A study of the relationship between physical activity and cardiovascular fitness and coronary heart disease risk factors in female adolescents

The association of measures of physical activity with coronary heart disease (CHD) risk factors in children, especially those for atherosclerosis, is unknown. The purpose of this study was to determine the association of physical activity and cardiovascular fitness with blood lipids and lipoproteins in pre-adolescent and adolescent girls.^ The study population was comprised of 131 girls aged 9 to 16 years who participated in the Children's Nutrition Research Center's Adolescent Study. The dependent variables, blood lipids and lipoproteins, were measured by standard techniques. The independent variables were physical activity measured as the difference between total energy expenditure (TEE) and basal metabolic rate (BMR), and cardiovascular fitness, VO$\rm\sb{2max}$(ml/min/kg). TEE was measured by the doubly-labeled water (DLW) method, and BMR by whole-room calorimetry. Cardiovascular fitness, VO$\rm\sb{2max}$(ml/min/kg), was measured on a motorized treadmill. The potential confounding variables were sexual maturation (Tanner breast stage), ethnic group, body fat percent, and dietary variables. A systematic strategy for data analysis was used to isolate the effects of physical activity and cardiovascular fitness on blood lipids, beginning with assessment of confounding and interaction. Next, from regression models predicting each blood lipid and controlling for covariables, hypotheses were evaluated by the direction and value of the coefficients for physical activity and cardiovascular fitness.^ The main result was that cardiovascular fitness appeared to be more strongly associated with blood lipids than physical activity. An interaction between cardiovascular fitness and sexual maturation indicated that the effect of cardiovascular fitness on most blood lipids was dependent on the stage of sexual maturation.^ A difference of 760 kcal/d physical activity (which represents the difference between the 25th and 75th percentile of physical activity) was associated with negligible differences in blood lipids. In contrast, a difference in 10 ml/min/kg of VO$\rm\sb{2max}$ or cardiovascular fitness (which represents the difference between the 25th and 75th percentile in cardiovascular fitness) in the early stages of sexual maturation was associated with an average positive difference of 15 mg/100 ml ApoA-1 and 10 mg/100 ml HDL-C. ^

The angiotensin-converting enzyme insertion/deletion polymorphism and its associations with carotid artery wall thickness and coronary heart disease: The atherosclerosis risk in communities study

Coronary heart disease (CHD) is the leading cause of death in the United States. Recently, renin-angiotensin system (RAS) was found associated with atherosclerosis formation, with angiotensin II inducing vascular smooth muscle cell growth and migration, platelet activation and aggregation, and stimulation of plasminogen activator inhibitor-1. Angiotensin II is converted from angiotensin I by angiotensin I-converting enzyme (ACE) and this enzyme is mainly genetically determined. The ACE gene has been assigned to chromosome 17q23 and an insertion/deletion (I/D)polymorphism has been characterized by the presence/absence of a 287 bp fragment in intron 16 of the gene. The two alleles form three genotypes, namely, DD, ID and II and the DD genotype has been linked to higher plasma ACE levels and cell ACE activity.^ In this study, the association between the ACE I/D polymorphism and carotid artery wall thickness measured by B-mode ultrasound was investigated in a biracial sample, and the association between the gene and incident CHD was investigated in whites and if the gene-CHD association in whites, if any, was due to the gene effect on atherosclerosis. The study participants are from the prospective Atherosclerosis Risk in Communities (ARIC) Study, including adults aged 45 to 65 years. The present dissertation used a matched case-control design for studying the associations of the ACE gene with carotid artery atherosclerosis and an unmatched case-control design for the association of the gene with CHD. A significant recessive effect of the D allele on carotid artery thickness was found in blacks (OR = 3.06, 95% C.I: 1.11-8.47, DD vs. ID and II) adjusting for age, gender, cigarette smoking, LDL-cholesterol and diabetes. No similar associations were found in whites. The ACE I/D polymorphism is significantly associated with coronary heart disease in whites, and while stratifying data by carotid artery wall thickness, the significant associations were only observed in thin-walled subgroups. Assuming a recessive effect of the D allele, odds ratio was 2.84 (95% C.I:1.17-6.90, DD vs. ID and II) and it was 2.30 (95% C.I:1.22-4.35, DD vs. ID vs. II) assuming a codominant effect of the D allele. No significant associations were observed while comparing thick-walled CHD cases with thin-walled controls. Following conclusions could be drawn: (1) The ACE I/D polymorphism is unlikely to confer appreciable increase in the risk of carotid atherosclerosis in US whites, but may increases the risk of carotid atherosclerosis in blacks. (2) ACE I/D polymorphism is a genetic risk factor for incident CHD in US whites and this effect is separate from the chronic process of atherosclerosis development. Finally, the associations observed here are not causal, since the I/D polymorphism is in an intron, where no ACE proteins are encoded. ^

