Welcome all seeking refuge from low carb dogma!

~ Charles Darwin (it's evolutionary baybeee!)

Saturday, March 7, 2015

Nina Teicholz Distorts the Fatty Acid Content of Wild Animals

direct link  African Buffalo
I have recently revisited Chapter 1, The Fat Paradox, in The Big Fat Surprise, and it's safe to say that Nina Teicholz's contentions about the diets of Native Americans are grossly inaccurate.  The "all the Indians ate meat" is rounded out by a British physician named Prentice who visited South Central Africa and attributed rampant meat eating to the natives there as well.  An then (begins at location 327 of 12033 in Kindle version):

... no savvy heart disease researcher can read these historical observations without raising a standard and reasonable objection, namely, that the meat from today’s domesticated animals is far more fatty— and a greater proportion of that fat is saturated— than was the meat from wild animals roaming around a hundred years ago. Experts argue that the meat from wild animals contained a higher proportion of polyunsaturated fats, which are the type found in vegetable oils and fish. IV  If wild animals contained less saturated fat, the argument goes, then early carnivorous populations would have consumed less of this fat than people eating meat from domesticated animals today.
Let's pause to object to the use of the term carnivorous.  Most human cultures, even tribes who based their diets on buffalo, were not carnivores.  Humans have been, and always will be, highly adaptable omnivores who will eat an all animal diet only if forced to by the environment.  Even then, as soon as contact is made with other cultures, this funny thing called trade always seems to happen to both bring variety and alleviate periods of extreme scarcity -- e.g. starvation.  

Let's also be instructed by Nina by her rare numbered-inline footnote:
IV. This objection reflects a reality about meat— that it contains a mixture of different kinds of fats . Half the fat in a typical cut of beef, for example, is unsaturated, and most of that fat is the same type (monounsaturated) that is found in olive oil.  Half of chicken fat is unsaturated, and 60 percent of lard is unsaturated. (Asserting that animal fats are synonymous with saturated fats is, therefore, a simplification, although because saturated fats are found mainly in animal foods, I will also resort to the same simplification in this book, for the sake of brevity.)
Ahh yes.  Those who counsel eating less animal food/fat as a means to lower saturated fats are oversimplifying things.  Those unscientific fools are trying to mislead you because Large Lardo didn't have the money to wine and dine folks like Big Olive did.   She, on the other hand, will take any shortcut she needs for brevity.  That's allowed you see.  And yet, as she fails to achieve brevity, she uses the simplification to distort facts over, and over, and over ... throughout the book.  Realize that the end of her Introduction includes a chart of fat sources (incomplete -- missing some obvious sources such as nuts and avocados -- and  inaccurate -- canola is over 60% MUFA, ~20% O6, ~10% O3 PUFA but she lists it under O6 PUFA while MUFA source lard is less than 50% MUFA)  before she launches into a listing of populations whom she claims eat mostly meat (listed on that chart under saturated fat).  The reader is reminded these are saturated with the Masai.  There is no mention that the fat the Inuit ate is highly UNsaturated.    But ... Now Teicholz is going to set the record straight on this wild animal are full of PUFA nonsense!

It is true that American beef from a cow raised on grain does have a different fatty-acid profile from an ox hunted in the wild. In 1968, the English biochemist Michael Crawford was the first to look at this question in detail. He had the Uganda Game Department send him the muscle meat from various kinds of exotic animals: the eland, hartebeest, topi, and warthog, plus a giraffe and a few others. He compared these meats to those of domesticated cows, chickens, and pigs in England and reported that the meat of the wild animals contained ten times more polyunsaturated fats than did the flesh of domesticated ones. Thus, on its surface, his paper seemed to confirm that modern-day people should not consider their domesticated meat to be anywhere near as healthy as hunted meat from the wild. And for the past forty-five years, Crawford’s paper has been widely cited, forming the general view of the subject.
As the paleos continue to fawn over the dairy fat promoting Teicholz, they ought to check their own grassfed tales ...  But the bolded part above is the set up.  Before I go on, here is the study to which she refers:  FATTY-ACID RATIOS IN FREE-LIVINGAND DOMESTIC ANIMALSPossible Implications for Atheroma.  Lancet, June 1968.  (request access)

You see, all of those *others* who cite Crawford in lock step following the mainstream line are doing just that ... blindly going along with the crowd.  And now for the main act in the center ring, Nina Teicholz will distort the work of yet another scientist while besmirching his character with her innuendo.  It's quite an act!!
What Crawford buries in his data, however, is that the saturated fat content of the wild and domesticated animal meats hardly differed at all.  In other words, the factor that was supposedly dangerous in red meat was no higher in the English cows and pigs than it was in Uganda’s beasts. 
No.  Crawford did NOT bury anything in his data.  The above is wrong.  For someone so fluent in percentage of percentages math, Teicholz is pretty bad at recognizing when applying some might be appropriate.  From Crawford:

Lipid Content of Meats, Wild and Domestic

Of note, this is the "muscle meat" with the usually associated fat from the butcher.   Even when the domestic meat is meticulously separated from any visible fat, e.g. lean meat, the fat content is more than twice that of the wild buffalo.  Before the removal of fat, the domestic meat has more than eight times the total fat content compared with wild buffalo.  Crawford also noted in the text that there was wide variation in the fat content from domestic cattle (SEM = 7.22 is over 25% of mean, wild SEM is less than 10%).  Note the highlight as well, that significantly larger samples of wild buffalo were required to obtain sufficient lipid for analysis.  Continuing on in the Crawford paper ...

