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Hi Dean!

Your diet seems great to me, as usual -- also, as I recall, you eat one meal a day -- probably a good idea.

  --  Saul

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I concur that Olive leaves may be a great idea , although in previous posts I was refering specifically to foods, whereas leaves and other supplements are not usually regarded as such.

Table olives have the obvious drawback of heterogeneity of content, and usually TPs are not available wheras in EVOO this info can be retrieved or even a sample sent to the lab where the tests are routine (I don't know abut olives). And, as written in another thead by Dean, NaOH curing or immersion in brine or other processing may sure alter the original content.

I've been quickly browsing olive leaves in Italian and it seems that it is well known as an herbal medicine. Extreme bitterness is cited as a major drawback, but it apaprently carries many, many benefits.

Some people associate the richness of secoiridoids to the longevity of the olive tree.

The Luras wild olive in Sardinia, Italy, has an estimated age o 3000 to 4000 years:

image.png.ce44b5532964fa74b05077690bcc4373.png

image.png.0f584bd690e5db6809d32f0982ef4d72.png

I

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I'm definitely leaning toward taking advantage of the properties of OLEs, after I've gathered some info. Maybe, as Sibiriak was thinking, adding olive leaves to EVOO may leverage the benefits of secoiridoids.

I've also seen there are quite a few non-alcoholic extracts in liquid form.

Edited by mccoy

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On 5/31/2019 at 7:43 AM, Ron Put said:

It's actually ironic that any weight is placed on it by people who are willing to disregard the considerable evidence that while EVOO may be BETTER than most common alternative dietary fats (animal or vegetable derived), it is nevertheless another processed fat, even if overall less harmful unless consumed only occasionally.  I'll repost a reputable source, for good measure:

"...any oil—including olive oil—is not a whole food and thus has little place in a whole food, plant-based diet. Like any other oil, olive oil is a processed, concentrated fat extract and thus has lost most of the nutritional value of its original form (the olive itself). If you want some nutritional value, you will find it by eating the whole olive—not by consuming it in its almost unrecognizable extracted oil form....

I agree that EVOO is not a whole food but, then, the supporters of this idea should only eat whole cereals. No bread, pasta, processed products. No soy milk, tofu, tempeh, only whole legumes. No cacao, coffe, tea, And so on and so forth. If said supporters are coherent with their talks at least I admire them for their stoicism.

Edited by mccoy

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I'm going to add any further considerations on OLe and OLP on the other thread linked by Dean, here it's a little OT.

My impression at present is that the OLE-OLP alternative to EVOO sure seems worthy to be explored. Caveats from MR still needing to be addressed thoroughly

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19 hours ago, mccoy said:

I agree that EVOO is not a whole food but, then, the supporters of this idea should only eat whole cereals. No bread, pasta, processed products. No soy milk, tofu, tempeh, only whole legumes. No cacao, coffe, tea, And so on and so forth. If said supporters are coherent with their talks at least I admire them for their stoicism.

And eating whole grains (steel cut oats, ground flax, etc.) is not such a bad idea.... One also does not have to regularly eat bread or pasta, in fact I almost never buy those at home. I do indulge when I go out, just as I do with olive oil if at a restaurant which serves it (and I feel weak that evening :) I enjoy cacao nibs daily, and it's worth noting that coffee and tea don't come wrapped in a sea of fat....

I also try not to eat desert, but I do that too, probably once a month or so. Many others seem to practice the same, and it's not all that hard or inconvenient.

Perhaps the analogy between EVOO and whole wheat bread is not that far fetched -- both are fine as replacements (EVOO to animal and most processed vegetable fats, and whole wheat bread to something like Wonder Bread).

As to the objections to olive leaf extract made above, the most damning was ""Hydroxytyrosol administration enhances atherosclerotic lesion development in apo E deficient mice" and after reading it, I am comfortable that it does not apply to most of us.

There were some bioavailability questions, but after a quick search I found a number of studies showing high human bioavailability from olive leaf extract (I posted a couple above). I did not find any studies which found low human bioavailability, BTW.

This is not an argument, I am merely trying to present the best facts I can find (if someone has better, I am happy to consider them) and each persons who reads them can make their own decisions.

Cheers.

Edited by Ron Put

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I never eat pasta or bread. I do eat oatmeal, 100% whole grain cereal, fruit, vegetables, legumes, nuts, seeds, coffee black, 1/2 cup Greek yogurt, 1 oz. salmon daily and one oyster for zinc. I found a milk product made with oats and bananas (yes very processed) it has no added calcium. Too much calcium is atherogenic and almond milks have tons of added calcium. So primarily Whole Foods but not entirely. Oh btw red wine daily and that is certainly processed.

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Yes, as you rightly point out, everything if not raw and untreated is processed.