The illness narratives of Hispanic American women with coronary heart disease (CHD): An ethnographic approach

Purpose. To provide a descriptive representation of the illness narratives described by Hispanic American women with CHD. ^ Design. Focused ethnographic design. ^ Setting. One outpatient general medicine clinic, one nurse-managed health promotion clinic, and informants' homes in a large metropolitan city located in southeast Texas. ^ Sample. Purposeful sampling from two different sites resulted in 17 interviews being conducted with 14 informants. ^ Method. Focused ethnographic techniques were employed in the designation of participants for the study, data collection, analysis and re-presentation. Audiotaped interviews and fieldwork were transcribed verbatim and analyzed through an iterative process of data reduction, data display, drawing conclusions and verification. ^ Findings. The developing conceptual framework that emerged from the data is labeled after the overarching experience described by informants, the experience of Embodied Exhaustion. Embodied Exhaustion, as described in this study, refers to an ongoing, dynamic, indeterminate experience of mind-body exhaustion resulting from a complex constellation of biologic, psychological and social distresses occurring over the life course. The experience consists of three categories: Taking Care of Others, Wearing Down and Hurting Hearts. Two stabilizing forces were identified: Collective Self and Believing in God. ^ Conclusions. The findings of this study emphasize the importance of framing all research, theory and practice targeting Hispanic women with CHD within a sociocentric paradigm. Nursing is challenged to provide care that extends beyond the physical body of the patient to include the social context of illness, especially the family. ^

Association between glycemic index and glycemic load and the risk of incident coronary heart disease among whites and African Americans with and without type 2 diabetes: The Atherosclerosis Risk in Communities study

Several studies have examined the association between high glycemic index (GI) and glycemic load (GL) diets and the risk for coronary heart disease (CHD). However, most of these studies were conducted primarily on white populations. The primary aim of this study was to examine whether high GI and GL diets are associated with increased risk for developing CHD in whites and African Americans, non-diabetics and diabetics, and within stratifications of body mass index (BMI) and hypertension (HTN). Baseline and 17-year follow-up data from ARIC (Atherosclerosis Risk in Communities) study was used. The study population (13,051) consisted of 74% whites, 26% African Americans, 89% non-diabetics, 11% diabetics, 43% male, 57% female aged 44 to 66 years at baseline. Data from the ARIC food frequency questionnaire at baseline were analyzed to provide GI and GL indices for each subject. Increases of 25 and 30 units for GI and GL respectively were used to describe relationships on incident CHD risk. Adjusted hazard ratios for propensity score with 95% confidence intervals (CI) were used to assess associations. During 17 years of follow-up (1987 to 2004), 1,683 cases of CHD was recorded. Glycemic index was associated with 2.12 fold (95% CI: 1.05, 4.30) increased incident CHD risk for all African Americans and GL was associated with 1.14 fold (95% CI: 1.04, 1.25) increased CHD risk for all whites. In addition, GL was also an important CHD risk factor for white non-diabetics (HR=1.59; 95% CI: 1.33, 1.90). Furthermore, within stratum of BMI 23.0 to 29.9 in non-diabetics, GI was associated with an increased hazard ratio of 11.99 (95% CI: 2.31, 62.18) for CHD in African Americans, and GL was associated with 1.23 fold (1.08, 1.39) increased CHD risk in whites. Body mass index modified the effect of GI and GL on CHD risk in all whites and white non-diabetics. For HTN, both systolic blood pressure and diastolic blood pressure modified the effect on GI and GL on CHD risk in all whites and African Americans, white and African American non-diabetics, and white diabetics. Further studies should examine other factors that could influence the effects of GI and GL on CHD risk, including dietary factors, physical activity, and diet-gene interactions. ^

