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FrederickSebastian

Problems with Olive Oil

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So,

 

Growing up (I'm 34) I remember hearing a lot about how extra virgin olive oil was really healthy for you, especially in Mediterranean-type diets... However, I recently read a webpage (http://www.whfoods.com/genpage.php?tname=george&dbid=56) that says that cooking with EVOO is NOT healthy for some reason... Also, I read somewhere that unless you get EVOO fresh that has NOT been exposed to oxygen, you will not reap the benefits...

 

Do I have anything to worry about?

 

Fred

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Frederick, you should make sure that EVOO is of the latest crop. In Europe crops are usually from late October- to early december. Avoid EVOOS from North Africa. Order High Polyphenols EVOOS from reliable providers. Use very little for cooking and add most of it after cooking (hi temperatures affect the EVOO polyphenols).

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On 9/16/2019 at 3:35 AM, mccoy said:

Frederick, you should make sure that EVOO is of the latest crop. In Europe crops are usually from late October- to early december. Avoid EVOOS from North Africa. Order High Polyphenols EVOOS from reliable providers. Use very little for cooking and add most of it after cooking (hi temperatures affect the EVOO polyphenols).

ok!

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As noted elsewhere, I have restricted my previously liberal use of EVOO and now consume it only occasionally, usually if in a restaurant which serves it (I enjoy with good Italian bread). I don't consider it particularly healthy, but it is healthier than animal fat and thus good as a replacement for it.

To get most of the benefits of EVOO, consider olive leaf extract, which contains most of the good stuff, but without the fat.

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Olive oil is not good!

 

JACC Vol. 36, No. 5, 2000 November 1, 2000:1455–60
Conclusions. In terms of their effects on postprandial endothelial function, the beneficial components of the Mediterranean and Lyon Diet Heart Study diets appear to be the antioxidant-rich foods—vegetables, fruits, and their derivatives such as vinegar, and omega-3-rich fish and canola oils—not olive oil. Canola oil may share some of the unique vasoprotective properties of other omega-3-rich oils, such as fish oil. Dietary fruits, vegetables, and their products appear to provide some protection against the direct impair- ment in endothelial function produced by high-fat foods, including olive oil

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From a study Al posted today:

Associations of fat and carbohydrate intake with cardiovascular disease and mortality: prospective cohort study of UK Biobank participants.
Ho FK, Gray SR, Welsh P, Petermann-Rocha F, Foster H, Waddell H, Anderson J, Lyall D, Sattar N, Gill JMR, Mathers JC, Pell JP, Celis-Morales C.
BMJ. 2020 Mar 18;368:m688. doi: 10.1136/bmj.m688.
PMID: 32188587 Free Article
https://www.bmj.com/content/bmj/368/bmj.m688.full.pdf
Abstract
OBJECTIVE:
To investigate the association of macronutrient intake with all cause mortality and cardiovascular disease (CVD), and the implications for dietary advice.
DESIGN:
Prospective population based study.
SETTING:
UK Biobank.
PARTICIPANTS:
195 658 of the 502 536 participants in UK Biobank completed at least one dietary questionnaire and were included in the analyses. Diet was assessed using Oxford WebQ, a web based 24 hour recall questionnaire, and nutrient intakes were estimated using standard methodology. Cox proportional models with penalised cubic splines were used to study non-linear associations.
MAIN OUTCOME MEASURES:
All cause mortality and incidence of CVD.
RESULTS:
4780 (2.4%) participants died over a mean 10.6 (range 9.4-13.9) years of follow-up, and 948 (0.5%) and 9776 (5.0%) experienced fatal and non-fatal CVD events, respectively, over a mean 9.7 (range 8.5-13.0) years of follow-up. Non-linear associations were found for many macronutrients. Carbohydrate intake showed a non-linear association with mortality; no association at 20-50% of total energy intake but a positive association at 50-70% of energy intake (3.14 v 2.75 per 1000 person years, average hazard ratio 1.14, 95% confidence interval 1.03 to 1.28 (60-70% v 50% of energy)). A similar pattern was observed for sugar but not for starch or fibre. A higher intake of monounsaturated fat (2.94 v 3.50 per 1000 person years, average hazard ratio 0.58, 0.51 to 0.66 (20-25% v 5% of energy)) and lower intake of polyunsaturated fat (2.66 v 3.04 per 1000 person years, 0.78, 0.75 to 0.81 (5-7% v 12% of energy)) and saturated fat (2.66 v 3.59 per 1000 person years, 0.67, 0.62 to 0.73 (5-10% v 20% of energy)) were associated with a lower risk of mortality. A dietary risk matrix was developed to illustrate how dietary advice can be given based on current intake.
CONCLUSION:
Many associations between macronutrient intake and health outcomes are non-linear. Thus dietary advice could be tailored to current intake. Dietary guidelines on macronutrients (eg, carbohydrate) should also take account of differential associations of its components (eg, sugar and starch).