The vegan doctors affirming that EVOO is processed wheras olives are natural seem to ignore that olives are cured in NAOH or cooked and that EVOO is press-filtered at low temperatures, so the beneficial chemicals are probably much more in the natural state in EVOO than in olives. Of course there is no fiber but this we usually ingest in ample amounts by vegetables, legumes and other food.

Also, unprocessed grains should be raw. Legumes, ditto. Cooking is by definition a processing procedure, which by the way makes grains and legumes digestible, but it is a processing nevertheless.

So not all processing is deleterious. I think the above would suggest a situation of religious fanaticism even by well respected MDs. The religion is the diet and the subjective beliefs on nutrition, sometimes are not really founded in science or even in basic rational thinking.

 

 

Edited by mccoy

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Al Pater just posted this. Doesn’t look good for olive oil to say the least!

Monounsaturated fat rapidly induces hepatic gluconeogenesis and whole-body insulin resistance.
Sarabhai T, Kahl S, Szendroedi J, Markgraf DF, Zaharia OP, Barosa C, Herder C, Wickrath F, Bobrov P, Hwang JH, Jones JG, Roden M.
JCI Insight. 2020 May 21;5(10):134520. doi: 10.1172/jci.insight.134520.
PMID: 32434996
Abstract
BACKGROUNDWhile saturated fat intake leads to insulin resistance and nonalcoholic fatty liver, Mediterranean-like diets enriched in monounsaturated fatty acids (MUFA) may have beneficial effects. This study examined effects of MUFA on tissue-specific insulin sensitivity and energy metabolism.METHODSA randomized placebo-controlled cross-over study enrolled 16 glucose-tolerant volunteers to receive either oil (OIL, ~1.18 g/kg), rich in MUFA, or vehicle (VCL, water) on 2 occasions. Insulin sensitivity was assessed during preclamp and hyperinsulinemic-euglycemic clamp conditions. Ingestion of 2H2O/acetaminophen was combined with [6,6-2H2]glucose infusion and in vivo 13C/31P/1H/ex vivo 2H-magnet resonance spectroscopy to quantify hepatic glucose and energy fluxes.RESULTSOIL increased plasma triglycerides and oleic acid concentrations by 44% and 66% compared with VCL. Upon OIL intervention, preclamp hepatic and whole-body insulin sensitivity markedly decreased by 28% and 27%, respectively, along with 61% higher rates of hepatic gluconeogenesis and 32% lower rates of net glycogenolysis, while hepatic triglyceride and ATP concentrations did not differ from VCL. During insulin stimulation hepatic and whole-body insulin sensitivity were reduced by 21% and 25%, respectively, after OIL ingestion compared with that in controls.CONCLUSIONA single MUFA-load suffices to induce insulin resistance but affects neither hepatic triglycerides nor energy-rich phosphates. These data indicate that amount of ingested fat, rather than its composition, primarily determines the development of acute insulin resistance.

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Very interesting study, maybe there really is the intramyocellular effect which lessens the muscle tissue uptake of glucose, maybe by glut4 inhibition.

The dosage is pretty high though, to me it would be about 80 grams of EVOO, alone, that is, absorbed faster than usual. Maybe the study should have compared the effects of different amounts and composition of fats. How do they know that the amount governs if there is no comparison with SAFAs?

Anyway, good news for the anti/EVOO vegan doctors, but I don-t know any people who ingest that dose of EVOO regularly. 

Edited by mccoy

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2 hours ago, Mike41 said:

Al Pater just posted this. Doesn’t look good for olive oil to say the least!

Monounsaturated fat rapidly induces hepatic gluconeogenesis and whole-body insulin resistance.
Sarabhai T, Kahl S, Szendroedi J, Markgraf DF, Zaharia OP, Barosa C, Herder C, Wickrath F, Bobrov P, Hwang JH, Jones JG, Roden M.
JCI Insight. 2020 May 21;5(10):134520. doi: 10.1172/jci.insight.134520.
PMID: 32434996  

A narrow metabolic study involving a single administration of , ~1.18 g/kg oil (=88.5 g of oil in a 75 kg adult person, ≈6.6 tablespoons) of a  canola oil (not even refined olive oil, let alone high-phenolic fresh EVOO) can't be held up against a mountain of high-quality prospective epidemiology and two large-scale randomized controlled clinical trials — particularly when that body of evidence specifically shows the benefit of EVOO in preventing and ameliorating the course of diabetes. Please stop wasting time with this shite.

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So everyone here is buying the 2L Kirkland Signature 100% Italian Extra Vrigin Olive Oil in the plastic bottle, right??

Edited by Clinton

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13 hours ago, Clinton said:

So everyone here is buying the 2L Kirkland Signature 100% Italian Extra Vrigin Olive Oil in the plastic bottle, right??

^No lol.