Systematic review of genetic risk score in coronary heart disease and other diseases

In order to better take advantage of the abundant results from large-scale genomic association studies, investigators are turning to a genetic risk score (GRS) method in order to combine the information from common modest-effect risk alleles into an efficient risk assessment statistic. The statistical properties of these GRSs are poorly understood. As a first step toward a better understanding of GRSs, a systematic analysis of recent investigations using a GRS was undertaken. GRS studies were searched in the areas of coronary heart disease (CHD), cancer, and other common diseases using bibliographic databases and by hand-searching reference lists and journals. Twenty-one independent case-control studies, cohort studies, and simulation studies (12 in CHD, 9 in other diseases) were identified. The underlying statistical assumptions of the GRS using the experience of the Framingham risk score were investigated. Improvements in the construction of a GRS guided by the concept of composite indicators are discussed. The GRS will be a promising risk assessment tool to improve prediction and diagnosis of common diseases.^

POLYCHOTOMOUS LOGISTIC REGRESSION ANALYSIS (HYPERTENSION, CORONARY HEART DISEASE)

The history of the logistic function since its introduction in 1838 is reviewed, and the logistic model for a polychotomous response variable is presented with a discussion of the assumptions involved in its derivation and use. Following this, the maximum likelihood estimators for the model parameters are derived along with a Newton-Raphson iterative procedure for evaluation. A rigorous mathematical derivation of the limiting distribution of the maximum likelihood estimators is then presented using a characteristic function approach. An appendix with theorems on the asymptotic normality of sample sums when the observations are not identically distributed, with proofs, supports the presentation on asymptotic properties of the maximum likelihood estimators. Finally, two applications of the model are presented using data from the Hypertension Detection and Follow-up Program, a prospective, population-based, randomized trial of treatment for hypertension. The first application compares the risk of five-year mortality from cardiovascular causes with that from noncardiovascular causes; the second application compares risk factors for fatal or nonfatal coronary heart disease with those for fatal or nonfatal stroke. ^

Effect of smoking on the association between periodontitis and incidence of coronary heart disease: The Atherosclerosis Risk in Communities Study