PUFA vs. SaFA+MUFA Content of Wild vs. Domestic Fat

It is interesting to note that the "parks" buffalo were essentially "grassfed".  While the pre-pop-era paleo line was one emphasizing the overall PUFA content of wild meats vs. domestic, it is important to understand that "grassfed" is at best the equivalent of the "parks" buffalo above.  Note that true wild buffalo (woodland) contain three times as much PUFA compared to even the "parks" variety.  While much closer than domestic, it is still a considerable difference.  

 Fun fact:  Wild buffalo contains more PUFA than canola oil 

Some Big Fat Fractions ...

Before moving on, a little check of the math here.  Elsewhere in the book, Teicholz insists that Americans have reduced dietary fat intake since the 1970's because fat used to comprise 43% of calories and now comprises 33%.  Leaving aside for a moment that this is a lie based on Teicholz's source for these values, those numbers have been further percentaged to claim a 25% reduction in fat intake.  Any way you look at it, though, percentages are a slice of a pie (cauliflower crusted stevia sweetened cow pie) and when one goes up, the other must go down and vice versa.  Since we're talking about different types of fat making up the whole here, as demonstrated in Table II above, when PUFA content is increased in proportion, the combined MUFA+SaFA content must be reduced.  

From Table I, we know that wild meat contains roughly one-ninth of the fat of domestic meat, and less than one-half the fat of meticulously separated domestic muscle.  One way the percentage of saturated fat could be greater in domestic animals vs. wild while the total saturated fat content remained the same between species would be if wild animals contained more total fat.  The opposite is actually the case.  So I've constructed a table based on data from Crawford:

As you can see, per 100 grams of meat, you're getting almost 25 grams combined of saturated and monounsaturated fat, while you get only 2 grams from the buffalo.  Even IF the ratios of SaFA to MUFA differ wildly, there is almost no mathematical way to support the contention that saturated fat did not differ.  If 100% -- all 2 grams -- of the combined amount is saturated in the wild buffalo, then the domestic cattle would have to contain 22.7 grams of MUFA, a value that would put MUFA:SFA ratio at 9:1 which is not in keeping with what we know about ruminant fats.  Rather, Crawford's data supports the statement that  domestic beef contains more than 10 times the saturated fat of wild buffalo. 

Teicholz's POOP

Having just demonstrated the near impossibility that the relative proportions of SaFA to MUFA could rescue the day, I'll return to the rest of Teicholz's discussion of the Crawford paper and what he is accused of hiding amidst his data.  She writes: 
Instead, the domesticated animals turned out to be higher in monounsaturated fats, which is the kind found predominantly in olive oil.  So whatever the differences between wild and domesticated animal meat, saturated fat was not the issue.
I'm adding this much emphasis here to accentuate just how brazen a lie this is.  Below is Figure 1 from Crawford, with some labeling added by me.

I did my best to estimate the percentages of the content for the beef and wild buffalo.  My totals come close for the wild but are a little low for the domestic by about 2 percent.  I can live with that.  Feel free to pad the MUFA for the domestic beef by 2% ;-) 

Yes, the oleic acid (18:1 MUFA) content of domestic beef is considerably higher than that of the wild buffalo ... roughly 10% of total fat content higher.  But both the total MUFA and the total SaFA contents are higher in the domestic beef.  

So I put this information together with the table I previously conducted from Tables I and II (I adjusted the totals to Crawford's percents though the 98.8 is likely a typo, it's inconsequential).

So ... according to Crawford's analysis, domestic beef in the UK in the mid-to-late 1960's, any way you look at it, saturated fat content is STILL an issue.  This is because:

  • While domestic cattle contains more SaFA and MUFA compared with wild buffalo, this is due to lower PUFA content.
  • The ratio between SaFA and MUFA in domestic vs. wild meat appears to be virtually unchanged.
  • While the PUFA:SaFA:MUFA percents for wild buffalo can be loosely rounded to 30:40:30, the pattern is dramatically different in domestic beef which is virtually devoid of PUFA and the ratios could be loosely rounded to 0:55:45.
  • The fatty acid distribution taken together with the overall fat content of domestic beef is 14% by weight for domestic beef and only a smidge over 1% by weight for wild buffalo.
Where did Teicholz get her statements?  Not from the Crawford paper.  Rather they were POOPed out.  

  POOP = Pulled Out Of Posterior 

At some point, this woman needs to be held to account for her gross mischaracterizations of her often difficult-to-obtain sources.  There was nothing hidden in Crawford's data, though as you can see through my analysis here, some of the comparisons needed to be teased out by presenting the same data in different formats.   None of this supports Teicholz's assertions.  Quite the opposite.

The Rest of Chapter 1 ...