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20 hours ago, Michael R said:

A narrow metabolic study involving a single administration of , ~1.18 g/kg oil (=88.5 g of oil in a 75 kg adult person, ≈6.6 tablespoons) of a  canola oil (not even refined olive oil, let alone high-phenolic fresh EVOO) can't be held up against a mountain of high-quality prospective epidemiology and two large-scale randomized controlled clinical trials — particularly when that body of evidence specifically shows the benefit of EVOO in preventing and ameliorating the course of diabetes. Please stop wasting time with this shite.

What large scale trials? Do you mean predimed? It was bogus. There was absolutely NO control low fat diet even though they claimed as much. So when we have a well conducted large clinical trial with a seriously low fat control we will continue to be in the dark wrt olive oil being an overall benefit.

Edited by Mike41

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14 minutes ago, Mike41 said:

What large scale trials? Do you mean predimed? It was bogus. There was absolutely NO control low fat diet even though they claimed as much. So when we have a well conducted large clinical trial with a seriously low fat control we will continue to be in the dark wrt olive oil being an overall benefit.

... an 'objection' covered in my original post, of course ...

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5 minutes ago, Michael R said:

... an 'objection' covered in my original post, of course ...

And not answered to my satisfaction

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7 minutes ago, Mike41 said:

And not answered to my satisfaction

Meanwhile, you evidently are "satisfied" by tiny, non-randomized and sometimes non-controlled studies involving low-fat diets with no hard outcomes and often confounded by things like smoking (Ornish, Esselstyn (sp) etc). It is a puzzlement.

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On 5/22/2020 at 2:57 PM, Mike41 said:

These data indicate that amount of ingested fat, rather than its composition, primarily determines the development of acute insulin resistance.

Unlike chronic insulin resistance with hyperinsulinemia acute insulin resistance is a non issue when insulin is low because there is little need for insulin if blood sugar remains in an ideal range.  My wife and I eat a high fat ketogenic diet, mostly animal fats but plenty of EVOO too and our fasting triglycerides and other markers of metabolic health are excellent, far far better than when we ate a low fat vegan diet.

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Mike,

I am going to stick my neck out a little here to break up a friendly debate 🙂

I like you was an olive oil skeptic.  After re-cultivating the habit of being systematic appraising the evidence and reading the primary publications - something I was doing in other areas of medical care but not in this universe - I have come around to the conclusion that for 99+% of the population EVOO is compatible with optimal health, though it is neither necessary nor sufficient.  Indeed, I would list among "Michael's Greatest Hits" the discourse that starts with this post: 

Nevertheless if I am truly reformed I would and certainly appreciate and encourage ongoing discourse as new evidence presents itself, and I think it is reasonable and appropriate to present new data and research findings.  Science is a process, not a conclusion, and I appreciate your & Al presenting data as it emerges.  

Though I fully endorse Michael's criticism of the study in question -  namely that there is little novel under the sun in the study in question and nothing that fundamentally undermines the overall EVOO evidence base with regard to actionable health optimization for our cadre here  I also fully concede ( leaving aside the matter of genetics which is a whole other ball of wax ) that PREDIMED included there has never been a well-conducted RCT with a true apples-to-apples comparison of an extreme Esselstyn or Ornish version with an equally healthy higher-fat EVOO and/or nuts equivalent comparison.  Though DIETFITS tried to reconcile  low-fat vs high-fat (  doi:10.1001/jama.2018.0245 ), ultimately the spread between the two was too narrow to satisfy either side of the debate ( caveat: yes I am conflating low/high fat vs. EVOO vs. ketogenic a bit but I am working with the very limited higher quality trials data that we do have available).

Given this state of affairs there is room for epidemiology ( Blue Zones - plagued with confounding by non-nutritional factors and problems with data quality and making inferences across non-controlled populations) and model organisms ( lovely controls and follow-up , yet alas mice are not little people with tails), and I concur with Valter Longo's reasonable appeal to identifying common themes across multiple different pillars ( categories of ) nutritional evidence including also centenarian studies, analogy to other complex systems / mechanisms of systems biology, etc.  

Though this holds no water at all, its always colorful to illustrate with personal examples and indeed, I have maintained detailed periodic biomarkers for years, including estoteric ones.  Anecdotally, I transitioned over years from a low fat diet to a relatively high fat Mediterranean diet - both whole foods based and plant-centered unscathed.   The only period when my fasting insulin rose above the very low single digits with comparable HOMA-IR ( while cholesterol have remained similarly near-optimal) was when the intervention was not an adjustment of the % macronutrients, but the total daily calories via meal size.  Barring individual differences ( https://doi.org/10.1016/j.cell.2015.11.001 ), diet quality trumps all within the common range.   My decision to edge towards higher fat was a personal one, albeit guided by my interpretation of less clear-cut data including basic science data, nutritional requirements / chronometer analysis, and yes even some interesting work at all levels on nutrient sensing pathways and intervention studies in rodents ( long term) and people ( short term, limited to surrogate variables).  But from a big picture perspective, both diets were compatible with good health at least as far as nutritional epidemiology and personal biomarkers go.

