David R Jacobs

University of Wollongong, City of Greater Wollongong, New South Wales, Australia

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Publications (697)4278.5 Total impact

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    ABSTRACT: Objective: To determine the associations of adiposity and insulin resistance with measures of vascular structure and function in children. Study design: A cross-sectional study included 252 children (age 15.1 ± 2.4 years; body mass index percentile 68.2 ± 26.5%; Tanner 2-5). Measurements of body fat percentage were obtained with dual-energy X-ray absorptiometry and visceral adipose tissue (VAT) with computed tomography. Insulin resistance was measured with hyperinsulinemic euglycemic clamp. Vascular measurements for endothelial function (brachial artery flow-mediated dilation [FMD]), vascular structure (carotid intima-media thickness [cIMT]), vascular stiffness (carotid incremental elastic modulus), and pulse wave velocity were analyzed by tertiles of adiposity and insulin resistance. Additional analyses with ANCOVA and linear regression were adjusted for Tanner, sex, race, and family relationship; FMD was also adjusted for baseline artery diameter. Results: FMD was positively associated with high adiposity (body mass index, body fat percentage, and VAT) (P < .01 all). Insulin resistance was not associated with FMD. cIMT was significantly, positively related to obesity, VAT, and insulin resistance (P < .05 all). No differences in carotid incremental elastic modulus and pulse wave velocity were observed in relation to adiposity or insulin resistance. Conclusions: The findings suggest that adiposity is associated with higher FMD, and insulin resistance and VAT are associated with higher cIMT in children. Further research is needed to clarify the progression of these relations.
    The Journal of pediatrics 10/2015; DOI:10.1016/j.jpeds.2015.08.034 · 3.79 Impact Factor
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    ABSTRACT: Obesity is linked to type 2 diabetes (T2D) and cardiovascular diseases; however, the underlying molecular mechanisms remain unclear. We aimed to identify obesity-associated molecular features that may contribute to obesity-related diseases. Using circulating monocytes from 1,264 Multi-Ethnic Study of Atherosclerosis participants, we quantified the transcriptome and epigenome. We discovered that alterations in a network of co-expressed cholesterol metabolism genes are a signature feature of obesity and inflammatory stress. This network included 11 body mass index (BMI)-associated genes related to sterol uptake (↑LDLR, ↓MYLIP), synthesis (↑SCD, FADS1, HMGCS1, FDFT1, SQLE, CYP51A1, SC4MOL) and efflux (↓ABCA1, ABCG1) - producing a molecular profile expected to increase intracellular cholesterol. Importantly, these alterations were associated with T2D and coronary artery calcium (CAC), independent from cardiometabolic factors including serum lipid profiles. This network mediated the associations between obesity and T2D/CAC. Several genes in the network harbored CpG dinucleotides (e.g. ABCG1/cg06500161) which overlapped ENCODE-annotated regulatory regions, and had methylation profiles that mediated the associations between BMI/inflammation and expression of their cognate genes. Taken together with several lines of previous experimental evidence, these data suggest that alterations of the cholesterol metabolism gene network represent a molecular link between obesity/inflammation and T2D/CAC. © 2015 by the American Diabetes Association. Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered.
    Diabetes 10/2015; 64(10):3464-3474. DOI:10.2337/db14-1314 · 8.10 Impact Factor
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    ABSTRACT: Objective: There is controversy about whether serum urate (sUA) predicts future cardiovascular disease (CVD) independently of classical risk factors, and the age at which any prediction starts. We studied the sUA-CVD association among generally healthy adults. Methods: CARDIA recruited 5115 black and white individuals aged 18-30 years in 1985-1986 (year-0). Fatal and nonfatal CVD events by year 27 (n = 164) were ascertained during annual contacts and classified using medical records. The association with sUA (year-0, 10, 15 and 20) was modeled using Cox proportional hazards regression, pooling over gender-specific quartiles. Results: Mean sUA concentration was higher in men than women, but increased over time in both genders. Those with elevated sUA had worse metabolic profiles that substantially deteriorated over time. Adjusting for demographic and lifestyle factors (the minimal model), baseline sUA concentration was positively associated with incident CVD (hazard ratio (HR) per mg/dL = 1.21; 95% confidence interval: 1.05, 1.39; P = 0.005). This positive association attenuated to nonsignificance in the full model accounting simultaneously for classical CVD risk factors (HR = 1.09; 0.94, 1.27; P = 0.24). Both the minimal and full models appeared to show stronger associations (than year-0 sUA) between year-10 sUA and incident CVD (HR = 1.27 and 1.12, respectively), but sUA was not statistically significant in the full model. Despite fewer events, year-15 sUA showed a significant sUA-CVD association pattern, with minimal model association magnitude comparable to year-10, and remained significant in the full model (HR = 1.19; 1.02, 1.40; P = 0.03). Hyperuricemia at year-15 strongly predicted CVD risk (HR = 2.11; 1.34, 3.33; P = 0.001), with some attenuation in the full model (HR = 1.68; P = 0.04). Conclusions: sUA may be an early biomarker for CVD in adults entering middle age. The prediction of CVD by sUA appeared to strengthen with aging. The potential complex relation of sUA with deterioration of a cluster of metabolic abnormalities warrants future exploration.
