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Good points about fatty acids. It drives me crazy when news outlets say nuts are high in omega 3. Only walnuts as you point out are. Nuts are high in arginine, plant sterols, vitamin E and fiber. All these may contribute to the cardiovascular connections with nut consumption would be my guess.

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I looked up the original green monkey study showing EVOO is still associated with atherosclerosis. Interestingly it found that:


"We found that dietary enrichment of monounsaturated fatty acids had the effect of keeping LDL-C lower and HDL-C higher in the primate model, a very similar outcome to that described for humans by Mattson and Grundy.2 At the same time, many of the changes in LDL particle composition induced by monounsaturated fat were noted to be those associated with exacerbated atherosclerosis in the primate model. When CAA was quantified at the end of the 5 years of atherosclerosis induction, the atherosclerosis extent in the monounsaturated fat group was similar to that in the saturated fat group, while the polyunsaturated fat-fed animals had less (Figs 3⇑, 4⇑, 6⇑, and 7⇑)."

Sorry, again from iPhone so no option to embed links: http://m.atvb.ahajournals.org/content/15/12/2101.full


The pritzkin citation from the previous post also notes "Now, if you had looked only at the blood lipids of the monkeys eating the monounsaturated-fat-rich diet in this study, you’d have thought they would have ended up with cleaner arteries than those that ate more saturated fat. Compared to monkeys fed the diet high in saturated fat, the monkeys fed the monounsaturated-fat-rich diet had lower LDL bad cholesterol levels and higher HDL good cholesterol levels (similar to what happens in studies with humans). And compared to monkeys fed a diet high in polyunsaturated fats, the monkeys fed the high-mono diet had HDLs that were nearly twice as high (again, just like humans)."


In other words even though they had a better lipid profile compared to the saturated fatty acid group, they still ended up with the same problems. I think this five year study highlights, at least for African Green monkeys, the dangers of extrapolating short term surrogate variables to long term outcomes. While in an animal model, this primate is a closer model than both, and the longer-term data, focus on clinically relevant variable ( atherosclerosis), and interventional design. Given the similarities in the animal model it would not be unreasonable to put more credence, given the interventional design and long-term nature of the study than short term studies in humans focusing on surrogate variables or a human observational study where there remains significant potential for residual confounding not adequately controlled for in the multivariate analysis.


While I'm very comfortable having a few ounces of nuts given the data we discussed above ( phew! I probably already have a good 5 oz/day now), I am more reluctant to incorporate substantial EVOO in light of this study and the human studies I've seen so far either not interventional ( i.e., cohort studies), or relying too much on surrogate variables and/or short-term in nature.


Some of my concerns are reiterated here: http://www.ncbi.nlm.nih.gov/m/pubmed/12544660/


I am interested in thoughts on this to test my own assumptions and thinking. Macronutrient % is a high yield CRON topic, this discourse has been very helpful.

Edited by Mechanism

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I thought you'd learned to read the material from the low-fat gurus like Dr. Pritikin (note correct spelling) with a healthy dose of skepticism?


Case in point, the Pritikin.com web page you point to provocatively titled What's Wrong With Olive Oil?, and the green monkey study [1] you looked up. Good job by the way - going to the original source. Now you just have to learn to read more carefully, and notice the hyperbole, subtle obfuscation and blurring of distinction that diet gurus often engage in - then you'll be golden.


Let's treat it as another good learning opportunity - shall we?


First off who actually wrote the copy for the web site? Was it Dr. Pritikin? If you look at the bottom of web page, we see a nice picture and short bio of the actual author - Eugenia Killoran:


Eugenia Killoran
Senior Editor & Writer
Eugenia Killoran has been the food and fitness journalist for the Pritikin Program since 1992. She has published more than 3,000 articles, lectures, and book chapters on a wide variety of healthy living and weight-loss topics.


Wow - she's been with the "Pritikin Program" since 1992. After almost 25 years with him, she must be the good Doctor's right-hand person.  And with "more than 3000 articles, lectures & book chapters", she sure sounds like an expert. Let's see how many publications Dr. Pritikin and Ms. Killoran have co-authored together. Hmmm - that's strange; A Pubmed search of "Pritikin Killoran" shows zero articles in which they share authorship. Well, perhaps the lack of connection between them is understandable, given the fact that Pritikin had been dead for seven years by the time Ms. Killoran says she joined the Pritikin program in 1992, according to her byline on that webpage.


But that's not right, since she is quoted as the spokesperson for Pritikin Program in this 1985 article about Pritikin's unfortunate suicide. Sure enough, her full bio on the Pritikin website has all the details. Apparently she's been with the Pritikin program since 1980 - over 35 years, but prior to 1992 she served as "Media Assistant to Dr. Pritikin" and "Marketing and Registration Director".  Apparently in 1992 she was promoted to Chief Spin Doctor, er, "Editor/Writer, Pritikin Programs and Newsletters".


Well that's ok, with 3000 articles to her credit, she must have published solo or with other authors/researchers besides Pritikin either before or since his untimely death - right? Hmmm that's strange; A Pubmed author search for Ms. Killoran again shows zero publications. In fact, there is only a single Pubmed-indexed publication by anyone by the name "E. Killoran", and that is a paper on medical library science by Elizabeth Killoran.


I guess that isn't too surprising, since clearly from her full-bio it appears her role with the Pritikin program isn't very technical. And she appears to have the training and the skills for what she does though. She's got a MA/BA in English, and bills herself in her LinkedIn profile as in "independent contractor" with skills that include "blogging", "creative writing" and "social media marketing". Now there is someone I'd go to for health advice...


But boy looking around Pritikin.com, they sure do have have a slick website, so she and her colleagues must be doing something right, keeping Pritikin's legacy alive 30 years after his death. And check out that resort in the background of her bio page. If they can afford that place, they must still be going strong. Sure enough, over 100,000 people having visited their "longevity center & spa". At $5k-10K a pop, they appear to be closing in on $1 Billion in revenue - yes, that's $1,000,000,000. Yeah, if it's not more hyperbole, I say from that figure they are still going strong...


But perhaps I'm being too harsh. Surely after over 35 years of working for, writing about, and apparently following the Pritikin program herself, Ms. Killoran must be an expert. Even if she herself is not a researcher per se, she must know how to read, fairly analyze and present technical health material - right? After all, she's writing copy for such a large and prestigious organization.


Let's see.


First off, what's with the picture of the chubby orangutan on the webpage where she bashes olive oil? That should raise a red flag right there. More explicitly, in discussing a study which she claims to show the cardiovascular harm associated with olive oil in green monkeys (left), Killoran show this orangutan photo (right). Anything wrong with this picture? Could she find an uglier, more sadly anthropomorphic orangutan photo? Perhaps a bit misleading and inflammatory? Yeah - I think so too.


T55a4DF.png   monkey-329x600.jpg  


Now let's look at the actual study in question [1], and compare it with what Killoran / Pritikin's ghost actually says, and how you appear to have bought into what they imply - hook, line, and sinker...


