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Effects of Omega-3 Docosapentaenoic Acid on Lipids and Other Risk Factors for Cardiovascular Disease (DPA)

The safety and scientific validity of this study is the responsibility of the study sponsor and investigators. Listing a study does not mean it has been evaluated by the U.S. Federal Government. Know the risks and potential benefits of clinical studies and talk to your health care provider before participating. Read our disclaimer for details. Identifier: NCT04088240
Recruitment Status : Recruiting
First Posted : September 12, 2019
Last Update Posted : September 12, 2019
Information provided by (Responsible Party):
Ann Skulas-Ray, University of Arizona

Brief Summary:

Elevated plasma triglycerides (TG) are due to an excess of TG-rich lipoproteins of several different types, most commonly of very-low-density lipoproteins (VLDL), but also intermediate-density lipoproteins (IDL, or VLDL remnants), chylomicrons, and/or chylomicron remnants. Epidemiologic evidence that a moderate elevation in TG is often associated with increased atherosclerotic cardiovascular disease (ASCVD) risk, and more recent evidence from Mendelian randomization studies has shown that elevated TG associated with genetic variants may be a causal factor for ASCVD and possibly for premature all-cause mortality.[1-6] Fasting plasma TG concentrations may be categorized as: normal (< 150 mg/dL ), borderline (150-199 mg/dL), high TG (HTG, 200-499 mg/dL), and very high TG (VHTG, ≥ 500 mg/dL).[7, 8] Risk of acute pancreatitis is increased in VHTG patients, especially those with TG ≥ 1000 mg/dL.[9] For VHTG, the primary goal of therapy is to reduce TG to < 500 mg/dL,[10] whereas there is no specific treatment goal for HTG nor prescription indication. However, the omega-3 fatty acids, EPA and DHA have well-established efficacy in reducing TG in the range of 150-500 when administered at doses of > or = 3 g/d EPA+DHA (reviewed in Skulas-Ray et al. in press). Importantly, administration of omega-3 fatty acids to people with TG in this range lead to a 25% reduction in major adverse cardiovascular endpoints in the recently completed "Reduction of Cardiovascular Events with EPA Intervention Trial" (REDUCE-IT).[11]

The results of REDUCE-IT provide compelling evidence for the use 3 g/d omega-3 fatty acid supplementation to reduce cardiovascular risk among patients with TG 150-500 mg/dL. The concentrated EPA supplement used in REDUCE-IT is just one of three long chain n-3 omega-3 fatty acids that influence lipids and lipoproteins and other aspects of cardiovascular risk.

Most research has focused on the evaluation of EPA and DHA, which are the two predominant n-3 FA in fish and in n-3 agents, but docosapentaenoic acid (DPA) is present in fish oil, as well, and accumulates in the blood at similar concentrations. The carbon length of the n-3 FA appears important for physiological effects. EPA has a carbon length of 20, DHA has a carbon length of 22, and DPA, the metabolic intermediate of EPA and DHA, is a 22-carbon n-3 FA. DPA may have significant potential for treating HTG and VHTG,[12, 13] but research on this fatty acid remains limited. In a 2-week open-label crossover comparison of 4 g/d of a DPA concentrate (containing unspecified amounts of free DPA and EPA) vs. 4 g/d EPA concentrate in people with HTG, plasma TG were reduced 33% by the DPA concentrate, which was significantly more than the 11% reduction with EPA.[13] Thus, a recent scientific advisory from the American Heart Association (Skulas-Ray et al, in press) concluded that more research is needed to elaborate the lipid and lipoprotein effects of DPA.

Additional biomarker research suggests DPA similarly can influence health outcomes that respond to EPA and DHA. For instance, decreased serum concentrations of DPA and DPA + DHA have been associated with increased risk of risk of acute coronary events[14] and myocardial infarction[15], respectively. Plasma DPA was also inversely associated with incident cardiovascular disease (CVD) in some ethnic groups.[16]

In conclusion evidence supports a potential role of DPA in improving health, but results from clinical supplementation studies are needed to clarify the effect of DPA supplementation on lipids and lipoproteins as well as other cardiovascular disease risk factors—relative to supplementation with EPA and DHA—to ascertain whether enrichment of omega-3 concentrates with DPA could offer health benefits above and beyond concentrates that only contain EPA and DHA.

