Quote from Andrew B on May 4, 2023, 2:14 am

@jessica2 One slight concern about eggs is that the USDA lists fried eggs as very high in trans fats. It's not the same with other cooked eggs. It could be the fat used to fry the eggs but it could be frying at too high a temperature. I've not encountered a problem with lightly frying or putting in pancakes and my digestive system is fully back to normal.

Quote from Inger on May 4, 2023, 4:00 am

Quote from Jessica2 on May 4, 2023, 3:11 am

@pattycake

I found this study interesting not only because dandelion prevented liver Fibrosis, but the study mentions malondialdehyde specifically too. Dandelion lowers levels of it in the liver.

https://basicandappliedzoology.springeropen.com/articles/10.1186/s41936-020-00177-9

great reminder, I am going to eat some dandelions from the garden this spring and summer again, have not done that for years! No wonder my liver and gallbladder function decreased 😉 🙂 Honestly I am going to eat some again 🙂

Quote from PJ on May 4, 2023, 9:13 pm

"To the earlier idea of non essential fats being used in cell membranes...yes isn't that the whole reason Trans fats are terrible? They get incorporated in cell membranes and allow permeability and impaired functions?" - @jessica2

It is my understanding that oxidized PUFA's do not allow permeability where there should be permeability.

"Do you also believe that normal digestive processing of a cold pressed non heated PUFA would generate it (malondialdehyde)?" @jessica2

There may be some damage when they are digested, as noted earlier in the presence of heme iron. But mainly endogenous production of the toxic by-products mostly occurs as a result of free radicals or reactive oxygen species (ROS).  Natural processes.  

"This study says >definitively< that Vitamin E and selenium protects against lipid peroxidation" @jessica2

Yeah, I intentionally did not list Vitamin E, because it is fat-soluble and generally speaking, it is naturally in whatever has PUFAs like you noted with nuts. 

 

Quote from PJ on May 4, 2023, 11:04 pm

"The take on fats depends a lot of whom one talks to, SFA is the holy grail and one should eat plenty, or SFA can be problematic and should not be eaten in excess (and a few who claims it is pure death but apparently those doesn't know jack shit about much) it is a very confusing area. Studies about the subject as well equally confusing." (quote taken from #21 of The false carotenoid conversion factors for vitamin A thread.) @liz

 

Stumbled on this article.

https://www.hsph.harvard.edu/news/press-releases/fats-stress-death-uncovering-the-toxic-effects-of-saturated-fatty-acids-on-cells/

spoiler alert, it involves the saturated fatty acid palmitate

I also found this statement rather interesting..."The study also provides new insights into how saturated fatty acids trigger cellular stress and showed that saturated fatty acids are less toxic to cells when they are combined with unsaturated fatty acids."

Found the study the article refers to.

https://www.cell.com/molecular-cell/fulltext/S1097-2765(19)30056-5

 

Quote from PJ on May 5, 2023, 3:39 pm

@salt

"It's a pretty complicated subject... My stance is first and foremost based on my own personal experimentation with what I eat but I think the scientific research is congruent with it. I started writing a long reply about PUFA in the other thread but ironing out the intricacies of this subject in a clear way is quite burdensome, especially when going through study after study and explaining what's incorrect, and why. I might finish it later, or maybe I wont. But some basic points are that the original studies "proving" the essentiality of the EFAs are about as well constructed as the studies "proving" the essentiality of VA, and that in just about every well-constructed study that includes an EFAD (D for deficient) control group, this control group has the best outcomes. The studies showing the "great effects" of EFAs don't have such a control group, they just have groups eating various amounts of various EFAs; the authors conclude that because people who ate more EFA A than EFA B had better results, we all require EFA A to be healthy. Oh and also that we need EFA B (in smaller amounts) for whatever reason." - Salt

I agree wholeheartedly it is a complicated subject. I wish you could share your personal experimentation/experience with PUFAs to help us understand where you are coming from and provide us with more insight.  I have only been looking at EFA's for the past 4 or 5 months, so not an expert,  especially compared to someone like Udo Erasmus whose research (if you include personal experience, his own n=1) encompasses the past 40 years. 

You say, ..."ironing out the intricacies of this subject in a clear way is quite burdensome, especially when going through study after study and explaining what's incorrect, and why."