For the remainder of the chapter, Teicholz goes on to bring up the usual arguments for why it isn't the meat we should be concerned with anyway.  We're told about the fatty organ meats, and how our ancestors were able to pick and choose year round from various species and herds to sample only the fattiest of animals from which to excise only the fattiest of parts, leaving the rest to the vultures.  I'll have at this romanticized paleonotion in a future post.  But since Teicholz cites the Crawford paper, I thought I'd leave you with the opening words from the paper itself:

THE amount and type of dietary fat may be related to atheroma (Ahrens et al. 1958, Funch et al. 1960). Death from arterial disease is correlated with a high intake of animal fat, protein, and calories (Yerushalmy and Hilleboe 1957) and it is likely that the animal fats and the calories are more relevant than the protein (Katz et al. 1958, Keys 1963). That the nature of the fat may be important is suggested by the fact that polyunsaturated fatty acids can protect the artery from damage in experimental situations (Thomas and Hartroft 1959, O’Neal et al. 1959, Wissler et al. 1962, Moore and Kon 1963, Kim et al. 1965).
The work on experimental atheroma tends to implicate, in some way, animal fat or carbohydrate (Sandler and Bourne 1963, Roberts and Strauss 1965). In this context, I have previously asked if, by examining data from a prosperous Western community, we may be dealing with an abnormal state (Crawford 1964, 1967).

Ahrens, Keys, Yerushalmy & Hilleboe, all together in one paragraph.   As we all know, however, it turns out carbohydrate is the real culprit in atheroma [ /sarcasm]


justjuliebean said...

I may have mentioned that I went to her book talk for this book, and I mentioned that although the percentage of carbs went up, in absolute terms everything went up, maybe just not as quickly, and she really looked at me blankly. I don't think she understands the difference. I no longer expect anyone to understand math, people can hardly make change, forget percentages, orders, interest.

MacSmiley said...

Solid gold, Evelyn!! I assume this is the whopper you were talking about?

Meanwhile, this is just Chapter ONE??? 😳

Curious: Is this recycled Gary Taubes falsification from GCBC or purely original Teicholz's mangling of the facts??

MacSmiley said...

Mathophobia is excuse. (OTOH, maybe she had Oxford math grad Zoe Harcombe proofread her numbers, whereupon it would be even more inexcusable.)

She's telling people compelling falsehoods in order to influence their dietary choices in ways which may adversely affect the health of many. It's her JOB to get the facts, as well as the math, straight, doggone it !!!

This book reeks of AGENDA!

macrauchenia said...

I don't think I'll ever read her book now. I was hoping to find a history of the low-fat nutritional recommendations and the subsequent low-fat diet fad that would be less tendentious then what came before. It's weird this stuff is endorsed by the Economist, she gets favorable coverage in Medscape, BMJ, WSJ, and an OP-ED in the NYT.

So I turned to some sources that are still popular but less mainstream that might challenge at least challenge the anti-Ancel Keys stuff. Dr. Hall on SBM took on Fed Up and does profiles of scientists. I'm impressed with Julia Belluz at Vox, they often interview Dr. Freedhoff and even had their intern write-up the Linus Pauling/vitamin C myth. That's when I found this *%#$@:

I lost weight by eating lots of bacon and cream. Here's a scientific explanation for why.

by Gregory Ferenstein on January 6, 2015
He didn't win me over when he linked Teicholz's WSJ piece first thing, but I was willing to give him the benefit of the doubt. But he just kept getting worse, attacking Ancel Keys, observational studies, finally linking to Mark Sisson. Et tu

Anyway, Vox accepts story tips and SBM might accept submissions. Maybe with Evelyn, Seth, and others advising we could get something on more sites like this to challenge the revisionist version of history?

Timar said...

"Fun fact: Wild buffalo contains more PUFA than canola oil"

Ehm, you probably meant "wild buffalo FAT". Otherwise it doesn't make any sense.

But, but, but... didn't you know that canola oil is made from toxic RAPEseed genetically modified by the Devil himself (right after creating the frankenwheat) as the most recent move in his grand plan to permanently expel mankind from its former Paleo Paradise? How dare you to compare God's most wholesome food, the very source of the Indians' good health and immortality, to the Devil's oily excrement?

David_Brown said...

"And yet, as she fails to achieve brevity, she uses the simplification to
distort facts over, and over, and over ... throughout the book."

Distort facts? How does that work? A fact is always true. However, truth itself can be distorted by selecting and organizing factual information. Perhaps you meant to say that Teicholz distorted the opinions of the likes of Prentice and Crawford.

carbsane said...

Distorts the facts in her presentation of them. IOW, presents distortions of the real facts as her own facts. I'm not going to get into a debate about my writing style here. This is a blog.

Crawford's chemical analyses are FACTS David. Teicholz distorted what his facts were with her biased opinions. Or, more likely, those of someone else.

carbsane said...

I'll address your first and last comments.

Your quote: "Death from arterial disease is correlated with a high intake of animal fat, protein, and calories and it is likely that the animal fats and the calories are more relevant than the protein."

Your commentary: >>> And they knew this for certain back in 1963? <<<

The problem you are having with being taken seriously by those you contact in the hopes of getting your ideas out there may be encapsulated in the above. The whole purpose of the beleaguered Seven Countries study was to investigate this further, along with studies of all sorts too numerous to list.