Outside that common broad range of reasonable options, there are other interesting phenomenon with a wider range of uncertainty and debate  ( e.g., cancer risk and methionine  & BCAA excess , ketogenic diets and metabolic syndrome and likely modest impact on some hallmarks of aging, etc).  So given this science and limitations in its study for the foreseeable future, I anticipate the forum and others like it will always have lots of interesting fodder for discussion and debate.

Edited by Mechanism

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Hi Mechanism, thanks for your input. My peRspective on EVOO is that it is empty calories and harmful in that it reduces flow mediated dilation as all higher fat meals do. As far as the polyphenols, these are easily obtained from Whole Foods like nuts and seeds that while fatty have numerous polys and nutrients unlike EVOO. Also of course red wine, teas, veggies, spices, fruits etc. Why eat a nutrient vacant high calorie substance based on a bunch of epidemiology that is following people who are eating as part of their diets, white bread, pasta, rice and other empty foods and so Of course they benefit when they eat some polyphenols from EVOO due to their suboptimal polyphenol diets. I don’t think most people eating a So-called Mediterranean  diet are eating  anything close to what we here consider an ideal diet. So if we are also limiting calories as most of us do then it makes sense to challenge EVOO as a smart choice IMO!

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Pretty much my thoughts too.  Non-essential fats -- including monoglycerides such as OO -- IMO are empty calories.

  --  Saul

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9 hours ago, Mike41 said:

. My peRspective on EVOO is that it is empty calories and harmful in that it reduces flow mediated dilation

Except EVOO calories are not empty,  and EVOO  is very likely to  increase FMD and improve endothelial function.  Of course,  it's not necessary to include EVOO in a healthy diet, (high fat, high calorie nuts are a good option),  and you make a good point  that the actual " Mediterranean  diet is not as ideal as often suggested.  What I'm objecting to is your repeated unsubstantiated assertion that  including a little polyphenol-rich EVOO  in a diet is going to be positively harmful  to  endothelial function.   The preponderance of evidence suggest otherwise.

Effects of Olive Oil on Markers of Inflammation and Endothelial Function—A Systematic Review and Meta-Analysis

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4586551/

Nutrients. 2015 Sep; 7(9): 7651–7675. Published online 2015 Sep 11. doi: 10.3390/nu7095356
PMCID: PMC4586551 PMID: 26378571
 
Quote

Abstract

The aim of the present systematic review was to synthesize data from randomized controlled trials investigating the effects of olive oil on markers of inflammation or endothelial function. Literature search in electronic databases Cochrane Trial Register, EMBASE, and MEDLINE was performed. Thirty studies enrolling 3106 participants fulfilled the selection criteria. Pooled effects of different interventions were assessed as mean difference using a random effects model. Olive oil interventions (with daily consumption ranging approximately between 1 mg and 50 mg) resulted in a significantly more pronounced decrease in C-reactive protein (mean difference: −0.64 mg/L, (95% confidence interval (CI) −0.96 to −0.31), p < 0.0001, n = 15 trials) and interleukin-6 (mean difference: −0.29 (95% CI −0.7 to −0.02), p < 0.04, n = 7 trials) as compared to controls, respectively.

Values of flow-mediated dilatation (given as absolute percentage) were significantly more increased in individuals subjected to olive oil interventions (mean difference: 0.76% (95% CI 0.27 to 1.24), p < 0.002, n = 8 trials).

These results provide evidence that olive oil might exert beneficial effects on endothelial function as well as markers of inflammation and endothelial function, thus representing a key ingredient contributing to the cardiovascular-protective effects of a Mediterranean diet. However, due to the heterogeneous study designs (e.g., olive oil given as a supplement or as part of dietary pattern, variations in control diets), a conservative interpretation of the results is necessary.

* * * * * *

4. Discussion

Synthesis of data available from RCTs in the present systematic review suggest that markers of inflammation (CRP, IL-6) and those characterizing endothelial function (FMD, sE-Selectin) were favorably affected following interventions with olive oil.

Although it is likely that no single biomarker is able to represent all the important risk information, most of the outcome parameters taken into consideration in this meta-analysis are regarded to be valid indicators of inflammation and endothelial dysfunction.

The association between serum CRP concentrations and cardiovascular risk has been suggested by various studies, and elevated CRP levels are regarded to be an independent risk factor for CVD [47,48]. The US Preventive Services Task Force performed a meta-analysis of 22 studies showing that CRP concentrations greater than 3.0 mg/L were associated with an approximate 60% excess risk of incident coronary heart disease as compared to levels less than 1 mg/L [49]. In addition, serum CRP levels can predict long-term risk of incidence of myocardial infarction, ischemic stroke, peripheral vascular disease and all-cause mortality [50]. Although the value of CRP as a predictor for CVD is still discussed controversially, decreases in CRP values found in the present meta-analysis may support the concept of a cardio-protective effect of olive oil intake. In addition to its function as a stimulator of CRP synthesis [51,52], IL-6 has been shown to correlate with an increased risk of coronary heart disease in prospective studies [53]. Moreover, increased baseline levels of IL-6 were found to predict future cardiovascular events [54].