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I am curious, what is the average intake and ratio of monounsaturated, polyunsaturated and saturated fat, as well as Omega-3 and and Omega-6 for those who track such things here?

Here is mine, averaged over the last 4 weeks. Top fat intake in descending order is from flax, almonds, avocado, walnuts and cacao nibs. The cholesterol is from tiramisu, pizza and butter (I lapse when I go out :)

2111799477_ScreenShot2020-04-01at17_09_28.png.715fcf5ffd4b65941e336b43b74147cc.png

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On 9/1/2019 at 6:59 PM, FrederickSebastian said:

I recently read a webpage (http://www.whfoods.com/genpage.php?tname=george&dbid=56) that says that cooking with EVOO is NOT healthy for some reason... Also, I read somewhere that unless you get EVOO fresh that has NOT been exposed to oxygen, you will not reap the benefits...

Do I have anything to worry about?


This reasonably narrow question got spun off into a whole discussion about the healthfulness of EVOO per se, with a bunch of random half-relevant assertions and data points ... please see here on EVOO as supreme health food (my post of July 3 — I would expect the main thing Gordo originally had in mind when linking the thread) and stop making assertions on lower-grade evidence.

Closer to the core question, see my post on EVOO freshness, storage, and cooking.

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Quote

A higher intake of monounsaturated fat (2.94 v 3.50 per 1000 person years, average hazard ratio 0.58, 0.51 to 0.66 (20-25% v 5% of energy)) and lower intake of polyunsaturated fat (2.66 v 3.04 per 1000 person years, 0.78, 0.75 to 0.81 (5-7% v 12% of energy)) and saturated fat (2.66 v 3.59 per 1000 person years, 0.67, 0.62 to 0.73 (5-10% v 20% of energy)) were associated with a lower risk of mortality

Wow, this goes on with intuition (I wouldn't touch PUFAs myself), but I thought PUFAs (in the population) are associated with lowered mortality? [simply b/c so much of the population still dies from heart disease]. How many studies show that more PUFAs increase [or at least don't decrease] mortality?

Edited by InquilineKea

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9 hours ago, InquilineKea said:

How many studies show that more PUFAs increase [or at least don't decrease] mortality?

Here is a good one:  The MCE (1968-73) is a double blind randomized controlled trial designed to test whether replacement of saturated fat with vegetable oil rich in linoleic acid reduces coronary heart disease and death by lowering serum cholesterol.

Re-evaluation of the traditional diet-heart hypothesis: analysis of recovered data from Minnesota Coronary Experiment (1968-73)

Quote

Results The intervention group had significant reduction in serum cholesterol compared with controls (mean change from baseline −13.8% v −1.0%; P<0.001). Kaplan Meier graphs showed no mortality benefit for the intervention group in the full randomized cohort or for any prespecified subgroup. There was a 22% higher risk of death for each 30 mg/dL (0.78 mmol/L) reduction in serum cholesterol in covariate adjusted Cox regression models (hazard ratio 1.22, 95% confidence interval 1.14 to 1.32; P<0.001). There was no evidence of benefit in the intervention group for coronary atherosclerosis or myocardial infarcts. Systematic review identified five randomized controlled trials for inclusion (n=10 808). In meta-analyses, these cholesterol lowering interventions showed no evidence of benefit on mortality from coronary heart disease (1.13, 0.83 to 1.54) or all cause mortality (1.07, 0.90 to 1.27).

Conclusions Available evidence from randomized controlled trials shows that replacement of saturated fat in the diet with linoleic acid effectively lowers serum cholesterol but does not support the hypothesis that this translates to a lower risk of death from coronary heart disease or all causes. Findings from the Minnesota Coronary Experiment add to growing evidence that incomplete publication has contributed to overestimation of the benefits of replacing saturated fat with vegetable oils rich in linoleic acid.

 

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I'm not a fan of any refined oils, but here [1] (with commentary [2]) is better evidence that goes the other way than the very old MCE trial, which among other confounders was done in the time when PUFA-rich margarines contained trans-fats. 

From the commentary [2]:

The top-line result from this meta-analysis [1] suggests a 7% lower risk of incident CVD when those in the top and those in the bottom fifth of [linoleic acid] in blood or adipose tissue lipids are compared. 