    PLoS ONE 09/2015; 10(9):e0138067. DOI:10.1371/journal.pone.0138067 · 3.23 Impact Factor
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    ABSTRACT: Background: High-density lipoprotein (HDL) particles have properties beyond reverse cholesterol transport. We hypothesized that their protection extends to inflammation-related disease. The predictive value of HDL particle subclasses and inflammatory markers was studied for noncardiovascular, noncancer chronic inflammation-related death and hospitalization, and for incident cardiovascular disease (CVD). Methods and results: A multiethnic, multicenter, prospective observational study was conducted in 6475 men and women (aged 45 to 84 years) free of known CVD at baseline with median follow-up of 10.1 years. Fasting venous samples were analyzed for baseline lipid profile and lipoprotein particles. We focused on the HDL family of variables (small-, medium-, and large-diameter HDL particles and HDL cholesterol). Analyses identified the sum of small- plus medium-diameter HDL particles as important. Small- plus medium-diameter HDL particles were inversely associated with diagnostic code-based noncardiovascular, noncancer chronic inflammation-related death and hospitalization (n=1054) independent of covariates: relative risk per SD 0.85 (95% CI: 0.79 to 0.91, P<0.0001). Small- plus medium-diameter HDL particles were also associated with adjudicated fatal and nonfatal coronary heart disease events (n=423): relative risk per SD 0.88 (95% CI 0.77 to 0.98, P=0.02). Conclusions: Small- plus medium-diameter HDL particles are an independent predictor for noncardiovascular, noncancer chronic inflammation-related death and hospitalization and for coronary heart disease events in subjects initially free of overt CVD. These findings support the hypothesis that smaller HDL particles of diameter <9.4 nm have anti-inflammatory properties in the general population.
    Journal of the American Heart Association 09/2015; 4(9). DOI:10.1161/JAHA.115.002295 · 4.31 Impact Factor
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    ABSTRACT: Objective: To determine whether duration and degree of weight gain is differentially associated with diabetes risk in younger versus middle-aged black and white adults. Research design and methods: We combined data from three cohort studies: Atherosclerosis Risk in Communities (ARIC), Coronary Artery Risk Development in Young Adults (CARDIA), and the Framingham Heart Study. A total of 17,404 participants (56% women; 21% black) were stratified by baseline age (younger: ≥30 and <45 years; middle aged: ≥45 and <60 years) and examined for incident diabetes (median follow-up 9 years). Duration and degree of gain in BMI was calculated as "BMI-years" above one's baseline BMI. Results: Diabetes incidence per 1,000 person-years in the younger and middle-aged groups were 7.2 (95% CI 5.7, 8.7) and 24.4 (22.0, 26.8) in blacks, respectively; and 3.4 (2.8, 4.0) and 10.5 (9.9, 11.2) in whites, respectively. After adjusting for sex, baseline BMI and other cardiometabolic factors, and age and race interaction terms, gains in BMI-years were associated with higher risk of diabetes in the younger compared with middle-aged groups: hazard ratios for 1-unit increase in log BMI-years in younger vs. middle-aged blacks were 1.18 (P = 0.02) and 1.02 (P = 0.39), respectively (P for interaction by age-group = 0.047); and in whites were 1.35 (P < 0.001) and 1.11 (P < 0.001), respectively (P for interaction by age-group = 0.008). Conclusions: Although middle-aged adults have higher rates of diabetes, younger adults are at greater relative risk of developing diabetes for a given level of duration and degree of weight gain.
    Diabetes care 09/2015; DOI:10.2337/dc14-2770 · 8.42 Impact Factor
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    ABSTRACT: Objective Lower C2, a continuous blood pressure waveform characteristic asserted to represent small artery elasticity, predicts future cardiovascular disease events. It is hypothesized that the paradoxical positive association between body mass index (BMI) and C2 may reflect muscle instead of excess fat.Methods In a multi-ethnic, community-living cohort of 1,960 participants, computed tomography scans of the abdomen were used to measure visceral adipose tissue (VAT) and total abdominal muscle tissue (TAMT), and applanation tonometry of the radial arteries was used to assess C2. The period cross-sectional associations between BMI, TAMT, and VAT with C2 were ascertained.ResultsThe mean age was 62 ± 9 years and 51% were male. After adjustments for age, gender, ethnicity, pack years smoking cigarettes, diabetes, hypertension, and total and HDL cholesterol, higher BMI (standardized beta = 0.09, P-value < 0.01) and more TAMT (standardized beta = 0.12, P-value < 0.01) were significantly associated with higher C2. In contrast, more VAT (standardized beta = −0.09, P-value < 0.01) was associated with lower C2.Conclusions In multivariable analysis, VAT, in contrast to TAMT and BMI, was associated with less compliant small arteries. Visceral fat may be a better marker for detrimental excess body fat than BMI.