First, what Killoran actually says in the introduction to her discussion of this study [1]:


“Better” cigarettes (those with less nicotine and toxic chemicals like benzo(a)pyrenes) still promote lung cancer. “Better” monounsaturated fats like olive oil may still lead to diseased arteries. When scientists fed a monounsaturated fat–rich diet to monkeys for five years, the monkeys developed extensive atherosclerotic plaques in their coronary arteries. (1)


Well that is a quite provocative statement - comparing "better" MUFU fats like olive oil to "better" cigarettes in terms of coronary artery disease. That apparently is meant to not only suggest that the analogy is an apt one, but that she's got the study to prove it. But notice she adds the weasel word 'may' to the olive oil half of the analogy, but not the cigarette half. That will be important later...


So let's start to look at [1], by first checking out the date - 1995. Hmmm... That's over 20 years ago, and a full 15 years prior to when Killoran created that Pritikin webpage, in 2011. Is a 20 (or 15) year-old study in monkeys the best evidence she can find against olive oil? It makes one wonder if she may not be trying to spin things...  But hey, according to Google Scholar, this paper has been cited 208 times by other publications. With that many citations, it must be a good study and show what Killoran says it does - right?


First let's look carefully at her exact words in introducing this study - “Better” monounsaturated fats like olive oil may still lead to diseased arteries. This statement suggests three things:

  1. Some people consider certain monounsaturated fats better than others.
  2. Olive oil is considered to be one such better monounsaturated fat.
  3. But here is the kicker - olive oil may still lead to clogged arteries.

If she's using [1] as evidence to back up her claim, one would naturally assume that the study actually tested good olive oil right? Mechanism, you seem to have bought this implication, hook, line and sinker, when you say:


I looked up the original green monkey study showing EVOO is still associated with atherosclerosis. 


Notice any difference between your statement, my statement, and Killoran's statement? I'll give you a hint, it doesn't stand for "Electric Vehicle".


That's right - you seem to have jumped to the conclusion that that green monkey study [1] fed monkey's extra virgin olive oil, exactly as Ms. Killoran hoped you would. After all, unless she can convince you that everything you thought you knew about a healthy eating (e.g. EVOO is healthy) is wrong, you won't be suckered into motivated to spend $10K on a 2-week visit to their "longevity spa" to learn what you should be eating instead.


You're thinking "They wouldn't feed the crappy stuff to their test animals would they? When they say 'monounsaturated fat' they mean EVOO - right?" Think again, as Michael pointed out just a couple days ago.


But believe it or not, it gets worse - much worse. Let's see how. 


OK you're saying, maybe they didn't use extra virgin olive oil, but they obviously must have use olive oil right? After all, Killoran & (the ghost of) Pritikin is basing their olive oil bashing on this study. Remember, they are using [1] to support the claim that - “Better” monounsaturated fats like olive oil may still lead to diseased arteries.


But alas, study [1] has nothing to do with olive oil. The methods section of the free full text clearly states:


The monounsaturated fat diet (primary source of fat, oleic acid–enriched safflower oil) contained over 70% of the fatty acids as oleic acid.


So not only was it not EVOO, it wasn't even OO in the green monkey study on which Killoran is basing the Pritikin case against olive oil...


And believe it or not, it gets even worse.


OK you're saying, maybe they didn't use olive oil, but in a diet study comparing MUFA, PUFA and SFA for their effects on the clogging of arteries - those must have been the types of fats that they fed the monkeys - right? In other words, the MUFA group got mostly MUFA (in the form of of high-oleic safflower oil) and the other two diets got some form of PUFA (actually low-oleic safflower oil) and SFA (actually palm oil) respectively, and nothing else in terms of fats that could potentially clog their arteries - right?


'Fraid not. From the full text of [1]:


[E]ach group was fed for about 5 years with experimental diets containing 35% of kilocalories as fat and 0.8 mg cholesterol/kcal; the diets differed only in fatty acid composition.


Well - what's so bad about a little cholesterol? After all, there has been a lot of controversy over the impact of cholesterol from eggs. If an occasional egg won't kill you, it shouldn't make much difference here - right? Think again. First, 0.8 mg of cholesterol / kcal is a heck of a lot - the human equivalent of 2000 mg of cholesterol per day. That's the equivalent of 12 eggs per day. Plus, even worse, from [2]:


[M]onkeys are hyperresponsive to dietary cholesterol compared with humans...


So they were shoveling the human equivalent of 12 eggs per day into poor creatures who are more sensitive to dietary cholesterol than humans are. See anything wrong yet?


And I know you aren't going to believe this, but it gets even worse.


Yup, study [3] showed that when green monkeys were fed very similar diets to the ones used in [1] - MUFA-rich, PUFA-rich and SFA-rich, but with little additional dietary cholesterol diet (0.05 mg/kcal), the serum LDL-cholesterol remained low in all three groups. But when they shoveled nearly as much cholesterol as used in [1] (i.e. 0.77 vs. 0.80 mg/kcal), the LDL-cholesterol of all three diet groups went through the roof; rising ~400%, from a level that would be healthy for both monkeys and humans (~70 mg/dl) to a Heart Attack Grill level of around ~300mg/dl. Notice that's LDL-cholesterol, not total-cholesterol.


The LDL levels in [1] weren't quite that high, at 272, 184 and 166 mg/dl for the SFA, MUFA, and PUFA groups, respectively. But that is still an LDL level which is 2.5 to 4 times higher than that of green monkeys, or humans for that matter, when fed a healthy diet. Are we surprised after five years on this toxic diet they had clogged arteries?


So Killoran points to [1] as the sole study in her argument that olive oil will clog your arteries, when [1] didn't even use olive oil, to say nothing of EVOO, to say nothing of high-polyphenol EVOO. And along with the non-OO fat, researchers in [1] shovelled enough dietary cholesterol into the poor cholesterol-sensitive monkeys to choke a horse, despite the fact that a diet high in MUFA should naturally be very low in dietary cholesterol, especially a diet consumed by anyone reading this.


Now you tell me Mechanism - does that seem like a fair and unbiased analysis of the data about olive oil on cardiovascular health?


But I will say one thing positive about Ms. Killoran. She's a good writer. Nowhere does she say anything blatantly false about study [1]. Instead, she uses her clever writing skills to deceive gullible victims normal folks into reading between the lines and drawing their own (false) conclusions about the data she is presenting. She's counting on them coming to believe they've been fooled all along by the so-called nutrition "experts", and then take out a second mortgage on their house so they can afford a week at the Pritikin Longevity Spa to find out what they really should be eating.


But don't feel bad Mechanism. You're far from the first to be misled by this kind of analysis, and in fact, by this particular study. A quick Google search of its PMID identifier (7489230) shows that study [1] even had our own James Cain "thinking that excess MUFA isn't completely neutral" in this post from 2012 on the Longecity forums. I trust James has learned a lot since then about how to read a study carefully.


Finally, for anyone coming new to these discussions in the middle - I'm not personally a big fan of olive oil. I much prefer to get my healthy fats from whole plant foods, in the form of nuts, seeds and avocados. But I'm even less of a fan of shoddy, or worse, deceptive analysis designed to mislead innocent people trying figure out what to eat to improve their health.