--Dean

---------

[1] Circulation. 2019;139:2422–2436

Biomarkers of Dietary Omega-6 Fatty Acids and Incident Cardiovascular Disease and Mortality
An Individual-Level Pooled Analysis of 30 Cohort Studies
Matti Marklund, Jason H.Y. Wu, Fumiaki Imamura, Liana C. Del Gobbo, Amanda Fretts, Janette de Goede, Peilin Shi, Nathan Tintle, Maria Wennberg, Stella Aslibekyan, Tzu-An Chen, Marcia C. de Oliveira Otto, Yoichiro Hirakawa, … See all authors 
Originally published11 Apr 2019

https://doi.org/10.1161/CIRCULATIONAHA.118.038908

Abstract
Background:
Global dietary recommendations for and cardiovascular effects of linoleic acid, the major dietary omega-6 fatty acid, and its major metabolite, arachidonic acid, remain controversial. To address this uncertainty and inform international recommendations, we evaluated how in vivo circulating and tissue levels of linoleic acid (LA) and arachidonic acid (AA) relate to incident cardiovascular disease (CVD) across multiple international studies.

Methods:
We performed harmonized, de novo, individual-level analyses in a global consortium of 30 prospective observational studies from 13 countries. Multivariable-adjusted associations of circulating and adipose tissue LA and AA biomarkers with incident total CVD and subtypes (coronary heart disease, ischemic stroke, cardiovascular mortality) were investigated according to a prespecified analytic plan. Levels of LA and AA, measured as the percentage of total fatty acids, were evaluated linearly according to their interquintile range (ie, the range between the midpoint of the first and fifth quintiles), and categorically by quintiles. Study-specific results were pooled using inverse-variance–weighted meta-analysis. Heterogeneity was explored by age, sex, race, diabetes mellitus, statin use, aspirin use, omega-3 levels, and fatty acid desaturase 1 genotype (when available).

Results:
In 30 prospective studies with medians of follow-up ranging 2.5 to 31.9 years, 15 198 incident cardiovascular events occurred among 68 659 participants. Higher levels of LA were significantly associated with lower risks of total CVD, cardiovascular mortality, and ischemic stroke, with hazard ratios per interquintile range of 0.93 (95% CI, 0.88–0.99), 0.78 (0.70–0.85), and 0.88 (0.79–0.98), respectively, and nonsignificantly with lower coronary heart disease risk (0.94; 0.88–1.00). Relationships were similar for LA evaluated across quintiles. AA levels were not associated with higher risk of cardiovascular outcomes; in a comparison of extreme quintiles, higher levels were associated with lower risk of total CVD (0.92; 0.86–0.99). No consistent heterogeneity by population subgroups was identified in the observed relationships.

Conclusions:
In pooled global analyses, higher in vivo circulating and tissue levels of LA and possibly AA were associated with lower risk of major cardiovascular events. These results support a favorable role for LA in CVD prevention.

 

-----

[2] Omega-6 Fatty Acids and Cardiovascular Disease
Are We Getting Closer to the Truth?
Thomas A.B. Sanders
Originally published20 May 2019

https://doi.org/10.1161/CIRCULATIONAHA.119.040331

Circulation. 2019;139:2437–2439

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21 hours ago, Dean Pomerleau said:

I'm not a fan of any refined oils, but here [1] (with commentary [2]) is better evidence that goes the other way than the very old MCE trial, which among other confounders was done in the time when PUFA-rich margarines contained trans-fats. 

From the commentary [2]:

The top-line result from this meta-analysis [1] suggests a 7% lower risk of incident CVD when those in the top and those in the bottom fifth of [linoleic acid] in blood or adipose tissue lipids are compared. 

--Dean

---------

[1] Circulation. 2019;139:2422–2436

Biomarkers of Dietary Omega-6 Fatty Acids and Incident Cardiovascular Disease and Mortality
An Individual-Level Pooled Analysis of 30 Cohort Studies
Matti Marklund, Jason H.Y. Wu, Fumiaki Imamura, Liana C. Del Gobbo, Amanda Fretts, Janette de Goede, Peilin Shi, Nathan Tintle, Maria Wennberg, Stella Aslibekyan, Tzu-An Chen, Marcia C. de Oliveira Otto, Yoichiro Hirakawa, … See all authors 
Originally published11 Apr 2019

https://doi.org/10.1161/CIRCULATIONAHA.118.038908

Abstract
Background:
Global dietary recommendations for and cardiovascular effects of linoleic acid, the major dietary omega-6 fatty acid, and its major metabolite, arachidonic acid, remain controversial. To address this uncertainty and inform international recommendations, we evaluated how in vivo circulating and tissue levels of linoleic acid (LA) and arachidonic acid (AA) relate to incident cardiovascular disease (CVD) across multiple international studies.

