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Saturated fat - a skeptic's view

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( Disclaimer: I'm not the skeptic!)

 

There was a terrific must-read AHA paper cited earlier by Al Pater intended to address the saturated fat debate which concluded saturated fats should be replaced by unsaturated fats to reduce the risk of CHD: http://circ.ahajournals.org/content/early/2017/06/15/CIR.0000000000000510

 

I just stumbled upon a must-listen to rebuttal ( which I hasten to add I do not advocate ) made by Chris Masterjohn. Although I am not convinced, I find it quite persuasive in instilling skepticism or at least some measure of reserving full judgement:

 

https://chrismasterjohnphd.com/2017/06/24/coconut-oil-killing-us/.

 

I would cheer on front row seats of a debate between Chris Masterjohn and MichaelR on this one!

Edited by Mechanism

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I agree that the sat fat controversy is interesting. 

 

Found this piece, all all places, from the paleo mom blog and was impressed with the balanced presentation.

https://www.thepaleomom.com/saturated-fat-healthful-harmful-or-somewhere-in-between/.

 

She starts off giving sat. fat a break but when the article is said and done the take away is far more con than pro.

 

I like the article cause it's a good review on sat fat from a number of different evidentury lines. 

 

I look forward to listening to Masterjohn's presentation. He's an interesting fellow. As I recall as a graduate student, he felt lousy eating a standard good diet.

After discovering Weston Price and adopting his ancestral diet ideas his physical woes were resolved. He's been try to give scientific credence to Price's ideas since.

 

Randy

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I believe that probably the proof lies in the pudding, at least from the CVD standpoint.

 

IF the lipids profile is all right, then it means that even a high consumption of SA fats does not impinge much upon the individual CV health (may not apply to other health hazards). In the Paleomom blog the author cites Dr Attia's references to individuals on a keto diet whose lipids would skyrocket.

 

On the other hand, on a podcast Dr. Esseltsyn cited one of his patients on a very low fat diet, no saturated fats, whose cholesterol could not drop below 200 mg/dL.

 

Individual response appears to govern.

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Thank you Randy, nice I agree fairly balanced article and an enjoyable read. I was not aware of some of the indiginous population data, specifically the carbohydrate content of blubber. Good quality info though I am not aware of strong causative data between mood ateratikns and low fat diet but thought this was based mostly on observational data rather than experimental designs that can better establish causality. If there are other resins to avoid excess PUFA, and I agree with these.

 

Given the RCT data highlighted by the AHA, I am more conservative for the time being, keeping my SFA lower than advised by this author ( < 10%).

 

Paleo Mom cites mostly a combination of animal model studies, basic science, and human natural populations observational studies. I prefer quality RCTs when available which is what the AHA used for its recommendations. What I find interesting is that though based on quality designs for the most part, Chris Masterjohn in his podcast raised some design nuance arguments to cast doubt on the validity I'd the RCTs meeting the inclusion criteria of their analysis. There was one not included he felt was higher quality. Confidence in the conclusion hinges on quality of the studies and if these proposed problems confounded the results, a null or inverse or worse yet association may be expected from the meta-analysis. The methodology appears to be far more controversial and precarious than first meets the eye - this is where a good debate can sometimes be helpful In arriving at a balanced perspective.

 

For my part it just makes me stick more with nuts / seeds / avocado / olives / some EVOO since both SFA and PUFA have their controversy -- even with epidemiology suggesting PUFA is superior to MUFA as the replacement fat in most of the point estimates from these meta-analysis when examining CHD as the outcome of concern ( note: possible malignancy & hepatic steatosis associations with PUFA but this is another matter). MichaelR's accelerated aging hypothesis also is consistent with this ( MUFA better than PUFA folllowing edequate EFA intake) approach.

