Introduction
Consider this a follow-up of sorts to my post and debate with Alan Flanagan (Goodrich, 2021a, 2021b), if you want some background.
Nick Hiebert (Hiebert, 2021a), whom I have been interacting with for several years on Twitter, thought he could do a better job than Alan did, and challenged me to a debate. After going through a little back-and-forth on format, it became clear that Nick wanted to debate me only if he could have a moderator that would take his side in his view of the facts and the logic. I proposed a standard Oxford-style debate, where such matters are handled by the debaters, and the moderator simply enforces the rules (time, taking turns, etc.).
Nick refused, and blocked me. And then apparently wrote this, “A Comprehensive Rebuttal of Seed Oil Sophistry” (Hiebert, 2021b). And then challenged me again to a debate (I’ve been told), which I couldn’t see, as he has continued to block me. Which is most amusing, but…
After several requests, I’ve decided to take a look at his post. I’m responding as I read it, as it’s 60-odd pages long*. I am doing this in the manner of an audit. I’m not going to go through the whole thing, but until I have a feeling that I can assess the quality of the argument to my satisfaction, and hopefully to that of the reader.
This post moved to Substack.
Brilliant as usual; thanks for all the work you do on this. I've personally seen great results cutting out seed oils, inspired in large part by you.
ReplyDeleteI wonder though how we can ever change the broader culture, where seed oils seem super-entrenched? I can't even convince my friends!
I think 99% of people just believe whatever the official line is; they are uninterested in diving into the issues themselves, and assume whatever is official policy must be an accurate summary of the latest science.
So maybe ultimately change needs to come from getting some influential in the establishment to take it seriously...
"I wonder though how we can ever change the broader culture, where seed oils seem super-entrenched? I can't even convince my friends!"
DeleteWe're working on it. It's coming.
Excellent work, Tucker. It takes many times the effort to kill a lie or misunderstanding, as you show. If have anything left, there is short TPN section. He tries to show that it is not soy oil LA but plant sterol that destroys the liver. "To recap, the fatty liver observed in children receiving IVLEs while on TNP is likely a function of the direct intravenous administration of phytosterols, and it is unlikely that LA has any unique role to play here."
ReplyDeleteSo, it is plant cholesterol AND Pufa-6 that mess up with your liver and your innate cholesterol synthetis, ending up as oxidised membrane particle. Your advice on this, avoid like a plague, affects to both parts of this equation.
Coconut oil, filled with stable fats, behaves a bit differently, and plant sterols may play a role together with shorter chain lengths? It remains as one of my favorites, though. Everything in moderation...
RGDS JR
The takeaway from my post is that Nick doesn't read studies, and misrepresents them.
Delete"Interestingly this study did not find ahepatotoxic effect of adding phytosterols to fish oil in enteral PN-induced liver injury. ...the composition of phytosterols added to fish oil approximated the types and amounts of phytosterols found in soybean oil."
"Alpha-tocopherol in intravenous lipid emulsions imparts hepatic protection in a murine model of hepatosteatosis induced by the enteral administration of a parenteral nutrition solution"
A short continuation, if you please, on TPN.
ReplyDeletehttps://pubmed.ncbi.nlm.nih.gov/22796064/ (ref 123 is this)
Soy oil vs fish oil. Both fed only pure is a bit problem. Thats why the developed a combi with soybean/MCT/olive/fish oil emulsion. This sounds like an emulation of a real fat! Note the inevitable phytosterols within soy and olives i guess.
Nick: "When tested in humans at matched, eucaloric dosages, there are no clinically meaningful differences between SO-IVLEs and FO-IVLEs [122-123]. Across all of the markers investigated by Nehra et al. (2014), the only significant changes were increases in alkaline phosphatase, but they occurred in both groups."
This is actually from the abstract (edited a bit):
Mean concentrations of(ALT), (AST) and total bilirubin, ..., were significantly lower with soybean/MCT/olive/fish (SMOF) oil emulsion after the treatment period compared to control. Eicosapentaenoic acid, docosahexaenoic acid and n-3/n-6 fatty acid ratio increased in the SMOF group, while they remained unchanged in the control in plasma and RBC. Serum α-tocopherol concentrations significantly increased in the study group compared to control (p = 0.0004). IL-6 and sTNF-RII levels did not change during the study period. Grade 4 (serious) adverse events occurred in 2/34 SMOF patients and in 8/39 control patients (p = 0.03).
So, "there are no clinically meaningful differences..."?
wonder what those would be then?
Falsus in omnibus
JR
"Falsus in omnibus"
DeleteBingo.
Good job Tucker. I appreciate your commitment on this issue and your thorough work. Look forward to your book.
ReplyDeleteThanks!
DeleteThank you Tucker for such a great rebuttal.