Methods:
We performed harmonized, de novo, individual-level analyses in a global consortium of 30 prospective observational studies from 13 countries. Multivariable-adjusted associations of circulating and adipose tissue LA and AA biomarkers with incident total CVD and subtypes (coronary heart disease, ischemic stroke, cardiovascular mortality) were investigated according to a prespecified analytic plan. Levels of LA and AA, measured as the percentage of total fatty acids, were evaluated linearly according to their interquintile range (ie, the range between the midpoint of the first and fifth quintiles), and categorically by quintiles. Study-specific results were pooled using inverse-variance–weighted meta-analysis. Heterogeneity was explored by age, sex, race, diabetes mellitus, statin use, aspirin use, omega-3 levels, and fatty acid desaturase 1 genotype (when available).

Results:
In 30 prospective studies with medians of follow-up ranging 2.5 to 31.9 years, 15 198 incident cardiovascular events occurred among 68 659 participants. Higher levels of LA were significantly associated with lower risks of total CVD, cardiovascular mortality, and ischemic stroke, with hazard ratios per interquintile range of 0.93 (95% CI, 0.88–0.99), 0.78 (0.70–0.85), and 0.88 (0.79–0.98), respectively, and nonsignificantly with lower coronary heart disease risk (0.94; 0.88–1.00). Relationships were similar for LA evaluated across quintiles. AA levels were not associated with higher risk of cardiovascular outcomes; in a comparison of extreme quintiles, higher levels were associated with lower risk of total CVD (0.92; 0.86–0.99). No consistent heterogeneity by population subgroups was identified in the observed relationships.

Conclusions:
In pooled global analyses, higher in vivo circulating and tissue levels of LA and possibly AA were associated with lower risk of major cardiovascular events. These results support a favorable role for LA in CVD prevention.

 

-----

[2] Omega-6 Fatty Acids and Cardiovascular Disease
Are We Getting Closer to the Truth?
Thomas A.B. Sanders
Originally published20 May 2019

https://doi.org/10.1161/CIRCULATIONAHA.119.040331

Circulation. 2019;139:2437–2439

Thanks Dean! Based on this one could choose walnuts as a preferred source of healthy fats. Also it is a whole unprocessed food and loaded with polyphenol and nutrition and Fibre unlike olive oil. Also Taste better 

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1 minute ago, Mike41 said:

Based on this one could choose walnuts as a preferred source of healthy fats. Also it is a whole unprocessed food and loaded with polyphenol and nutrition and Fibre unlike olive oil. Also Taste better 

Agreed Mike. Nuts, seeds and avocado are my sources of concentrated fats for the reasons you outline. 

--Dean 

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17 hours ago, Mike41 said:

Also Taste better 

If taste is a factor, I beg to differ on that. The taste of Hi-poly EVOO is a taste of its own, which makes a dish of boiled spinachs an absolute culinary specialty. If I mix avocados or nuts to vegetables it is not the same thing as to dress it with a very good EVOO which permeates the vegetables.

We can agree of course that tastes are subjective and that they can be trained, or tamed. I absolutely hate the taste of white sugar, but I remember I trained myself to hate it over 40 years ago.

Edited by mccoy

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On 1/17/2021 at 2:07 PM, Dean Pomerleau said:

but here [1] (with commentary [2]) is better evidence that goes the other way than the very old MCE trial

...

Methods:
We performed harmonized, de novo, individual-level analyses in a global consortium of 30 prospective observational studies from 13 countries.

Observation is a weaker form of evidence than intervention.  You can observe correlation but interventional trials are better for establishing causation.

The MCE was an interventional trial with special properties.  Because it was done to a captive institutionalized population the issue of compliance was reduced while blinding the participants to the fact they were being experimented upon.  The researchers were also blinded to who was subjected to the intervention diet.  Thus significant changes in outcome can be more readily attributed to the intervention as effects of placebo, bias and confounding are minimized.  This was a large expensive trial designed to provide evidence that replacing saturated fat from animal sources with plant sourced polyunsaturated fats would reduce LDL cholesterol and heart disease as hypothesized.  The intervention was designed to test this swap of fats isolated as much as practical from other changes such as changes in protein, carbs or calories.

Unfortunately the researchers appeared more married to promoting their hypothesis than engaging in science as they buried the results of their crime instead of publishing and raising questions of why their intervention was so harmful which might have lead to earlier and better understanding of the potential problems of trans fats and unstable pufas.  To this day many believe in the primacy of lowering LDL to reduce heart disease and promote doing it by cutting saturated fat while the best evidence to date suggests the opposite.  And thus we may have people commiting slow suicide eating foods fried in vegetable oils dying happy because their LDL was decimated.

Edited by Todd Allen

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