Age-Related Changes in Body Composition
|First Submitted Date||January 24, 2012|
|First Posted Date||January 25, 2012|
|Last Update Posted Date||October 17, 2017|
|Start Date||January 2, 2012|
|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 NCT01517113 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||Age-Related Changes in Body Composition|
|Official Title||Age-Associated Changes in Regional Adiposity and Novel Cardiovascular Risk Factors|
- Advancing age is associated with greater risk of heart disease. High blood pressure and hardening of the arteries also have more complications with age. Studies suggest that age-related inflammation may affect fatty tissue in the body. If this fat develops in the muscles or around the heart, it may increase risks of heart disease. Researchers will study body composition in older adults to see if age-related changes in body fat are related to higher risks of heart disease.
- To study the relationship between fat deposits and aging, and greater risks of heart disease.
Advancing age is associated with an increasing prevalence, incidence, and complications of cardiovascular diseases, particularly hypertension and atherosclerosis. The reasons why age is associated with increased susceptibility to cardiovascular diseases are not understood but recent literature suggests that systemic inflammation, by affecting endothelial function, vascular stiffening, diastolic dysfunction and insulin resistance may be an important contributing cause. Aging is also associated with substantial changes in body composition, primarily an increase in fat mass and a decline in lean body mass. Studies in animal models and in humans have shown that the adipose tissue is an important source of pro-inflammatory mediators and suggested that changes in body composition may be the primary cause of the pro-inflammatory state of aging. A number of gene expression studies in animal models show that genes of several pro-inflammatory cytokines are over-expressed with aging, especially in the adipose tissue. The overproduction of pro-inflammatory cytokines have important systemic effects, including (1) endothelial dysfunction, one of the earliest features of atherosclerosis; (2) vascular stiffening, the primary etiology for isolated systolic hypertension in the elderly; and (3) insulin resistance, the principal metabolic abnormality associated with cardiovascular risk. Fat infiltration in the liver also promotes chronic inflammation both directly and by inducing apoptosis of hepatocytes with consequent inflammatory response and deterioration of liver function.
Limited data exists suggesting that deposition of adipose tissue in specific districts but not in others is associated with high circulating levels of pro-inflammatory markers. For example, in humans central adiposity, including fat accumulation surrounding the heart, and fat infiltration in the muscle, opposed to subcutaneous adiposity seems to be particularly pro-inflammatory. However, this information comes from small studies, or studies limited to a very narrow age-range. In addition, the assessment of regional adiposity was mostly based on anthropometrics. Indeed, non-invasive methodology for the assessment of regional lipid deposition profiles has become available only recently.
We propose to complement the BLSA population with a group of individuals with established CAD because the inclusion of this group may help to determine whether, and if so the extent to which, the expected relationships between body adiposity, inflammation, endothelial dysfunction, arterial stiffness and insulin resistance are different in healthy individuals compared to age-matched individuals with clinically overt vascular disease.
As a side hypothesis, we will also verify whether changes in Testosterone with age are associated with changes in regional fat accumulation. To test this hypothesis we will measure total, free and biovailable Testosterone in all participants.
|Study Design||Time Perspective: Prospective|
|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.
|Estimated Completion Date||October 13, 2017|
|Primary Completion Date||Not Provided|
In addition, for CAD participants (Group B):
In addition, for CAD participants in whom arterial and hepatic vein inflammatory mediators will be obtained:
- Scheduled for clinically indicated right or left heart catheterization, no contraindication for the procedure, and consented to the research procedure.
In addition, for BLSA participants:
- Known coronary artery disease by prior history, examination, or resting or stress electrocardiogram testing.
In addition, for CAD participants undergoing arterial and hepatic vein inflammatory mediator sampling:
|Ages||50 Years to 90 Years (Adult, Senior)|
|Accepts Healthy Volunteers||Yes|
|Contacts||Contact information is only displayed when the study is recruiting subjects|
|Listed Location Countries||United States|
|Removed Location Countries|
|Other Study ID Numbers||120019
|Has Data Monitoring Committee||Not Provided|
|U.S. FDA-regulated Product||Not Provided|
|IPD Sharing Statement||Not Provided|
|Responsible Party||National Institutes of Health Clinical Center (CC) ( National Institute on Aging (NIA) )|
|Study Sponsor||National Institute on Aging (NIA)|
|PRS Account||National Institutes of Health Clinical Center (CC)|
|Verification Date||October 13, 2017|