That's why, despite all the intricacies I touched on above, this discussion remains relevant to the topic of this thread. There is so much dietary misinformation out there, even by people like Pritikin and other low fat gurus who aren't supposed to be beholden to "Big Food" or other special interests. It's very hard for your average person to know who to trust.


That's why the article I started this thread off with is such a gem - it summarizes in an easy-to-read form what I'm confident are good recommendations for a healthy diet and lifestyle, all back up by solid science.





[1] Arterioscler Thromb Vasc Biol. 1995 Dec;15(12):2101-10.

Compared with dietary monounsaturated and saturated fat, polyunsaturated fat
protects African green monkeys from coronary artery atherosclerosis.
Rudel LL(1), Parks JS, Sawyer JK.
Atherogenic diets enriched in saturated, n-6 polyunsaturated, and monounsaturated
fatty acids were fed to African green monkeys for 5 years to define effects on
plasma lipoproteins and coronary artery atherosclerosis. The monkeys fed
polyunsaturated and monounsaturated fat had similar plasma concentrations of LDL 
cholesterol, and these values were significantly lower than for LDL in the
animals fed saturated fat. Plasma HDL cholesterol concentrations were comparable 
in animals fed saturated and monounsaturated fat and were significantly higher
than in animals fed polyunsaturated fat. Thus, the monounsaturated fat group had 
the lowest LDL/HDL ratio. LDL particle size was largest in the saturated and
monounsaturated fat groups, significantly larger than in the polyunsaturated fat 
group. LDL particle enrichment with cholesteryl oleate was the greatest in the
animals fed monounsaturated fat, next greatest in the saturated fat-fed animals, 
and was least in the polyunsaturated fat-fed animals. Coronary artery
atherosclerosis as measured by intimal area was less in the polyunsaturated fat
compared with the saturated fat groups, was less in the animals fed
polyunsaturated fat compared with the monounsaturated fat-fed animals, but did
not differ between the monounsaturated and saturated fat groups. Cholesteryl
ester, particularly cholesteryl oleate, accumulation in the coronary arteries was
also similar between groups fed monounsaturated and saturated fat but was minimal
in the animals fed polyunsaturated fat. In sum, the monkeys fed monounsaturated
fat developed equivalent amounts of coronary artery atherosclerosis as those fed 
saturated fat, but monkeys fed polyunsaturated fat developed less. The beneficial
effects of the lower LDL and higher HDL in the animals fed monounsaturated fat
apparently were offset by the atherogenic shifts in LDL particle composition.
Dietary polyunsaturated fat appears to result in the least amount of coronary
artery atherosclerosis because it prevents cholesteryl oleate accumulation in LDL
and the coronary arteries in these primates.
PMID: 7489230
[2] J Nutr. 1998 Jul;128(7):1104-13.
Dietary cholesterol affects serum lipids, lipoproteins and LDL metabolism in
cynomolgus monkeys in a dose-dependent manner.
Stucchi AF(1), Nicolosi RJ, Karge WH 3rd, Ausman LM, Ordovas JM.
Author information: 
(1)Center for Cardiovascular Disease Control, Department of Health and Clinical
Sciences, University of Massachusetts-Lowell, Lowell, MA 01854, USA.
To examine the mechanism(s) underlying the cholesterolemic response to dietary
cholesterol and saturated fatty acids, low density lipoprotein (LDL) metabolism
was studied in two groups of cynomolgus monkeys fed diets containing 30 or 36% of
total energy as fat. At each dietary fat level, the same group of monkeys was
sequentially fed three dietary cholesterol concentrations as egg yolk in the
following sequence: low (0.01 mg/kJ), medium (0.03 mg/kJ) and high (0.05 mg/kJ)
for 30, 32 and 24 wk, respectively. Dietary polyunsaturated and monounsaturated
fatty acids were the same in the two groups; the 6% difference in fat was due to 
the saturated fatty acids, 12:0 and 14:0. Serum total cholesterol, LDL
cholesterol and LDL apolipoprotein B concentrations increased (P < 0.05) with
dietary cholesterol in a dose-dependent manner in both fat groups. These
elevations were the result of generally increasing LDL apolipoprotein B
production rates, concomitant with reduced LDL apolipoprotein B fractional
clearance at the high cholesterol intake. Serum HDL cholesterol and HDL
apolipoprotein A-I concentrations were not affected in a consistent manner. These
results demonstrate that cynomolgus monkeys are hyperresponsive to dietary
cholesterol compared with humans, suggesting that this model may be useful in
identifying metabolic and genetic predictors for hyperresponsiveness to dietary
cholesterol in humans as well as assessing the metabolic heterogeneity of
responses to dietary cholesterol.
PMID: 9649592
[3]  J Lipid Res. 1992 Apr;33(4):559-68.
Reduction of cholesterol absorption by dietary oleinate and fish oil in African
green monkeys.
Parks JS(1), Crouse JR.
Author information: 
(1)Department of Biochemistry, Bowman Gray School of Medicine, Wake Forest
University, Winston-Salem, NC 27157-1040.
To determine whether diets enriched in monounsaturated or n-3 fatty acids cause a
reduction in cholesterol absorption relative to those more enriched in saturated 
fatty acids, we measured cholesterol absorption in 18 African green monkeys fed
diets enriched in lard, oleinate (oleic acid-rich safflower oil), or fish oil at 
two levels of dietary cholesterol (0.05 vs. 0.77 mg/kcal). All animals were
initially challenged with the lard, high cholesterol diet to ascertain their
responsiveness to dietary cholesterol. Based on the results of this challenge,
low versus high responders were equally distributed in assignation to the low (n 
= 6) and high (n = 12) cholesterol regimens. Within each level of dietary
cholesterol animals consumed all three dietary fats in random sequences during
three experimental phases each lasting 9-12 months with a monkey chow washout
period between each phase, so that each animal served as its own control. During 
each dietary phase measurements of plasma lipids and cholesterol absorption were 
performed. The animals fed the higher versus lower level of dietary cholesterol
had significantly higher plasma total cholesterol and low density lipoprotein
(LDL) cholesterol concentrations and lower percentage cholesterol absorption;
high density lipoprotein (HDL) cholesterol levels were not affected by the level 
of dietary cholesterol. Dietary fish oil resulted in a 20-30% reduction (P less
than 0.01) in total plasma and LDL cholesterol and a 30-40% reduction (P less
than 0.01) in HDL cholesterol concentrations compared to lard and oleinate
regardless of the level of dietary cholesterol. At the high level of cholesterol 
intake, the oleinate and fish oil diets resulted in significantly lower
percentage cholesterol absorption compared to the lard fat diet (35 +/- 2%, 34
+/- 3%, 41 +/- 4%, respectively). At the lower level of dietary cholesterol,
percentage cholesterol absorption values were higher than those at the high
cholesterol intake (45-52% vs. 34-41%) but were not affected by the type of
dietary fat. There was a significant positive correlation between plasma LDL
cholesterol concentrations and percentage cholesterol absorption for the oleinate
and lard diets at the high level of dietary cholesterol and a significant inverse
association between plasma HDL cholesterol and percentage cholesterol absorption.
We conclude that the type of dietary fat can influence cholesterol absorption in 
African green monkeys and that oleinate and fish oil reduce cholesterol
absorption relative to lard when a high amount of cholesterol (0.77 mg/kcal) is
present in the diet.
PMID: 1527479

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Additional piece of advice, although it is pretty well publicized already would be:


Practice sun protection!


