Dose Response Effects of Marine Omega-3 Fatty Acids on Inflammation

Inflammation Clinical Trial

Official title:

Dose Response Effects of Marine Omega-3 Fatty Acids on Inflammation

Clinical Trial Details — Status: Completed

Administrative data

• NCT number: NCT01078909
• Other study ID #: PKE LPS
• Status: Completed
• Phase: Phase 3
• Start date: October 2011
• Est. completion date: April 2014

Study information

• Verified date: August 2023
• Source: Penn State University
• Contact: n/a
• Is FDA regulated: No
• Study type: Interventional

Clinical Trial Summary

The purpose of this study is to determine the lowest effective dose of EPA + DHA (300, 600, 900 and 1,800 mg/day delivered as fish oil supplements) that significantly attenuates the inflammatory response to in vivo and ex vivo endotoxin challenge as measured by the production over time of several inflammatory markers.

Description:

Inflammation is an important biological process initiated by the immune system in response to injury, irritation or infection. Prolonged or chronic inflammation is involved in the etiology of several diseases such as cardiovascular disease (CVD), diabetes, rheumatoid arthritis, cancer, and neurodegenerative diseases such as Alzheimer disease. The evidence base clearly demonstrates benefits of diet in ameliorating inflammation and reducing the burden of chronic disease. With respect to marine-derived omega-3 fatty acids and various markers of inflammation related to cardiovascular disease (CVD), both population studies and randomized controlled supplementation trials have yielded mixed results.

Some studies have demonstrated a dose-response relationship between dietary eicosapentaenoic acid and docosahexaenoic acid (EPA + DHA) and increased membrane (phospholipid) EPA and DHA. Red blood cell (RBC) EPA + DHA content has been proposed as a potential, modifiable marker for coronary heart disease (CHD) risk. It is well established that these fatty acids are precursors of series-3 prostanoids, thromboxanes, 5-series leukotrienes, and novel lipid mediators such as resolvins and protectins that have anti-inflammatory effects. We hypothesize that nutritionally-relevant intakes of omega-3 fatty acids are able to blunt the usual response to an inflammatory stimulus. We propose to test this hypothesis using both in vivo (i.v. endotoxin challenge) and ex vivo (endotoxin-stimulated monocytes) models in a 6-month, dose-response study with marine-derived omega-3 fatty acid supplements in healthy volunteers.

Recruitment information / eligibility

• Status: Completed
• Enrollment: 125
• Est. completion date: April 2014
• Est. primary completion date: November 2012
• Accepts healthy volunteers: Accepts Healthy Volunteers
• Gender: All
• Age group: 20 Years to 45 Years

Eligibility

Inclusion Criteria:

• Healthy men and non-pregnant/lactating women between the ages of 20 and 45

• BMI >19.9 and <30.0

• Able to give written informed consent and willing to comply with all study- related procedures.

Exclusion Criteria:

• Previous history of heart disease or diabetes

• Renal Insufficiency

• Chronic anti-inflammatory use

• Systolic blood pressure < 90

• Individuals currently using tobacco products or have done so in the previous 30 days

• Individuals taking Omega-3 fatty acid supplements or their usual intake of fish is greater than 3-4 servings per month.

Related Conditions & MeSH terms

• Cardiovascular Disease
• Cardiovascular Diseases
• Inflammation

Intervention

Biological:
• Eicosapentaenoic Acid and Docosahexaenoic Acid (EPA + DHA)
Comparison of 4 doses of EPA+DHA on in vivo and ex vivo (monocytes) response to an inflammatory stimulus (endotoxin) following a 6 month supplementation period

Locations

Country	Name	City	State
United States	Penn State University	University Park	Pennsylvania

Sponsors (2)

Lead Sponsor	Collaborator
Penn State University	United States Department of Agriculture (USDA)

Country where clinical trial is conducted

United States, 

Outcome

Type	Measure	Description	Time frame	Safety issue
Primary	Mean Concentrations of Inflammatory Markers (TNF-alpha and IL-6) Following 5 Months of Treatment		5 months
Primary	Mean Concentrations of CRP Following 5 Months of Treatment		5 months
Secondary	Change in Lipid Mediators	0 Participants Analyzed; Lipid mediators were unable to be detected therefore there are no data to report.	1, 2, 3 and 5 days post LPS administration