I'm hoping we all remember Sauer. If not there's a post here:
Sauer vs Lisanti
And a brief summary at the start of this one:
Sauer and 13-HODE
Sauer demonstrated that food withdrawal from rats carrying tumour xenografts makes those tumours grow like wildfire. He went on to show that it was 13-HODE which made the tumours grow and that either linoleic acid or arachidonic acid (both 13-HODE precursors) were essential for tumour growth in his model. Fasting released these carcinogenic PUFA from adipocytes when the rats were starved.
You cannot make 13-HODE without linoleic acid. Or arachidonic acid if you prefer.
Do you want to make a tumour grow? Feed your model linoleic acid. It's easy. Or you could try using a Ketocal based ketogenic diet for glioblastoma multiforme management in real live humans. There was a trial doing this recently:
Ketogenic diet treatment as adjuvant to standard treatment of glioblastoma multiforme: a feasibility and safety study
which didn't really pick up any benefit, it was only a pilot study. Serious concern about the composition of the ketogenic diet was expressed in this letter to the editor:
Problems associated with a highly artificial ketogenic diet: Letter to the Editor Re: van der Louw EJTM, Olieman JF, van den Bemt PMLA, et al. ‘Ketogenic diet treatment as adjuvant to standard treatment of glioblastoma multiforme: a feasibility and safety study’
link tweeted by Miki Ben-Dor.
Much of the diet was Ketocal based "consisting of refined vegetable oils from sunflower, soy, and palm fruit..."
This looks like an excellent source of the 13-HODE precursor linoleic acid, which Sauer might have recognised as the growth promoter in his rat models.
I would suspect that the ketogenic diet supplied benefit from ketosis, but this was largely offset by tumour promotion from the linoleic acid content.
Is there any end to the damage done by the lipid hypothesis?
Probably not.
Peter
So maybe a high-stearic-acid keto diet would be preferable to fasting if one was trying not to feed a tumor.
ReplyDeleteI wonder if there's any way to tell how much stored linoleic might be lurking in one's adipocytes. Say in a non-overweight person who's avoided veg oils religiously for some years. But then there's chicken and pork, right?
Your second link, "Sauer and 13-HODE", is broken. Maybe you meant this one?
ReplyDeletehttps://high-fat-nutrition.blogspot.com/2013/09/omega-3s-and-g-protein-coupled-receptors.html
The letter is from Colin Champ, an oncologist I talk to on Twitter.
ReplyDeleteNot too long ago he said he didn't think fat had anything to do with cancer. After some back and forth, he seems to have reconsidered somewhat.
cave, yes, yes and yes. Last one was a copy-paste error!. Oh, and eggs (gasp). Plenty of linoleate in modern eggs. If push comes to shove. It begs the question of how low in PUFA does one have to go. That's a current question to me. That might be an individual thing...
ReplyDeleteOver the years I have thought about weight stability to reduce linoleic acid efflux from adipocytes and shift fatty acid metabolism to dietary stearate. The only issue I can see is whether eating enough saturated fat to maintain bodyweight might have to work via inducing enough insulin secretion to suppress lipolysis. Then the possible benefits of stearate are offset by increased growth promotion by insulin. The rodent models do find benefit from stearate irrespective of insulin levels so...
Tucker, should there be a link there?
Peter
Hi Peter,
ReplyDeleteyou know the work of S. Cunnane? In his paper "Problems with essential fatty acids: time for a new paradigm?" he discusses how LA/PUFAs are readily oxidized during caloric deficiency/fasting.
He also discusses how ALA dramatically reduces the need for LA and how symptoms of LA deficiency disappear before tissue is saturated with LA. The latter being the reference for recommendations of LA intake.
He's a very analytical thinker.
"Plenty of linoleate in modern eggs." Do you mean modern in terms of what commercial chickens eat, or as a result of modern breeds regardless of feed? My eggs are from a neighbor whose chickens wander around outside all day in a pasture.
ReplyDeleteCan't remember how you feel about Ray Peat – this high-density 2013 article is rather fascinating, if accurate, and serves only to reinforce your comment "Is there any end to the damage done by the lipid hypothesis?...Probably not."