This again needs to be unpacked. Most people think in terms of using sunscreen, but it's not so simple: even just regarding sunscreen, you need to pay attention to the SPF, whether it protects against the broader spectrum of UV, whether it contains toxic substances, and being cognizant of time limits i.e. you can't just put in on in the morning and stay out in the sun all day, or even jump in the ocean - it needs to be re-applied regularly, and make sure it covers areas you may not think of, like tips of ears etc. Remember, you can get sun damaged from light that gets bounced, so for example, just because you wear a broad-rimmed hat doesn't mean your face is off the hook because it is not in direct sunlight - sunlight that bounces off the concrete pavement is still very damaging, sunlight that pours through a glass window (like f.ex. a car) is too (unless the glass is specifically UV protected - which usually only happens in museums). Best bet is to protect yourself with clothing - note how sun protection is practiced in the Middle East desert regions, full dress from head to toe including face protection, not like Westerners who show up in shorts and a T-shirt "because it's hot". But not all clothes are made equal when it comes to sun protection - a lot of shirts and pants and the like are loosely woven and you get a ton of direct sunlight on your skin, so make sure your clothes truly protect against the sun. Your sunglasses ought to have reliable UV rating - and make sure the frames and glass truly protect your eyes... the damage is cumulative, and it's very often that the very old are blind or severely sight compromised (even Jean Calment).


Skin cancer can be disfiguring (and is the most common cancer in humans), and it can also kill (melanoma, the rates of which are quite high). For a variety of reasons, the rates of skin cancer, including very fast growing lethal cancers are skyrocketing - not only are we spending more time in the sun, but with the ozone layer depletion you are getting a lot more UV than you'd have gotten 50 years ago. Some regions are especially dangerous (Australia). Avoid unprotected sun exposure at hours of particularly intense UV radiation (midday). Obviously, avoid lunacy like suntanning salons. Therefore the next piece of advice:


Visit a dermatologist regularly, for a full body scan - as you get older, past 60 or so, do so yearly. Skin cancer rates explode in later age, especially in areas habitually exposed to the sun, such as scalp, face, neck, ears, forearms (especially the left arm, for you, car drivers in countries with the steering wheel on the left). If you catch a skin cancer early, it's eminently treatable, the longer you wait, the worse it'll get, especially with dangerous cancers such as melanoma. So: regular dermatologist visits for a full body scan! Remember: skin cancer is the most likely cancer you'll get.


Now, if you are super careful with sun exposure, there is a flip side: you must pay attention to your vitamin D3 status, and supplement if necessary. In Saudi Arabia there are many people who are vit. D deficient, particularly women, due to a rigid dress-code... ironic in a country where you have a huge vit. D generator in the sky year round. Get your vit. D from food and supplements, be careful about getting it from the sun.


But there is some controversy about sun exposure. We can't prove that the vit. D you get through sun exposure might not work somewhat differently physiologically, or that there can't be other health benefits (including mental health!). There was a study recently where people who regularly sunbathed outlived those who avoided the sun - but there are confounders galore. So if you do elect to have some sun exposure, be very careful, and be aware of the risks - skin cancer, including deadly skin cancer, is incredibly common; be particularly careful if you are light skinned, red-haired, blue-green-gray eyed, if your skin doesn't tan easily but burns instead, if you are of Northern European extraction (Celt, Scandinavian, etc.). 

Edited by TomBAvoider

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Dean, my respect for you has gone up a notch - and that's hard to do with your track record. When I got the part " choke a horse" I laughed out loud, mostly out of pity for those poor African Green Monkeys. Great analysis. Before posting I found some other concerning cues besides the conflict of interest you so eloquently summarized and my reference to their misleading use of a study on better extrapolating to EVOO. For example, one of the studies cited inefficacy of monounsaturated fat intervention relative to walnuts which is a far cry away from demonstrating harm from EVOO ( rather, it can be relative benefit ) as they implied... actually after your post I better double check they really used EVOO at all (and if so, the sourcing...). In any case, with the preponderance of the data while I prefer to see it in nuts/seeds/avocado/olives to increase phytonutrients/fiber, reduce potential unknown toxicities, and reduce unknowns departing from whole foods, I increasingly see room for EVOO in the diet ( it has been our preferred cooking oil all along but we may get a higher quality sources EVOO at your suggestion) provided that it does not push out good nutrients out or increase calories too high. This has been enlightening... but it is only first in the 1,000 mile journey for this CRON newbie, with full agreement on the pertinent "next steps" you detailed above.


I do still have a quibble with nuts in the list corresponding to your article because many centenarian cultures have no or minimal nuts at all ( as seen by the macronutrient breakdown in my Okinawan link ). Make no mistake, I think they are great and have a ton myself, I just don't see data that they are necessary or sufficient (which is my personal criteria for them to make the cut for the list, but may not be yours).


Given the Okinawan ( 6% fat) and other data, what say you to my concern, given the black box of long-term health effects, of departing above the % fat content of Mediterranean diets? I cut & paste my argument from above, and would love for you to tear it to pieces if you feel it lacks merit - I am not married to the idea, and am interested in challenging my assumptions to see how the hold up:



"While short to low-intermediate term studies may suggest acceptability of higher fat diets, the long-term implications are less well studied, and there is some measure of avoidable risk extrapolating surrogate variables indefinitely into the future. One way to address this is to ask how much the %fat varies across blue zone cultures. The presence of blue zone cultures with substantially higher fat content ( that is, substantially higher than for the % at for a prototypical Mediterranean diet similar to Sardinia's version at the time) would lend greater credence to a long-term higher % oil diet. In the absence of such cultures I pose the question: would it not be unreasonable, to be conservative, to keep the % calories from oil/fat at or under the percent witnessed by blue zones populations?"


My experience is that just as with some of the CR study data you have presented in other threads -- which is mixed on the implications of CR on immunity and tumor progression -- that translation from basic science to clinical outcomes is neither straightforward nor reliably predictable, so addressing the above paragraph I think is key if we extended above that % fat macronutrients in the diet.

Edited by Mechanism

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Since the risks of sun exposure for skin cancer were just introduced by Tom, the below papers describe the risks in detail by body parts exposed and the risks of sunburn.