You last link is to a PhD Thesis entitled: The Associations Among Dietary Fatty Acids, Plasma Fatty Acids, and Clinical
Markers in Postmenopausal Women with Diabetes.

So we're talking circulating fatty acids in those with existing disease. This is where nonsense like fear of BCAAs comes from. In any case, your excerpt left out some important findings:

>>> We had anticipated correlations for linoleic acid, C18:2n6, an essential fatty
acid, and for elaidic, C18:1n9, the most common industrially produced trans fat in the
diet since neither are synthesized in the body; however, dietary and plasma level
correlations of linoleic acid and elaidic acid were not shown.
Instead, dietary myristic
acid, C14:0, was positively correlated with its plasma fatty acid. These data were
unable to show a consistent relationship between diet and plasma fatty acid
composition. <<<

Of course there was significant dietary under-reporting that pretty much nullifies all of the diet/circulating relationships. As discussed in the thesis, but you neglected to mention.

>>>Long chain omega 6 and omega 3 fatty acids including C:20:4n6, C20:5n3, and
C22:6n3, were correlated with positive health markers. Arachidonic acid, an omega 6
fatty acid required in the pro-inflammatory pathway of eicosanoid production, had no
unhealthy correlations.
Levels of arachidonic acid were inversely related to the ratio of
total cholesterol to HDL. <<<

Funny how the non-HDL or TC/HDL ratios are identified as significant biomarkers.

>>> Plasma fatty acids were indeed
related to health markers. Levels of non-esterified fatty acids in the plasma positively
predicted for both trunk and total body fat.

You don't say ;-)

carbsane said...

Sorry for delayed reply (really need to find a way to respond inline on Disqus on my phone!) ... I stand corrected ;-) and laughed at your chastisement for my comparison. :-)

carbsane said...

When one watches her TEDx talk and her media appearances, it becomes clear that she's been very well coached since, or has some background in public speaking and the like that had gone rusty, was dusted off and polished up post haste.

David_Brown said...

Again, "real facts" is redundant, like saying "true facts." And I'm not talking about your writing style. We're all capable of being sloppy in terms of choosing information as well as careless in our use of words. That has nothing to do with writing style. What you do here is of great value because you point out the sloppy thinking and careless (Let's pause to object to the use of the term carnivorous.) use of words. I'm just trying to do for you what you 've been doing for Teicholz.

With that in mind, a belief is whatever a person chooses to accept as true. As you know, it is foolish to embrace an opinion without familiarizing oneself with the facts upon which opinion is based. However, when new facts come to light, it makes sense to abandon the opinion if it does not adequately explain the phenomenon under investigation. Case in point is the connection between dietary fatty acid intake and plasma fatty acid profile. Depending on the type of digestive system, the microbiota profile, the micronutrient profile, fiber content, and the macro-nutrient percentages, fatty acids in food may appear in the plasma, be converted to another form, be incorporated into the cell membranes of the microbes inhabiting the digestive tract, or they may be excreted intact. I could be mistaken but those who comment on this blog don't seem to have given these matters much study or thought.

carbsane said...

Thank you again for the semantics lesson. I didn't claim carelessness, simply that anything written in a blog post is not by nature of the venue subject to the same scrutiny as those written in a book of the nature of BFS. Teicholz calls herself a carnivore on Twitter so take that up with her. If you want to do for me what I am doing for Teicholz, you are failing miserably by focusing on phraseology rather than what I am saying.

Don't give me the new facts come to light angle here. We are talking about the OLD facts upon which Teicholz lays out a "new" argument. Crawford's results (the fatty acid analyses) are fact. Teicholz's discussion in the book would lead one to believe that these facts were indeed different than they objectively are. So I used the phrase "distorts the facts" as in she misrepresents what those facts are.

Please refrain from guessing what anyone who reads or comments here is thinking. It's rude. It also has NOTHING to do with the topic of this post, which is the adipose tissue content of various fatty acids in wild vs. domesticated versions of similar animals that can be attributed to diet. The human body doesn't care why wild buffalo have higher PUFA, only that they do.

David_Brown said...

>>>Don't give me the new facts come to light angle here. We are talking
Crawford's results (the fatty acid analyses) are fact. Teicholz's
indeed different than they objectively are. So I used the phrase
"distorts the facts" as in she misrepresents what those facts are.<<<

Point taken. Teicholz made some careless mistakes which you have pointed out to her. Good job on that. However, if you are truly concerned about improving our collective understanding of how the real world works, I suggest you incorporate the NEW facts into your thinking.

>>> Please refrain from guessing what anyone who reads or comments here is thinking. It's rude.<<<

I didn't mean to insult anyone. I said, "I could be mistaken but those who comment on this blog don't seem to have given these matters much study or thought." I thought I was issuing a challenge to prove me wrong. Thus far there's been little interest in refuting my opinions.

carbsane said...

Yes, of course they want to salvage their grant funded work. It's human. But that degree of error in reporting brings ALL correlations into enough question as to nullify them.

>>>Thusfar there's been little interest in refuting my opinions.<<<

I wonder why.