    Obesity 09/2015; DOI:10.1002/oby.21221 · 3.73 Impact Factor
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    ABSTRACT: To explore the relations of parent-child cardiometabolic risk factors and assess the influence of adiposity on these associations. Associations of adiposity, blood pressure (BP), lipids, fasting insulin and glucose, and a risk factor cluster score (CS) were evaluated in a cross-sectional study of 179 parents and their children (6-18 years, N = 255). Insulin resistance was assessed by euglycemic clamp in parents and children aged 10 years or older. Metabolic syndrome in parents was defined by National Cholesterol Education Program's Adult Treatment Panel III criteria. CSs of the risk factors were created based on age-specific z-scores. Analyses included Pearson correlation and linear regression, adjusted for parent and child age, sex, race, and body mass index (BMI), accounting for within-family correlation. We found positive parent-child correlations for measures of adiposity (BMI, BMI percentile, waist, subcutaneous fat, and visceral fat; r = 0.22-0.34, all P ≤ .003), systolic BP (r = 0.20, P = .002), total cholesterol (r = 0.39, P < .001), low-density lipoprotein cholesterol (r = 0.34, P < .001), high density lipoprotein cholesterol (r = 0.26, P < .001), triglycerides (r = 0.19, P = .01), and insulin sensitivity (r = 0.22, P = .02) as well as CSs (r = 0.15, P = .02). After adjustment for BMI all parent-child correlations, except systolic BP, remained significant. Although adiposity is strongly correlated between parents and children, many cardiometabolic risk factors correlate independent of parent and child BMI. Adverse parental cardiometabolic profiles may identify at-risk children independent of the child's adiposity status. Copyright © 2015 Elsevier Inc. All rights reserved.
    The Journal of pediatrics 08/2015; DOI:10.1016/j.jpeds.2015.07.053 · 3.79 Impact Factor
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    ABSTRACT: Individuals with high levels of hostility may be more susceptible to the influence of television on violence and risk taking behaviors. This study aimed to examine whether hostile personality trait modifies the association between TV viewing and injuries. It is a prospective study of 4,196 black and white adults aged 23 to 35 in 1990/1. Cross-lagged panel models were analyzed at three 5-year time periods to test whether TV viewing predicted injuries. Covariates were gender, race, and education. Individuals who watched more TV (0 hours, 1-3 hours, 4-6 hours, and ≥7 hours) were more likely to have a hospitalization for an injury in the following 5 years across each of the three follow-up periods [OR = 1.5 (95%CI = 1.2, 1.9), 1.5 (1.1, 1.9), and 1.9 (1.3, 2.6)]. The cross-lagged effects of TV viewing to injury were significant in the high hostility group [OR = 1.4 (95%CI = 1.1, 1.8), 1.3 (1.0, 1.8), and 2.0 (1.3, 2.9)] but not in the low hostility group [OR = 1.3 (95%CI = 0.6, 2.2), 1.1 (0.6, 2.1), and 1.4 (0.7, 2.8)]. Additionally, a statistically significant difference between the two models (P < 0.001) suggested that hostility moderated the relationship between TV watching and injury. These findings suggest that individuals who watch more TV and have a hostile personality trait may be at a greater risk for injury.