Edited by Mechanism

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Weston Price is a crank, and anyone who bases their theories on him, does not enhance their credibility. That said, the whole fatty acids science is in a state of flux and firm recommendations are hard to come by. I always keep in mind that there appears tremendous personal variation to such dietary components, perhaps due to microbiome or whatnot. I personally avoid SFA like the plague (including stearic acid which supposedly does not elevate LDL as much as other SFA), but my LDL is persistently elevated no matter what I do (high 120's), so combined with my high HDL, my TC is pushed above 200 (I have never gotten it below 203 or so). So there you go - I avoid SFA but my LDL is still through the roof, I exercise, and my LDL is still through the roof, I consume metric tons of fiber (including daily psyllium), and my LDL is through the roof - the point being, is that how your particular body reacts to SFA may be completely different from what the statistical construct of the "average" person does in all those studies of FA (and the same for individual reactions to exercise or any other lifestyle component). We are different. Getting hung up on f.ex. exercise, when you are seeing no results only leads to futile frustration - I have a friend who exercises diligently, and seems only the worse for it - I pointed out to him that there are many studies showing that some 20% of people are non-responders to exercise, and some for whom exercise seems to actually end up being a negative (worse blood sugar control!). So just because you read all those studies showing the benefits of exercise doesn't mean you should conclude that it will definitely apply to you. Eskimos and Himalayans apparently react differently to FA in general - but even if you are not a member of those ethnic groups, you may react to dietary FA in ways contrary to study results.

 

Bottom line - it's not just about whether there exists a scientific consensus abou the health effects of dietary SFA, it's about whether those findings apply to you, or to what degree they may or may not. In short, dietary science, including SFA, is a land of contrasts (is how we end our high school papers).

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Some get high LDL from their diet, but your body itself produces about 75% of the LDL in it at any given time, so for some high LDL is a result of their body either producing too much LDL or not efficiently destroying excess LDL, there are a number of genetic defects related to this and as far as genetic defects go, these are pretty common (1 in 400 at a minimum).

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I think that in the whole CV-Health subject it is difficult to tell which is correlation and which is causation.

 

From what I learned from various sources, the image presented to me is that both the saturated-fat-intake as well as the levels of LDL-cholesterol are biomarkers that predict the occurrence of CV-events but are not the inherent cause of it.

 

Elevated LDL levels in the absence of dietary cholesterol simply means an adjustment to fat-metabolism. LDL and HDL are Lipoproteins, which means they are fat-ferries that are used to deposit fat in the tissue or bring it from the tissue to the liver in order to be converted into ketone-bodies.

 

People who are losing weight will always have increased levels of that even if they don't consume fat simply because the fat needs to be ferried to the liver.

 

For some reason I can't paste a link here, but there's relatively recent science looking at the role of TMAOs in the development of CV. TMAOs are an inflammation-inducing waste-product produced by certain types of gut-bacteria when digesting certain types of food. This type of gut-bacteria is mostly non-existent in the guts of people eating a plant-based-diet which would offer an alternative explanation for the difference in CV-rates between them and others apart from both saturated fat and cholesterol.

Edited by AIL

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Hi Tom, great points on bioindividuality. Though the kind of extreme variation in lipid metabolism such as seen in the intuit and Polynesian populations are rare and more associated with isolated populations - hence in my assessment there still some value for general recommendations such as put out by AHA, ADA, etc. - there'res enough variation that you need to see if it applies to you, and looking at biomarker responses is one helpful modality. Another example: in lipid metabolism, FTO gene variants make some more vulnerable to fat, ESP saturated fat. I happen have a rare PPAR-gamma mutation myself which also influences this, and appreciated your sharing your own situation with your elevated LDL with presumably other genetic and/or epigenetic +/- microbiome influences. Though I suppose in your case it does not change the advice ( what you are doing with exercise may not help much but it does not hurt and probably helps at least a little ... have you tried a variation of this diet - more powerful than statins: https://www.crsociety.org/topic/11672-near-perfect-diet-study/page-1. ).

 

Thanks for the stats / link Gordo... I suspect TomB has other (epi)genetic influences though I cannot rule out a milder familial hypercholesterolemia, which for many of them have far more dramatic ( average) lipid panel numbers than he reported. The only way to tell is to map out the SNPs and see. Your excellent point stands & I agree again re: the importance of individual differences in interpreting recommendations for "average" members of a population.

