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Dean Pomerleau

DHA/EPA and ALA for Cardiovascular Disease & All-Cause Mortality

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All,

 

As discussed in this thread, evidence suggests ALA may be beneficial for brain health in most people, while DHA/EPA may be a mixed blessing - only helpful for avoid Alzheimer's disease (but not other forms of dementia) in those with the APOE4 allele. And as discussed in this thread, fatty fish high in DHA/EPA may be detrimental for cardiovascular health if contaminated with PCBs, as was the case in several studies of Swedish fish eaters. 

 

But this new study [1] shared by Al Pater (thanks Al!) found in another population of fish eaters, this time from Spain, dietary DHA/EPA may in fact be beneficial for avoiding cardiovascular mortality. But dietary DHA/EPA was not significantly beneficial for all-cause mortality. For dietary Alpha Linolenic Acid (ALA) which is an omega-3 from plants (e.g. walnuts, olive oil, flax, chia seeds) the opposite was the case. Namely, dietary ALA reduced all-cause mortality, but not cardiovascular mortality risk. 

 

Putting the two together, people who met the dietary recommendations for both DHA/EPA and ALA had the lowest all-cause mortality risk - 37% lower than those who didn't meet either recommendation.

 

Perhaps the fish from Spain have less PCBs than Swedish fish (no - I don't mean the candy :-) ). The full text of the study did not address DHA/EPA supplements - DHA/EPA intake was assessed solely from dietary sources. So it is not clear if a similar beneficial effect could be achieved through a combination of ALA from plant sources and DHA/EPA supplements as fish oil or algae oil, both of which are less likely to be contaminated with mercury or PCBs than the flesh of whole fish.

 

--Dean

 

------

[1] J Am Heart Assoc. 2016 Jan 26;5(1). pii: e002543. doi: 10.1161/JAHA.115.002543.

 

Dietary Alpha-Linolenic Acid, Marine Omega-3 Fatty Acids, and Mortality in a Population With High Fish Consumption: Findings From the PREvención con DIeta MEDiterránea (PREDIMED) Study.

 

Sala-Vila A, Guasch-Ferré M, Hu FB, et al.

http://jaha.ahajournals.org/content/5/1/e002543.long
http://jaha.ahajournals.org/content/5/1/e002543.full.pdf+html

Abstract

BACKGROUND:

Epidemiological evidence suggests a cardioprotective role of Alpha-linolenic acid (ALA), a plant-derived Omega-3 fatty acid. It is unclear whether ALA is beneficial in a background of high marine Omega-3 fatty acids (long-chain n-3 polyunsaturated fatty acids) intake. In persons at high cardiovascular risk from Spain, a country in which fish consumption is customarily high, we investigated whether meeting the International Society for the Study of Fatty Acids and Lipids recommendation for dietary ALA (0.7% of total energy) at baseline was related to all-cause and cardiovascular disease mortality. We also examined the effect of meeting the society's recommendation for long-chain n-3 polyunsaturated fatty acids (=/>500 mg/day).

METHODS AND RESULTS:

We longitudinally evaluated 7202 participants in the PREvención con DIeta MEDiterránea (PREDIMED) trial. Multivariable-adjusted Cox regression models were fitted to estimate hazard ratios. ALA intake correlated to walnut consumption (r=0.94). During a 5.9-y follow-up, 431 deaths occurred (104 cardiovascular disease, 55 coronary heart disease, 32 sudden cardiac death, 25 stroke). The hazard ratios for meeting ALA recommendation (n=1615, 22.4%) were 0.72 (95% CI 0.56-0.92) for all-cause mortality and 0.95 (95% CI 0.58-1.57) for fatal cardiovascular disease. The hazard ratios for meeting the recommendation for long-chain n-3 polyunsaturated fatty acids (n=5452, 75.7%) were 0.84 (95% CI 0.67-1.05) for all-cause mortality, 0.61 (95% CI 0.39-0.96) for fatal cardiovascular disease, 0.54 (95% CI 0.29-0.99) for fatal coronary heart disease, and 0.49 (95% CI 0.22-1.01) for sudden cardiac death. The highest reduction in all-cause mortality occurred in participants meeting both recommendations (hazard ratio 0.63 [95% CI 0.45-0.87]).

CONCLUSIONS:

In participants without prior cardiovascular disease and high fish consumption, dietary ALA, supplied mainly by walnuts and olive oil, relates inversely to all-cause mortality, whereas protection from cardiac mortality is limited to fish-derived long-chain n-3 polyunsaturated fatty acids.