    International Journal of Injury Control and Safety Promotion 08/2015; DOI:10.1080/17457300.2015.1061560 · 0.67 Impact Factor
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    ABSTRACT: To evaluate lactation duration in relation to subsequent atherosclerosis in women during midlife. The Coronary Artery Risk Development in Young Adults study is a multicenter prospective cohort that enrolled 2,787 women in 1985-1986 (ages 18-30 years, 52% black, 48% white), of whom 2,014 (72%) attended the 20-year follow-up examination in 2005-2006. We selected 846 women (46% black) without heart disease or diabetes at baseline who delivered one or more times after the baseline evaluation, had cardiometabolic risk factors measured at baseline, and had maximum common carotid intima-media thickness (mm) measured at the 20-year follow-up examination in 2005-2006. Lactation duration was summed across all postbaseline births for each woman and (n, women) categorized as: 0 to less than 1 month (n=262), 1 to less than 6 months (n=210), 6 to less than 10 months (n=169), and 10 months or greater (n=205). Multiple linear regression models estimated mean common carotid intima-media thickness (95% confidence interval) and mean differences among lactation duration groups compared with the 0 to less than 1-month group adjusted for prepregnancy obesity, cardiometabolic status, parity, and other risk factors. Lactation duration had a graded inverse association with common carotid intima-media thickness; mean differences between 10 months or greater compared with 0 to less than 1 month ranged from -0.062 mm for unadjusted models (P trend <.001) to -0.029 mm for models fully adjusted for prepregnancy body mass index (BMI) and cardiometabolic risk factors, parity, smoking, and sociodemographics (P trend=.010). Stepwise addition of potential mediators (BMI, systolic blood pressure at the 20-year follow-up examination) modestly attenuated the lactation and common carotid intima-media thickness association to -0.027 and -0.023 mm (P trend=.019 and .054). Shorter lactation duration is associated with subclinical atherosclerosis independent of prepregnancy cardiometabolic risk factors and traditional risk factors. The magnitude of differences in carotid artery intima-media thickness may represent greater vascular aging. Lactation may have long-term benefits that lower cardiovascular disease risk in women. II.
    Obstetrics and Gynecology 08/2015; 126(2):381-390. DOI:10.1097/AOG.0000000000000919 · 5.18 Impact Factor
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    ABSTRACT: Periodontal infections have been linked to cardiovascular disease, including atherosclerosis, and systemic inflammation has been proposed as a possible mediator. Secretory phospholipase A2 (s-PLA2) and Lipoprotein-associated PLA2 (Lp-PLA2) are inflammatory enzymes associated with atherosclerosis. No data are available on the association between oral microbiota and PLA2s. We studied whether a relationship exists between periodontal microbiota and the activities of these enzymes. The Oral Infection and Vascular Disease Epidemiology Study (INVEST) collected subgingival biofilms and serum samples from 593 dentate men and women (age 68.7 ± 8.6 years). 4561 biofilm samples were collected in the two most posterior teeth of each quadrant (average 7/participant) for quantitative assessment of 11 bacterial species using DNA-DNA checkerboard hybridization. Mean concentration of s-PLA2 and activities of s-PLA2 and Lp-PLA2 were regressed on tertiles of etiologic dominance (ED). ED is defined as the level of presumed periodontopathic species/combined level of all eleven species measured, and represents the relative abundance of periodontopathic organisms. Analyses were adjusted for age, sex, race/ethnicity, education, smoking, BMI, diabetes, LDL cholesterol and HDL cholesterol, and systolic blood pressure. Higher levels of s-PLA2 activity were observed across increasing tertiles of etiologic dominance (0.66 ± 0.04 nmol ml(-1) min(-1), 0.73 ± 0.04 nmol ml(-1) min(-1), 0.89 ± 0.04 nmol ml-1 min-1; p < 0.001), with also a trend of association between Lp-PLA2 activity and ED (p = 0.07), while s-PLA2 concentration was unrelated to ED. Increasingly greater s-PLA2 activity at higher tertiles of etiologic dominance may provide a mechanistic explanatory link of the relationship between periodontal microbiota and vascular diseases. Additional studies investigating the role of s-PLA2 are needed. Copyright © 2015. Published by Elsevier Ireland Ltd.
    Atherosclerosis 07/2015; 242(2):418-423. DOI:10.1016/j.atherosclerosis.2015.07.039 · 3.99 Impact Factor
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    ABSTRACT: Early menarche has been linked to risk of several chronic diseases. Prospective research on whether the intake of soft drinks containing caffeine, a modulator of the female reproductive axis, is associated with risk of early menarche is sparse. We examined the hypothesis that consumption of caffeinated soft drinks in childhood is associated with higher risk of early menarche. The National Heart, Lung, and Blood Institute Growth and Health Study recruited and enrolled 2379 (1213 African American, 1166 Caucasian) girls aged 9-10 y (from Richmond, CA; Cincinnati, OH; and Washington, DC) and followed them for 10 y. After exclusions were made, there were 1988 girls in whom we examined prospective associations between consumption of caffeinated and noncaffeinated sugar- and artificially sweetened soft drinks and early menarche (defined as menarche age <11 y). We also examined associations between intakes of caffeine, sucrose, fructose, and aspartame and early menarche. Incident early menarche occurred in 165 (8.3%) of the girls. After adjustment for confounders and premenarcheal percentage body fat, greater consumption of caffeinated soft drinks was associated with a higher risk of early menarche (RR for 1 serving/d increment: 1.47; 95% CI: 1.22, 1.79). Consumption of artificially sweetened soft drinks was also positively associated with risk of early menarche (RR for 1 serving/d increment: 1.43; 95% CI: 1.08, 1.88). Consumption of noncaffeinated soft drinks was not significantly associated with early menarche (RR for 1 serving/d increment: 0.88; 95% CI: 0.62, 1.25), nor was consumption of sugar-sweetened soft drinks (RR for 1 serving/d increment: 1.15; 95% CI: 0.95, 1.39). Consistent with the beverage findings, intakes of caffeine (RR for 1-SD increment: 1.22; 95% CI: 1.08, 1.37) and aspartame (RR for 1-SD increment: 1.20; 95% CI: 1.10, 1.31) were positively associated with risk of early menarche. Consumption of caffeinated and artificially sweetened soft drinks was positively associated with risk of early menarche in a US cohort of African American and Caucasian girls. © 2015 American Society for Nutrition.
