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The optimal type of oil to prevent cardiovascular disease (CVD) is uncertain. In general, unsaturated oils with higher content of cis-monounsaturated fatty acids (MONO) or cis-polyunsaturated fatty acids (PUFA) are preferable over those rich in saturated fatty acids. However, unsaturated oils can vary in their relative contents of n-6 and n-3 fatty acids (specifically alpha-linolenic acid (ALA)). Some investigators advocate that oils rich in ALA are cardioprotective, while others suggest that optimal cardioprotective effects can only be obtained when oils are lower in n-6 fatty acids (mainly linoleic acid) in addition to being higher in ALA. It is hypothesized that increased ALA would result in beneficial effects on inflammatory markers. The objective of this trial is to establish definitively the biological effects of ALA with and without reductions in linoleic acid on inflammatory markers linked to CVD.
This study is a dietary trial that examines the effects of increasing ALA by 2 gr or 4 gr per day, with and without decreasing linoleic acid, on inflammatory markers linked to CVD. Trial participants (n=136), approximately 50% women, 50% men) are age 50 and older and living in the town of Montana, Bulgaria during the study. The study uses a double-blinded placebo-controlled, randomized cross-over design. Combinations of two oils that are considered healthy (sunflower and olive) and an ALA supplement containing either 2 or 4 gr of ALA (supplied as flaxseed oil) or placebo are consumed for 6 weeks each: sunflower-ALA (high linoleic-low ALA), sunflower-placebo (high linoleic-low ALA), olive-ALA (low-linoleic-high ALA) and olive-placebo (low linoleic-low ALA). The participants are indicated to keep their usual diet and physical activity through-out the study. The primary endpoints are plasma levels of inflammatory markers. Secondary endpoints include systolic and diastolic blood pressure, and plasma levels of LDL cholesterol, HDL cholesterol and triglycerides.
To determine the effect of increasing ALA by 2 or 4 gr per day in the context of a diet that that is high in linoleic acid (~13% energy) on inflammatory markers. The ALA effect will be tested by comparing ALA supplement vs. placebo while using sunflower oil for cooking at home. We hypothesize that ALA has favorable effects on inflammatory markers in the context of a diet that is high in linoleic acid.
To determine the effect of increasing ALA by 2 or 4 gr per day in the context of a diet that that is low in linoleic acid (~6% energy) on inflammatory markers. The ALA effect will be tested by comparing ALA supplement vs. placebo while using olive oil for cooking at home. We hypothesize that ALA has favorable effects on inflammatory markers in the context of a diet that is low in linoleic acid.
To determine the effect of reducing linoleic acid from a high level (~13% energy) to a low level (~6% energy) while keeping ALA at a high level (2 or 4 gr per day) on plasma levels of inflammatory markers. The reduction in linoleic acid will be tested by comparing sunflower to olive oil while taking the ALA supplement. We hypothesize that reducing linoleic acid does not affect inflammatory markers when ALA intake is high.
To determine the effect of reducing linoleic acid from a high level (~13% energy) to a low level (~6% energy) while keeping ALA at a low level (placebo) on plasma levels of inflammatory markers. The reduction in linoleic acid will be tested by comparing sunflower to olive oil while taking the placebo. We hypothesize that reducing linoleic acid does not affect inflammatory markers when ALA intake is low.
To determine whether the intervention contrasts specified in the specific aims and secondary aims 1 & 2 affect plasma levels of LDL cholesterol, HDL cholesterol and triglycerides and blood pressure.
We hypothesize that ALA has favorable effects on plasma triglycerides and blood pressure compared to placebo regardless of whether linoleic acid is high or low.
We hypothesize that lowering linoleic acid has favorable effects on plasma HDL cholesterol but unfavorable effects on LDL cholesterol,regardless of whether ALA is high or low.
Allocation: Randomized, Control: Placebo Control, Intervention Model: Crossover Assignment, Masking: Double Blind (Subject, Caregiver, Investigator), Primary Purpose: Prevention
Flaxseed oil-Olive oil, Olive oil-olive oil, Flaxseed oil-sunflower oil, Olive oil-sunflower oil
Harvard School of Public Health
Published on BioPortfolio: 2014-08-27T03:19:43-0400
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Oil extracted from fruit of the OLIVE TREE (genus Olea).
A plant genus of the family OLEACEAE. The olive fruit is the source of olive oil.
A genus of Old World monkeys, subfamily COLOBINAE, family CERCOPITHECIDAE, that inhabits the forests of Africa. It consists of eight species: C. angolensis (Angolan colobus), C. badius or C. rufomitratus (Red or Bay colobus), C. guereza (Guereza or Eastern black-and-white colobus), C. kirkii (Kirk's colobus), C. polykomos (King colobus or Western black-and-white colobus), C. satanas (Black colobus), and C. verus (Olive colobus). Some authors recognize Procolobus as a separate genus and then the olive colobus is recognized as the species P. verus.
A genus in the family BROMOVIRIDAE containing one species: Olive latent virus 2.
Oil derived from the seeds of SUNFLOWER plant, Helianthus.
Cardiovascular disease (CVD)
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