 

The saturated fat is not bad ( or even good) camp often make the argument that LDL is a poor surrogate variable for mortality and go in, usually reminding us the important roles cholesterol plays in immune function and membrane fluidity including in the brain, to emphasize they think high LDL is fine as long as it doesn't get oxidized so is just fine with an anti-inflammatory diet.

 

Has anyone here listened to the full podcast I linked to above? It is really quite interesting. I agree that Weston Price appears to be centered around an ideology and literature not always evidence based, but Chris Masterjohn's argument was of interest as I was not aware of the apparently significant in some cases confounders in the major studies comprising the backbone of the AHA meta-analysis.

 

If the arguments from the full podcast link in my original post are believable they raise a real concern that the AHA saturated fat recommendations may be premature or misguided - individual genetic or microbiome considerations aside. This is where the perspective of other researchers in the field ( how serious are the study design faults Dr Masterjohn raised?) would be helpful.

 

AIL, thank you I have seen the TMAO work, this could translate to another mechanism whereby saturated fat can be deleterious through that camp also is quick to point out cooking method cooking with veggies, vinegar, etc. mitigate the TMAO rise with these food sources. For my part I play cautious avoiding too much SFA and avoiding too much PUFA but started the thread to address / dialogue Chris Masterjohns's specific methodologic criticims of the methodology employed in the RCTs comprising the AHA meta-analysis on which they based the recommendation to replace SFA with unsaturated fat.

Edited by Mechanism

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( Disclaimer: I'm not the skeptic!)

 

There was a terrific must-read AHA paper cited earlier by Al Pater intended to address the saturated fat debate which concluded saturated fats should be replaced by unsaturated fats to reduce the risk of CHD: http://circ.ahajournals.org/content/early/2017/06/15/CIR.0000000000000510

 

I just stumbled upon a must-listen to rebuttal ( which I hasten to add I do not advocate ) made by Chris Masterjohn. Although I am not convinced, I find it quite persuasive in instilling skepticism or at least some measure of reserving full judgement:

 

https://chrismasterjohnphd.com/2017/06/24/coconut-oil-killing-us/.

 

I would cheer on front row seats of a debate between Chris Masterjohn and MichaelR on this one!

 

From the AHA paper:  Replacement of saturated with unsaturated fats lowers low-density lipoprotein cholesterol, a cause of atherosclerosis, linking biological evidence with incidence of CVD in populations and in clinical trials.

 

But here's a meta study that suggests high LDL is not so bad:

Lack of an association or an inverse association between low-density-lipoprotein cholesterol and mortality in the elderly: a systematic review

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4908872/

 

I think the discussion in the Chris Masterjohn podcast of recent research pointing to oxidized LDL as the bigger culprit might eventually resolve some of the conflicting evidence on LDL.

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I eat cacao nibs every day. They provide the bulk of my 20g-22g per day saturated fat intake (flax is in a relatively distant second place). I just read another study about saturated fat:

"Not all saturated fats are equal when it comes to heart health

People whose diets contain relatively little palmitic and stearic acid -- saturated fats composed of 16 or more carbon atoms (longer-chain saturated fats) that are typically found in meats -- and eat plant-based proteins instead have decreased chances of myocardial infarction."

Part of me is wondering if I should cut down on cacao nibs and maybe switch to cacao powder, which contains considerably less saturated fat. Notably, cacao beans (and nibs) contain precisely stearic and palmitic fats and while proportionately lower than beef, the fat profile of cacao nibs is apparently close to the of mutton (I read this somewhere). 😞

On the other hand, I also seem to recall reading that the stearic and palmitic fats in cacao nibs have much lower bioavailability than animal fats.

Since I've started trying to maintain my Omega-3 and Omega-6 ratio at 1:1, my total cholesterol has dropped to the low 150s and my LDL/HDL ratio is 1:1. My average fat intake is about 34% and 143% of what Cronometer suggests as minimum daily value.

I am happy with this, so I am leery of tinkering with what I do and abandoning cacao nibs in favor of cacao powder (I initially switched to nibs because they are a more "whole" food and also because powders generally have higher cadmium/lead content.

Any input from anyone who may have considered this?