Multiple studies have shown an association between periodontitis and coronary heart disease due to the chronic inflammatory nature of periodontitis. Also, studies have indicated similar risk factors and patho-physiologic mechanisms for periodontitis and CHD. Among these factors, smoking has been the most discussed common risk factor and some studies suggested the periodontitis - CHD association to be largely a result of confounding due to smoking or inadequate adjustment for it. We conducted a secondary data analysis of the Dental ARIC Study, an ancillary study to the ARIC Study, to evaluate the effect of smoking on the periodontitis - CHD association using three periodontitis classifications namely, BGI, AAP-CDC, and Dental-ARIC classification (Beck et al 2001). We also compared these results with edentulous ARIC participants. Using Cox proportional hazard models, we found that the individuals with the most severe form of periodontitis in each of the three classifications (BGI: HR = 1.56, 95%CI: 1.15 – 2.13; AAP-CDC: HR = 1.42, 95%CI: 1.13 – 1.79; and Dental-ARIC: HR = 1.49, 95%CI: 1.22 – 1.83) were at a significantly higher risk of incident CHD in the unadjusted models; whereas only BGI-P3 showed statistically significant increased risk in the smoking adjusted models (HR = 1.43, 95%CI: 1.04 – 1.96). However none of the categories in any of the classifications showed significant association when a list of traditional CHD risk factors was introduced into the models. On the other hand, edentulous participants showed significant results when compared to the dentate ARIC participants in the crude (HR = 1.56, 95%CI: 1.34 – 1.82); smoking adjusted (HR = 1.39, 95%CI: 1.18 – 1.64) age, race and sex adjusted (HR = 1.52, 95%CI: 1.30 – 1.77); and ARIC traditional risk factors (except smoking) adjusted (HR = 1.27, 95%CI: 1.02 – 1.57) models. Also, the risk remained significantly higher even when smoking was introduced in the age, sex and race adjusted model (HR = 1.38, 95%CI: 1.17 – 1.63). Smoking did not reduce the hazard ratio by more than 8% when it was included in any of the Cox models. ^ This is the first study to include the three most recent case definitions of periodontitis simultaneously while looking at its association with incident coronary heart disease. We found smoking to be partially confounding the periodontitis and coronary heart disease association and edentulism to be significantly associated with incident CHD even after adjusting for smoking and the ARIC traditional risk factors. The difference in the three periodontitis classifications was not found to be statistical significant when they were tested for equality of the area under their ROC curves but this should not be confused with their clinical significance.^

Analysis of interval -censored events in hypertension studies: Evaluation of treatment of coronary heart disease

Many statistical studies feature data with both exact-time and interval-censored events. While a number of methods currently exist to handle interval-censored events and multivariate exact-time events separately, few techniques exist to deal with their combination. This thesis develops a theoretical framework for analyzing a multivariate endpoint comprised of a single interval-censored event plus an arbitrary number of exact-time events. The approach fuses the exact-time events, modeled using the marginal method of Wei, Lin, and Weissfeld, with a piecewise-exponential interval-censored component. The resulting model incorporates more of the information in the data and also removes some of the biases associated with the exclusion of interval-censored events. A simulation study demonstrates that our approach produces reliable estimates for the model parameters and their variance-covariance matrix. As a real-world data example, we apply this technique to the Systolic Hypertension in the Elderly Program (SHEP) clinical trial, which features three correlated events: clinical non-fatal myocardial infarction, fatal myocardial infarction (two exact-time events), and silent myocardial infarction (one interval-censored event). ^

THE DECLINE OF ISCHEMIC HEART DISEASE MORTALITY IN TEXAS: HEALTH PLANNING IMPLICATIONS

This is a report on an empirical study of the decline of ischemic heart disease mortality in the State of Texas. The study period was from 1970 to 1977. The data was collected and analyzed at three different levels of analysis: state, health service area (HSA), and county. The study was designed to test five main hypotheses. They serve to test the role of the medical care system as a possible factor associated with the changing ischemic heart disease mortality trends.^ The principal findings of the study were that a reasonable relationship could be found between the number of emergency medical care personnel, the number of icu-ccu beds, the number of medical specialists and the percent of hospitals with icu-ccu and the decline in ischemic heart disease mortality for the State of Texas. However, non significant relationships were found between variables in the medical care system and ischemic heart disease mortality trends, at the health service area level of analysis. More specifically, the number of coronary care unit beds was found to be negatively correlated with the decline in ischemic heart disease mortality at the county level.^ While being limited in its scope, the study suggests that certain factors (emergency medical service, icu-ccu beds, percent of icu-ccu units, and medical specialists) have been shown to be associated with the observed decline in ischemic heart disease mortality. The study also suggests many avenues of future research that need to be explored. ^

Does cigarette smoking modify the association between change in body mass index during young adulthood and risk of coronary mortality during middle-age in men? Twenty-five year follow-up results from the Chicago Western Electric Study