Condition or disease Intervention/treatment Phase
Elevated Triglycerides Cardiovascular Risk Factor Dietary Supplement: DPA enriched n-3 Dietary Supplement: n-3 control Dietary Supplement: Placebo Not Applicable

  Show Detailed Description

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Study Type : Interventional  (Clinical Trial)
Estimated Enrollment : 20 participants
Allocation: Randomized
Intervention Model: Crossover Assignment
Masking: Quadruple (Participant, Care Provider, Investigator, Outcomes Assessor)
Primary Purpose: Prevention
Official Title: Effects of Omega-3 Docosapentaenoic Acid on Lipids and Other Risk Factors for Cardiovascular Disease
Actual Study Start Date : September 4, 2019
Estimated Primary Completion Date : May 31, 2020
Estimated Study Completion Date : May 31, 2020

Arm Intervention/treatment
Experimental: DPA enriched n-3
4 g/d DPA enriched n-3 concentrate (~980 mg DPA, 380 mg EPA, 1720 mg DHA)
Dietary Supplement: DPA enriched n-3
4 g/d DPA enriched n-3 concentrate (~980 mg DPA, 380 mg EPA, 1720 mg DHA)

Active Comparator: n-3 control
4 g/d n-3 control (~980 oleic acid, 380 mg EPA, 1720 mg DHA)
Dietary Supplement: n-3 control
4 g/d n-3 control (~980 oleic acid, 380 mg EPA, 1720 mg DHA)

Placebo Comparator: Placebo
4 g/d placebo control ("light" olive oil)
Dietary Supplement: Placebo
4 g/d placebo control ("light" olive oil)

Primary Outcome Measures :
  1. Triglycerides [ Time Frame: 6-8 weeks ]
    Fasting blood work (triglycerides)

Secondary Outcome Measures :
  1. Pulse Wave Velocity (PWV) [ Time Frame: 6-8 weeks ]
    As measured by SphygmoCor device

  2. Augmentation Index [ Time Frame: 6-8 weeks ]
    augmentation index corrected for heart rate

  3. Other lipids [ Time Frame: 6-8 weeks ]
    Fasting blood work (HDL-C, total cholesterol, and LDL-C)

  4. Glucose [ Time Frame: 6-8 weeks ]
    Fasting glucose

  5. Insulin [ Time Frame: 6-8 weeks ]
    Fasting blood work (insulin)

  6. Non-HDL-C [ Time Frame: 6-8 weeks ]
    Fasting blood work (non-HDL-C)

  7. Central blood pressure [ Time Frame: 6-8 weeks ]
    systolic and diastolic blood pressures

Other Outcome Measures:
  1. DPA-derived pro-resolving lipid mediators [ Time Frame: 6 weeks ]
    Fasting blood work (lipid mediators)

  2. Inflammatory markers [ Time Frame: 6-8 weeks ]
    Fasting blood work (CRP, TNF-α)

Information from the National Library of Medicine

Choosing to participate in a study is an important personal decision. Talk with your doctor and family members or friends about deciding to join a study. To learn more about this study, you or your doctor may contact the study research staff using the contacts provided below. For general information, Learn About Clinical Studies.

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Ages Eligible for Study:   18 Years to 65 Years   (Adult, Older Adult)
Sexes Eligible for Study:   All
Accepts Healthy Volunteers:   Yes

Inclusion Criteria:

  • Elevated fasting TG (150-500 mg/dL)
  • BMI of 18-40 kg/m2
  • Consistent dosage for any medication/supplements taken for elevated lipids, blood pressure, glucose, or inflammatory conditions
  • Ability to abstain from alcohol for 48 hours prior to lab testing
  • Low fish consumption (<2 servings/week)

Exclusion Criteria:

  • Pregnant or lactating
  • Use of blood thinning medications
  • Adherence to a weight loss program
  • Allergy to fish

Information from the National Library of Medicine

To learn more about this study, you or your doctor may contact the study research staff using the contact information provided by the sponsor.

Please refer to this study by its identifier (NCT number): NCT04088240

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Contact: Research Coordinator (520) 621-5382

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United States, Arizona
University of Arizona Recruiting
Tucson, Arizona, United States, 85721
Contact: Research Coordinator    520-621-5382   
Principal Investigator: Ann C Skulas-Ray, PhD         
Sponsors and Collaborators
University of Arizona

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Responsible Party: Ann Skulas-Ray, Assistant Professor, University of Arizona Identifier: NCT04088240     History of Changes
Other Study ID Numbers: 1907850505
First Posted: September 12, 2019    Key Record Dates
Last Update Posted: September 12, 2019
Last Verified: September 2019
Individual Participant Data (IPD) Sharing Statement:
Plan to Share IPD: No

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Studies a U.S. FDA-regulated Drug Product: No
Studies a U.S. FDA-regulated Device Product: No
Keywords provided by Ann Skulas-Ray, University of Arizona:
Additional relevant MeSH terms:
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Cardiovascular Diseases
Lipid Metabolism Disorders
Metabolic Diseases