The other inflammatory markers investigated in this systematic review were unaffected by olive oil interventions. Although TNF-α is a relevant trigger during the inflammatory response, it has only rarely been assessed in epidemiological studies [55]. Likewise, data on a potential association between adiponectin and CVD risk are inconclusive [56,57,58]. An independent association of hypoadiponectinaemia with endothelial dysfunction measured by FMD has been observed by Tan et al. [59] in diabetic patients. Changes in TNF-α and adiponectin did not differ between olive oil interventions and respective controls in the present meta-analyses, which might be explained by the low number of study participants enrolled in the RCTs assessing these parameters.

To assess endothelial function, one of the standard non-invasive tools is FMD, which is regarded to reflect the local bioavailability of endothelium-derived vasoactive substances such as nitric oxide or endothelin-1. Reduced values of FMD are regarded to be early markers of atherosclerosis [60] as well as a predictor of future CVD events [8,61]. The association between reduced FMD and cardiovascular risk in individuals with varying baseline risk was demonstrated by several studies [62,63,64]. In a meta-analysis by Inaba and co-workers [8] synthesizing data of 5,500 participants of observational studies, each 1% reduction of FMD was associated with a 13% risk increase for cardiovascular events. This would equal an approximately 10% risk reduction given the effects of olive oil on FMD in the present meta-analysis.

Selectins are primary adhesion molecules in the inflammatory process expressed on the surfaces of activated endothelial cells, platelets, and leukocytes upon stimulation by TNF-α, IL-6, and other pro-inflammatory cytokines [65]. Elevated concentrations of E-selectin were found to be associated with ischemic events independent of traditional risk markers in the PRIME study [66,67]. ICAM-1 and VCAM-1 promote the adhesion of leukocytes to the endothelium. They are both up-regulated by pro-inflammatory cytokines, although VCAM-1 is considered to be expressed in more advanced states of atherosclerosis. This might explain at least in part why, in contrast to ICAM-1, reductions in VCAM-1 levels were not significantly more pronounced following olive oil interventions in the present systematic review.

Vascular reactivity is affected by food intake. Atherosclerotic events may be slowed down by anti-oxidant compounds in food via limiting oxidative damage and restoring endothelial function [68]. Thus, polyphenol intake has been associated with low mortality rates caused by coronary heart disease [69]. Other studies indicate that endothelial function and lipid profile were improved by anti-oxidant and anti-inflammatory polyphenols [70]. Therefore, the phenolic compounds present in extra virgin olive oil might mediated the beneficial effects observed in the present meta-analyses. Extra virgin olive oil polyphenols demonstrated strong anti-oxidant properties in experimental studies [3,13]. In vivo studies in healthy volunteers and patients with hypercholesterolemia or stable coronary heart disease have demonstrated that polyphenols improve ischemic reactive hyperemia blood pressure as well as inflammatory status [4,71].

Another potential health-promoting ingredient of olive oil is oleic acid. High oleic acid content of olive oil was demonstrated to affect metabolic functions and cardiovascular risk factors [72]. In various meta-analyses and meta-regressions, beneficial effects of monounsaturated fatty acids such as oleic acid on cardiovascular risk factors have been reported although the data available at present are still ambiguous [5,9,73].

 

The Mediterranean Diet, its Components, and Cardiovascular Disease

Quote

Two randomized, blinded crossover trials have assessed the antioxidant effect of dietary supplementation of extra virgin olive oil in humans: EUROLIVE (47) and the Virgin Olive Oil Study (VOLOS) (48). The Italian VOLOS trial (48) studied the inflammatory protective potential of olive oil in 22 mildly dyslipidemic patients. After a seven week treatment period, levels of thromboxane B2 (an index of maximal platelet activation) and total antioxidant capacity of plasma were both reduced with administration of olive oil without change in overall serum lipid profiles. In the The Effect of Olive Oil on Oxidative Damage in European Populations (EUROLIVE) study (47), a randomized, crossover controlled trial performed at six research centers across five European studies, patients received olive oil with low, medium or high phenolic content for three weeks with intervening two week washout periods. There was a linear decrease in markers of oxidative stress with increasing phenolic content by 1.21 to 3.21U/L.