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Ron, your blood lipids are apparently pretty good, so why are you thinking about changing a regime which is already optimized?

The lipids scenario is confused, but, as I wrote in an earlier post, the proof lies in the pudding. Whatever lipids you are eating, if your inflammation markers are all right, your lipid markers are all right, then what you are eating is all right for you.

One word of caution for those who support the paleo narrative is that one of the most renowned, if not the most renowned practical and experimental specialist in preventive medicine applied to longevity, Dr. Peter Attia (not a low-fat activist, on the contrary), does believe that blood lipids are important for CVD prevention. actually, he gives pretty stringent guidelines as far as triglicerides and LDL are concerned.

 

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It's interesting how the low-carbers are reviewing some of their previous fanatical assertions, in a more moderate and sensible way. I still receive e-mails from the diet doctor site, the main low-carbers site to which I used to subscribe. Just today I received this one, which warns that even low carbers should mind their LDL, if it shows too high in blood analyses.

A little while ago I received a similar article stating that even low carbers should mind their calories: myths shattered, in a self-criticizing way, which is good after all.

 

Quote

 

Does LDL matter for our heart health?

Many social media posts suggest that LDL is irrelevant for low-carb eaters. Interestingly, for most of us, dismissing LDL as a heart disease risk factor is just not necessary to justify low carb because most research studies show that LDL does not increase on a low-carb diet.

But what about when LDL does go up? Should we be concerned?

A new study published in JAMA says yes, we should pay attention to lifetime exposure to LDL as well as systolic blood pressure (the higher number of a blood pressure reading).

JAMA: Association of genetic variants related to combined exposure to lower low-density lipoproteins and lower systolic blood pressure with lifetime risk of cardiovascular disease

The study is a so-called Mendelian randomization study. This is a bit of a misnomer, as there is no real randomization, but since it looks at people with different genetic markers, it is considered that they were “randomized” at birth based on who has certain genetic traits and who does not. The authors put this into perspective by saying:

Ideally, this question would be addressed by conducting a randomized trial to minimize the effect of confounding that can occur in observational studies. However, a randomized trial evaluating the association between maintaining prolonged exposure to both lower LDL-C levels and lower SBP with the risk of cardiovascular disease would take several decades to complete, and therefore is unlikely to ever be conducted.

The study evaluated over 430,000 subjects with a mean age of 65 with follow up ranging from 8 to 12 years (but since these were genetic differences, the assumption was that they had these traits since birth and therefore the follow up is six or more decades). Those with genetic predisposition towards lower LDL cholesterol levels, on average 15mg/dl lower, had a 26% relative lower risk of a cardiac event (defined as either a heart attack, stent or cardiac death). In addition, those with a genetic tendency toward lower blood pressure, on average 3 mmHg, had a 17% relative decreased risk of cardiac events.

That all seems straight forward and suggests that lifelong exposure to lower LDL and lower blood pressure reduced cardiac events. But now for the trickier part. What about overall mortality? A study this size is perfect for reporting overall mortality risk, not just cardiac events. But that was not done.

Although knowing the relative risks is nice, what were the absolute risks? Did the risk of a cardiac event go from 2.00% to 1.48%? Or from 30.0% to 22.2%? Both of these examples represent 26% reductions, but they mean something very different to the individual.

Another reasonable question is how much can we generalize these findings to those without a genetic predisposition to lower LDL or blood pressure? The authors recognize this nuance with the following quote:

This study does not provide evidence that outcomes associated with intrinsic physiological findings, such as naturally occurring lower levels of LDL-C or SBP, are the same as outcomes that would be associated with extrinsic drug treatment or other interventions to achieve similar plasma LDL-C or SBP levels.

While their data supports the LDL hypothesis, it does not speak to whether or not lowering LDL with drugs would be beneficial.

Also, what about the subjects’ baseline health? Since this was essentially a “randomized” trial, all of the baseline data was the same, so we don’t have to worry about healthy user bias or obvious confounding variables.