Teicholz's "mistakes" are not careless. One could presume so on a benefit-of-doubt basis, but her "correction" on the buffalo eating Native Americans of the Southwest would unequivocally demonstrate otherwise.

Are you defending her here? Or claiming any sort of parallels to my analyses with hers?

Catweazle said...

Omg, that means all these vegan mothers in Tamil Nadu having over hundreds of generations brainless babys? Or does it mean that hundreds or thousends of western scientists having some limitations in the brains that they dont see the 800 pound gorilla in the room?

carbsane said...

I read the paper where they discussed the error in underreporting. Did you?

David_Brown said...

Which paper? The Masters Thesis by Nancy Carol Baker or some other paper about reporting errors.

David_Brown said...

Actually, vegan diets produce healthy brains in the babies of mothers who can tolerate vegan diets as long as the mom hasn't been consuming excessive linoleic acid prior to pregnancy.

It's the elephant in the room. And an overweight Gorilla weighs 450 pounds, not 800. When Cleveland Zoo gorillas stopped eating vegan primate biscuits containing wheat, sugar, and 6.6% soybean oil, they doubled their caloric intake and lost 60 pounds. Apparently, even low intake of linoleic acid derived from seed oils can be deadly in a context of sugar and wheat intake.

carbsane said...

I have to laugh at the "quietly replacing" nonsense. The "high oleic" has been around for a very long time and it's to parallel the fatty acids in olive oil.

macrauchenia said...

macrauchenia said...

This is something I have wondered about looking at bottles on the store shelves. Safflower oil supposedly has the highest n-6 PUFA, but the product label in stores is pretty much entirely MUFA. The only one's that I could find that are high in PUFA are grape seed oil and walnut oil, and soybean oil which is usually labeled vegetable oil has some combination. I suspect that so few have high PUFA has to do with cooking properties of MUFA or the tendency of PUFA to become rancid. I think it probably seems so quiet because the average consumer has little knowledge beyond poly, mono, and omega-3.

macrauchenia said...

I don't believe I've failed to consider anything or have any interest in proving you wrong. Maybe it's because I came upon the conversation in the middle or because I have never taken a class in biochemistry, but to be honest, I don't find your comment to be expressed in a way that is easily understandable. I see citations of studies and suggestions to google this and google that without explanation of the relevance. I just don't think you are connecting the dots very well here.

With biohydrogenation, it's interesting, but I don't see anything to express a problem for dietary LA in the study. It was ex-vivo so it's hard to know if it would be even be applicable in vivo. Also, I think I pointed out before that a small percent of LA would make it to the colon anyway.

By the way, what technical help and expertise did you provide the authors of the biohydrogenation study?

David_Brown said...

You're correct to say that "high oleic" has been around for a long time. "Florida first applied for a patent on the high-oleic peanut in 1987." However, "It still may be a few years before consumers find themselves checking labels to be sure they are getting high-oleic peanut butter and other peanut products on grocery store shelves, but Gorbet says, "Things are starting to come together to position ourselves in the world marketplace for high-oleic peanuts."

From another article: "The success of this commitment has been remarkable, she says. In 2011, only 6 percent of the U.S. peanut crop was planted in high-oleic varieties. Today, that number had quadrupled, to approximately 24 percent.

"Quietly replacing nonsense"? Allow me to explain what I meant by that remark. While at least some of the other oil seed companies admit that high linoleic acid content of seed oils poses problems, Dupont carefully avoids mention of LA. "Health-conscious consumers expect foods with labels that say 0g trans fat. Food manufacturers and fast food restaurants are working to find oils that can meet this demand without sacrificing performance—or the taste that keeps their customers coming back. Farmers want a soybean with strong agronomics and increased demand. Enter Plenish®—a Pioneer® brand soybean with a healthier oil profile and increased oil stability. Plenish® high oleic soybean oil has 0g trans fat, less saturated fat and the highest amount of heart-healthy monounsaturated fat available in soy."

Monsanto so not quite so circumspect. "Monsanto boasts that Vistive Gold oil is “a golden opportunity for better health,” touting that the new oil has higher oleic (monounsaturated fat), and lower linolenic (polyunsaturated) and palmitic and stearic (saturated fat) content than the non-modified soybean seeds."

The peanut oil industry apparently has no qualms about bashing linoleic acid. "Same fatty acid profile as olive oil – even better as higher in Oleic Acid (the good acid!) and lower in Linoleic Acid (the bad acid!)"

Lastly, I've had a Google Alert in place for "Omega-6 linoleic acid" these past five years. Had the high oleic acid oils been publicized with any mention of linoleic acid, I would have gotten wind of it.

Glad you had a laugh. Laughing is healthy.

David_Brown said...

>>>LA intake. NOTHING else. Right?<<<
I didn't say that. "The roles of both LA and fructose in the current obesity epidemic are
under intense scrutiny but are not well understood and seldom compared

billy the k said...

Hey, David—I've been following with interest your recent exchanges here with Evelyn (and others) regarding linoleic acid. You've amassed quite a wealth of info on this subject, and I was wondering what your thinking was concerning the views of two guys who both share your (current) conclusion of the dangers of excessive Omega-6,—despite their wildlyopposed views on the question of fats vs carbs: Peter D (over at Hyperlipid) maintains a very low-carb diet and likes to run on mostly FFA's, along with some ketones; Ray Peat shares Peter's fondness for dairy fat, but regards sugar as the cat's ass of good things to eat:
What's your thinking concerning the arguments of these two characters?