A recent randomized crossover trial in a small group of healthy patients demonstrated that not only does the Mediterranean Diet (rich with olive oil) improve endothelial function and reduce systemic inflammation, but it also improves endothelial progenitor cell numbers which the authors report as a marker of increased endothelial repair (49). Ex-vivo observations in healthy volunteers showed that, in contrast to butter- and walnut-rich meals, consumption of an olive oil-rich meal does not induce the postprandial activation of NF-kB pathway in monocytes (50), thus suggesting an anti-inflammatory effect.

Recent data from our lab indicates a beneficial effect of olive oil supplementation on endothelial function in low-moderate risk patients (51).

Olive oil and health effects: from epidemiological studies to the molecular mechanisms of phenolic fraction   (2014)

https://www.ocl-journal.org/articles/ocl/full_html/2014/05/ocl140029/ocl140029.html

Quote

Endothelium dysfunction: in different human trials, the consumption of meals with phenolic rich olive oil was shown to improve endothelium function in the postprandial period (Vogel et al., 2000; Karatzi et al., 2008; Fuentes et al., 2008; Ruano et al., 2007). Experimental studies carried out in different animal models of atherosclerosis, hypertension, hypercholesterolemia supported the link between endothelial dysfunction and oxidative stress.

The different actions of polyphenols on endothelial and smooth muscle cells through nitric oxide (NO) stimulation have been reviewed (Andriantsitohaina et al., 2012). OOP’s were reported to contribute to increased NO levels and prevent the powerful oxidant peroxynitrite forming (Perona et al., 2006).

Moreover, OOP’s were found to decrease homocysteine, which has been linked to increased adhesiveness of the endothelium (Manna et al., 2009).

The role of noninvasive cardiovascular testing, applied clinical nutrition and nutritional supplements in the prevention and treatment of coronary heart disease

Ther Adv Cardiovasc Dis. 2018 Mar; 12(3): 85–108.
PMID: 29316855

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5933539/

 

Quote

Olive oil was associated with a decreased risk of overall mortality and an important reduction in CVD mortality in a large Mediterranean cohort of 40,622 participants.

For each increase in olive oil by 10 grams per day there was a 13% decrease in CV mortality. In the highest quartile of olive oil intake, there was a 44% decrease in CV mortality.60

One of the mechanisms by which the traditional Mediterranean diet (TMD), particularly if supplemented with virgin olive oil at 50 grams per day, can exert CV health benefits is through changes in the transcriptomic response of genes related to CV risk that include genes for atherosclerosis, inflammation, oxidative stress, vascular immune dysfunction, T2DM and hypertension.

This includes genes for ADR-B2 (adrenergic beta 2 receptor), IL7R (interleukin 7 receptor), IFN gamma (interferon), MCP1 (monocyte chemotactic protein), TNFα (tumor necrosis factor alpha), IL-6 and hsCRP.56,6163

 

 2018 Feb;269:50-56.
doi: 10.1016/j.atherosclerosis.2017.12.012. Epub 2017 Dec 8.

Mediterranean Diet Improves Endothelial Function in Patients With Diabetes and Prediabetes: A Report From the CORDIOPREV Study

 

Quote

Abstract

Background and aims: Endothelial dysfunction (ED) plays a key role in the development of atherosclerotic cardiovascular disease (ASCVD). Likewise, type 2 diabetes (T2D) is a major CVD risk factor. Therefore, our objective was to explore whether long-term consumption of a Mediterranean diet (MedDiet) rich in olive oil or a low-fat diet (LF diet) was associated with an improvement in ED and whether the potential benefits were similar in patients with or without T2D in the CORDIOPREV clinical trial (NCT00924937).

Methods: Endothelial function was measured in 805 participants who had completed follow-up ultrasound image studies, using ultrasonography of brachial artery to calculate flow mediated vasodilatation (FMD) before and after 1.5 years of intervention with a MedDiet [35% of calories from fat (22% monounsaturated) and 50% from carbohydrates] and LF diet [28% fat (12% monounsaturated) and 55% of calories from carbohydrates]. We categorized participants as patients with T2D, prediabetes, and without T2D according to the American Diabetes Association (ADA) criteria.

Results: MedDiet increased FMD in patients with T2D [5.2 ± 0.4 at 1.5 years vs. 3.8 ± 0.4 at baseline; p=0.04] and prediabetes [4.9 ± 0.4 vs. 3.8 ± 0.4; p=0.04] and induced an improvement in FMD compared to LF diet in patients with diabetes [5.2 ± 0.4 (MedDiet) vs.3.7 ± 0.4 (LF diet); p=0.01]; whereas both diets maintained FMD stable in patients without diabetes.

Conclusions: Habitual consumption of a MedDiet rich in extra virgin olive oil improves endothelial function in patients with prediabetes and diabetes. This takes great importance given that diet must be the cornerstone of treatment of patients with diabetes at high cardiovascular risk.