Many persons in the U.S. gain weight during young adulthood, and the prevalence of obesity has been increasing among young adults. Although obesity and physical inactivity are generally recognized as risk factors for coronary heart disease (CHD), the magnitude of their effect on risk may have been seriously underestimated due to failure to adequately handle the problem of cigarette smoking. Since cigarette smoking causes weight loss, physically inactive cigarette smokers may remain relatively lean because they smoke cigarettes. We hypothesize cigarette smoking modifies the association between weight gain during young adulthood and risk of coronary heart disease during middle age, and that the true effect of weight gain during young adulthood on risk of CHD can be assessed only in persons who have not smoked cigarettes. Specifically, we hypothesize that weight gain during young adulthood is positively associated with risk of CHD during middle-age in nonsmokers but that the association is much smaller or absent entirely among cigarette smokers. The purpose of this study was to test this hypothesis. The population for analysis was comprised of 1,934 middle-aged, employed men whose average age at the baseline examination was 48.7 years. Information collected at the baseline examinations in 1958 and 1959 included recalled weight at age 20, present weight, height, smoking status, and other CHD risk factors. To decrease the effect of intraindividual variation, the mean values of the 1958 and 1959 baseline examinations were used in analyses. Change in body mass index ($\Delta$BMI) during young adulthood was the primary exposure variable and was measured as BMI at baseline (kg/m$\sp2)$ minus BMI at age 20 (kg/m$\sp2).$ Proportional hazards regression analysis was used to generate relative risks of CHD mortality by category of $\Delta$BMI and cigarette smoking status after adjustment for age, family history of CVD, major organ system disease, BMI at age 20, and number of cigarettes smoked per day. Adjustment was not performed for systolic blood pressure or total serum cholesterol as these were regarded as intervening variables. Vital status was known for all men on the 25th anniversary of their baseline examinations. 705 deaths (including 319 CHD deaths) occurred over 40,136 person-years of experience. $\Delta$BMI was positively associated with risk of CHD mortality in never-smokers, but not in ever-smokers (p for interaction = 0.067). For never-smokers with $\Delta$BMI of stable, low gain, moderate gain, and high gain, adjusted relative risks were 1.00, 1.62, 1.61, and 2.78, respectively (p for trend = 0.010). For ever-smokers, with $\Delta$BMI of stable, low gain, moderate gain, and high gain, adjusted relative risks were 1.00, 0.74, 1.07, and 1.06, respectively (p for trend = 0.422). These results support the research hypothesis that cigarette smoking modifies the association between weight gain and CHD mortality. Current estimates of the magnitude of effect of obesity and physical inactivity on risk of coronary mortality may have been seriously underestimated due to inadequate handling of cigarette smoking. ^

Physical activity and survival after a first myocardial infarction: The Corpus Christi Heart Project

