, and the AMY1 shows extensive copy number variations which directly affect differences in salivary and serum amylase amount and activity. Recent evidence suggests associations of low serum amylase levels and obesity. We investigated whether the copy number related AMY1 genotypes were associated with 2-year changes of adiposity in response to weight-loss diet intervention. Methods: This study included 692 obese individuals with data on AMY1 variant rs11185098 who were randomly assigned to 1 of 4 diets varying in macronutrient contents. Changes of body weight (BW) and waist circumference (WC) over 2 years during the intervention were evaluated according to the genotype. Results: We found that changes in BW and WC were significantly different according to the AMY1 genotype (Figure). After adjustment for age, sex, ethnicity, diet groups and value for the respective outcome traits at baseline, carrying the minor A allele (which indicates higher amylase amount and activity-associated allele) of rs11185098 was significantly associated with greater reduction of BW at 6, 12, 18, and 24 months (β (SE), p value; -0.7 (0.35), 0.04; -1.21 (0.46), 0.009; -1.63 (0.52), 0.0017; -1.27 (0.49), 0.0095, respectively). Also, increasing number of allele A was associated with a greater decrease of WC at 6, 12, 18 and 24 months (p <0.05 for all). The genetic effects on these outcomes did not significantly differ across the diet groups. Conclusions: Our study indicated that the genetic variant responsible for starch metabolism significantly influenced on the response to weight-loss dietary intervention. Obese individuals carrying the AMY1 genotype that associated with higher salivary amylase activity may benefit from greater weight loss and the improvement of central adiposity in response to low-calorie diet interventions. [ABSTRACT FROM AUTHOR]

Background: A history of asthma from childhood has been related to various risk factors affecting left ventricular (LV) remodeling; however, no prospective study has analyzed the impact of asthma on markers of LV remodeling. Methods: Prospective analyses were performed among 1177 Bogalusa Heart Study participants (average age at follow-up: 36.3±8.3), with a baseline history of self-reported asthma collected since childhood (mean first diagnosed age: 25.2±10.3). LV mass was assessed using 2-dimensional guided M-mode echocardiography, and indexed for body height (m2.7) as LV mass index (LVMI, g/m2.7). A multivariate linear mixed model was fitted for the repeated measures. Results: After an average of 9.1 years follow-up, participants with a history of asthma showed significantly greater LV mass (166.9 vs. 156.3, p=0.007) and LVMI (40.1 vs. 37.1, p=0.002) than those without asthma, with adjustment for age, gender, race, smoking status, antihypertensive medicine, heart rate and systolic blood pressure (SBP) at follow-up. Also, we found significant interactions between SBP and asthma on LV mass and LVMI (p for interaction= 0.008 and 0.006). The associations between asthma and LV measures appeared to be stronger among prehypertensive participants (SBP≥130 mm/Hg) compared with those with normal SBP (<130 mm/Hg) [regression coefficient: 26.12 vs. -0.79 for LV mass; and 6.75 vs. 0.29 for LVMI]. Conclusions: Our findings indicate that a history of asthma is associated with higher LV mass, and such association is stronger among individuals with prehypertension. [ABSTRACT FROM AUTHOR]

Background: Elevated serum uric acid (UA) is commonly found in subjects with metabolic syndrome (MetS). This study assessed the hypothesis that UA is associated with levels of individual MetS components and the degree of their clustering patterns in different age periods. Methods: The study sample consisted of 2614 children (1577 whites, 1037 blacks; 1333 males; aged 4-18 years) and 2447 adults (1682 whites, 1765 blacks; 1072 males; aged 19-54 years) examined during 1987-2010. The adverse levels of MetS components, including body mass index (BMI), mean arterial pressure (MAP), triglycerides to HDL cholesterol ratio (TG/HDLC), and homeostasis model assessment of insulin resistance (HOMA), were defined as >75th percentile specific for age, race and sex. Observed/expected (O/E) ratio and intra-class correlation (ICC) were used as a measure of the degree of clustering of categorical and continuous variables, respectively. Results: UA was significantly positively associated with only BMI in children, and with all four components in adults. Odds ratios of UA associated with MetS were 1.74 in children and 1.92 in adults (p<0.001 for both), adjusted for race, sex and age. Trends in O/E ratios with UA quartiles are shown in the figure below. ICCs of 3- and 4-component clusters increased with increasing UA quartiles in children; however, only BMI-MAP-HOMA cluster showed an increasing trend of ICC in adults. Conclusions: The results suggest an important role of UA in the development of MetS in pediatric and adult populations. The findings provide further insights into the potential pathophysiological mechanisms of MetS and have implications for identification and treatment of high risk individuals for MetS in early life. [ABSTRACT FROM AUTHOR]

Objective To validate the World Health Organization (WHO) non-laboratory-based cardiovascular disease risk prediction model in regions of China. Methods We performed an external validation of the WHO model for East Asia using the data set of China Kadoorie Biobank, an ongoing cohort study with 512 725 participants recruited from 10 regions of China from 2004-2008. We also recalculated the recalibration parameters for the WHO model in each region and evaluated the predictive performance of the model before and after recalibration. We assessed discrimination performance by Harrell's C index. Findings We included 412 225 participants aged 40-79 years. During a median follow-up of 11 years, 58 035 and 41 262 incident cardiovascular disease cases were recorded in women and men, respectively. Harrell's C of the WHO model was 0.682 in women and 0.700 in men but varied among regions. The WHO model underestimated the 10-year cardiovascular disease risk in most regions. After recalibration in each region, discrimination and calibration were both improved in the overall population. Harrell's C increased from 0.674 to 0.749 in women and from 0.698 to 0.753 in men. The ratios of predicted to observed cases before and after recalibration were 0.189 and 1.027 in women and 0.543 and 1.089 in men. Conclusion The WHO model for East Asia yielded moderate discrimination for cardiovascular disease in the Chinese population and had limited prediction for cardiovascular disease risk in different regions in China. Recalibration for diverse regions greatly improved discrimination and calibration in the overall population. [ABSTRACT FROM AUTHOR]