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- Olive (Olea europaea, Oleaceae) Oil
- Coronary Artery Disease
- Inflammation
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Date:
05-31-2018 | HC# 111743-593
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Re: Cardioprotective and Anti-inflammatory Properties of Olive Oil Phenolic Compounds
Souza PAL, Marcadenti A, Portal VL. Effects
of olive oil phenolic compounds on inflammation in the prevention and treatment
of coronary artery disease. Nutrients.
2017;9(10):1087. doi: 10.3390/nu9101087.
Cardiovascular (CV) diseases are the leading
cause of world mortality, with 7.4 million of their 17.7 million annual deaths due
to coronary artery disease (CAD). CAD risk factors include diabetes mellitus
(diabetes type 2 [DT2]), hypertension, dyslipidemia, obesity, poor diet,
tobacco (Nicotiana tabacum, Solanaceae) smoking, lack of exercise,
and alcohol abuse. Acute myocardial infarction and death—two primary effects
associated with CAD—account for more than 90% of all CAD-related outcomes. Atherosclerotic
plaques form when vascular endothelial cells express chemotactic and adhesion
molecules, starting the inflammatory process crucial to CAD's pathogenesis.
Within a healthy diet, cardioprotective foods can modulate expression of
proinflammatory cytokines and inflammation markers and help control risk
factors like DT2, hypertension, dyslipidemia, and obesity. Phenolic compounds
and unsaturated fats found in olive (Olea
europaea, Oleaceae) oil (OO) show benefits in this area and may improve CV outcomes
overall. Virgin OO (VOO) is produced by mechanical processes alone, while
refined OO (ROO) is subjected to mechanical and chemical processes. This
influences the concentration of phenolic compounds, with extra VOO (EVOO) retaining
significantly more phenolics than ROO, while both oils have similar fatty acid
content. VOOs are divided into EVOO, virgin (fine), and lampante according to the amount of acidity (ratio of free fatty
acids to total oleic acid) as follows: ≤0.8%, ≤2%, and >2%, respectively).
EVOO's sensory and physicochemical properties are superior to those of other
VOOs.
VOOs have saponifiable and unsaponifiable
fractions; the former about 98% of total content, with monounsaturated oleic
acid comprising 55-83% of that fraction. VOOs also have polyunsaturated fatty
acids, such as linoleic acid (3.5-21%), and saturated fatty acids, like
palmitic (7.5-20%) and stearic acids (0.5-5%). Unsaponifiable fractions, 1-2%
of total content, include over 230 compounds, such as sterols, hydrocarbons,
volatile molecules, triterpenic and aliphatic alcohols, pigments, and phenolics.
The latter, secondary metabolites created during plant development or under
stress, occur when fruits are crushed for oil extraction. Their presence is
directly related to glycosides in fruit tissue and both hydrolytic and
oxidative enzymes. Structurally, they have one or more hydroxyl and an aromatic
ring. Phenolic compounds may be lipophilic or hydrophilic. Among lipophilic
compounds in VOO, α-tocopherol is most important, with a mean level of 150.7
mg/kg, up to 400 mg/kg. At least 36 hydrophilic compounds in OO are grouped
into six categories by chemical structure; these are not described. VOO phenolic
content varies with cultivar, growth location (altitude), maturity at harvest,
fruit storage conditions, oil extraction procedures, and commercial storage.*
Phenolics are mostly responsible for
organoleptic qualities of olive fruit and OO's oxidative stability. Hydroxytyrosol
(HT; 3,4-DHPEA) and its derivatives, including oleuropein complex, tyrosol (p-HPEA), and especially the secoiridoid
derivatives (dialdehyde forms of decarboxymethyl elenolic acid linked to HT [oleacein;
3,4-DHPEA-EDA] and tyrosol [oleocanthal; p-HPEA-EDA],
aglycones of oleuropein [3,4-DHPEA-EA], and ligstroside [p-HPEA-EA]), are the most abundant phenolics in OO (90% of phenolic
content). HT and tyrosol are the primary phenols responsible for producing VOO's
antiatherosclerotic effects. Aglycones of oleuropein, created by hydrolysis
during fruit maturation, oil extraction, and storage, are in part responsible
for EVOO's complex flavors. Lignans also occur at high levels. Phenolic acids,
the first compounds identified in OO with at least 14 described,** usually
occur at <1 mg/kg. Flavones luteolin and apigenin, OO's main flavonoids,
also occur at relatively low levels. Hydroxy-isocromans have been found in
commercial VOOs, formed from HT's reactions with benzaldehyde and vanillin.
Phenolic alcohols also occur. Phenolic compounds are metabolized after
ingestion, first by hydrolysis in the stomach and small intestine, then by conjugation
by gut microbiota in the small intestine and enzymatically in the liver.
Oleuropein, however, is metabolized by colonic microbiota to HT. In a rather
startling study cited of OO absorption in healthy subjects, a group who had
received ileostomies and another group with intact colons were included. OO
absorption was estimated at 55-66% of the total dose, with no difference stated
between groups. Absorption of HT varies with the food matrix. It is noted that
supplementation with OO is associated with other changes in dietary patterns,
including consumption of other phenolic-rich foods with compounds that may
influence phenolic absorption, affect gut microbiota, and themselves modify CAD
risk factors.
In vitro and in vivo studies report benefits
of phenolic compounds in general and OO compounds specifically against
inflammation. Human primary prevention studies show an association between daily
EVOO intake and reduced risk of major CV events in at-risk patients; consumption
of 50 mL/day EVOO cut risks of CAD by 37%, and of major CV events by 30%. Anti-inflammatory
effects of EVOO have been seen at different stages of atherosclerosis. They
include modulation of the arachidonic acid cascade, effects on signaling
pathways and receptors, improvement of vascular function, and reduced cytokines
and adhesion molecules. In some studies, EVOO has been combined or compared with
other anti-inflammatory foods (including the "Mediterranean diet") or
with other OOs and/or dietary oils. Most report the superiority of EVOO with
high HT. Short-term studies show less definite benefits, but one study with seven
weeks of supplementation found ongoing benefits in reduced inflammatory markers
at five years' follow-up. Most trials have been quite small; the largest
population shown was 82 subjects. More long-term trials, specifically in
established CAD, would be useful. Evidence for EVOO's benefits against CAD is
strong, and its lack of any toxicity makes clinical use compelling.
—Mariann
Garner-Wizard
*
While unmentioned by these authors, post-purchase storage and use of OO is crucial
to the quality of OO consumed dietarily. Light and/or heat quickly degrade OO's
phenolic and fatty acid contents.
** But just 12 are listed in an accompanying table.
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