An interventional study of 4 g prescription omega-3 concentrate and Placebo in Inflammatory Responses, sponsored by Penn State University. Completed at 1 site in United States. Open to male participants aged 20 Years to 45 Years, including healthy volunteers. Per ClinicalTrials.gov, last updated 2023-08-21.
Sponsored by Penn State University · Not applicable, Interventional, and Basic science
The purpose of this study is to assess whether the marine omega-3 fatty acids can attenuate inflammatory responses to endotoxin challenge.
Controlled endotoxin infusion has been used widely as a model system to evaluate anti-inflammatory mediators and therapies in a controlled, in vivo setting. It is well established that infusion of bacterial endotoxin (also known as lipopolysaccharide or LPS) in humans results in a marked increase in inflammatory cytokines, most notably TNF-α, IL-1, IL-6 and IL-8, CRP, granulocyte colony stimulating factor (GCSF); eicosanoids, such as prostaglandin (PG) E2 and other mediators. Administration of endotoxin, even at a low dose (0.6 ng/kg) elevates circulating concentrations of inflammatory cytokines, and mimics the inflammatory effects of chronic diseases. This model has been used for decades and has proved to be safe and informative for evaluating anti-inflammatory therapeutic interventions on human inflammation and downstream consequences.
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's 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. It is well established that these omega-3 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 supplementation of omega-3 fatty acids will blunt the response to an inflammatory stimulus and/or enhance the resolution phase.
We propose to test this hypothesis using an in vivo endotoxin challenge with a pharmacological dose of omega-3 fatty acid ethyl esters (P-OM3, 3.4 g/d EPA + DHA) in healthy volunteers. Our proposed approach is novel in that we will provoke an in vivo inflammatory response by infusing human subjects with a low dose (0.6 ng/kg body weight) of sterile endotoxin (lipopolysaccharide [LPS]) in contrast to studies that have attempted to reverse established inflammatory pathology. Results from our proposed research will advance our understanding of the effect of omega-3 fatty acids on prevention/attenuation of an inflammatory response.
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This study's enrollment of 21 is below the median of 50 across 2,437 interventional studies indexed under Inflammation.
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Of its 13 completed or terminated interventional studies of FDA-regulated products, 10 (77%) have results posted.
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Inclusion Criteria:
The specific exclusion criteria are:
Identical olive oil capsules
Drug: Placebo
4 g prescription omega-3 concentrate (4 g/d prescription omega-3 fatty acid concentrate taken orally for 8-12 weeks)
Drug: 4 g prescription omega-3 concentrate
4 g/d prescription omega-3 fatty acid concentrate taken orally for 8-12 weeks
Also known as: Lovaza, Omacor
olive oil
Also known as: No other name (control)
Change in C Reactive Protein (CRP)
Change in blood levels of CRP at 24 hours post endotoxin administration, after each 8 week intervention
Time frame: 24 hours post endotoxin administration, following each 8 week intervention
Tumor Necrosis Factor-α (TNF-α)
Change in the plasma concentration of TNF-α at 2 hours post endotoxin administration, after each 8 week intervention
Time frame: 2 hours post endotoxin administration, following each 8 week intervention
Interleukin-6 (IL-6)
Change in the plasma concentration of TNF-α at 2 hours post endotoxin administration, after each 8 week intervention
Time frame: 2 hours post endotoxin administration, following each 8 week intervention
| Milestone | Placebo (8 Weeks), Then Omega-3 Fatty Acids (8 Weeks) | Omega-3 Fatty Acids (8 Weeks), Then Placebo (8 Weeks) |
|---|---|---|
| Started | 10 | 11 |
| Completed | 10 | 10 |
| Not completed | 0 | 1 |
Change in blood levels of CRP at 24 hours post endotoxin administration, after each 8 week intervention
| mg/L | Placebo (8 Weeks) | Omega-3 Fatty Acids (8 Weeks) |
|---|---|---|
| Change in C Reactive Protein (CRP) | 17.2 ± 1.8 | 17.1 ± 1.8 |
Change in the plasma concentration of TNF-α at 2 hours post endotoxin administration, after each 8 week intervention
| pg/mL | Placebo (8 Weeks) | Omega-3 Fatty Acids (8 Weeks) |
|---|---|---|
| Tumor Necrosis Factor-α (TNF-α) | 58.3 ± 8.1 | 59.9 ± 8.1 |
Change in the plasma concentration of TNF-α at 2 hours post endotoxin administration, after each 8 week intervention
| pg/mL | Placebo (8 Weeks) | Omega-3 Fatty Acids (8 Weeks) |
|---|---|---|
| Interleukin-6 (IL-6) | 90.6 ± 14.0 | 99.9 ± 14.0 |
Collected over Adverse event data was collected over a period of 1 year.. Non-serious events are listed at a 0% frequency threshold.
| Group | Deaths | Serious | Other |
|---|---|---|---|
| Placebo, Omega-3 | — | 0/10 (0%) | 0/10 (0%) |
| Omega-3, Placebo | — | 0/11 (0%) | 0/11 (0%) |
Only the 20 participants who completed the study are included in the baseline characteristics analysis
| Age, Continuous(years) | Baseline |
|---|---|
| Mean | 27 ± 1 |
| Sex: Female, Male(Participants) | Baseline |
|---|---|
| Female | 0 |
| Male | 20 |
Plan to share: No
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Penn State University