KEYWORDS:

fatty acid; nutrition; sudden cardiac death

PMID: 26813890

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For over a year I have consumed a significant amount of Omega-3 rich foods, such as flax and chia (about 30g daily) and according to Cronometer, my intake balance is about 1:2 Omega-3 and Omega-6.

But my blood test shows AA/EPA ratio of 8:1, which is of course sub-optimal. I have since started taking 300mg EPA and 600mg DHA from algae (my blood DPA is already higher than "normal," as is my ALA).

I am curious about how CR practitioners here fare in terms of Omega-3/Omega-6 balance.

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On 10/2/2020 at 12:20 AM, Ron Put said:

For over a year I have consumed a significant amount of stanozolol dose, Omega-3 rich foods, such as flax and chia (about 30g daily) and according to Cronometer, my intake balance is about 1:2 Omega-3 and Omega-6.

what used to be your balance before starting to have high intake of Omega-3?

Edited by ohth
grammar

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4 hours ago, ohth said:

what used to be your balance before starting to have high intake of Omega-3?

Unfortunately, I did not take an Omega-3/6 measurement before I changed my diet. This is the first time I've done it.

But my cholesterol dropped almost 40 points down, to less than 140.  At the same time, I stopped consuming olive oil at home, which I credit with contributing to the lower cholesterol.

Anyway, part of the reason I am curious about the AA/EPA ratio of others here is that I am trying to see where other vegan/vegetarian CR practitioners are at.

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Fwiw I take 2TBSP of ground flaxseeds for ALA, about 1oz (1/4) cup of almonds and a couple of fish oil capsules every day (500 EPA 250 DHA) each.

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On 10/2/2020 at 4:20 AM, Ron Put said:

....my blood test shows AA/EPA ratio of 8:1, which is of course sub-optimal.

[...] my cholesterol dropped almost 40 points down, to less than 140.  At the same time, I stopped consuming olive oil at home, which I credit with contributing to the lower cholesterol.

Most likely your cessation of olive oil consumption contributed to your worsened AA/EPA ratio. 

On the other hand,  it is extremely unlikely that cessation of olive oil consumption (assuming it was EVOO) contributed to lowered  cholesterol,  since it is an established fact that EVOO intake decreases LDL,  decreases or maintains TC,  while  increasing or maintaining HDL.   This has been demonstrated in numerous studies without contradiction.  (EVOO also decreases LDL oxidation, ,  promotes reverse cholesterol transport, and improves endothelial function)

Edited by Sibiriak

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On 10/2/2020 at 6:40 PM, Sibiriak said:

Most likely your cessation of olive oil consumption contributed to your worsened AA/EPA ratio. 

On the other hand,  it is extremely unlikely that cessation of olive oil consumption (assuming it was EVOO) contributed to lowered  cholesterol,  since it is an established fact that EVOO intake decreases LDL,  decreases or maintains TC,  while  increasing or maintaining HDL. 

Thanks, Sibiriak, but based on what I have read, I would have to respectfully disagree. Virtually all studies that tout olive oil, are comparing it to commonly used animal and vegetable oils and I don't dispute that olive oil is better than stuff like butter or a bit better than coconut oil,.  But as the study linked in the previous sentence shows, it doesn't mean that it will lower cholesterol for those on sensible low-fat diets.

As to the AA/EPA ratio specifically, take a look at this: 

Effect of randomized supplementation with high dose olive, flax or fish oil on serum phospholipid fatty acid levels in adults with attention deficit hyperactivity disorder

1268970254_ScreenShot2020-10-04at17_47_54.png.cde727238dfef10fcccd062efa360365.png

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4 hours ago, Ron Put said:

it doesn't mean that it will lower cholesterol for those on sensible low-fat diets.

Not the point.  The issue is   your  claim that eliminating EVOO consumption   radically reduced your cholesterol levels. 

There's no evidence to support that prima facie  entirely implausible notion.  Of course, we can't rule out that you personally suffered from  some very rare,  heretofore unreported kind of reactivity to EVOO.   Individuals are different.

 

Quote

Olive oil contained extremely low  levels of α-LNA, and no EPA, DHA or other omega-3 fatty acids. The 60 g daily dose of flax oil contained approximately
34 g of α-LNA, but no measurable EPA or DHA. The daily dose of fish oil contained approximately 23 g of EPA and 12 g of DHA.