However, the baseline TG:HDL ratio of the group averaged 2.7. That is a potential marker of insulin resistance or metabolic dysfunction. Other studies have shown that the correlation of LDL with heart disease depends on HDL levels and TG:HDL ratios. Would these results be different in subjects with TG:HDL ratios of 1 or less? Or in those following a healthy low-carb diet? I sure would like to know the answer to those questions!!!

In the absence of those answers, however, we have to register this new data as a result that favors paying attention to LDL and blood pressure rather than dismissing either as categorically unimportant. While that may be an unpopular conclusion in the low-carb world, it is still supported by certain lines of evidence.

Make sure you discuss your lipids, blood pressure and overall health with your physician to find out what the right approach is for you!

Thanks for reading,
Bret Scher, MD FACC

 

 

Edited by mccoy

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Ron,   I basically agree with Mccoy.   I don't see the palmitic acid being a problem given you don't have  elevated LDL-C levels, and your overall fat intake seems okay.

 

Quote

The oil in cacao, referred to as cocoa butter, is a mixture of monounsaturated and saturated fatty acids. In the monounsaturated fraction, oleic acid predominates, as it does in olive oil (26). The majority of the saturated fatty acids are palmitic acid and stearic acid. In general, saturated fatty acid consumption has been associated with an increased risk of coronary heart disease as saturated fatty acids elevate total cholesterol and LDL (10, 280). A single meal containing relatively high levels of saturated fat may destabilize coronary plaque and impair endothelial function (128, 198, 275). Stearic acid is unusual in that it does not elevate serum lipid levels to the same degree that other saturated fatty acids do (112). Thus, whereas shorter-chain saturated fatty acids such as myristic acid (14:0) and palmitic acid (16:0) are associated with increased LDL and atherogenesis, stearic acid is not (32, 124, 223). Although the lipid content of chocolate is relatively high, one-third of the lipids in cocoa butter is stearic acid (18:0), which is believed to be nonatherogenic and to exert a neutral cholesterolemic response in humans (26). The 2010 Dietary Guidelines Advisory Committee specifically acknowledged stearic acid's unusual nature and has recommended that it be considered separately from cholesterol-raising fats (262).   https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4696435/

On the other hand,  if you still ascribe to the Pritikin-promoted theory you defended during the discussion on olive oil -- that all dietary fat intake is essentially  bad for cardiovascular health and should therefore be minimized-- it would be logical for you  to lower your fat intake by consuming cocoa powder rather than nibs.

Personally, since I eat a reasonable amount of nuts and olive oil and would prefer not to have the added fat and calories from cacao nibs,  I consume a modest amount of low-fat cocoa powder, sometimes augmented with cocoa flavanol extracts (eg. CocoaWell or CocoaVia).

Estimates for flavanol  (and procyanidin) intake by the Kuna people  go as high as 1,880 mg/day,   while cocoa flavanol studies typically use dosages around 900 mg/day.    Unless I am mistaken,  you  need to eat a lot of cocoa powder, nibs, chocolate etc.  to get those kinds of levels.  That's something that doesn't fit well with my eating patterns,  not to mention the potential problems with cadmium and/or fat intake.   In any case,  I believe there are other routes to optimal cardiovascular health apart from the Kuna approach.  (Also,  my  skepticism is triggered a bit by the fact that so much of the cacao research and cacao hype is funded by chocolate companies such as Hershey and Mars.)

Obviously it's  a personal choice.  Mccoy, for example,  is sitting in an Italian villa eating mountains of cacao  mashed into luscious bananas, dressed as a Kuna bride.   He's in cacao heaven!

 

Edited by Sibiriak

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3 hours ago, Sibiriak said:

Obviously it's  a personal choice.  Mccoy, for example,  is sitting in an Italian villa eating mountains of cacao  mashed into luscious bananas, dressed as a Kuna bride.   He's in cacao heaven!

Sibiriak, I wish it were as picturesque as you depicted it!

I'm restraining myself now, rarely going beyond 40 grams daily of cacao powder. Plus some dark chocolate. Fact is that unprocessed cacao is pretty flavanol-dense and that tends to satiate, probably a neurological signal which reminds to remain within the hormetic region. 