Ray Peat:

Peter D (over at Hyperlipid):
also here:

carbsane said...

Do feel free to share your views on Peter's ideas on his blog :-)

billy the k said...

I hear you.
Sorry to see there's no longer any leeway for a side-excursion on the CarbSane Highway.

There used to be.

carbsane said...

I have no probs with side excursions -- feel free to go all Peaty here etc, b/c Ray Peat will not take offense. Peter OTOH doesn't take kindly to discussions of his ideas on this blog, so I'm just trying to avoid conflict. Sorry ;-)

billy the k said...


carbsane said...

BTW, I don't have the full text of this, but tis interesting:

>>>The authors analyzed blood metabolites in nine children with epilepsy prior to starting the ketogenic diet (KD) and 3 to 4 weeks after KD therapy. Elevated β-hydroxybutyrate and cortisol levels were observed in all children on the KD. <<<

Maybe some of the stressed out irritable ketos should wean themselves occasionally ;-) But what more caught my eye vis a vis PUFA:

>>>Free fatty acids increased 2.2-fold on the KD, with significant elevations in most polyunsaturated fatty acids (PUFA; arachidonate increased 1.6- to 2.9-fold and docosahexaenoate increased 1.5- to 4.0-fold). The rise in total serum arachidonate correlated with improved seizure control. Elevated PUFA may represent a key anticonvulsant mechanism of the KD.<<<

Arachidonic acid generally gets a bad rap.

David_Brown said...

Hi Billy,

Thanks for your question. I think the fats vs carbs controversy needs to be framed in terms of how individuals respond to various macronutrient mixes of fat and carbohydrate. Two good books discussing these matters are "Biochemical Individuality" by Roger J. Williams and "Nutrition and Your Mind" by George Watson.

In my opinion, to achieve optimal nutrition, the issues are appropriateness, adequacy and toxicity.

Appropriateness: It's the one-man's-meat-is another-man's carbohydrate principle. It all has to do with the cellular machinery, as Williams puts it, and how the various glands and digestive organs are configured. It's like we've got all these different chemical factories inside us that vary in size, input requirements, and output capacities. Along these lines:

Adequacy: In order for chemical reactions to proceed to completion there must be sufficient amounts of all the required chemical reactants. Mineral imbalances and deficiencies can be avoided if the food is mineral-rich. Refined sugars and grains are not mineral-rich. Perhaps that's why Americans spend 10s of billions on supplements annually with hopes of furnishing enough vitamins and minerals to ward off disease.

Toxicity: Supplementation and even really good quality, mineral-rich food cannot totally mitigate the toxic effects of a highly reactive molecule such as linoleic acid. However, a diet that promotes the proliferation of bacteria that biohydrogenate linoleic acid to other species of fatty acid more benign than linoleic acid may make it possible to consume rather large amounts of linoleic acid for quite a while without apparent harm. If a person's linoleic acid intake is very low and his mineral intake is adequate, a reasonably high sugar intake will likely be well tolerated. As I understand it, however, releasing energy derived from carbohydrate uses up more mineral resources than does releasing energy from fats. In other words, separated fats such as butter do less to deplete minerals stored in cellular reserves than refined carbohydrates such as sugar.

A person can learn a lot from both Ray and Peter.

billy the k said...

Hey David,—thanks for replying. And thanks for more links to check out.

You said: " a person can learn a lot from both Ray and Peter." The websites I frequent are the ones I have in fact benefitted from; I've learned things of value to me from bloggers and commenters having diametrically opposed views on choiceworthy diets.

You mentioned: "...the toxic effects of a highly reactive molecule such as linoleic acid." As I understand it, both Omegas—the 6's and the 3's—are indeed highly reactive molecules; Omega 6 is the one most often regarded as dangerous for just this reason, but Omega 3's are reputedly even more highly reactive, yet are routinely recommended,—either to "balance" the omega 6 in one's diet, or for their own purported beneficial value (Peat is the only guy I can think of whose advice is to generally minimize both; even Peter D joins his polar opposite Dean Ornish in knocking back fish-oil capsules).

But this matter of reactivity leads me then to wonder about glucose—which is another highly reactive molecule and one even more critical to life. This reactivity aspect leads many low-carb folks to regard glucose—along with linoleic acid—as another dangerously reactive substance, which—for that reason—should also be minimized in the diet: ("go low carb: you don't want your body proteins glycated, do you??!!!")

So the question looks to be about how best to reconcile these two factors,—namely the [purported?] danger of taking in highly reactive substances,—but substances which are nevertheless required: the indisputable essentiality of glucose and the [purported?] essentiality of the Omegas.

Hence the perennial questions: How much per day? How much per meal?
(the final answers don't appear to be in, just yet...)

David_Brown said...

Hi Billy,

Recently, Verner Wheelock suggested Gary Fettke's blog at Previous to this, I had not heard of Fettke. I'm finding his commentaries interesting.

Jane Karlsson said...

