Scientific Basis for Olive Oil, Monounsaturated Fatty Acids and LDL Oxidation

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Scientific Basis for Olive Oil, Monounsaturated Fatty Acids, Anti-

oxidants, and LDL Oxidation

http://www.food-info.net/uk/products/olive/olive04.htm

 

 

Summary from

http://europa.eu.int/comm/agriculture/prom/olive/medinfo/de/factsheet

s/fact4.htm

 

Author : Eurosciences Communication in cooperation with the

Institute for Arteriosclerosis Research, University of Münster,

Germany

 

Introduction

 

Low-density lipoprotein (LDL) is the major cholesterol-carrying

particle in blood plasma. There is wide agreement that increased

levels of LDL are causally related to atherosclerosis and the

development of coronary heart disease (CHD). There is increasing

evidence that LDL in its `native' state is not harmful; however,

when it is altered by oxidation, it becomes a real threat within the

arterial wall. The susceptibility of LDL to oxidation is determined

by both internal (endogenous) and external (exogenous) factors.

Among the latter, nutritional factors are extremely important,

particularly the types of fatty acids and anti-oxidant vitamins in

the diet. This Fact Sheet reviews the mechanisms of LDL oxidation

and the role of nutritional factors in its prevention.

 

LDL oxidation (in atherogenesis)

 

Half of the cholesterol in the blood is carried in LDL, which is a

spherical fat-protein particle consisting of an outer monolayer

containing the protein apolipoprotein B (apo B), which surrounds a

core containing triglycerides and/or cholesterol esters (non-polar

fats). One LDL particle contains about 3600 fatty acids, half of

which are polyunsaturated fatty acids (PUFAs). LDL also contains

anti-oxidants, the most important being (alpha) a-tocopherol

(vitamin E).

 

LDL oxidation (peroxidation) is a chain reaction initiated by free

radicals, a mainly reactive oxygen species. PUFAs are very

susceptible to lipid peroxidation and breakdown to a variety of by-

products which bond to LDL apo B. LDL can be oxidised in vitro by

exposing them to smooth muscle and endothelial cells, macrophages

(derived from large cells called monocytes), or metal ions (Copper

or Iron). LDL oxidation in vivo is poorly understood, and it may be

reduced by the presence of anti-oxidants, e.g., ascorbic acid

(vitamin C) in plasma. It is therefore likely that LDL oxidation

occurs in the artery wall rather than in the blood stream. Vitamin E-

enriched LDL is significantly more difficult to oxidise. LDL

oxidation is likely to occur when the anti-oxidant `defences' are

down, especially when a-tocopherol is depleted.

 

LDL oxidation and atherosclerosis

 

The essential step in the development of atherosclerosis begins as

LDLs filter into the arterial wall and become entrapped in the

intima, where they may undergo oxidative modification. Macrophages

(cells formed when monocytes permeate the artery wall from the

bloodstream) avidly take up this modified LDL, which contributes to

their transformation to foam cells. The accumulation of foam cells

in the intima results in the formation of fatty streaks. These do

not produce significant obstruction of the artery, but they are

gradually converted into fibrous plaques by a mechanism similar to

scar formation. These, in turn, are gradually transformed into

atherosclerotic lesions which underlie most clinical events.

 

 

 

Olive oil and LDL oxidation

 

There are several potential ways by which dietary fatty acids may

influence the oxidation of LDL. The amount and composition of

dietary fats affect the amount of LDL in the artery wall.

Replacement of dietary saturated fats with monounsaturated fats

(MUFAs) or PUFAs lowers LDL levels, thereby decreasing the amount of

LDL entering the artery wall and so reducing the amount (and

composition) available for oxidation. Because of its high MUFA

content, olive oil appears to offer some protection against LDL

oxidation (see Section entitled " Effects of dietary fatty acids on

LDL oxidation " ). Olive oil may afford additional protection by

supplying LDL with potent anti-oxidants, such as vitamin E and

phenolic compounds, which will be described later.

 

Effects of dietary fatty acids on LDL oxidation.

 

Various studies have investigated the role of MUFA and PUFA in

reducing susceptibility to LDL oxidation. Studies in the rabbit

model show that oleate-rich (oleic acid is the predominant fatty

acid of olive oil) LDL is remarkably resistant to oxidation. Dietary

studies in humans support this finding and show that the linoleic

acid (the major dietary PUFA which is predominant in vegetable oils)

content of LDL is strongly related to the rate and extent of

oxidation, with LDL oxidation rate being increased during the

studies involving the PUFA diet, compared to the MUFA diet. Further

studies have tried to address whether such effects are due to PUFA-

induced enhancement or a MUFA-induced inhibition of LDL oxidation.

Dietary supplementation of olive oil suggests that the linoleic acid

content of LDL is reduced and that there is less cellular uptake by

macrophages and reduced susceptibility of LDL to oxidation.