Ron, there are defatted cocoa powders which are very low in fats, but I never tasted them, they're not available here. Also I don't know if you can find defatted+undutched, but it is probably worth some search time. The article posted by Sibiriak on stearic acid is very interesting, the issue would then be just the energy balance.

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5 hours ago, Sibiriak said:

I basically agree with Mccoy.   I don't see the palmitic acid being a problem given you don't have  elevated LDL-C levels, and your overall fat intake seems okay.

 

1 hour ago, mccoy said:

there are defatted cocoa powders which are very low in fats, but I never tasted them, they're not available here. Also I don't know if you can find defatted+undutched, but it is probably worth some search time. The article posted by Sibiriak on stearic acid is very interesting, the issue would then be just the energy balance.

Thank you both. I think I am going to stick to my cacao nibs, fat and all. Part of the reason why minimally processed cacao ends up in the beneficial column overall may be that the high fiber content limits gut absorption of lipids.

Also, I am thinking that cacao nibs, even when chewed, are not easily digested and the fats are not easily absorbed.

For what it's worth, my uBiome results (excerpts of which I posted elsewhere) indicates that overall my microflora is a bit less efficient in absorbing fats, too. So, I am about to order another large bag of nibs -- I also really like the crunchy texture and the taste, when consumed with a banana and a few walnuts 🙂

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Mccoy: Fact is that unprocessed cacao is pretty flavanol-dense

I'm curious, do you happen to know the flavanol mg/g content of the product your  using?  

I was just looking at  Navitas Organic Cacao Nibs at iHerb.com

Quote

Contains 23 mg of Flavanols per serving [30g]

And Navitas Organic Cacao Powder
 

Quote

Contains 17 mg of Flavanols per serving [15g]

Seems pretty low,  and if I'm not mistaken doesn't match the info from the 2014 Consumer Lab report posted here.

Realistically,  should you expect to get something like  30mg/g flavanols from an unprocessed cacao/cocoa powder? 

Edited by Sibiriak

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Sibiriak, I've not the data for the El Ceibo cacao I'm consuming. I can tell you it's pretty rich in flavanols by its taste, which is significantly bitter, astringent and pungent but of course the exact amount is not detectable by the taste buds. I collected some statistical data and posted elsewhere from literature but I have to retrieve them and check them, since the flavanols include diversified groups of molecules like catechins and epicatechins, but the latter are the most characteristic of cacao. We can obtain more catechins from tea, although it must be seen if they (epigallocatechingallate) are the same as the catechins in cocoa.

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According to Comer Lab, Navitas nibs contain about 35.3 mg/g of flavanols and Navitas powder contains about 25.8.

But my understanding is that cacao is very nutritionally complex, so I'd be leery of focusing on just one aspect of it.

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I retrieved the Andres-Lacueva et al. 2008 article, which I'll start posting now with a few quick comments to develop later.

Flavanols (catechins and epicatechins) are by far higher than flavonols. Epicatechins average thrice the concentration of catechins in undutched powders, and the epicatechine content in undutched powders (2 mg/g) is over thrice the content in alkalized powders (0.6 mg/g).

The overall, average content in flavanols in natural (unprocessed) cacao powders is 1.9+0.6 = 2.5 mg/g.

  •  a 15 g serving = 37.5 mg flavanols
  • a 30 g serving = 75 mg flavanols

which is more than twice the amount of the data cited by Sibiriak.

Re complexity: probably there is some unknown synergy within compounds, some flavonols could increase the efficacy of flavanols, and there are also caffeine and theobromine which could provide the overall effect of this formidable cocktail of phytochemicals.

 

 

image.png.0712fe4d1464072f4765cf374b3b6542.png

 

Edited by mccoy

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Mccoy: The overall, average content in flavanols in natural (unprocessed) cacao powders is 1.9+0.6 = 2.5 mg/g.

Ron Put: According to Comer Lab, Navitas nibs contain about 35.3 mg/g of flavanols and Navitas powder contains about 25.8.

That's quite a disparity.   Perhaps it can be explained by the distinction between   "cocoa powder," which is roasted, and "raw cacao powder",  which is unroasted   (sun-dried, cold-pressed),  discussed previously here.    Roasting arguably diminishes polyphenol content.