So it's a no-brainer that that olive  oil would not raise  EPA/DHA levels.    That's why olive oil was used basically as a control in the study,  and the aim was to compare flax oil with fish oil.

Thus:

Quote

As expected, there were no changes in serum fatty acid composition with olive oil supplementation

 

And the study's conclusion:

Quote

the increase in EPA and other omega-3 fatty acids observed  with flax oil supplementation was not significant as compared with the changes observed with fish oil supplementation.

In your case, if you substituted olive oil (low in AA) with any  foods  with greater AA content (many nuts and seeds),  then that could have contributed to your  "sub-optimal" AA/EPA ratio.    Just a possibility.

Most likely the problem is that your intake of flax and chia was not increasing your omega-3 levels, so   it makes sense for  you to take a supplement.

Personally,  I'm more concerned about  getting adequate absolute levels  of omega-3's,  including DHA,  particularly in regards to brain health.  I regularly eat a small amount  of oily red fish   or supplement.

See detailed posts on EPA/DHA,  problematic ALA conversion,  Michael Rae's,  Jack Norris',  Dean P.'s vegan recommendations etc.  here here, here, here and here.

 

 

 

Edited by Sibiriak

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44 minutes ago, Sibiriak said:
In your case, if you substituted olive oil (low in AA) with any  foods  with greater AA content (many nuts and seeds),  then that could have contributed to your  "sub-optimal" AA/EPA ratio.    Just a possibility.

Let's keep this in perspective: the average European or American has an AA/EPA ratio in the 15:1 - 20:1 vicinity.  The average Western vegan has a ratio of about 11:1 if I recall correctly.

I don't know my ratio back when I consumed EVOO, it may well gave been higher than 8:1, as both my DPA and ALA are now higher than normal.

As I mentioned, I am taking algae-derived DHA and EPA and I will run another test in the next few weeks to see if it having the effect I expect.

 

44 minutes ago, Sibiriak said:

Not the point.  The issue is   your  claim that eliminating EVOO consumption   radically reduced your cholesterol levels. 

Actually, this is the main point.  I did not reduce my daily fat consumption overall, it remained at about 35% of my daily calories.  I simply replaced EVOO with mostly flax meal or at times, chia seeds. And to me at least, replacing EVOO with flax, which is high in Omega-3 and ALA, would suggest an eventual drop in LDL cholesterol. The study comparing butter, coconut oil and olive oil essentially implies the same:

"LDL-C concentrations were significantly increased on butter compared with coconut oil (+0.42, 95% CI 0.19 to 0.65 mmol/L, P<0.0001) and with olive oil (+0.38, 95% CI 0.16 to 0.60 mmol/L, P<0.0001), with no differences in change of LDL-C in coconut oil compared with olive oil (-0.04, 95% CI -0.27 to 0.19 mmol/L, P=0.74). Coconut oil significantly increased HDL-C compared with butter (+0.18, 95% CI 0.06 to 0.30 mmol/L) or olive oil (+0.16, 95% CI 0.03 to 0.28 mmol/L). Butter significantly increased TC/HDL-C ratio and non-HDL-C compared with coconut oil but coconut oil did not significantly differ from olive oil for TC/HDL-C and non-HDL-C. There were no significant differences in changes in weight, BMI, central adiposity, fasting blood glucose, systolic or diastolic blood pressure among any of the three intervention groups."

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1 hour ago, Ron Put said:

replacing EVOO with flax, which is high in Omega-3 and ALA, would suggest an eventual drop in LDL cholesterol

 

1) Although high intakes of omega-3- rich  oils  have been shown to decrease circulating triglyceride levels (mostly in individuals with high baseline TG levels),   omega-3 intake  tends to slightly INCREASE  LDL levels,  or have a neutral effect,  but do NOT substantially reduce them.

 

Quote

Systematic reviews.... Wei and Jacobson compared the efficacy of DHA to EPA and found that individuals who consumed either DHA or EPA experienced reductions in serum TG of 18.5 % and 32 %, respectively. Individuals also exhibited significantly elevated serum low density lipoprotein cholesterol (LDL-c) levels by 5 % after DHA consumption, while those consuming EPA had a non-significant reduction in serum LDL-c of 1 % [20].

Additionally, Bernstein et al. concluded that DHA from algal oil plays a role in reducing serum TG while elevating serum LDL-c [21].