Previous studies have demonstrated that habitual physical activity is associated with a reduced risk of incident coronary heart disease (CHD). However, the role of physical activity in lowering the risk of all-cause mortality, CHD mortality, reinfarction, or receipt of a revascularization procedure after a first myocardial infarction (MI) remains unresolved, particularly in minority populations. To investigate the associations between physical activity and risk of all-cause mortality, CHD mortality, reinfarction, and receipt of a revascularization procedure, this study was conducted among Mexican-American and non-Hispanic white women and men who survived a first MI. The Corpus Christi Heart Project, a population-based cardiovascular surveillance study, provide data which included vital status, survival time, medical history, CHD risk factor information, including level of physical activity among Mexican-American and non-Hispanic white adults who had experienced a first MI between May, 1988 and April, 1990. MI patients were interviewed at baseline and annually thereafter until their death or through May, 1995. A categorical variable was created to reflect change in level of physical activity following the first MI; categories included (1) sedentary with no change, (2) decreased activity, (3) increased activity, and (4) moderate activity with no change (the referent group). Proportional hazards regression analyses were used to assess the relationship of level of physical activity and risk of death, reinfarction, or receipt of a revascularization procedure adjusting for age, sex, ethnicity, severity of MI, and CHD risk factor status. Over a 7-year follow-up period, the relative risk (95% confidence intervals) of all-cause mortality was 4.67 (2.27, 9.60) for the sedentary-no change group, 2.33 (0.96, 5.67) for the decreased activity group, and 0.52 (0.11, 2.41) for the increased activity group. The relative risk of CHD mortality was 6.92 (2.05, 23.34) for the sedentary-no change group, 2.40 (0.55, 10.51) for the decreased activity group, and 1.58 (0.26, 9.65) for the increased activity group. The relative risk for reinfarction was 2.50 (1.52, 4.10) for the sedentary-no change group, 2.26 (1.24, 4.12) for the decreased activity group, and 0.52 (0.21, 1.32) for the increased activity group. Finally, the relative risk for receipt of a revascularization procedure was 0.65 (0.39, 1.07) for the sedentary-no change group, 0.45 (0.22, 0.92) for the decreased activity group, and 1.01 (0.51, 2.02) for the increased activity group. No interactions were observed for ethnicity or severity of first MI. These results are consistent with the hypothesis that moderate physical activity is independently associated with a lower risk of all-cause mortality, CHD mortality, and reinfarction, but not revascularization, among Mexican-American and non-Hispanic white, female and male, first MI patients. These results also support the current recommendation that physical activity plays an important role in the secondary prevention of CHD. ^

Are functional and genetic components of platelets linked to coronary artery disease: A case-control study

Coronary artery disease (CAD) is a multifactorial disease process involving behavioral, inflammatory, clinical, thrombotic, and genetic components. Previous epidemiologic studies focused on identifying behavioral and demographic risk factors of CAD, but none focused on platelets. Current platelet literature lacks the known effects of platelet function and platelet receptor polymorphisms on CAD. This case-control analysis addressed these issues by analyzing data collected for a previous study. Cases were individuals who had undergone CABG and thus had been diagnosed with CAD, while the controls were volunteers presumed to be CAD free. The platelet function variables analyzed included fibrinogen Von Willebrand Factor activity (VWF), shear-induced platelet aggregation (SIPA), sCD40L, and mean platelet volume; and the platelet polymorphisms studied included PIA, α2 807, Ko, Kozak, and VNTR. Univariate analysis found fibrinogen, VWF, SIPA, and PIA to be independent risk factors of CAD. Logistic regression was used to build a predictive model for CAD using the platelet function and platelet polymorphism data adjusted for age, sex, race, and current smoking status. A model containing only platelet polymorphisms and their respective receptor densities, found polymorphisms within GPIbα to be associated with CAD, yielding an 86% (95% C.I. 0.97–3.55) increased risk with the presence of at least 1 polymorphism in Ko, Kozak, or VNTR. Another model included both platelet function and platelet polymorphism data. Fibrinogen, the receptor density of GPIbα, and the polymorphism in GPIa-IIa (α2 807) were all associated with CAD with odds ratios of 1.10, 1.04, and 2.30 for fibrinogen (10mg/dl increase), GPIbα receptors (1 MFI increase), and GPIa-IIa, respectively. In addition, risk estimates and 99% confidence intervals adjusted for race were calculated to determine if the presence of a platelet receptor polymorphism was associated with CAD. The results were as follows: PIA (1.64, 0.74–3.65); α2 807 (1.35, 0.77–2.37); Ko (1.71, 0.70–4.16); Kozak (1.17, 0.54–2.52); and VNTR (1.24, 0.52–2.91). Although not statistically significant, all platelet polymorphisms were associated with an increased risk for CAD. These exploratory findings indicate that platelets do appear to have a role in atherosclerosis and that anti-platelet drugs targeting GPI-IIa and GPIbα may be better treatment candidates for individuals with CAD. ^

