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Hi All,

Healthy fats in foods and their oils are described and compared below for

their

effects on health in the below three papers that are not in Medline yet, the

last of

which only is pdf-available.

Why do we initiate CRON? Many do so who are healthy, have good diets before

CR

and have a long-life family history. So is it not for me, and some others. The

first paper represented for the below abstract suggests the superiority of fish

oil

versus alpha-linolenic acid, it seems.

First, a review that is free full-text for the atherogenic lipoprotein

phenotype

is:

Twickler TB, Dallinga-Thie GM, Cohn JS, Chapman MJ.

Elevated remnant-like particle cholesterol concentration: a characteristic

feature

of the atherogenic lipoprotein phenotype.

Circulation. 2004 Apr 27;109(16):1918-25. Review. No abstract available.

PMID: 15117861

http://circ.ahajournals.org/cgi/content/full/109/16/1918

Here, is the first of the three in press papers.

Influence of a-linolenic acid and fish-oil on markers of cardiovascular risk

in

subjects with an atherogenic lipoprotein phenotype

Atherosclerosis, In Press, Corrected Proof, Available online 3 February 2005,

Wilkinson, Clare Leach, E. Ah-Sing, Nahed Hussain, J. ,

D.

Joe Millward and Bruce A.

Abstract

We tested the hypothesis that dietary a-linolenic acid (ALA) can exert effects

on

markers of cardiovascular risk similar to that produced by its longer chain

counterparts in fish-oil. A dietary intervention study was undertaken to examine

the

effects of an ALA-enriched diet in 57 men expressing an atherogenic lipoprotein

phenotype (ALP). Subjects were randomly assigned to one of three diets enriched

either with flaxseed oil (FXO: high ALA, n = 21), sunflower oil (SO: high

linoleic

acid, n = 17), or SO with fish-oil (SOF n = 19) for 12 weeks, resulting in

dietary

intake ratios of n-6:n-3 PUFA of 0.5, 27.9 and 5.2, respectively. The relative

abundance of ALA and EPA in erythrocyte membranes increased on the FXO diet (p <

0.001), whereas both EPA and DHA increased after fish-oil (p < 0.001). There

were

significant decreases in total plasma cholesterol within (FXO -12.3%, p = 0.001;

SOF

-7.6%, p = 0.014; SO -7.3%, p = 0.033) and between diets (p = 0.019), and

decreases

within diets after 12 weeks for HDL cholesterol on flaxseed oil (FXO -10%, p =

0.009), plasma TG (-23%, p < 0.001) and small, dense LDL (-22% p = 0.003) in

fish-oil. Membrane DHA levels were inversely associated with the changes in

plasma

TG (p = 0.001) and small, dense LDL (p < 0.05) after fish-oil. In conclusion,

fish-oil produced predictable changes in plasma lipids and small, dense LDL

(sdLDL)

that were not reproduced by the ALA-enriched diet. Membrane DHA levels appeared

to

be an important determinant of these fish-oil-induced effects.

Second, is an abstract for a paper, the title of which was lost, on the use of

genetic approaches to examine the importance of the n-6/n-3 ratio for health,

using

different fats in the diet to achieve the appropriate ratios. It was seemingly

surprising that the ratio should be so small.

... Homozygous apoE-/- LDLR-/- double knockout mouse (DKO mice,

129XC57BL/6J

background) and male C57BL/6 mice aged 6 weeks were divided into four groups.

Each

group was fed a diet containing a different n-6/n-3 ratio (Group l: 0.29; Group

2:

1.43; Group 3: 5.00; Group 4: 8), prepared with high linolenic (LNA) flaxseed

oil

(n-3 rich) and high linoleic (LA) safflower oil (n-6 rich). ... After 16 weeks,

plasma triglyceride and LDL levels in Group 1 were significantly lower than in

the

other groups. Conversely, HDL was the highest. After 8 and 16 weeks, ... n-6/n-3

ratio had a dose-dependent antithrombotic effect (thrombus volume decreased 23%,

Group 1 vs. Group 4), In addition, the extent of atherosclerosis was less in the

animals fed a low n-6/n-3 ratio compared with the high n-6/n-3 ratio group

(atherosclerotic area decreased 40%, Group 1 vs. Group 4). The lowest n-6/n-3

ratio

tested (0.29) was the most effective in suppressing the thrombotic and

atherosclerotic parameters in these DKO mice.

The last of the three in press papers is presented in full, and the

discussion

centers of control oil that was used for fish oil in a study that was commented

upon. Using the healthy olive oil as a control is purported to be a poor choice

and

alternative choices are suggested.

Omega-3 and depression research: Hold the olive oil

Prostaglandins, Leukotrienes and Essential Fatty Acids, In Press, Corrected

Proof,

Available online 21 April 2005,

Alan C. Logan

I read with great interest the paper of Silvers et al. which examined the

effect

of commercial tuna oil on depressive symptoms [1]. The authors acknowledge that

the

omega-3 make up of this particular oil, high in docosahexaenoic acid and low in

eicosapentaenoic acid, may have influenced the outcome. The authors chose to use

olive oil as a placebo despite the previous suggestions in the psychiatric

literature that this may not be an appropriate choice of placebo lipid in mood

research [2].

Silvers and colleagues quickly dismiss the idea that olive oil and fish oil

might

both significantly influence mood. Published research however supports the

notion

that oleic acid (from olive oil) can be readily biosynthesized into oleamide

[3], a

lipid which can induce sleep, increase pain thresholds, alter serotonin

receptors to

enhance binding, alter food intake, and limit seizure potential [4], [5], [6],

[7]

and [8].

An additional consideration is that olive oil is naturally rich in

antioxidant

polyphenolic chemicals which have reported neuroprotective properties [9]. For

example, olive oil, and not safflower oil, has been shown to improve antioxidant

status and preserve the important lipid antioxidant coenzyme Q10 [10]. Given the

emerging research which has shown patients with depression are under increased

oxidative stress and that oxidative stress is associated with severity of

depression

[11], administration of a high-phenolic oil may have additional untold effects

over

the course of 3 months. In turn, dietary antioxidant intake may also influence

essential fatty acid status [12].

While it is understood that the choice of a lipid placebo is difficult in

psychiatric research, utilization of corn or safflower oils may be more

appropriate.

These oils, with more than four times the amount of linoleic acid of olive oil,

are

more suited to test the hypothesis that changes to the modern diet and linoleic

acid

over-consumption are influencing chronic conditions such as depression. While

corn

or safflower oil as a placebo may limit dietary omega-3 metabolism in the

placebo

group, such is the case with a diet top-heavy in linoleic acid. Perhaps its time

investigators removed olive oil from the placebo list in psychiatric research

and

provide a placebo which matches the background diet.

References

[1] K.M. Silvers, C.C. Woolley, F.C. Hamilton, P.M. Watts and R.A. ,

Randomized double-blind placebo-controlled trial of fish oil in the treatment of

depression, Prostaglandins Leukot. Essent. Fatty Acids 72 (2005), pp. 211–218.

....

Al Pater, PhD; email: old542000@...

__________________________________________________

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