    American Journal of Clinical Nutrition 07/2015; 102(3). DOI:10.3945/ajcn.114.100958 · 6.77 Impact Factor
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    ABSTRACT: Few studies have examined the longitudinal associations of fitness or changes in fitness on the risk of developing dyslipidemias. This study examined the associations of (1) baseline fitness with 25-year dyslipidemia incidence and (2) 20-year fitness change on dyslipidemia development in middle age in the Coronary Artery Risk Development in Young Adults Study (CARDIA). Multivariable Cox proportional hazards regression models were used to test the association of baseline fitness (1985-1986) with dyslipidemia incidence over 25 years (2010-2011) in CARDIA (N=4,898). Modified Poisson regression models were used to examine the association of 20-year change in fitness with dyslipidemia incidence between Years 20 and 25 (n=2,487). Data were analyzed in June 2014 and February 2015. In adjusted models, the risk of incident low high-density lipoprotein cholesterol (HDL-C); high triglycerides; and high low-density lipoprotein cholesterol (LDL-C) was significantly lower, by 9%, 16%, and 14%, respectively, for each 2.0-minute increase in baseline treadmill endurance. After additional adjustment for baseline trait level, the associations remained significant for incident high triglycerides and high LDL-C in the total population and for incident high triglycerides in both men and women. In race-stratified models, these associations appeared to be limited to whites. In adjusted models, change in fitness did not predict 5-year incidence of dyslipidemias, whereas baseline fitness significantly predicted 5-year incidence of high triglycerides. Our findings demonstrate the importance of cardiorespiratory fitness in young adulthood as a risk factor for developing dyslipidemias, particularly high triglycerides, during the transition to middle age. Copyright © 2015 American Journal of Preventive Medicine. Published by Elsevier Inc. All rights reserved.
    American journal of preventive medicine 07/2015; DOI:10.1016/j.amepre.2015.04.022 · 4.53 Impact Factor
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    ABSTRACT: Cumulative blood pressure (BP) exposure may adversely influence myocardial function, predisposing individuals to heart failure later in life. This study sought to investigate how cumulative exposure to higher BP influences left ventricular (LV) function during young to middle adulthood. The CARDIA (Coronary Artery Risk Development in Young Adults) study prospectively enrolled 5,115 healthy African Americans and whites in 1985 and 1986 (baseline). At the year 25 examination, LV function was measured by 2-dimensional echocardiography; cardiac deformation was assessed in detail by speckle-tracking echocardiography. We used cumulative exposure of BP through baseline and up to the year 25 examination (millimeters of mercury × year) to represent long-term exposure to BP levels. Linear regression and logistic regression were used to quantify the association of BP measured repeatedly through early adulthood (18 to 30 years of age) up to middle age (43 to 55 years). Among 2,479 participants, cumulative BP measures were not related to LV ejection fraction; however, high cumulative exposure to systolic blood pressure (SBP) and diastolic blood pressure (DBP) were associated with lower longitudinal strain rate (both p < 0.001). For diastolic function, higher cumulative exposures to SBP and DBP were associated with low early diastolic longitudinal peak strain rate. Of note, higher DBP (per SD increment) had a stronger association with diastolic dysfunction compared with SBP. Higher cumulative exposure to BP over 25 years from young adulthood to middle age is associated with incipient LV systolic and diastolic dysfunction in middle age. Copyright © 2015 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.