History of Severe Sunburn and Risk of Skin Cancer Among Women and Men in 2 Prospective Cohort Studies.
Wu S, Cho E, Li WQ, Weinstock MA, Han J, Qureshi AA.
Am J Epidemiol. 2016 Apr 3. pii: kwv282. [Epub ahead of print]
PMID: 27045074
"Dr. Abrar A. Qureshi serves as a consultant for AbbVie
Inc. (North Chicago, Illinois), Novartis International AG
(Basel, Switzerland), Janssen Pharmaceuticals (Titusville,
New Jersey), and Pfizer, Inc. (New York, New York) and receives
research funding from Regeneron Pharmaceuticals,
Inc. (Tarrytown, New York)."
Few studies have assessed the relationship between sunburn and risk of different skin cancers (melanoma, squamous cell carcinoma (SCC), and basal cell carcinoma (BCC)) in prospective studies simultaneously, and little is known about the association of severe sunburns at different body sites with skin cancer risk. We used data on 87,166 women in the Nurses' Health Study (1982-2010) and 32,959 men in the Health Professionals Follow-up Study (1992-2010) to investigate skin cancer risk associated with history of severe sunburns at different body sites (face/arms, trunk, and lower limbs). After adjustment for other risk factors, overall baseline history of severe sunburn was more apparently associated with risk of melanoma than with risk of SCC and BCC in men (multivariable-adjusted hazard ratios were 2.41 (95% confidence interval (CI): 1.32, 4.41) for melanoma, 1.48 (95% CI: 1.08, 2.03) for SCC, and 1.18 (95% CI: 1.06, 1.32) for BCC) but not in women. Sunburn on the trunk appeared to be more closely associated with melanoma risk, but not risk of SCC and BCC, when compared with sunburns at other body sites (face/arms and lower limbs). These differences were more apparent in men than in women. Pending further investigation, our findings add novel insights to the existing literature on sunburn history and skin cancer risk.
cohort studies; melanoma; skin cancer; sun exposure; sunburn
Risk factors for melanoma by body site.
Cho E, Rosner BA, Colditz GA.
Cancer Epidemiol Biomarkers Prev. 2005 May;14(5):1241-4.
PMID: 15894679 Free Article
It has been hypothesized that cutaneous melanoma at different anatomic sites develops through divergent pathways. We examined this hypothesis prospectively. We followed 152,949 women and 25,204 men free of cancer at baseline for up to 14 years in three large prospective studies. We examined risk factors for melanoma by anatomic location (head or neck, trunk, upper extremity, and lower extremity). Polytomous logistic regression was used to test the difference among risk factors by location of melanoma. A total of 511 incident cases of invasive melanoma (49 head or neck, 188 trunk, 98 upper extremity, and 176 lower extremity) were included in the analysis. Compared with females, males had a higher risk of developing melanoma on the head or neck and trunk. History of severe and painful sunburn was most strongly related to melanoma of upper extremity; individuals with >10 burns had a 6.86-fold (95% confidence interval, 2.62-18.00) higher risk of melanoma of upper extremity compared with those with no burns (P for trend < 0.0001; P for difference by body site = 0.04). Number of moles was most strongly related to melanoma of the trunk; the multivariate relative risk for having >10 moles was 4.67 (95% confidence interval, 3.07-7.11) compared with having no moles (P for trend < 0.0001; P for difference by body site = 0.04). Age, family history of melanoma, and hair color did not statistically differ by anatomic site of the cancer. These data support divergent etiologic pathways of melanoma development by anatomic sites.

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Tom (and Al),


Thanks for adding the caution against (excessive) sun exposure to the list of sensible health & longevity advice. I completely concur, especially the parts about avoiding sunburns, intentional tanning & tanning salons, and UV protective eyewear.


The only thing I worry about is the point that you made Tom, that there may be benefits of sun-derived vitamin D, or other benefits of sun exposure, that people may miss out on if they go overboard avoiding the sun.


When I run outdoors as I do for about 30min per day, I do so in shorts and no shirt and without sunblock, in order to get a prudent amount of sun exposure for my (rather northerly) latitude, always making sure to wear UV-protective sunglasses, i.e. these or these, depending on how intense the sun.  At other times when I'm out in the sun I wear a good SPF30 sunscreen. My red-haired daughter needs to be especially careful.


The problem of optimizing sun exposure reminds me of the whole "hygiene hypothesis", and how we Americans have gone overboard avoiding germs - with over prescription of antibiotics, antibacterial soap and preventing our kids from playing in the dirt etc. What's resulted is not better health for ourselves or our children, but instead people who are allergy prone and have poor gut health, not to mention mental health problems from not being exposured to nature enough.


I can imagine a similar realization dawning in 10-15 years, that we've gone overboard by eschewing the sun entirely, impairing rather than improving our long-term health through our well-intentioned diligence.


But Tom I think you struck a very good balance in your discussion, showing both the major cons as well as the modest pros of sun exposure.


Thanks again,



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You asked:

would it not be unreasonable, to be conservative, to keep the % calories from oil/fat at or under the percent witnessed by blue zones populations?"


Here is a good rule to follow. Keeping protein on the low side until one's elder years, when one should boost protein (and calories) to compensate for absorption issues and prevent sarcopenia. Beyond that, the evidence (including the so-called "Blue Zones") suggests that people can thrive on a wide range of percentages for the other two macronutrients - healthy carbs and healthy fats.  


I personally think if one is going to focus on one long-lived population, it's the Adventists Blue Zone (Loma Linda, CA) who best represent folks like me, and others who are likely to be reading this - as they have the most similar genetics, social structures, cultural background, lifestyle habits etc. In addition, their lifestyle seems the most sustainable of any of the Blue Zones - i.e. it isn't disappearing like (all?) the others. Plus, they've been the most carefully studied, by researchers other than Buettner.  Finally, many of them are vegan and eat a lot of nuts .


To learn in detail what the Adventists eat and how they live, check out this post and this entire thread, along with this one. The long-lived Adventists get about 30-35% of their calories from (mostly) healthy, plant fats, especially nuts & seeds.


So my answer to your question is:

  • You could do worse than model your diet on one of the Blue Zones
  • IMO, the most appropriate Blue Zone for a westerner to model is Loma Linda, CA (the Adventists)
  • The Adventists eat about 30-35% of calories from mostly healthy fats.


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I agree, a balance needs to be struck. And when giving advice about skin protection, it really is important to give some context, because most people don't have a clear idea of what is involved. For example, I have the glasses in your second link - but under what circumstances should you wear eye protection? Most people wear sunglasses to protect against glare, with UV being a secondary - if noticed at all - consideration. And so, they won't wear eye/skin protection on a cloudy day. Yet, in some ways UV radiation can be even more intense on a cloudy day. Here's a pop article from American Scientist:





"Investigators have known since 1964 that clouds can have paradoxical effects on incident UV radiation. In more than a dozen studies since then, every data set includes at least some examples of what is known as cloud enhancement of UV. For people hoping to avoid skin photoaging and cancer, this can be a confounding characteristic."


So when should you wear sunscreen? Or sunglasses? Dermatologists frequently simply advise: "every time you step outside" - in other words, constantly. Is is overkill? Is there a place for some selective sun exposure? As we see, this is a controversial issue. But if you are worried about your eyes - as we should be - how much UV is too much? Some would say, since the damage is cumulative - any UV is too much UV for your eyes. I know that here in Los Angeles, I wear sunglasses even on the (infrequent) overcast days, because there is intense glare here even with cloudy skies, but I do it in addition because of the UV.


