Epidemiology of Stress and the Metabolic Syndrome

To examine the effects of psychological stress on the metabolic syndrome.

Study Overview

• Status: Completed
• Conditions: Heart Diseases; Cardiovascular Diseases; Hypertension; Obesity; Insulin Resistance; Hyperinsulinism; Metabolic Syndrome X

Detailed Description

BACKGROUND:

The metabolic syndrome identifies the clustering of lipid abnormalities, hypertension, hyperglycemia and abdominal obesity. It is a common and strong contributor to heart disease and diabetes and disproportionably affects older persons. Animal and small clinical studies have suggested that psychosocial stress is a risk factor for the metabolic syndrome. Underlying mechanisms may be through activation of the hypothalamopituitary-adrenal (HPA) axis causing hypercortisolemia, and, partly in turn, elevated inflammation and decreased sex hormone levels. However, longitudinal data showing that psychosocial stress indeed contributes to the onset and sequelae of the metabolic syndrome in the population at large, are lacking.

DESIGN NARRATIVE:

The primary objectives are to conduct data-analyses and biological sample analyses to examine the effect of psychosocial stress, as indicated by mood problems (depressive symptoms) and stressful social circumstances (poverty, negative life events, occupational stress, lack of emotional support), on the onset and sequelae of the metabolic syndrome. Secondary objectives are to examine underlying biological mechanisms in the effect of psychosocial stress on the metabolic syndrome. The investigators will use available data from two ongoing longitudinal community-based studies among older persons: the Health Aging and Body Composition (Health ABC) study (n=3,075, mean age=74 years, 52%=female, 42% African American) and the InChianti study (n=1,453, mean age=69 years, 56%=female). In both studies psychosocial stress and the metabolic syndrome are well defined, longitudinal data on sequelae (CVD events and diabetes onset) and onset of the metabolic syndrome are available, and potentially underlying biological variables were, or will be, assessed including 24-h urinary cortisol, serum sex steroid hormones (estradiol, testosterone, SHBG, DHEAS) and inflammatory markers (IL-6, IL-10, TNF-alpha, CRP, and various soluble cytokine receptors). The results of this study will help in designing future intervention trials that evaluate whether reducing stress and/or its physiological consequences, either by pharmacological treatment or behavioral intervention, could reduce incidence of the metabolic syndrome in the older general population.

• Study Type: Observational
• Enrollment (Actual): 3075

Participation Criteria

Eligibility Criteria

• Ages Eligible for Study: 70 years to 79 years (Older Adult)
• Accepts Healthy Volunteers: No
• Genders Eligible for Study: All

• Sampling Method: Non-Probability Sample

Study Population

Older persons

Description

Age >70 years Community swelling

Study Plan

How is the study designed?

What is the study measuring?

Primary Outcome Measures

Outcome Measure	Time Frame
There is no primary outcome	There is no time frame

Collaborators and Investigators

• Sponsor: University of Florida
• Collaborators: National Heart, Lung, and Blood Institute (NHLBI)
• Investigators: Principal Investigator: Marco Pahor, University of Florida

Study record dates

Study Major Dates

• Study Start: September 1, 2003
• Primary Completion (Actual): August 1, 2008
• Study Completion (Actual): August 1, 2008

Study Registration Dates

• First Submitted: December 8, 2003
• First Submitted That Met QC Criteria: December 9, 2003
• First Posted (Estimate): December 10, 2003

Study Record Updates

• Last Update Posted (Estimate): August 12, 2013
• Last Update Submitted That Met QC Criteria: August 8, 2013
• Last Verified: August 1, 2013

More Information

Terms related to this study

• Additional Relevant MeSH Terms: Pathologic Processes; Glucose Metabolism Disorders; Metabolic Diseases; Disease; Heart Diseases; Cardiovascular Diseases; Syndrome; Metabolic Syndrome; Insulin Resistance; Hyperinsulinism
• Other Study ID Numbers: 1239; R01HL072972 (U.S. NIH Grant/Contract)