    Journal of the American College of Cardiology 06/2015; 65(25):2679-87. DOI:10.1016/j.jacc.2015.04.042 · 16.50 Impact Factor
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    Se-A Kim · Yu-Mi Lee · Ho-Won Lee · David R Jacobs · Duk-Hee Lee
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    ABSTRACT: Although cognitive decline is very common in elders, age-related cognitive decline substantially differs among elders and the determinants of the differences in age-related cognitive decline are unclear. We investigated our hypothesis that the association between age and cognition was stronger in those with higher serum concentrations of organochlorine (OC) pesticides, common persistent and strongly lipophilic neurotoxic chemicals. Participants were 644 elders aged 60-85, participating in the National Health and Nutrition Examination Survey 1999-2002. Six OC pesticides (p,p'-dichlorodiphenyltrichloroethane (DDT), p,p'-dichlorodipenyldichloroethylene (DDE), β-hexachlorocyclohexane, trans-nonachlor, oxychlordane, and heptachlor epoxide) were evaluated. "Lower cognitive function" was defined as having a low Digit-Symbol Substitution Test (DSST) score (<25th percentile of DSST score, cutpoint 28 symbols substituted). Higher levels of β-hexachlorocyclohexane, trans-nonachlor, oxychlordane, and heptachlor epoxide modified the associations between age and lower cognitive function (Pinteraction<0.01, 0.03, <0.01, and 0.02, respectively). Elders in the 3rd tertile of these chemicals demonstrated a greater risk of lower cognitive function with aging, compared to those in the combined 1st and 2nd tertiles. Among those with highest OC pesticides (3rd tertile), the odds ratio for the risk of lower cognitive function was about 6 to 11 for the highest quintile of age (80-85 years) vs. the first quintile of age (60-63 years), while the association between age and lower cognitive function became flatter in those with lower OC pesticides (combined 1st and 2nd tertiles). Both DDT and DDE showed no interaction, with lower DSST scores for higher age irrespective of serum concentrations of DDT or DDE. Even though DSST score measures only one aspect of cognition, several OC pesticides modified aging-related prevalence of low cognitive score, a finding which should be evaluated in prospective studies.
    PLoS ONE 06/2015; 10(6):e0130623. DOI:10.1371/journal.pone.0130623 · 3.23 Impact Factor
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    ABSTRACT: The relationship between carotid artery intima-media thickness (IMT) and cognitive function in midlife remains relatively unexplored. We examined the association between IMT and cognitive function in a middle-aged epidemiological cohort of 2618 stroke-free participants. At the year 20 visit (our study baseline), participants from the Coronary Artery Risk Development in Young Adults study had IMT measured by ultrasound at the common carotid artery. Five years later, participants completed a cognitive battery consisting of the Rey Auditory-Verbal Learning Test of verbal memory, the Digit Symbol Substitution Test of processing speed, and the Stroop test of executive function. We transformed cognitive scores into standardized z scores, with negative values indicating worse performance. Mean age at baseline was 45.3 years (SD, 3.6). Greater IMT (per 1 SD difference of 0.12 mm) was significantly associated with worse performance on all cognitive tests (z scores) in unadjusted linear regression models (verbal memory, -0.16; 95% confidence interval [CI], -0.20 to -0.13; processing speed, -0.23; 95% CI, -0.27 to -0.19; and executive function, -0.17; 95% CI, -0.20 to -0.13). In models adjusted for sociodemographics and vascular risk factors that lie earlier in the causal pathway, greater IMT remained negatively associated with processing speed (-0.06; 95% CI, -0.09 to -0.02; P, 0.003) and borderline associated with executive function (-0.03; 95% CI, -0.07 to 0.00; P, 0.07) but not with verbal memory. We observed an association between greater IMT and worse processing speed-a key component of cognitive functioning-at middle age above and beyond traditional vascular risk factors. Efforts targeted at preventing early stages of atherosclerosis may modify the course of cognitive aging. © 2015 American Heart Association, Inc.
    Stroke 06/2015; 46(8). DOI:10.1161/STROKEAHA.115.008994 · 5.72 Impact Factor
  • David R Jacobs · Linda C Tapsell
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    ABSTRACT: Given scientific and public debate about optimal diet to prevent cardiovascular disease, and interest in diet and other chronic diseases, we propose that following a few simple dietary principles would reduce chronic disease incidence. Nutrition research has been criticized for focusing on individual nutrients and foods, treated like drug therapy. With a few important exceptions, clinical trials of supplemental nutrients have not shown benefit. Although highly specific nutrition information is elusive, diet patterns have provided consistent answers, important for public health. Observational cohort studies have found that some dietary patterns are reported with high reliability over long periods and predict future cardiovascular and other inflammatory-related diseases. Two randomized clinical trials confirmed this finding. There are many common features of Mediterranean and prudent diets, particularly the plant-centered aspect, coupled with variety of foods eaten. A dietary pattern characterized by high fruit, vegetable, legume, whole grain, nut, berry, seed, and fish intakes, and possibly by intakes of dairy, coffee, tea, chocolate, and alcohol (not in excess), but low meat and detrimentally processed foods is associated with reduced incidence of cardiovascular disease and rates of noncardiovascular, noncancer chronic inflammatory-related mortality. A plant-centered diet may be broadly recommended.