And it gets worse. From personal experience, let me issue a warning - you have no idea where you may be exposed to intense and damaging UV: I am frequently involved in film/video production, and lights are used routinely in the course of filming - there are some lights that put out tremendous - truly huge - amounts of UV radiation, to the point where you can get a "sunburn" within seconds of exposure. In order to protect the skin - and primarily the eyes - of the crew and actors, there is a special glass put in front of these bulbs. Well, sometimes these glass filters break, because of heat or accidents. We have replacement glass. One day a lighting technician was complaining about skin peeling and feeling raw from the lights. Quickly, tests were performed. It transpired that the new lights we got in from China, and new glass filters (also from China) for the old lights were not compliant with UV protection specs! It was a nightmare. We had to replace the lights with ones from Germany at 6 times the cost, and there were legal consequences and a lawsuit. 


Now, let me ask you: have you taken a spectrometer to the various lights you are exposed to during the day as you go about your business? You'd be surprised. You have no idea where the lights came from and to what spec they've been built to. I'd rather be laughed at or seen as an eccentric when I put on my orange sunglasses at the dentist, as I lay under the harsh overhead light that the dentist uses to see into my mouth, than to suffer eye damage. You wouldn't laugh at such precautions, if you ever visited one of those old people homes for folks who worked in the film industry here in LA, and saw all the old light techs and cinematographers who are blind. Poor eyesight in the elderly everywhere is at least partially mediated through UV exposure - when they were young or adults, sunglasses were often not something commonly worn. Today we have options to protect our eyes - we'd be wise to do so, rather than take the convenient route today and regret it in later years. Protect your eyes, people! The dangers often lurk where you may not think they are - in broad light. 

Edited by TomBAvoider

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Thank you for the tip on the Adventist - I will be using them as a case study for one model of optimal diet.


Accommodating new paradigms takes time, and when different experts disagree, it is often because the data is murky.  Still, you did such a stellar job tearing apart the green monkey study (your post should be required reading for CRON newcomers) , I'm curious what you have to say regarding this...


[ FYI I tried googling for previous discussions on this paper using: "site:crsociety.org 15182405" where the string corresponds to the PMID number of the reference below ... this search turned up empty].


So in this thread, Jeff Novick, at the bottom of the page, makes a case it is not the olive oil per se that has health benefits, but rather due to confounding by other dietary and lifestyle factors that go with it.  Here he refers to  Br J Nutr. 2004 Jun;91(6):1013-9 

where he comments:


"There is a fairly recent study done on the Isle of Crete, where the original famous Mediterranean diet of the 1960's came from. They looked at 304 patients In Crete, 152 patients with heart disease vs 152 without heart disease. The patients with heart disease had significantly higher daily intakes of monounsaturated fats (Olive Oil). The patients without heart disease had higher intakes of carbohydrates, fiber, folate & omega 3’s. The more mono unsaturated fat (olive oil) consumed, The more heart disease." [...he concluded..] "Those in the Mediterranean countries were healthy because they walked everywhere, did hard physical labor and ate an unrefined plant based diet. They were not healthy because of the olive oil in their diet but in spite of it."  


I'm interested in your take on the study, as the relationship was inverse that we hope to see if olive oil is protective.


His contention seems to be supported by


Role of vegetables and fruits in Mediterranean diets 
to prevent hypertension. European Journal of Clinical Nutrition (2008), 1–8 

which found the benefit of fruits / vegetable consumption was lost in the high olive oil consuming group, and 


Despite some promising research suggesting a beneficial effect, there is biological plausibility for a concerning inverse health effect via intermediation by cholesteryl oleate, as he summarizes here.


In any case, your thoughts regarding the Br J Nutr.  reference quoted from above appreciated - I wonder whether this page should be indexed for consumption as there is a lot of great discourse over a major controversy in ON if such indexing appears ( still familiarizing myself with the site ).

Edited by Mechanism

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Sorry Mechanism,


Here is where I get off this olive oil train... As I've said repeatedly, I'm not very interested in OO. I've got other (metaphorical) fish to fry. Perhaps a diehard high-polyphenol EVOO proponent will step in to carry the torch with/for you. I'd flash the bat (or is it BAT ) signal for Michael, but alas, it appears to be futile... ☹.


Alternatively, perhaps you can study these Pubmed search results for "extra virgin cardiovascular" and report back to us what you find/conclude. But I suggest you start a different thread since we're definitely straying from the "sensible advice" theme of this thread with these deeper and deeper dives into the pros and cons of olive oil.



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No problem Dean, sounds good.  I find debate a great form of learning and I hope this thread helped others too.  Thank you for the link and helpful posts.

Edited by Mechanism

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Good idea Tom.


I'll post to "Cool Tools" about the sunglasses, with a link to this thread.

Thanks for the interesting post, I was not so aware of the risk of UV rays for eyes.

Regarding UV exposition in the car, UVA only goes through the window, and  when I have long travels by car in summer I use these sleeves UPF 50 +: Sleeves Coolibar    (could be another "cool Tools" ?  :)xyz )


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FWIW, the response to monounsaturated fatty acids (and hence EVOO), might be dependent on your genetic profile. For example rs1801282:


"Several studies have shown that rs1801282 (also known as the Pro12Ala variant in the PPARG gene) influences whether an individual benefits from a diet high in monounsaturated fat. (This type of diet is often called a "Mediterranean"-style diet because olive oil is a good source of monounsaturated fat.) In people of European descent carrying at least one copy of the G version of rs1801282, increasing intake of just monounsaturated fat was associated with reductions in body mass index (BMI). In addition, a low fat diet led to an increase in waist circumference in people with the G version but a diet high in monounsaturated fat protected against this effect. The protection was even stronger in people with type 2 diabetes."


In general, one reason why different studies might come to different conclusions about the effect of FA - or for that matter any aspect of any diet - might be all down to the fact that in most such studies they don't break down the subjects according to their genetic profiles, or for that matter science may as yet not know which genetic profile responds do what aspect of any given diet. There is a lot of talk about "personalized medicine", but that is liable to be just as true of "personalized diet". 


So when I read contradictory studies, I often say myself: well, maybe we are dealing with different mixes of different genetic profiles in these subjects in study A vs study B.

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Thank you TomBAvoider, that's a great point.  I'm looking into 23andme and will likely pursue SNP mapping sometime this year.  The more I read the more valued this service seems.  I was was just listening to a podcast at SigmaNutrition interviewing Nanci Guest RD on nutrigenomics and I can see we have really come a long way with profiling results increasingly relevant and actionable.

Edited by Mechanism

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Be careful to get a reputable sunscreen:




"More concerns raised about quality of American sunscreens


WASHINGTON — The Environmental Working Group is out with its annual ratings and said most of the sunscreens available in this country are not nearly as good as they should be, and that some may contain worrisome ingredients.


The EWG analysis came exactly one week after Consumer Reports issued its annual guide to sunscreens. Consumer Reports tested more than 60 lotions, sprays and sticks and found 28 failed to meet the SPF claim on their labels."