"Fats, functions & malfunctions—Saturated fatty acids terminate the stress reactions, polyunsaturated fatty acids amplify them.
—The most highly unsaturated fats, including DHA, accumulate with aging, and their toxic fragments are increased in Alzheimer's disease. — The most highly unsaturated fats found in fish oil break down into chemicals that block the use of glucose and oxygen. — The ratio of saturated fatty acids to polyunsaturated fatty acids is decreased in cancer. Omega-3 fats promote metastasis."
http://www.raypeat.com/articles/articles/fats-functions-malfunctions.shtml
cave, many years ago Ray blotted his copy book very badly. In one of his essays he had three references supporting some point. One may have been a typo as it had nothing to do with the point in question and the other two were on-topic but did not contain the information to support his point. That's a hard situation to recover from.
ReplyDeleteI think you might want to know as much as possible about your personal circumstances before you do serious planning food choices. Someone commented elsewhere on the blog that a trial of beef, salt and water would be a good start for any medical problem. I'd have thought it extreme a year ago but nowadays I'm much less dismissive...
Peter
Re eggs, USA databases presumably document USA eggs. What happens with grass-feeding and omega 3 eggs? Dunno on those...
Alex, no, I'd missed that paper (along with an infinite supply of other gems). I have the text now and will have a read...
ReplyDeletePeter
Lots of PUFA in the paleolithic if I read table 2 correctly. NAFLD must have been rampant.
ReplyDeletehttps://www.nature.com/articles/srep07926
Also Peter, isn't this adiposity less than dogs?
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5744898/
Cavenewt, glad the surgery went good.
Alta, if I read table 2 correctly the samples were around 15% fatty acids and of this most were palmitic and stearic acids, around 70-80%, looking at the white samples rather than brown adipose tissue. Table 3 suggests that in white adipose tissue LA was undetectable or, in one sample, it was 0.4% of the total of the FAs in the tissue. One sample of brown fat had almost 2% of LA and 4% of ALA but all of the rest of the samples were under 1% or undetectable. I note oleic acid is pretty low too, around 10%ish. Pour that olive oil down the drain!
ReplyDeleteAssuming bulk calories for hunters came from white adipose tissue rather than brown fat the tables suggest a max of 0.0-0.5% LA with somewhere around 0.0-1.0% ALA. Maybe slightly higher to allow for degradation in the permafrost.
Great find! Not making we want to drink corn or flax oil!
Personally I’d been looking at data from modern wild African elephants and 1% LA with 2% ALA look reasonable average values from here https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3954733/.
Stearic acid rules, along with my fave, palmitic acid.
Peter
Quick and probably easy question: are omega-3 fats good to have in the diet? I understand at some minimal level they're (probably) necessary, but do higher levels help or hurt? If these are burned for energy, they're not going to produce much in the way of ROS and therefore aren't any better than the omega-6 fats from a "protons" viewpoint. I've heard O3 are good for fighting inflammation in the body (opposite function of O6). Overall thoughts on O3 vs O6?
ReplyDeleteI have an overall impression that buffalo hump fat was a prized delicacy which primitive hunters went for first. The Siberian samples appear to have been taken from under the belly skin. I wonder if brown or white fat predominated in the hump.
ReplyDeleteThe article finally made clear to me the difference between brown and white fat. Also the differences in fat production between ruminants and single-stomached animals. Fascinating!
Altavista, thanks.
Unknown. That is far from a simple question. We probably need some DHA and arachidonic acid. Probably as much as come from eating our share of a large herbivore. Many would disagree.
ReplyDeletePeter
Alta, re body fat %, yes. No idea why that should be...
ReplyDeletecave, it's not quite that simple. Elephants (and I'd guess Wooly Mammoths too, our historic preferred food in temperate zones) are hind gut fermenters so I wonder if their fat might be less saturated than ruminant fat. No chance to check at the moment.
Peter
Ron Rosedale has this to say about the argument between
ReplyDeletegenetic and metabolic cause of cancer:
https://www.youtube.com/watch?v=F5HXCfimEa4
He appears to be saying protein drives cancer growth.
I'd really like to know what you think of his info?