Gary Fettke says

"Something has happened to our dietary intake in the last 100 years or so to account for the massive shifts in diseases experienced by modern society. Fructose and Polyunsaturated Oils look to be the major contributors to most of our Modern diseases including obesity, diabetes, heart disease, dementia, cancer and a raft of other conditions."

David, you have just shot yourself in the foot. Again.

ZM said...

"I frequently write to authorities who bash saturated fats. Below is a response to a message I sent explaining why I don't buy the cholesterol hypothesis."

David, I'm curious to know who is behind that response.

David_Brown said...

In my second email to the person quoted, I asked for permission to quote his response with attribution. I'll get back to you on that if permission is granted. I'll include the article that brought that individual to my attention.

billy the k said...

Speaking of "not buying the cholesterol hypothesis", my own early skepticism of Keys, et. al., only increased after reading Ravnskov's arguments, but I have Nigel Kinbrum to thank for introducing me to the following paper on Neovascularization—which (for me) pretty much nailed the coffin shut on the ubiquitious view of how atherosclerosis is caused by the elevated LDL cholesterol in the blood flowing through our arteries:

a. If—as the common view has it—low density lipoprotein cholesterol (LDL-C) invades the coronary artery wall from the coronary lumen, then the initial depositions ought to be most proximal to blood, i.e., in the inner part of the artery wall. The facts show that the opposite is true, and lipids are initially deposited in the outer layer. The normal artery wall is avascular, receiving nutrients by diffusion from the lumen, whereas in coronary atherosclerosis (CA) the outer part of the artery wall is ALWAYS neovascularized.

b. small as they are, the LDL-C particle size—at 20 X 10⁻⁹m—i.e., 20 nm!—is too large to pass from the inner to the outer part of the artery wall by diffusion. But once the normally avascular outer layer has been neovascularized, LDL-C can now enter the wall via this new (and abnormal) blood supply route into the artery wall.

These facts are what now come to mind each time I see another instance of the phrase: "artery-clogging saturated fats.

Jane Karlsson said...

That paper is very interesting indeed. Where is Nigel, do you know? I wish he'd come back.

billy the k said...

Dunno, Jane...I hope that karaoke hasn't taken over his life!

David_Brown said...

I've been reading the paper with minimal comprehension. My maternal grandfather used to say that Latin and typing are courses every high school student ought to take. I can see the wisdom of that advice. I taught myself to type about 20 years ago using a computer program. Now I'm having to learn some Latin terms to understand this paper.

It's interesting that the Subbotin paper (2012) has been cited by only one other paper (2014). I'm going to be studying that one as well.

Billy, what led you to the Subbotin paper? Was it an article? I would like to read that as well. Thanks for inserting this into the discussion.

billy the k said...

Q. Why does the outer layer of the artery wall become neovascularized in the first place?
A. The process begins when the cells in that area are stimulated to proliferate,—and this proliferation results in the requirement to vascularize the newly thickened cellular layer in order to provide oxygen:
"...the cells in the coronary tunica intima respond by proliferating to any stimuli, exogenous or endogenous. Regardless of the nature and magnitude of stimuli/ insults, cells that appear in the arterial intimal compartment always proliferate in response. An increase in cell numbers inevitably expands intimal thickness, which occurs with aging [119,181]. Expanded intimal thickness impairs diffusion of oxygen, as diffusion is inversely proportional to the square of the distance. Insufficient oxygen diffusion would inevitably result in hypoxia, specifically of cells in the outer layer of the artery wall (DIT), because this tissue compartment is the most distant from the lumen and adventitial vasa vasorum...[and] when the intima of the coronary artery exceeds a certain thickness, parts must either die or develop secondary blood supply: i.e., neovascularization.

My candidate for the initiating insult that stimulates the cellular proliferation is not linoleic acid but the calcium shift phenomenon: 1. calcium deposits are, after all, what provides the hardening of atherosclerosis; 2. an insufficient supply of dietary calcium leads to a shifting of calcium from bone to the soft tissues:

"Calcium deficiency is a constant menace to land-abiding animals, including mammals. Humans enjoying exceptional longevity on earth are especially susceptible to calcium deficiency in old age. Low calcium and vitamin D intake, short solar exposure, decreased intestinal absorption, and falling renal function with insufficient 1,25(OH)2 vitamin D biosynthesis all contribute to calcium deficiency, secondary hyperparathyroidism, bone loss and possibly calcium shift from the bone to soft tissue, and from the extracellular to the intracellular compartment, blunting the sharp concentration gap between these compartments. The consequences of calcium deficiency might thus include not only osteoporosis, but also arteriosclerosis and hypertension due to the increase of calcium in the vascular wall, amyotrophic lateral sclerosis and senile dementia due to calcium deposition in the central nervous system, and a decrease in cellular function, because of blunting of the difference in extracellular-intracellular calcium, leading to diabetes mellitus, immune deficiency and others (Fig. 6).

It's a primary reason why I follow the great pioneering nutritionist Elmer McCollum's 100 year old recommendation for everyone—including adults—to have one quart of milk per day.
"Drink up!"

David_Brown said...

That makes sense in terms of hardening of the arteries which raises blood pressure. However, heart attack involving unstable plaque is likely related to excessive linoleic acid intake.

billy the k said...