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Earlier in this thread I inquired about Jeff Novick's objection to EVOO as an additive in excess (excess of course being the in the eye of the beholder), as opposed to a substitute for saturated fat. Below I quote the relevant parts:


Mechanism, on 04 May 2016 - 7:00 PM, said: [...]


So in this thread, Jeff Novick, at the bottom of the page, makes a case it is not the olive oil per se that has health benefits, but rather due to confounding by other dietary and lifestyle factors that go with it. Here he refers to Br J Nutr. 2004 Jun;91(6):1013-9 where he comments:


"There is a fairly recent study done on the Isle of Crete, where the original famous Mediterranean diet of the 1960's came from. They looked at 304 patients In Crete, 152 patients with heart disease vs 152 without heart disease. The patients with heart disease had significantly higher daily intakes of monounsaturated fats (Olive Oil). The patients without heart disease had higher intakes of carbohydrates, fiber, folate & omega 3’s. The more mono unsaturated fat (olive oil) consumed, The more heart disease." [...he concluded..] "Those in the Mediterranean countries were healthy because they walked everywhere, did hard physical labor and ate an unrefined plant based diet. They were not healthy because of the olive oil in their diet but in spite of it."




Despite some promising research suggesting a beneficial effect, there is biological plausibility for a concerning inverse health effect via intermediation by cholesteryl oleate, as he summarizes here.




Since that post quoted above I have done a bit more investigating:


At least one other source has cited the Br J. Nutrition publication I mention above as evidence that EVOO as an additive is not healthful and may be deleterious (as opposed to using it as a substitute for saturated fat).


Referring to the original research in Crete that put the Mediterranean diet on the map, the authors contend (quote between ###)




"It was true that residents of Crete consumed olive oil – about three tablespoons per day. But they also practiced many other healthy habits – they consumed lots of fruits, vegetables and whole grains, and their physical activity levels were very high – the equivalent of nine miles of walking per day (most residents were engaged in some form of agriculture at that time). Their health status certainly could not be attributed to the consumption of olive oil alone, and one could argue that the other healthy habits practiced by these people helped to overcome what we now know are the detrimental effects of regularly consuming oils of any ty pe. In my opinion, the conclusion that olive oil was responsible for the health status of these people is an error of attribution; a practice that is becoming more common in interpreting studies of nutrition and health." "One relatively recent study of people living on the island of Crete determined that patients with heart disease consumed more monounsaturated fat daily than patients without heart disease. The more olive oil consumed, the more heart disease they developed."




So I examined the Br. J Nutr case control study myself, and methodology seemed fairly sound (objectors please feel free to chime in). Rather, the greatest limitation of the study may be the inherent weaknesses of case control studies as a research design in general (compared with prospective cohort studies and better yet randomized controlled trials) coupled with the fact this was only one study and it is the preponderance of the evidence that governs best evidence and many other studies coming to the opposite conclusion.


These objections to the study do not dismiss its finding outright, so I was curious how Nutrition Action, the journal of the Center for Science in the Public Interest (CSPI) weighed in on the subject of EVOO as they have a long history of not accepting advertisements in their journal which in theory reduces at least one potential source for conflict of interest. They certainly are not without their thorns and Jeff Novick published a critique of the rationale for their "dirty dozen" vegetables, and I seem to remember another crsociety raised similar concerns. However, I appreciate that they also have a scientific panel and tend to cite original manuscripts. I found two references from them


Here, in 2014, (pages 5-6), they report: "We don’t have the solid evidence for monos that we have for polys. We do have evidence that replacing saturated fat with monounsaturated fat lowers LDL cholesterol, though not as much as polys do. And the default assumption should be that if you lower your LDL cholesterol, you lower your risk of heart disease.That would be reason enough to say, “If you like olive oil, go ahead—it’s very likely that it will lower your heart disease risk.” Also, the countries where people eat huge amounts of olive oil have low heart dis­ ease risk, so that makes it more plausible."


I found the qualification on the limited data above intriguing, along with subsequent commentary that "In the high quality controlled experiments that have been done over the last five or ten years, the omega3s from fish oil—EPA and DHA—have shown less and less of an effect on heart disease." font]


(FYI, the last page has a beautiful summary of composition of common oils which is worth taking a peek at!)


The 2nd Nutrition Action source, albeit a bit dated ( 2002) noted (Quotes Between ###):




"In the early 1970s, corn oil was king. Researchers had just confirmed that highly polyunsaturated fats (like corn, soy, and sunflower oil) could lower total cholesterol. (We call them polys, but all fats are really a mixture of polys, monos, and sat fat. See “Oil in the Family,” p. 7.) In contrast, highly saturated fats (like butter and beef) raised cholesterol, while highly monounsaturated fats (like canola and olive oil) were neutral. (Monos are neutral when researchers compare them to carbohydrates. But if you substitute monos for saturated fats, monos will lower your cholesterol.) “After corn oil lowered total cholesterol in the Los Angeles Veterans Administration Diet Study, some researchers recommended that every

one take a tablespoon or two a day,” says Connor. But by the 1990s, the pendulum had swung towards monos. In part, the enthusiasm was fueled by lavish conferences for researchers and the media sponsored by the olive oil industry. The science looked promising, too. “People got very excited about monos because, unlike polys, they didn’t cause oxidation of LDL in test-tube studies,” explains Lichtenstein. Oxidized LDL is more likely to clog arteries. “Some researchers also argued that, unlike polys, monos don’t lower HDL, the so-called good cholesterol,” she adds. But those arguments have lost some credence. For one thing, it became clear that polys lowered HDL more than monos only when ingested in huge quantities. “If you feed people reasonable amounts of polys,” Lichtenstein explains, “their HDL is not much dif ferent than when you feed them monos. And even though monos didn’t cause oxidation of LDL in test tubes, all bets are off in the body.” Meanwhile, researchers rediscovered that polys have more power to lower cholesterol than monos. And studies found cleaner arteries in monkeys that were fed polys than in those that were fed monos."


### (Dean's brilliant rebuttal to the green monkey study noted -- noteworthy that they were not using EVOO per se but another monounsaturated fats along with other methodoloy concerns)


While the above passage does not directly address the point made in the first Nutrition Action citation (which was from 2014 so quite up-to-date) that the evidence that EVOO is beneficial is weak, it does raise concerns that pharmaceutical sponsorship on a grand scale may have played some role in the evolution of the nutrition literature. In my own search I see a number of meta-analyses showing favorable effects from EVOO for a variety of outcome measures, but if the olive industry funds this work disproportionately, while not damning by itself, it does give pause regarding accepting the preponderance of that data in the absence of independent RCTs (ie, no funding by olive industry) confirming the findings.


Now, given the concern regarding sponsorship/funding of the studies, if we stratify research into those not funded by the olive oil industry and independent RCTs, I am not sure the latter would come to the same effect size, and possibly even conclusion as the former.