 

 

Polyphenol fraction of extra virgin olive oil protects against endothelial dysfunction induced by high glucose and free fatty acids through modulation of nitric oxide and endothelin-1

 

Quote

Abstract

Epidemiological and clinical studies have reported that olive oil reduces the incidence of cardiovascular disease. However, the mechanisms involved in this beneficial effect have not been delineated. The endothelium plays an important role in blood pressure regulation through the release of potent vasodilator and vasoconstrictor agents such as nitric oxide (NO) and endothelin-1 (ET-1), respectively, events that are disrupted in type 2 diabetes.

Extra virgin olive oil contains polyphenols, compounds that exert a biological action on endothelial function. This study analyzes the effects of olive oil polyphenols on endothelial dysfunction using an in vitro model that simulates the conditions of type 2 diabetes. Our findings show that high glucose and linoleic and oleic acids decrease endothelial NO synthase phosphorylation, and consequently intracellular NO levels, and increase ET-1 synthesis by ECV304 cells. These effects may be related to the stimulation of reactive oxygen species production in these experimental conditions.

Hydroxytyrosol and the polyphenol extract from extra virgin olive oil partially reversed the above events. Moreover, we observed that high glucose and free fatty acids reduced NO and increased ET-1 levels induced by acetylcholine through the modulation of intracellular calcium concentrations and endothelial NO synthase phosphorylation, events also reverted by hydroxytyrosol and polyphenol extract.

Thus, our results suggest a protective effect of olive oil polyphenols on endothelial dysfunction induced by hyperglycemia and free fatty acids.

 

 

 

 

Edited by Sibiriak

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It may not be just the powerful polyphenols which  make  EVOO  demonstrably good for endothelial function and cardiovascular health:

Oleic acid inhibits stearic acid-induced inhibition of cell growth and pro-inflammatory responses in human aortic endothelial cells

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Abstract

Saturated fatty acids (SFAs), significant components of both enteral/parenteral nutritional formulations (including diet), are linked to cardiovascular disease complications, such as atherosclerosis. We investigated whether oleic acid (C18:1n-9) reduces the growth inhibitory and pro-inflammatory effects of the stearic acid (C18:0) in human aortic endothelial cells (HAEC).

Stearic acid induced growth inhibition at concentrations less than 50 μM, whereas higher concentrations invoked cytotoxicity. Stearic acid-induced growth inhibition and cytotoxic effects were eradicated upon cosupplementation with oleic acid (25 μM). Oleic acid (as low as 5 μM) also inhibited the stearic acid-induced increase in intercellular adhesion molecule-1 (ICAM-1) expression. Stearic acid-induced phosphorylation of nuclear factor-kappa B (NF-κB), a transcriptional regulator of ICAM-1, was also reduced by oleic acid.

HAECs supplemented with either stearic or oleic acid resulted in cellular incorporation of C18:0 and C18:1n-9, respectively. Stearic acid primarily incorporated into phospholipids without increasing the total fatty acid content in HAECs. In contrast, oleic acid, with or without stearic acid, incorporated into both phospholipids and triglycerides, with a significant increase in total fatty acid amounts in triglycerides.

Our data suggest that oleic acid has the ability to reduce the inflammatory effects of long-chain SFAs in HAECs through reducing cellular stearic acid incorporation and NF-κB activation.

 

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These results indicate that long-chain SFAs are potentially damaging to endothelial cells; however, if SFAs are presented to endothelial cells with at least a moderate quantity of oleic acid, the SFA-induced pro-inflammatory and eventual cytotoxic effects can be averted.

Our results provide mechanistic support to the benefit of diets containing elevated levels of oleic acid (i.e., Mediterranean diet) on the development of inflammatory and cardiovascular diseases.

Unsaturated fatty acids selectively induce an inflammatory environment in human endothelial cells

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In contrast with linoleic and linolenic acids, which exerted strong or moderate proinflammatory responses, respectively, oleic acid diminished inflammatory gene mRNA levels in endothelial cells.

These data agree with previous reports on antioxidant effects mediated by oleic acid. For example, a diet enriched in oleic acid markedly decreases LDL susceptibility to oxidation and LDL-protein modification in mildly hypercholesterolemic patients (10). Similar results were obtained in experimental animals fed a diet enriched in oleic acid (52).

Extensive evidence also indicates the protective and antioxidant effects of oleic acid on endothelial cell activation. Cellular treatment with this fatty acid protects endothelial cells against cytokine-induced VCAM-1, ICAM-1, or E-selectin overexpression (53).

In addition, supplementation with oleic acid protects endothelial cells against hydrogen peroxide– induced cytotoxicity (16) and against dysfunction of the endothelial barrier as mediated by oxidized LDL (54).