"However, heart attack involving unstable plaque may be more related to excessive linoleic acid intake than calcium deficiency."

The paper cited (from AHA's Circulation: Cardiovascular Genetics) in support of the statement above provides an analysis of the lipid composition present in human lesions, and just as you say, linoleic acid is seen to be selectively enriched in cholesterol ester (CE) species, but it doesn't follow from this that the problem was therefore one of linoleic acid intake. The examined plaques were selectively enriched not just in linoleic acid, but also in oleic acid, and if dietary intake per se was responsible for it getting there then Walter Willett and all the other Mediterranean Dieters would have to stop glugging their beloved—and purportedly heart-healthy—Extra Virgin Olive Oil.

There's lots of stuff that ends up being in atherosclerotic plaques: the analysis (in that same paper) "...revealed 24 (of a total of 150) distinct lipid species that were differentially identified in the atherosclerotic plaques." The key question remains: Not: What ends up being inside the plaques? but What is the initiating event that starts the atherosclerosis process in the first place?

Calcium is also present in plaques, but it surely doesn't get there as a result of dietary intake, and reducing one's intake to zero will not guarantee the absence of calcium in plaques (indeed, I am persuaded the opposite is the case!). Likewise, despite the well known and well publicized pro-inflammatory problems of linoleic acid—and its presence in atherosclerotic plaques—I don't think the evidence to date warrants avoiding the use of Hellman's mayo on my occasional tuna salads. Or using olive oil on tossed salads.

Ω-6LA is, after all, an essential fatty acid. Since David Brown does enjoy "two to three pounds of butter a week"—(a bit more, but not that much more, than yours truly)—I'm pretty sure that you're thereby already getting your RDA for Ω-6LA.
(But I just can't see the benefit of leaving off the olive oil on a tossed salad, or buttering a tuna salad!)

David_Brown said...

>>>The examined plaques were selectively enriched not just in linoleic acid, but also in oleic acid and if dietary intake per se was responsible for it getting there then Walter Willett and all the other Mediterranean Dieters would have to stop glugging their beloved—and purportedly heart-healthy—Extra Virgin Olive Oil.<<<

Perhaps I didn't make it clear. Linoleic acid makes the plaques unstable due to it's toxic effects. Oleic acid, even though selectively enriched in plaques, does not make them unstable. Even the Masai have atheromas but they don't have heart attacks. Why? Willett would say that enlarged coronary arteries due to constant exercise it the answer. I'd say it is the low linoleic acid content of the Masai diet.

Note that circulating oleic and linoleic acids are not necessarily related to dietary intakes due to biohydrogenation and de novo lipogeneis (DNL).

"We had anticipated correlations for linoleic acid, C18:2n6, an essential fatty acid, and for elaidic acid, C18:1n9, the most common industrially produced trans fat in the diet since neither are synthesized in the body; however, dietary and plasma levels of linoleic acid and elaidic acid were not correlated. Instead, dietary myristic acid, C14:0, was positively correlated with its plasma fatty acid. These data were unable to show a consistent relationship between diet and plasma fatty acid composition."

"DNL may produce lipid species with bioactivities distinct from those of lipids derived predominantly from the diet (1).

David_Brown said...

Graham MacGregor wrote the response.

In a second message he ignored my request for permission to quote him with attribution. Since he didn't tell me not to quote him, here's what he said:

"... the facts are that it is clear from 50 years of data now, that saturated fat puts up cholesterol which is a major cause of atheroma and there is no doubting that.

Whether some other factors influence it to some extent or not is really what the debate is about, not whether sugar is uniquely damaging, for which there is little evidence, or that fat is. We need to have a balanced approach to this. We need to reduce both trans fats, saturated fat, total fat intake and sugar intake to deal with the obesity and type 2 diabetes crisis and the atheroma that is the third cause of death in the world – and reduce salt which is the main factor putting up our blood pressure which is the biggest cause of death, even greater than tobacco.

There can be no disagreement about this. There are slight nuances between some factions and others are rather desperate and they don’t help the overall message which is to stop the food industry slowly killing us and to get more healthy food from them so we can live longer and suffer less from strokes, heart attacks and heart failure."

ZM said...

Thanks David, some strong words from MacGregor in those replies, though they are easy to refute.

Have you seen the recent review Ramsden was involved in? -

David_Brown said...

I hadn't seen that review. Thanks ZM. I requested the full text article.

I told Dr. MacGregor I wouldn't send him any more messages if he indicated he was not interested in linoleic acid research. However, if anyone else cares to importune him: Graham MacGregor

Jane Karlsson said...

I just looked up this MacGregor person. He's a big shot professor with 400 publications to his name. Doesn't stop him from being a complete idiot. Salt is the main factor in hypertension? What about magnesium? Sodium isn't the problem, it's the sodium-potassium balance, which is controlled by magnesium. Surely MacGregor knows that both magnesium and potassium are in short supply in the modern diet due to something awfully simple: they get deliberately removed from refined carbs.

David_Brown said...

The sad thing is, it is thought leaders of this sort that shape public nutrition policy, not people like yourself who are familiar with the science.

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