 

Pro-oxidant activities of dietary fatty acids

 

Certain dietary fatty acids can change the monocyte membrane

composition, thereby enhancing free radical production, and

producing pro-oxidant effects. A study compared the effects of

dietary supplementation with MUFA and n-3 (found in fish oils) or n-

6 (linoleic acid) PUFA on superoxide anion (a free radical)

generation in monocytes and macrophages. Only n-3 fatty acids

reduced free radical production, while the monocytes from the MUFA

or n-6 PUFA showed no change or increased levels. The mechanisms for

this are unknown, and these results have not been reproduced. More

studies on the role of different fatty acids on cellular pro-oxidant

activity are needed; however, MUFA-enriched cells are less

susceptible to oxidative damage (in direct comparison to n-6 PUFA),

probably as a result of cell membrane fatty acid composition.

 

Antioxidant constituents of olive oil

 

Oxidative stress may play an important role in the development of

several chronic diseases such as CHD and cancer. The possibility

that dietary anti-oxidants, such as those found in olive oil, may

protect against LDL oxidation has led to epidemiological and

intervention studies.

 

Vitamin E (a-tocopherol)

 

Epidemiological studies have shown that high doses of vitamin E over

at least two years, can significantly reduce CHD risk (31-65%).

Short-term studies using lower doses have not shown this, however.

This is also the finding from the majority of randomised

intervention trials with vitamin E; however, these trials were not

designed to assess cardiovascular end-points, their treatment

duration was too short, and they employed sub-optimal doses of the

vitamin. Several ongoing large-scale trials may help to resolve this

issue. To date, only the Cambridge Heart Antioxidant Study (CHAOS)

has been completed. This double-blind, placebo-controlled study of

2000 patients with established CHD, reported that high-dose vitamin

E supplementation significantly reduced the incidence of non-fatal

heart attacks but had no impact on cardiovascular or all-cause

mortality.

 

Intervention trials have been criticised on the grounds that a few

years of treatment may be inadequate to demonstrate benefit of anti-

oxidants, and that anti-oxidant supplementation may be needed over

20 or more years, before any clinical benefit ensues.

 

Several studies have demonstrated that vitamin E supplementation

results in increased levels of a-tocopherol both in plasma and in

LDL particles. Furthermore, LDL showed a higher resistance against

in vitro oxidation compared to the pre-study baseline. The degree of

resistance was closely related to the vitamin dose received.

Oxidative resistance is also higher in non-supplementing individuals

who have higher plasma levels of a-tocopherol, than those with

naturally occurring lower levels.

 

Phenolic compounds

 

In addition to vitamin E, olive oil contains a variety of

constituents which are responsible for its unique taste. Among these

(comprising 2-3% of unrefined oil) are phenolic compounds, which are

also found in vegetable foods and are biologically extremely

important. These include simple phenols and phenolic acids e.g.

flavonoids. These play a vital role to scavenge and detoxify free

radicals, and can provide increased resistance to LDL oxidation and

inhibit lipid peroxidation. Phenolic compounds have additional anti-

inflammatory and anti-haemorrhagic effects.

 

Health benefits derived from potent phenolic flavonoids, also

present in fruits and beverages such as tea and wine, have been

observed in the Seven Countries and the Zutphen Elderly studies,

where the average intake of flavonoids was inversely and

independently correlated with CHD mortality. However, more studies

are needed to confirm the cardioprotective properties of flavonoids.

 

Summary and conclusions

 

There is extensive evidence that oxidative modifications of LDL play

a crucial role in atherogenesis. Oxidation of LDL begins with

peroxidation of PUFA in the LDL particle. Thus the LDL fatty acid

composition undoubtedly contributes to LDL oxidation. The fatty acid

composition (and therefore, susceptibility to oxidation) of LDL is

influenced by dietary fatty acids. Diets rich in MUFAs render LDL

more resistant to LDL oxidative modification compared with diets

rich in PUFAs, e.g., linoleic acid. In addition, the fatty acid

composition of cell membranes is diet-dependent, and MUFA-rich diets

also lead to a higher MUFA content of cell membranes and therefore

higher cellular resistance to oxidative damage.

 

Dietary anti-oxidants such as vitamins E and C, flavonoids, etc.,

provide additional protection against oxidative stress. Recent

studies indicate that not only a-tocopherol, but also phenolic

compounds in olive oil may inhibit LDL oxidation and reduce the risk

of atherosclerosis. Further research is needed to fully elucidate

the mechanisms of action of phenolic compounds in vivo.

 

Much of the focus of attention on the Mediterranean diet has been on

the cardiovascular benefits associated with a reduced saturated fat

intake, and its high MUFA levels, as well as complex carbohydrate

and fibre. Current evidence suggests that additional components, in

abundance in the Mediterranean diet, namely anti-oxidants derived

from fruit and vegetables, but additionally, from olive oil, may

contribute to protection from CHD, cancer and other chronic

disorders.

 

High intakes of MUFAs from olive oil consumption in the

Mediterranean diet, may combine the advantages of lowering

cholesterol and decreasing LDL and cell susceptibility to oxidation.

_________________

JoAnn Guest

mrsjoguest

www.geocities.com/mrsjoguest/Genes