At 2.5mg/g it would take a whopping 360 grams of non-alkalized cocoa powder to obtain the minimal 900 mg/d of flavanols attributed to the Kuna (is that correct?)  and used in various cocoa flavanol studies like this one cited by Dean Pomerleau.   At 25.8 mg/g it would take only about 35 g of raw cacao powder (still a lot).

FWIW,  in this Hershey Co. funded study  the non-alkalized  cocoa powder  tested produced these results:

image.png.cd8c860fc66610621b62f9f18cb825e3.png

 

 
Quote
Figure 1

Antioxidant capacity and polyphenol and flavanol content of various fruit powders. A. ORAC antioxidant capacity per gram of various fruit powders. Acai, acai powder; Blue, blueberry powder; Cran, cranberry powder; Pom, pomegranate powder; Cocoa, cocoa powder. Data are expressed as the mean ± SEM. Columns not sharing superscripts are significantly different, p > 0.05. B. Total polyphenol content measured in gallic acid equivalents per gram of various fruit powders. Acai, acai powder; Blue, blueberry powder; Cran, cranberry powder; Pom, pomegranate powder; Cocoa, cocoa powder. Data are expressed as the mean ± SEM. Columns not sharing superscripts are significantly different, p > 0.05. C. Total flavanol content per gram of various fruit powders by the DMAC method. Acai, acai powder; Blue, blueberry powder; Cran, cranberry powder; Pom, pomegranate powder; Cocoa, cocoa powder. Data are expressed as the mean ± SEM. Columns not sharing superscripts are significantly different, p > 0.05.

 

In any case,  if  you wanted to substantially increase your cocoa flavanol intake while minimizing fats and/or cadmium,  one way would be add in some concentrated cocoa powder extract, such as CocoaVia:

image.png.71f85dfb64eaae32203bc4245ebecf41.png

 

One does have to ask, however,    if you're already eating a  very polyphenol rich diet,  is it really necessary or advisable to add in on top of that the super  high cocoa flavanol intake of the Kuna people?    There does come a point, presumably,  when polyphenol intake  becomes  excessive and counterproductive.

Edited by Sibiriak

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While the saturated fat debate rages on, often rife with oversimplifications,  one thing has become clear to me:  atherosclerosis is an extemely  complex,  multifactorial inflammatory disease.  Recently,  researchers have been studying the role of M2 macrophages.    The following article is long and dense and  goes into this in great detail:

M2 Macrophages as a Potential Target for Antiatherosclerosis Treatment (2019)

 

Quote

Abstract

Atherosclerosis is a chronic progressive inflammation course, which could induce life-threatening diseases such as stroke and myocardial infarction. Optimal medical treatments for atherosclerotic risk factors with current antihypertensive and lipid-lowering drugs (for example, statins) are widely used in clinical practice. However, many patients with established disease still continue to have recurrent cardiovascular events in spite of treatment with a state-of-the-art therapy. Atherosclerotic cardiovascular disease (ASCVD) remains the leading cause of mortality worldwide. Hence, current treatment of atherosclerosis is still far from being satisfactory.

Recently, M2 macrophages have been found associated with atherosclerosis regression. The M2 phenotype can secrete anti-inflammatory factors such as IL-10 and TGF-β, promote tissue remodeling and repairing through collagen formation, and clear dying cells and debris by efferocytosis. Therefore, modulators targeting macrophages' polarization to the M2 phenotype could be another promising treatment strategy for atherosclerosis. Two main signaling pathways, the Akt/mTORC/LXR pathway and the JAK/STAT6 pathway, are found playing important roles in M2 polarization.

In addition, researchers have reported several potential approaches to modulate M2 polarization. Inhibiting or activating some kinds of enzymes, affecting transcription factors, or acting on several membrane receptors could regulate the polarization of the M2 phenotype. Besides, biomolecules, for example vitamin D, were found to affect the process of M2 polarization. Pomegranate juice could promote M2 polarization via unclear mechanism. In this review, we will discuss how M2 macrophages affect atherosclerosis regression, signal transduction in M2 polarization, and outline potential targets and compounds that affect M2 polarization, thus controlling the progress of atherosclerosis.

image.png.b812b716c3b4b85cab8f2ec89ac4fee3.png

How M2 macrophages affect atherosclerosis development.