ReplyDeleteWhat I found especially interesting was the SFA rich diet being unable to lower LA concentrations of the LDL lipid membrane. Only the MUFA rich diet was able to do that, although both diets were low in LA.
Does that maybe mean that beyond eliminating seed oils from our diet, we should try to include foods that have higher MUFA content?
Yes, when the body constructs fats (comprised of two or three fats in a triglyceride or diglyceride) it typically puts a SFA in one position and a UFA in another. So if you want to replace the UFA (say an omega-6 fat) you have to proved another UFA (like a MUFA).
DeleteSo if you are looking to reduce oxidizability, you have to restrict n-6 PUFA and provide MUFA (SFAs like stearic acid that quickly convert to MUFA might also do the trick, but I haven't seen a paper demonstrating that yet).
Most sources of animal fat have plenty of oleic acid. Butter has 32%, more than any other fatty acid in butter, for instance.
ReplyDeleteIf you are looking to recover from a high n-6 diet, then more oleic may be beneficial short term.
Hi, Tucker.
DeleteWhat would you suggest as a good formulation for a TPN product? SFA is stable and healthy, but TPN needs to be liquid (at least at body temperature, and probably at room temperature as well).
Hi, if kids are also eating the same omega 6 diet as adults, why do they not get the same health problems... Why does it take until middle age for most of the diseases of civilization to show up? I am wondering if it must include something about iron overload slowly developing over the years... the middle-aged adults have been accumulating the iron for a long time, and maybe that has a role, in addition to the omega 6 fats?
ReplyDeleteThere is something called "ferroptosis", which is the process by which iron oxidizes omega-6 fats into toxins. So it's certainly plausible that increasing iron could lead to health issues.
DeleteWe also have a phenomenon where we now have previously unknown diseases (ACL tears, non-alcoholic fatty liver disease), or diseases that were condsidered to be disease of old age (type 2 diabetes, some cancers, diverticulitis) becoming common in young people, which is likely due to increasing seed oil intake and the resultant damage to our bodies.
Excellent read, thank you 👍
ReplyDeleteSomething that puzzles me: how does oxidation increases LDL-C as measured by a conventional LDL assay? This question because a few in vivo studies in mice show that LDL, and not only Ox-LDL, skyrockets after oxidation. Why that?
Oxidized LDL has a different clearance pathway than LDL. That could account for what you describe, although I haven't seen the results that you are describing. Could you post them here?
DeleteHere is a recent one with H2O2 induced oxidation:
Deletehttps://archrazi.areeo.ac.ir/article_124866.html
I remember reading an old study where Cu2+ induced oxidation was used but I can't find it anymore.
Not sure why my reply didn't go through...
DeleteHere is a recent article:
https://pubmed.ncbi.nlm.nih.gov/35096330/
with H2O2 used for oxidation. I remember older studies using Cu2+ instead but can't find them anymore.
It didn't go through because when you include a link, Blogger interprets it as spam (often correct) and puts it in the penalty box for my review.
DeleteOk thank you. Would still appreciate to get your opinion on why LDL-C is also increased in oxidation studies. Or an artifact?
DeleteLDL is not increased in oxidation studies.
Delete"Total cholesterol decreased significantly in both study groups and LDL cholesterol decreased 24.5% in the linoleate group and 18.5% in the oleate group."
"Effects of oleate-rich and linoleate-rich diets on the susceptibility of low density lipoprotein to oxidative modification in mildly hypercholesterolemic subjects."
"Since many potent peroxisome proliferators do not bind directly to the PPAR (Peroxisome Proliferator Activated Receptor), it seems probable that a natural ligand for the PPAR exists; in this regard it is interesting to note that natural fatty acids, and especially polyunsaturated fatty acids, activate PPAR as potently as does hypolipidaemic drug Wy-14643, the most effective activator known so far (Ref 1, Ref 2)."
ReplyDeleteExcerpt Page 217
Title: The peroxisome: a vital organelle
Author: Colin Masters; Denis Crane
Publisher: Cambridge, Mass. Cambridge University Press 1995
Ref 1:
Fatty acids activate a chimera of the clofibric acid-activated receptor and the glucocorticoid receptor.
Author: M Göttlicher; E Widmark; Q Li; J A Gustafsson
Publication: Proceedings of the National Academy of Sciences of the United States of America, v89 n10 (19920515): 4653-4657
Ref 2:
Fatty acids and retinoids control lipid metabolism through activation of peroxisome proliferator-activated receptor-retinoid X receptor heterodimers.
Author: H Keller Affiliation: Institut de Biologie animale, Université de Lausanne, Switzerland.; C Dreyer; J Medin; A Mahfoudi; K Ozato;
Publication: Proceedings of the National Academy of Sciences of the United States of America, v90 n6 (19930315): 2160-4