    Current opinion in lipidology 06/2015; 26(4). DOI:10.1097/MOL.0000000000000184 · 5.66 Impact Factor
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    ABSTRACT: Periodontitis and type 2 diabetes mellitus are known to be associated. The relationship between periodontal microbiota and early diabetes risk has not been studied. We investigated the association between periodontal bacteria and prediabetes prevalence among diabetes-free adults. ORIGINS (the Oral Infections, Glucose Intolerance and Insulin Resistance Study) cross sectionally enrolled 300 diabetes-free adults aged 20 to 55 y (mean ± SD, 34 ± 10 y; 77% female). Prediabetes was defined as follows: 1) hemoglobin A1c values ranging from 5.7% to 6.4% or 2) fasting plasma glucose ranging from 100 to 125 mg/dL. In 1,188 subgingival plaque samples, 11 bacterial species were assessed at baseline, including Aggregatibacter actinomycetemcomitans, Porphyromonas gingivalis, Treponema denticola, Tannerella forsythia, and Actinomyces naeslundii. Full-mouth clinical periodontal examinations were performed, and participants were defined as having no/mild periodontitis vs. moderate/severe periodontitis per the definition of the Centers for Disease Control and Prevention / American Academy of Periodontology. Modified Poisson regression evaluated prediabetes prevalence across bacterial tertiles. Prevalence ratios and 95% confidence intervals for third vs. first tertiles are presented. All analyses were adjusted for cardiometabolic risk factors. All results presented currently arise from the baseline cross section. Prediabetes prevalence was 18%, and 58% of participants had moderate/severe periodontitis. Prevalence ratios (95% confidence intervals) summarizing associations between bacterial levels and prediabetes were as follows: A. actinomycetemcomitans, 2.48 (1.34, 4.58), P = 0.004; P. gingivalis, 3.41 (1.78, 6.58), P = 0.0003; T. denticola, 1.99 (0.992, 4.00), P = 0.052; T. forsythia, 1.95 (1.0, 3.84), P = 0.05; A. naeslundii, 0.46 (0.25, 0.85), P = 0.01. The prevalence ratio for prediabetes among participants with moderate/severe vs. no/mild periodontitis was 1.47 (0.78, 2.74), P = 0.23. Higher colonization levels of specific periodontal microbiota are associated with higher prediabetes prevalence among diabetes-free adults. © International & American Associations for Dental Research.
    Journal of dental research 06/2015; 94(9 Suppl). DOI:10.1177/0022034515590369 · 4.14 Impact Factor
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    ABSTRACT: Obesity is highly heritable. Genetic variants showing robust associations with obesity traits have been identified through genome-wide association studies. We investigated whether a composite score representing healthy diet modifies associations of these variants with obesity traits. 32 BMI- and 14 waist-hip ratio (WHR)-associated SNPs were genotyped and genetic risk scores (GRS) calculated in 18 cohorts of European ancestry (n=68,317). Diet score was calculated based on self-reported intakes of whole grains, fish, fruits, vegetables, nuts/seeds (favorable) and red/processed meats, sweets, sugar-sweetened beverages, fried potatoes (unfavorable). Multi-variable adjusted, linear regression within each cohort, followed by inverse variance-weighted fixed-effects meta-analysis was used to characterize: a) associations of each GRS with BMI and BMI-adjusted WHR; b) diet score modification of genetic associations with BMI and BMI-adjusted WHR. Nominally significant interactions (P=0.006-0.04) were observed between the diet score and WHR-GRS (but not BMI-GRS), two WHR loci (GRB14 rs10195252; LYPLAL1 rs4846567), and two BMI loci (LRRN6C rs10968576; MTIF3 rs4771122), for the respective BMI-adjusted WHR or BMI outcomes. Although the magnitudes of these select interactions were small, our data indicated that associations between genetic predisposition and obesity traits were stronger with a healthier diet. Our findings generate interesting hypotheses; however, experimental and functional studies are needed to determine their clinical relevance. © The Author 2015. Published by Oxford University Press.