 

Effects of Oleic Versus Linoleic Acids on Adhesion Molecule Expression in Glucose-Treated Vascular Endothelial Cells

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The oleic acid-rich Mediterranean diet in contrast to linoleic acid-rich diets may protect against atherosclerosis by improving endothelial function

. This study evaluated the effects of oleic acid versus linoleic acid on adhesion molecule expression in glucose-treated endothelial cells.[br]Endothelial cells were cultured in normal (5 mmol/l; NG) or high (25 mmol/l; HG) D-glucose for 6 days. Oleic or linoleic acid was added to the medium (final conc 0.2 mmol/l) using fatty acid free BSA as a carrier (6:1) for the final 3 days of culture prior to TNF[alpha] stimulation (10 ng/ml; 4-12 hr). The cell surface expression of adhesion molecules was quantified in fixed cells by ELISA and real time PCR was used to quantify gene expression. All results were expressed relative to the control (NG + BSA). [br]TNF[alpha] stimulation induced the cell surface and mRNA expression of the adhesion molecules E-selectin, VCAM-1 and ICAM-1 as well as the mRNA expression of the chemokine MCP-1.

Linoleic acid significantly increased TNF[alpha]-stimulated E-selectin cell surface expression in NG and HG whereas addition of oleic acid resulted in a decrease in expression. TNF[alpha]-stimulated cell surface expression of ICAM-1 and VCAM-1 was also reduced by oleic acid but linoleic acid had no additional effect in comparison to control.

Oleic acid decreased mRNA expression of E-selectin, MCP-1 and ICAM-1 but increased VCAM-1 expression in TNF[alpha]-stimulated cells. Linoleic acid had variable effects on the mRNA expression of the adhesion molecules and MCP-1. HG alone increased TNF[alpha]-stimulated mRNA expression of both MCP-1 and E-selectin. [br]

In conclusion, the monounsaturated oleic acid may exert its anti-atherogenic effect via reducing the expression of MCP-1 and E-selectin, both early mediators in atherogenesis.

In contrast, linoleic acid may be considered pro-atherogenic as it promotes increased cell surface expression of E-selectin.

 

Monounsaturated fatty acids protect against palmitate-induced lipoapoptosis in human umbilical vein endothelial cells (2019)

PLoS One. 2019; 14(12): e0226940.

PMID: 31891641

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The cellular effects of fatty acids vary depending on the chain length and saturation state. For example, high dietary intake of long chain saturated fatty acids such as palmitate (C16:0) and stearate (C18:0) is associated with elevated risk of CVD and diabetes [16, 17]. Palmitate, the most prevalent saturated fatty acid in circulation [17], also impairs endothelium-dependent vasodilation [7] and is a potent stimulator of endothelial cell lipoapoptosis [18].

Conversely, diets high in mono- and polyunsaturated fatty acids are generally cardioprotective [16]. Interestingly, the addition of unsaturated fatty acids to hepatocytes [19, 20] and pancreatic β-cells [21] has been shown to protect against saturated fatty acid-mediated lipoapoptosis.

In endothelial cells, the monounsaturated fatty acid oleate prevents palmitate- and stearate-induced cell toxicity [22, 23] although the effects on apoptosis are unknown.

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The monounsaturated fatty acid oleate has garnered particular focus because of its presence in olive oil and importance to the Mediterranean diet [37, 38]. In vitro studies have supported human trials by demonstrating that unsaturated fatty acids are less toxic than long chain saturated fatty acids in various cell types, including endothelial cells [23, 35, 39, 40]. For example, Harvey et al. and Artwohl et al. demonstrated that endothelial cell dysfunction caused by the saturated fatty acid stearate (C18:0) was mitigated by co-incubation with oleate or eicosapentanoic acid [23, 39].

These studies coincide with work in other cell types, such as hepatocytes and pancreatic β-cells, in which oleate has been shown to mitigate saturated fatty acid cell toxicity [19, 20, 41].

 

 

 

 

Edited by Sibiriak

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To be honest, I've long since taken the position that showing benefits to X (whatever that may be, foods, medications etc. - in this case, say EVOO) in the context of ameliorating some other damage due to suboptimal diet or lifestyle factors is a complete non-starter in the case of people like us. In fact, it may be actively destructive.

That was one of my - many - problems with resveratrol, for example. When it was not possible to show much in the way of benefits for life extension in normal mice, the fallback position of the resveratrol touts was that it showed great benefit for mice on a very poor diet (high saturated fat, high levels of sugar etc.). Fine - but of what good is it to me? I'm not on a very poor diet. So what good is resveratrol for me? 

Tremendous numbers of "beneficial" foods and compounds fall into this category - they lower BP... but only if your BP is very high, or they show some other benefit in the context of some disease process. But if you are not in that category - nothing doing.

There's some suspicion that this is in the case of alcohol (or red wine) - it'll show benefits if you are suboptimal along some axis - but if you're a very healthy individual, perhaps it might even be destructive.

Therefore I would really like to see more studies of things like EVOO in subjects who don't have CVD vulnerabilities and the like. Otherwise it's difficult to make a good evaluation of the advisability of any given intervention. 

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