 

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(8) Conjugated Linoleic Acid (CLA). Conjugated linoleic acid (CLA) which was first found to inhibit chemically induced cancer has been reported to regress atherosclerosis plaques by some researchers [166168]. McCarthy et al. indicated further that CLA supplementation increased IL-10 expression and induced macrophages to skew to an anti-inflammatory M2 phenotype in vitro or in vivo [169]. In addition, CLA can act as an agonist of PPARs and is involved in modulating inflammation. Bruen et al. recently reported that CLA reduced the level of the M1 macrophage marker CD68 and alleviated some M2 markers including CD163 and mannose receptors in human peripheral blood mononuclear cell-derived macrophages [170]. Besides, they confirmed that CLA could limit foam cell formation, reduce inflammation mediators, and affect atherosclerosis lesion development. This suggest CLA as a potential compound for atherosclerosis treatment.

 

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(10) Pomegranate Juice and Polyphenols. In the evidence of the anti-inflammation function of pomegranate, Aharoni et al. investigated the association of pomegranate juice (PJ) as well as its polyphenols and macrophage phenotypes [174]. They reported that the secretion of IL-10 was promoted by PJ and polyphenols in a dose-dependent manner. Mice supplemented with PJ, comparing to the control group supplemented with water, showed a 36% decrease and a 41% decrease in TNFα secretion and IL-6 secretion, respectively, indicating a macrophage shift towards the M2 phenotype. Besides, ApoE-KO mice treated with PJ decreased the progressive inflammation in the aorta atherosclerotic lesion with aging. The study suggests that PJ or its polyphenols may result in macrophage polarization towards the M2 phenotype and lead to antiatherosclerosis effect.

Edited by Sibiriak

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On 9/13/2019 at 9:55 PM, Ron Put said:

According to Comer Lab, Navitas nibs contain about 35.3 mg/g of flavanols and Navitas powder contains about 25.8.

Are those mg/serving or mg/g? It would seem it's the former

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1 hour ago, Sibiriak said:

At 2.5mg/g it would take a whopping 360 grams of non-alkalized cocoa powder to obtain the minimal 900 mg/d of flavanols attributed to the Kuna (is that correct?)  and used in various cocoa flavanol studies like this one cited by Dean Pomerleau.   At 25.8 mg/g it would take only about 35 g of raw cacao powder (still a lot).

I checked the original article: 

 
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J Am Soc Hypertens. Author manuscript; available in PMC 2013 Nov 20.
 
Published in final edited form as:
PMCID: PMC3835452
NIHMSID: NIHMS525697
PMID: 20409950

Flavanols, the Kuna, Cocoa Consumption, and Nitric Oxide

Norman K. Hollenberg, M.D., Ph.D.,1 Naomi D.L. Fisher, M.D.,2 and Marjorie L. McCullough, Sc.D., R.D.3

 

 
 
The authors write:
 
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Kuna cocoa sources (home-grown and Columbian cocoa powder) were shown to be high in certain flavonoids, especially the flavanols and procyanidins (7, 8). We estimate that the Kuna consume approximately 1,880 mg per day. The several glasses of cocoa consumed daily by island-dwelling Kuna leads to what is probably the highest flavanol intake of any community on earth.

They add:

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The cocoa “dose” employed was that calculated from our studies in the Kuna to provide about 900 mg of epicatechin per day. 

 

So clearly, from the Lacueva et al statistical analysis of natural cacaco powder, containing 2000 micrograms/g epicatechin = 2 mg/g epicatechin on average, it would ensue that the kuna indians ate 450 grams of cacao powder per day (one pound!!) which would appear to be an absurdely inordinate amount.

So I don't know what to say, maybe the units in the Hollenberg et al. article are wrong. Maybe the Kuna Indians really went over the board with that.

To me, that quantity would surely fall into the toxicity domain. 

 

Edited by mccoy

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