The results of a systematic review by Eslick et al. showed that 3.25 g/day of fish oil (1.9 g of EPA and 1.35 g of DHA) reduced serum TG by 14 %, yet cholesterol levels were not altered beyond a clinically insignificant increase in LDL-c [22].

Similar results were obtained in systematic reviews by Balk et al. and Mori et al., both of which assessed studies in which individuals consumed either fish, algal EPA or algal DHA oils [23, 24].

While results from the previously identified systematic reviews indicate that DHA contributes to slight increases in LDL-c and EPA contributes to minor reductions in LDL-c, both n-3 PUFA were established to be efficacious in significantly lowering serum TG levels.

https://lipidworld.biomedcentral.com/articles/10.1186/s12944-015-0049-7

 

2) It appears unlikely that your flax/chia intake  substantially increased your omega-3 levels.

3) Having said that,  it's quite possible that flax/ chia seed  soluble fibers/ lignans contributed to a reduction on LDL. (Flax oil, although rich  in ALA, would  not have that effect).

 If so,  it was the addition of those factors, not the removal  of EVOO which was causal.  If you believed you needed to maximally lower LDL  levels,  then substituting flax/chia meal  for olive oil could  well have been an effective move. 

In my view,  your LDL levels are plenty low enough,  if anything lower than necessary for lifespan extension.  But that's been discussed elsewhere.

Edited by Sibiriak

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Sibiriak, I might agree with your point 3.  Although my total fiber intake has not increased substantially, as I was eating more steel cut oats before.

I was coming back to post something interesting I found, comparing olive oil with seed oils.  It appears that most seeds oils are better with respect to cholesterol:

Effects of oils and solid fats on blood lipids: a systematic review and network meta-analysis.

 

1275539498_ScreenShot2020-10-04at21_23_07.png.5b6947cb77d43f3364f2a5a98bfb048a.png

 

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4 hours ago, Ron Put said:

my total fiber intake has not increased substantially,

The soluble fibers/lignans in flax might be particularly effective,  compared to just fiber  in general.   I've run out of time at the moment to look into it.

 

4 hours ago, Ron Put said:

, comparing olive oil with seed oils

Generic "olive oil" ≠ EVOO.       Multiple studies confirm the difference;   multiple studies  confirm  EVOO  decreases LDL,  decreases LDL oxidation, ,  promotes reverse cholesterol transport, and improves endothelial function.

In any case,  your  blood lipid levels are not a concern,  and you're not going to  be switching safflower oil, sunflower oil etc. into your diet, if for nothing else because  of your  concern about your AA /EPA ratio.    The whole issue seems overblown to me.

   Arguing about whether seed oils or generic olive are at best marginally better for lipid  levels is a waste of time, imo. If your lipid  levels are sub-optimal,  you need  to look at other causes and other solutions.

YMMV

Edited by Sibiriak

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1 hour ago, Ron Put said:

I was coming back to post something interesting I found, comparing olive oil with seed oils.  It appears that most seeds oils are better with respect to cholesterol:

Effects of oils and solid fats on blood lipids: a systematic review and network meta-analysis.

 

1275539498_ScreenShot2020-10-04at21_23_07.png.5b6947cb77d43f3364f2a5a98bfb048a.png

MMmmm..., only butter and sunflower oil satisfy the significance criterion, in all other data the CI of the mean includes the unity, so the correct interpretation of the above study would be that a generic olive oil (not a specific EVOO), whose secoiridoids content is unknown, is better than butter and a little worse than sunflower oil, as far as blood lipids go. All other comparisons are statistically not significant.

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Mmm, the problem with the above line of reasoning is that I haven't seen a significant difference between "olive oil" and EVOO, as far as I can remember. :)  Based on that, I personally take the claims of night and day difference between the two olive oil versions with some suspicion.

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I was a skeptic at first too Ron (a great health and scientific literacy quality I might add), but looking deeper into the matter, I ultimately came to the conclusion that while yet unproven, there are likely additional benefits ( not by oleic acid alone)!  
 

For a sense of perspective, if faced with a choice I would prioritize keeping EVOO (vs refined lower quality OO) much higher than the need for cold exposure . This, even and perhaps especially for those with substantial metabolic dysfunction & metobesity for whom there remains the greatest plausibility for material CE health outcome benefits.

