Neural Mechanisms in Asthma

Asthma is a chronic disease that affects nearly 13% of adults in the U.S., causing substantial impairment that is reflected in the tens of millions of missed days of work, and doctors' and emergency room visits it leads to annually. Those who have asthma are twice as likely to develop depression and anxiety, which are associated with more frequent and severe asthma symptoms, especially in those under chronic stress. The project proposed here seeks to understand the role of the brain in these associations and to evaluate the neural mechanisms through which a safe, low-cost intervention, that influences the function of body via the mind, may diminish the expression of asthma symptoms.

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Key information

Conditions

Asthma Bronchial Diseases Hypersensitivity Hypersensitivity, Immediate Immune System Diseases Lung Diseases Lung Diseases, Obstructive Respiratory Hypersensitivity Respiratory Tract Diseases

Age range

18 year–45 year

Sex eligibility

All sexes

Study type

Observational

Primary location

University of Wisconsin-Madison

Madison, Wisconsin, 53715, United States

Who can participate

Healthy volunteers accepted: Yes

Only the study team can determine whether someone qualifies for participation.

Inclusion criteria

Asthmatics:

Physician diagnosed asthma with previous use of asthma medication
Controls:

negative skin-prick test to cat dander or house dust mite and have no history of asthma
Chronic Stress:

score 3 or above on any subscale of the UCLA (University of California Los Angeles) chronic stress interview

No chronic stress:

score 1.5 or below on all subscales of the UCLA chronic stress interview

Exclusion criteria

Individuals with severe asthma, or those whom currently require the use of corticosteroids
Individuals with significant medical problems
Individuals who smoke cigarettes
Individuals a previous adverse reaction to corticosteroids, a recent (< 1 month) viral illness, a history of severe asthma or anaphylaxis.
Breastfeeding women or women who are, suspect they might be or are trying to become pregnant

Treatment and study plan

Primary outcomes

Neural activity in response to stress

Time frame: duration of stress (30 minutes)

positron emission tomography
inflammation

Time frame: 24 hours

infiltration of eosinophils into lung sputum, percentage of blood eosinophils, exhaled nitric oxide, glucocorticoid sensitivity of peripheral blood leukocytes
lung function

Time frame: 24 hours

peak expiratory volume in 1 sec effort
peripheral acute stress reactivity

Time frame: 60 minutes

salivary cortisol and alpha amylase in response to acute stressor

Sponsors and collaborators

Lead sponsor

University of Wisconsin, Madison

Other

Registry information

Official study title

Neural Mechanisms by Which Chronic Stress Regulates Inflammation in Asthma

Important dates

Study start: 2011
Primary completion: 2014
Study completion: 2014
First posted: Jul 2, 2010
Registry last updated: Oct 2, 2015

OpenTrials presents study information sourced from ClinicalTrials.gov. The official registry record should be consulted for the latest information.

View the official ClinicalTrials.gov record (opens in a new tab)

This listing is for discovery and informational purposes only. It is not medical advice, does not guarantee that a study is recruiting, and does not determine eligibility. Contact the study team and a qualified healthcare professional when considering participation.

Published trials that share one or more normalized conditions with this study.

Completed