Adiposity and the perilipin gene: The role of single locus and multilocus variation, obesity-related quantitative traits, and disease-related phenotypes in the Atherosclerosis Risk in Communities (ARIC) study

Obesity is a complex multifactorial disease and is a public health priority. Perilipin coats the surface of lipid droplets in adipocytes and is believed to stabilize these lipid bodies by protecting triglyceride from early lipolysis. This research project evaluated the association between genetic variation within the human perilipin (PLIN) gene and obesity-related quantitative traits and disease-related phenotypes in Non-Hispanic White (NHW) and African American (AA) participants from the Atherosclerosis Risk in Communities (ARIC) Study. ^ Multivariate linear regression, multivariate logistic regression, and Cox proportional hazards models evaluated the association between single gene variants (rs2304794, rs894160, rs8179071, and rs2304795) and multilocus variation (rs894160 and rs2304795) within the PLIN gene and both obesity-related quantitative traits (body weight, body mass index [BMI], waist girth, waist-to-hip ratio [WHR], estimated percent body fat, and plasma total triglycerides) and disease-related phenotypes (prevalent obesity, metabolic syndrome [MetS], prevalent coronary heart disease [CHD], and incident CHD). Single variant analyses were stratified by race and gender within race while multilocus analyses were stratified by race. ^ Single variant analyses revealed that rs2304794 and rs894160 were significantly related to plasma triglyceride levels in all NHWs and NHW women. Among AA women, variant rs8179071 was associated with triglyceride levels and rs2304794 was associated with risk-raising waist circumference (>0.8 in women). The multilocus effects of variants rs894160 and rs2304795 were significantly associated with body weight, waist girth, WHR, estimated percent body fat, class II obesity (BMI ≥ 35 kg/m2), class III obesity (BMI ≥ 35 kg/m2), and risk-raising WHR (>0.9 in men and >0.8 in women) in AAs. Variant rs2304795 was significantly related to prevalent MetS among AA males and prevalent CHD in NHW women; multilocus effects of the PLIN gene were associated with prevalent CHD among NHWs. Rs2304794 was associated with incident CHD in the absence of the MetS among AAs. These findings support the hypothesis that variation within the PLIN gene influences obesity-related traits and disease-related phenotypes. ^ Understanding these effects of the PLIN genotype on the development of obesity can potentially lead to tailored health promotion interventions that are more effective. ^

The effect of genotype-by-environment interaction on longitudinal triglyceride profiles in the Bogalusa Heart Study

Triglyceride levels are a component of plasma lipids that are thought to be an important risk factor for coronary heart disease and are influenced by genetic and environmental factors, such as single nucleotide polymorphisms (SNPs), alcohol intake, and smoking. This study used longitudinal data from the Bogalusa Heart Study, a biracial community-based survey of cardiovascular disease risk factors. A sample of 1191 individuals, 4 to 38 years of age, was measured multiple times from 1973 to 2000. The study sample consisted of 730 white and 461 African American participants. Individual growth models were developed in order to assess gene-environment interactions affecting plasma triglycerides over time. After testing for inclusion of significant covariates and interactions, final models, each accounting for the effects of a different SNP, were assessed for fit and normality. After adjustment for all other covariates and interactions, LIPC -514C/T was found to interact with age3, age2, and age and a non-significant interaction of CETP -971G/A genotype with smoking status was found (p = 0.0812). Ever-smokers had higher triglyceride levels than never smokers, but persons heterozygous at this locus, about half of both races, had higher triglyceride levels after smoking cessation compared to current smokers. Since tobacco products increase free fatty acids circulating in the bloodstream, smoking cessation programs have the potential to ultimately reduce triglyceride levels for many persons. However, due to the effect of smoking cessation on the triglyceride levels of CETP -971G/A heterozygotes, the need for smoking prevention programs is also demonstrated. Both smoking cessation and prevention programs would have a great public health impact on minimizing triglyceride levels and ultimately reducing heart disease. ^