The work since this 06’ classic paper (1) has done much more to support than to undermine the evidence:

https://onlinelibrary.wiley.com/doi/full/10.1111/j.1538-7836.2006.01963.x

(1) Pacheco YM, López S, Bermúdez B, Abia R, Muriana FJ. Extra-virgin vs. refined olive oil on postprandial hemostatic markers in healthy subjects. J Thromb Haemost. 2006 Jun;4(6):1421-2. doi: 10.1111/j.1538-7836.2006.01963.x. PMID: 16706995.

 

Edited by Mechanism

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On 10/5/2020 at 1:06 AM, mccoy said:

MMmmm..., only butter and sunflower oil satisfy the significance criterion, in all other data the CI of the mean includes the unity, so the correct interpretation of the above study would be that a generic olive oil (not a specific EVOO), whose secoiridoids content is unknown, is better than butter and a little worse than sunflower oil, as far as blood lipids go.

And here is a study discussing how sunflower oil reduces apoptosis in cardiomyocytes but unfortunately does so by increasing necrosis resulting in a much worse outcome...  At least the rats could die happy knowing their LDL was reduced.

Brief episode of STZ-induced hyperglycemia produces cardiac abnormalities in rats fed a diet rich in n-6 PUFA

Quote

In an effort to determine the elements that induce necrosis, we measured the cardiac free fatty acid species and determined that sunflower oil feeding increased cardiac n-6 PUFA, predominantly linoleic acid. In clinical studies, accumulation of linoleic acid has been strongly associated with an increased inflammatory response in endothelial cells, in addition to an augmented risk of myocardial infarction and necrosis (46). Additionally, in vitro, linoleic acid precipitates necrosis via proinflammatory pathways in various cell types (44, 45).

 

But what about in people?  Here's an analysis of the Sydney Diet Heart Study RCT:

Use of dietary linoleic acid for secondary prevention of coronary heart disease and death: evaluation of recovered data from the Sydney Diet Heart Study and updated meta-analysis

Quote

In this cohort, substituting dietary n-6 LA in place of SFA increased the risks of death from all causes, coronary heart disease, and cardiovascular disease. An updated meta-analysis of LA intervention trials showed no evidence of cardiovascular benefit. These findings could have important implications for worldwide dietary advice to substitute n-6 LA, or PUFAs in general, for SFA.

 

Edited by Todd Allen

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Todd, yet sunflower seeds oil may have its properties, like a high concentration of tocopherols. Also, whole sunflower seeds, as you surely know, are a mine of vitamins and minerals. 

My personal inclination at present is not to eat sunflower oil but eat 20-30 grams of sunflower seeds per day, in addition to other nuts and seeds, in addition to EVOO, in addition to peanut butter.

After all the above, there may be a little room in my stomach for SAFAs, which I will not disdain, in moderate amounts, pending the results of my next blood lipids analysis. 

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21 hours ago, Mechanism said:

The work since this 06’ classic paper (1) has done much more to support than to undermine the evidence:

https://onlinelibrary.wiley.com/doi/full/10.1111/j.1538-7836.2006.01963.x

(1) Pacheco YM, López S, Bermúdez B, Abia R, Muriana FJ. Extra-virgin vs. refined olive oil on postprandial hemostatic markers in healthy subjects. J Thromb Haemost. 2006 Jun;4(6):1421-2. doi: 10.1111/j.1538-7836.2006.01963.x. PMID: 16706995.

Mechanism, very interesting article and one of the few which clearly reports the content of polyphenols in the tested oils. Here EVOO has a huge amount of polyphenols (1125 mg kg-1) rarely seen in commercial oils. The trial has been designed in such a manner to isolate the effects of carotenoids-tocopherols and polyphenols  in EVOO, from the refined OO, where such compounds were absent (not detectable).

The amounts of oil administered are pretty large though. My body surface area is 1.8 m2, so they would have administered me 90 grams of EVOO, or ROO. Such a quantity goes way beyond what average guys can eat in a meal. I usually eat 30 to 40 grams of EVOO in a day, but very rarely in a single meal.

For people who wish to follow a ketogenic, plant-based diet though, 90 grams of EVOO per meal may be realistic, and it did not show adverse effects in the postprandial hemostatic system 

 

Quote

ROO was obtained by physical refining of EVOO and had no detected minor compounds with antioxidant activity, whereas the contents (in mg kg−1) of carotenoids, tocopherols and polyphenols in EVOO were 22, 350 and 1125, respectively. The fatty acid composition and TG molecular species were identical for EVOO and ROO. 