I can empathize with that.  I went to the original Burr & Burr studies because of Ray Peat's articles...I also went to several of the sources that Ray Peat cited in his articles (very tedious) and I found some disparities between what he said vs what the article said.  What I think is ironic is that he found the error in the early LA study, but missed it with the VA.  As brilliant as he sounded he was still just like you and me, trying to figure out how to feel our best. 

You say, ..."My stance is first and foremost based on my own personal experimentation" 

That is really all that matters.  I feel the same way.  For whatever reason, incorporation of the EFA's into my diet has been nothing but beneficial FOR ME!  It is certainly not going to be the same for everyone.   I recently learned about some genetic conditions associated with lipid metabolism.  If someone were to have MCAD (medium chain acyl coa dehydrogenase) deficiency, which is a disorder that affects the way the body breaks down fats, they may get lipid accumulation in the liver, which would be bad. @lil-chick were you the one that mentioned past frequent vomiting? as this is a symptom of MCAD deficiency, I think you probably would have figured that out pretty early in life though.   Then there is also something called x linked adrenoleukodystrophy.  (Ninja Nerd discusses these at the end of his Fatty Acid Oxidation vid. https://www.youtube.com/watch?v=jxylGoJP9jY) 

You say..."But some basic points are that the original studies "proving" the essentiality of the EFAs are about as well constructed as the studies "proving" the essentiality of VA, and that in just about every well-constructed study that includes an EFAD (D for deficient) control group, this control group has the best outcomes. The studies showing the "great effects" of EFAs don't have such a control group, they just have groups eating various amounts of various EFAs; the authors conclude that because people who ate more EFA A than EFA B had better results, we all require EFA A to be healthy. Oh and also that we need EFA B (in smaller amounts) for whatever reason"  

I get what you are saying here.  I have read that same sort of critique. Chris Masterjohn points out that only after linoleic acid was added in intravenous TPN infusions that  "suddenly a new deficiency was born." (referring to ALA) Makes you stop to think.

I would like to point out that sometimes it is hard to tell in studies the quality of EFA that was used which may be a factor.  A lot of, especially the older studies, would have potentially used commercially produced oils. 

These well-constructed studies can only go on for so long though.  I know my food history for my entire life (51 years).  I know that for much of my life, I have consumed oxidized oils and trans fats when younger.  It has only been about the last 10 years that I have really focused on health and nutrition at which point I was not necessarily consuming oxidized oils but kept a relatively low fat with more of a focus on the saturated fats.  So my long-term n=1 study equates to a very poor intake of healthy functional EFA's.  

You say..."in just about every well-constructed study that includes an EFAD (D for deficient) control group, this control group has the best outcomes."

Could you please point me to these well-constructed studies?  I am interested in reading them. TIA

Quote from puddleduck on May 23, 2023, 4:14 am

@christian Here’s a paper explaining one of the reasons why the “PUFAS are the root cause of inflammatory disease” hypothesis became popular:

https://academic.oup.com/advances/article/6/3/293S/4568626?login=false

An excerpt from that:

“So an important question is why did the evidence from human clinical trials fail to support the theory that dietary LA promotes inflammation?

“One reason might be that the ‘LA-proinflammatory paradigm’ relies on an overly simplified model of LA metabolism. Originally, most of the proinflammatory activity of dietary LA was thought to be a consequence of an accumulation of AA, which leads to greater production and release of proinflammatory eicosa- noids, such as PGE2 and leukotriene B4 (LTB4).

“A review of the clinical literature by Rett and Whelan (47) indicated that increasing LA up to 6-fold within the context of a typical Western diet failed to increase tissue AA. Surprisingly, reducing dietary LA down to 10% of control was without effect on circulating AA. Therefore, for those who currently advocate for large reductions in dietary LA, their emphasis has shifted to the potential adverse effects of oxidized forms of this PUFA.

“Recent advances in analytical capabilities (i.e., lipidomics) have greatly expanded our knowledge of LA-derived metabolites (48). Yet, our understanding of the bioactivity and physiologic role of each of these novel metabolites remains incomplete.

“Figure 2 [attached to this post] is meant to capture some of this complexity, at least as it relates to LA. Unfortunately, this author is unaware of a single publication that describes a research study in which all of the possible bioactive metabolites of LA and other important FAs have been measured and accounted for. Two excellent reviews related to this topic were recently published (49,50).”