Having said all that we use EVOO in our household as the primary cooking oil, :)xyz Bu,t given:


1) Nutrition Action's 2014 qualification of the evidence in the 1st citation and


2) Impact of the oil industry in sponsoring a material number of olive oil studies that go into the meta-analysis (again, not a fatal flaw, but a wide scope of research suggests this may introduce subjective bias despite best efforts to avoid this, aside from more direct mechanisms such as failure to publish null findings on EVOO benefits),




I am less confident of the absolute (if any) benefit of EVOO and hence use it more of a substitute for less healthful choices to make for delicious cooking and/or add calories to the diet without pushing %calories from protein or blood sugar too high.


Rebuttals, balanced thoughts, perspectives, etc., invited here by EVOO advocates and aficionados and lovers of Truth and evidence-based nutrition. I am not pegged into any dogma but given the state of the science I thought that playing devil's advocate would be helpful.

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Thanks for digging into the evidence (or lackthereof) for benefits of EVOO. As I've said several times, these days I avoid EVOO and any oils in favor of nuts, seeds & avocados for my healthy fats - hence my disappointment at the CR Conference meals where high quality olive oil was plentiful, but where there were no other sources of healthy fat on offer.


As far as I can tell the only person who strongly believes in the benefits of EVOO around here is Michael, who (sadly) is unlikely to come to its defense - I say in hopes of goading him into responding...



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There are problems with studying any oils. One problem is the focus on biomarkers as surrogates for health outcomes. That may or may not be valid. Yes, polyunsaturated fatty acids lower TC and LDL. But does that by itself tell us all we need to know - this is no substitute for all-cause mortality outcomes. For example, see the recent study that showed polys as coming off worse than saturated fatty acids in all cause mortality as I highlighted in this thread:




The objections such as they were, focused on which polys were used (Dean), but there was a good rebuttal to that objection by Al P. in that thread. And I think we all are familiar with the problematic nature of excess n-6 FA vs n-3. But it's all very complicated - see for example the study Dean referenced about peanuts in this thread: 




One particular study - PMID: 25730101 - showed benefits specific to peanuts, and most likely a substantial portion of those were roasted, which goes against the whole philosophy of oxidising oils and destructive heat treatments. So were the benefits due to the FA component of nuts, or other parts of the nuts (a point I explored in other posts).


And be careful about studies done in animals (like monkeys EVOO and atherosclerosis). In rabbits peanuts/oils promote atherosclerosis - but in certain monkeys, peanut oil actually reverses atherosclerosis that's been induced by diet, so it's like a cure (alert: pdf):


Peanut Oil Reduces Diet-Induced Atherosclerosis in Cynomolgus Monkeys


So as you can see, studies in animals contradict each other depending on which animal species is involved. And nothing says that results in monkeys are translatable to humans anyhow. It's gotten to the point where if I see a study has been conducted in animals or in vitro, I immediately become enervated, depressed and discouraged. Give me results in humans, and in vivo, please.


The EVOO defense, such as I've seen from Michael, centers around other components of EVOO than the mono FA aspect. I am NOT speaking for Michael, and this is only my recollection, but as I recall - and he's welcome to chime in here to contradict, agree or clarify :) - his take is that the mono FA aspect of EVOO is merely neutral from a health point of view, and the positive health benefits are entirely due to the other components of EVOO... which is why it is critical that in evaluating the health effects of EVOO we should know the characteristics of the EVOO consumed, which is mostly impractical in such broad ecological studies (which are low quality evidence to begin with); and so he puts a great deal of emphasis on the EVOO being of the highest quality with appropriate numbers of those other components, properly stored, fresh etc. It is entirely possible that if you are simply using OO of some dodgy quality, you might not derive many or any health benefits.


And then there may be different effects depending on your genetic profile as I pointed out in a post a few above this one. All in all, trying to discern the optimal kind of FA and manner of consumption for humans is too fraught to make any very strong statements (except perhaps regarding transfats) - see even the recent saturated FA attempts at rehabilitation. There is too much noise in the data for me to draw firm conclusions. But since I must take in some FA anyway, I'm basically speculating - and my practice is: 1.3 oz almonds daily, about 1tbsp (of the very highest quality) EVOO daily (according to Michael possibly inadequate amount to derive health benefits), 1tbsp of ground flaxseeds daily, fatty fish twice a week (small amounts, salmon once/week and sardines once/week); I try my best to eliminate SFA and TFA as far as I can. But I freely admit it's purely speculation as to best practices.

Edited by TomBAvoider

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Thank you Tom, the threads you linked to were truly gems, I appreciate the time you took to compile them.  I particularly enjoyed the one you started dubbed "Re-evaluating Saturated Fat" as I too have been surprised how little discourse there has been on this key macronutrient in light of multiple recent studies including now a second major re-evaluation of the previous datasets that originally demonized saturated fat and elevated MUFA & PUFA such as that summarized by the BMJ piece that AlPater posted. 


Given a sizable literature using very different methodology / design, from basic science and animal studies up through clinical data supporting at least some concern regarding SFAs, I am not ready to absolve them, albeit I now suspect that the magnitude of harm, particularly for better sourced SFAs consumed by non-metabolic syndrome active lifestyle lower BMI individuals, to be somewhat overestimated.  While still avoiding saturated fats personally, try to have most of my fats in whole food form via nuts/seeds/olives/avocados, and my wife fortunately favors EVOO for most of her cooking which makes up the lion's share of the rest. 


As an aside, I have noticed that the functional nutrition community has taken on higher % fats and loves coconut oil with zest ( zeal?), but I remain wary enough regarding saturated fats in the absence of more reassuring data and therefore avoid coconut oil, which has a sizable portion of longer chain saturated fat as well as the newly touted 'healthy" medium chain saturated fatty acids, for the time being.


In the face of uncertainty, I focus on basic principals: I follow a primarily whole foods plant-based unprocessed or minimally processed approach to nutrition (with a bit of fish) and use the % oils for weight titration (to titrate my weight UP due to my naturally fast metabolism). 


Given the observational data ( e.g., blue zones), it appear that a wide variety of practices promote optimal compression of morbidity, a contention supported by the distillation of research Dean has compiled in his devil's advocate thread asking how CR may benefit individuals above and beyond a non-obesogenic healthy lifestyle.  There is more than one road to Dublin as they say.  As I find the fat/oil literature almost as murky as the microbiome data that is coming out, I am following the ongoing SFA/PUFA/MUFA research with great interest to see where it takes us.

Edited by Mechanism

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I also gargle with my homemade mouth rinse (water, baking soda, xylitol, erythritol, & amla powder) several times throughout the day to make my mouth inhospitable to bacteria.


Dean, do you know of any existing commercial mouthwash that is made with these ingredients, or some close enough approximation?

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Welcome (belatedly) to the CR Forums!


Unfortunately I don't know of any commercially available mouthwashes with anywhere near that combination of ingredients. I couldn't find any mouthwashes on Amazon.com that contain erythritol and certainly not amla, but there are plenty containing the combination of baking soda (sodium bicarbonate) and xylitol. Here is the search result. You could pick one of these (perhaps this one or this one), and add erythritol and/or amla yourself, or not. They are both pretty expensive though...



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