    Human Molecular Genetics 05/2015; DOI:10.1093/hmg/ddv186 · 6.39 Impact Factor
  • David R Jacobs
    Nature Reviews Endocrinology 05/2015; 11(7). DOI:10.1038/nrendo.2015.76 · 13.28 Impact Factor
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    ABSTRACT: To examine the association of menarche timing with cardiometabolic risk factors into early to mid-adulthood, comparing African American and White women. Analyses included 2583 women (African American = 1333; White = 1250) from the Coronary Artery Risk Development in Young Adults cohort study over 25 years of follow-up (1985-2011). Outcomes included type 2 diabetes, metabolic syndrome, adiposity, glucose, insulin, blood pressure, and blood lipids. Cox models or repeated measures linear regression models estimated the association between age at menarche and the outcomes. Each 1-year earlier age at menarche was associated with higher mean body mass index among African American (0.88 ± 0.12 kg/m(2), P < .0001) and White (0.89 ± 0.10 kg/m(2), P < .0001) women. After body mass index adjustment, each 1-year earlier age at menarche was associated with higher triglycerides (2.26 ± 0.68 mg/dL, P = .001) and glucose (0.34 ± 0.11 mg/dL, P = .002), and greater risk for incident impaired fasting glucose (hazard ratio = 1.13, 95% CI 1.04-1.20) and metabolic syndrome (hazard ratio 1.19, 95% CI 1.11-1.26) among White women only. Excess adiposity associated with earlier menarche is sustained through mid-adulthood, and primarily drives higher cardiometabolic risk factor levels. However, White women with earlier menarche had increased risk of a number of insulin-resistance related conditions independent of adiposity. The cardiometabolic impact of earlier menarche was weaker in African American women despite higher average adiposity. Weight maintenance would likely reduce but may not completely eliminate the elevated cardiometabolic risk of earlier menarche. Copyright © 2015 Elsevier Inc. All rights reserved.
    The Journal of pediatrics 05/2015; 167(2). DOI:10.1016/j.jpeds.2015.04.032 · 3.79 Impact Factor

Publication Stats

37k Citations
4,278.50 Total Impact Points


  • 2015
    • University of Wollongong
      City of Greater Wollongong, New South Wales, Australia
  • 2006–2015
    • University of Oslo
      • • Department of Nutrition
      • • Division of Medicine
      Kristiania (historical), Oslo, Norway
    • Johns Hopkins University
      Baltimore, Maryland, United States
  • 1976–2015
    • University of Minnesota Duluth
      • • Medical School
      • • Laboratory Medicine and Pathology
      • • Department of Family Medicine and Community Health
      Duluth, Minnesota, United States
  • 2014
    • Loma Linda University
      • Center for Health Research
      Loma Linda, California, United States
  • 2013
    • University of California, San Francisco
      • Department of Epidemiology and Biostatistics
      San Francisco, California, United States
    • Bastyr University
      Kenmore, Washington, United States
    • University of Western Australia
      Perth City, Western Australia, Australia
  • 2005–2013
    • Kyungpook National University
      • Department of Preventive Medicine
      Daikyū, Daegu, South Korea
    • University of Toronto
      Toronto, Ontario, Canada
    • University of Vermont
      Burlington, Vermont, United States
  • 2003–2013
    • University of Minnesota Twin Cities
      • Division of Epidemiology and Community Health
      Minneapolis, Minnesota, United States
  • 2012
    • University of Bergen
      • Department of Biology
      Bergen, Hordaland Fylke, Norway
  • 2003–2011
    • Northwestern University
      • Department of Preventive Medicine
      Evanston, IL, United States
  • 1990–2011
    • University of Alabama at Birmingham
      Birmingham, Alabama, United States
  • 2010
    • Tufts University
      Georgia, United States
    • University of Washington Seattle
      Seattle, Washington, United States
  • 2002–2010
    • Columbia University
      • • Department of Epidemiology
      • • Division of General Medicine
      New York City, NY, United States
    • University of Rochester
      • School of Medicine and Dentistry
      Rochester, New York, United States
  • 1993–2010
    • University of North Carolina at Chapel Hill
      • Department of Nutrition
      Chapel Hill, NC, United States
    • Stanford University
      Palo Alto, California, United States
  • 2009
    • San Francisco VA Medical Center
      San Francisco, California, United States
    • Carnegie Mellon University
      • Department of Psychology
      Pittsburgh, PA, United States
  • 2008
    • University of Texas Health Science Center at Houston
      Houston, Texas, United States
  • 2007
    • Exponent
      San Mateo, California, United States
    • National Institute for Public Health and the Environment (RIVM)
      • Centre for Prevention and Health Services Research (PZO)
      Utrecht, Utrecht, Netherlands
  • 2002–2007
    • University of Michigan
      • • Center for Social Epidemiology and Population Health (CSEPH)
      • • Division of Pediatric Genetics
      Ann Arbor, MI, United States
  • 2004
    • University of Greifswald
      • Institute of Epidemiology and Social Medicine
      Griefswald, Mecklenburg-Vorpommern, Germany
  • 2001–2003
    • Kosin University
      • College of Medicine
      Pusan, Busan, South Korea
  • 1999
    • Wayne State University
      Detroit, Michigan, United States
  • 1995
    • University of Alabama
      Tuscaloosa, Alabama, United States
  • 1989
    • University of Houston
      Houston, Texas, United States