 

Edited by mccoy

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McCoy! Great to hear from you. Hope you and family are all well- and into Covid round 2+ ( if there ever was a lull).

yes, that’s a lot of EVOO- if nothing else places into context concerns re: FMD. Indeed, the initial reports may have been I. Part from using refined oil and without vitamins ( summary of those details here, worth the read for anyone not familiar): https://www.oliveoiltimes.com/world/uc-davis-researcher-advises-opt-out-of-olive-oil/51579

 

 

Regarding dosing in PREDIMED, “Participants in the group assigned to a Mediterranean diet with extra-virgin olive oil received 1 liter of the oil per week per household, with the recommendation to consume at least 4 tablespoons per day of extra-virgin olive oil per person” though real consumption was less (https://www.nejm.org/doi/full/10.1056/NEJMoa1800389).

I owe my initial introduction to EVOO to Michael. Though I think it is possible to have a healthy diet without EVOO, if choosing an oil, EVOO is the best bet.
 

MR’s choice?   “I insist on verifiably superior EVOO qualities: high (≥76%) oleic acid content (for oxidative stability, and see above on DHA-accelerated aging hypothesis: olives from different cultivars and regions can vary from 55-83% oleic acid); low peroxide value (<9, and preferably <6 meq/kg), and high (≥350 mg/kg) total phenolics, assayed using caffeic acid equivalents. ”

His own take on the literature and I do not disagree is: 

“The epidemiology strongly suggests 2-3 T/d. I get an average of 5-6 tsp (ie, 2 T or just a bit shy of it); I also get a lot of additional MUFA from nuts (also on 'the list'), Peruvian olives, and occasional avocado, tho' of course EVOO is not just a MUFA source.”

By contrast, Valter Longo - hedging his bets a bit the other way [ I won’t mention the flawed / lower quality low-far vegan school of thought data as not to invoke the ire of MR... though I would not dismiss it out of hand either] as a compromise, as detailed in his Longevity Diet book), has advised in the ballpark of 3T/d.   There is no perfect data out there but as a whole foods purist (I still prefer nuts!) I have been thoroughly persuaded harm, if any, is minor in the context of a healthy diet/lifestyle and that evidence and statistics favor moderate EVOO as a net positive in the vast majority of diets via in large part from polyphenols, MUFA, and substitution effect for low quality / high GL carbohydrates & “true” nasty refined elements.

Mechanism

 

Edited by Mechanism

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https://www.cardiovascularbusiness.com/topics/lipids-metabolic/ornish-beats-mediterranean-best-heart-healthy-diet

best diet for heart disease is not olive oil based.

BTW, contrary to what usnews criticizes it for I FIND IT much easier to follow than any diet I have ever been on. As a former obese food addict that is saying a lot. I literally have to work at keeping my weight from dropping. Why u might ask simply this. Fat is loaded with calories that one does not chew nor does it take up much space. High Fibre, whole plant foods are much more satisfying 

Edited by Mike41

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Fact is that we don't know if a low-fat diet has benefits over other diets. There are no trials that I know. Intuitively, low fat diets are high-carbs so they should be unfavourable to blood ar values. But again, who has proven or disproven this hypothesis?

And, it's not easy for everyone to eat lowfat. For example, all the nonfat dressings cited by Ornish in his recipes are not available in Italy.

 

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McCoy there is good reason why usnews chose the Ornish diet. It has the real evidence not junk predimed science comparing butter and cheese eaters to EVOO. They claim it’s SO SO hard to follow and that the Mediterranean is SO SO easy to follow and for that reason they are hesitant, but it is by far the most substantiated diet to reverse heart disease and all the other bad stuff that results from atherosclerosis. And anyone on this list that’s over 18 probably already has it even though they don’t know it. And that’s probably because it may not be in an advanced state. Hopefully!

Edited by Mike41

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On 11/8/2020 at 10:03 PM, Mike41 said:

They claim it’s SO SO hard to follow

I find it hard to follow and it may raise blood sugar. Nothing is usually as good as the hardcore supporters like to present it.

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I’ve checked my blood sugar multiple times 35% fat vs 15% no difference whatsoever. Each person would need to do this of course. The key here is whole plant based high Fibre, but if one compares say nuts to white bread or say cheese and white bread or crackers etc. of course those carbs will look awful glucose wise. The whole anti carb thing is basically a problem of putting all carbs in one basket which of course is very misleading.

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I would add that of course finding a diet that works for you personally is crucial to successfully following it. Hopefully that embodies a whole, minimally processed strategy.

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