|First Submitted Date||May 25, 2000|
|First Posted Date||May 26, 2000|
|Last Update Posted Date||May 13, 2016|
|Start Date||August 1989|
|Primary Completion Date||Not Provided|
|Current Primary Outcome Measures||Not Provided|
|Original Primary Outcome Measures||Not Provided|
|Change History||Complete list of historical versions of study NCT00005247 on ClinicalTrials.gov Archive Site|
|Current Secondary Outcome Measures||Not Provided|
|Original Secondary Outcome Measures||Not Provided|
|Current Other Outcome Measures||Not Provided|
|Original Other Outcome Measures||Not Provided|
|Brief Title||Nutritional Determinants of Cardiovascular Disease|
|Official Title||Not Provided|
|Brief Summary||To define the role of nutritional and dietary variables in determining atherogenic traits and morbidity and mortality due to coronary heart disease as observed in the Framingham Heart Study cohort and the Framingham Offspring Study cohort.|
A major component of the prevention and treatment of coronary heart disease is the attenuation of its major underlying process, atherosclerosis, which brings about myocardial ischemia. In exploring the determinants of atherosclerosis, a diet-heart hypothesis has emerged. Simply stated, the hypothesis is that the excessive ingestion of dietary fat, notably total fat, saturated fat and cholesterol and lowered intakes of other nutrients including unsaturated fatty acids and possibly soluble fiber lead to the elevation of serum LDL-cholesterol which causes atherosclerosis. Support of the diet-heart hypothesis is available from epidemiologic, laboratory, and clinical research.
In spite of a broad range of data supporting the diet-heart hypothesis, the importance of diet is often challenged. Cited in this controversy are population-based, cross-sectional studies which have provided conflicting data. Several studies including an early report from Framingham and the Tecumseh Study have failed on cross-sectional analysis to link dietary variables to serum cholesterol, lipoproteins or coronary heart disease rates. The genetic and possible dietary homogeneity in these populations and methodological weaknesses inherent in singe serum cholesterol and dietary assessments have been posed as possible explanations for these differing results.
Difficulties in confirming the diet-heart hypothesis across existing literature may arise for several reasons: methodological problems inherent in estimating nutrient intake; difficulties associated with characterizing a behavior as complex as food purchasing; wide intraindividual variation in nutrient intake that make single day estimates of nutrient intake difficult to interpret; dissimilarities among dietary data collection techniques; varying lengths of followup for the observation of outcome variables in longitudinal epidemiologic studies; differing methods of lipid measurement or the lack of lipoprotein subfractionation. The Framingham data provide a unique opportunity to test the diet-heart hypothesis both cross-sectionally and longitudinally, to develop models for studying diet and heart disease relationships, and to establish the importance of dietary variables in atherogenesis and the morbidity and mortality of heart disease.
The associations between nutritional variables and major atherogenic risk factors including dyslipidemia, elevated blood pressure, impaired glucose tolerance, and overweight were investigated cross-sectionally in the total Framingham Offspring Study cohort of 3,800. The independent, quantitative effects of dietary factors on the prediction of cardiovascular morbidity and mortality were explored longitudinally in two samples of the original Framingham cohort at 20 and 30 years of follow-up. Six major steps were followed in each set of analyses: dimension reduction using cluster and factor analysis; zero order independent nutrition variable analyses; stepwise multiple regression of independent variables; specification of overall regression models; stability and validity testing; the addition of intervening variables using multiple regression techniques. Multivariate analyses of the dependent variables were conducted to determine associations and interactions among these variables.
The study completion date listed in this record was obtained from the "End Date" entered in the Protocol Registration and Results System (PRS) record.
|Study Design||Not Provided|
|Target Follow-Up Duration||Not Provided|
|Sampling Method||Not Provided|
|Study Population||Not Provided|
|Study Groups/Cohorts||Not Provided|
* Includes publications given by the data provider as well as publications identified by ClinicalTrials.gov Identifier (NCT Number) in Medline.
|Completion Date||July 1992|
|Primary Completion Date||Not Provided|
|Eligibility Criteria||No eligibility criteria|
|Ages||up to 100 Years (Child, Adult, Senior)|
|Accepts Healthy Volunteers||No|
|Contacts||Contact information is only displayed when the study is recruiting subjects|
|Listed Location Countries||Not Provided|
|Removed Location Countries|
|Other Study ID Numbers||1129
R01HL039144 ( U.S. NIH Grant/Contract )
|Has Data Monitoring Committee||Not Provided|
|U.S. FDA-regulated Product||Not Provided|
|IPD Sharing Statement||Not Provided|
|Responsible Party||Not Provided|
|Study Sponsor||National Heart, Lung, and Blood Institute (NHLBI)|
|PRS Account||National Heart, Lung, and Blood Institute (NHLBI)|
|Verification Date||May 2000|