Arachidonic acid seems controversial in some ways. The scientists (!) over at wikipedia say this : 'Increased consumption of arachidonic acid will not cause inflammation during normal metabolic conditions unless lipid peroxidation products are mixed in. '
ReplyDeleteand lipid peroxidation lands you right back to looking at the linoleate cascade, food preparation, cooking, iron/lead etc via Gerard Spiteller. (And many others.)
I have never noticed if there is much marrow in chicken bones but marrow in general is a high fat source eg 26g fat in 28g of caribou marrow plus other useful nutrients. It's amusing to see sliced cow bones cooked and sitting on a plate with delicate trimmings in a gourmet restaurant. There was a sciencey newspaper article doing the rounds recently about the discovery of stores of marrow bones somewhere near Miki Ben Dor's areas of interest. Seems that it is literally a good storage form of fatty food ie doesn't go off too quickly. (Dogs worked that out long ago.) Hoards of deer bones were found in caves associated with early humans. As my wife said at the time
"Dear bones, I miss you."
Peter, thanks re woolly mammoth hind guts. Nothing in this universe is as simple as it seems! Since my local market doesn't seem to carry mammoth meat anyway, it's good to know that ruminant fat might be a better choice at least for the immediate future.
ReplyDeleteCurious about who these hind gut fermenters might be? Here's the lowdown from Wikipedia: "Hindgut fermentation is a digestive process seen in monogastric herbivores, animals with a simple, single-chambered stomach. Cellulose is digested with the aid of symbiotic bacteria.[1] The microbial fermentation occurs in the digestive organs that follow the small intestine: the large intestine and cecum. Examples of hindgut fermenters include proboscideans and large odd-toed ungulates such as horses and rhinos, as well as small animals such as rodents, rabbits and koalas.[2] In contrast, foregut fermentation is the form of cellulose digestion seen in ruminants such as cattle which have a four-chambered stomach,[3] as well as in sloths, macropodids, some monkeys, and one bird, the hoatzin.[4]"
As for my buffalo hump comment, I'm wondering if buffalo hump fat is/was white (i.e.saturated) fat, which might explain why it was so prized. Ancestral wisdom and all that.
The Nature paper depends upon an assumption of RDA for DHA+EPA of 250 mg and 0.5%E of ALA.
ReplyDeleteHow valid are these values? Is DHA+ EPA really an essential nutrient?
India has many vegetarians, all apparently biologically successful, who consume only dairy as animal food. How much DHA are they getting?
The paper speaks also of
ReplyDelete"the n-3 PUFAs needed for the maintenance of long-term health and prevention of specific chronic diseases."
What may be these "specific chronic diseases"?
Passthecream,
ReplyDeleteMy oldest and I love marrow from ruminants. We also love eating the ends off chicken bones. The marrow is hard to get at though. I am blown away by how soft the bones of industrial raised/breed chickens are compared to my slow growing backyard flock. The bones of my chickens are like concrete. Lol! Cornish crosses are ready for sloughter in about six weeks.
They are true freaks of nature. All that selective breeding sure paid off. I think I just might have to roast some bones tonight!
@ Gyan
ReplyDeleteIndia is a hot spot for FADS1 gene variants which enables carries to synthesize omegas better from plant-based fats. They might indeed need less of the animal-derived fatty acids.
In contrast, native Greenlandic people have a variant that protects them from too many O3s.
some refs: 28333262, 29094686, 28193867
Hi Bill,
ReplyDeleteI could spend days discussing this presentation. There never was an oxygen holocaust. Nick Lane is convincing on this. GH promotes insulin resistance and inhibits muscle catabolism. Insulin resistance is my forte, keeping my muscles in old age seems good too. So I like GH. Insulin controls the production of IGF-1 in response to GH. Simple Atkins induction lowers insulin and lowers IGF-1 in real live humans compared to the SAD. Leptin drops with any diet producing weight loss, Atkins induction will be no different. Low mTOR is apparently needed for ketosis. If you are in dietary ketosis does that mean mTOR signalling is low? Even on 2g/kg protein as part of a 2:1 PKD diet?
But on some things he is spot on. Growth factors matter, insulin and IGF-1 no doubt. Hyperglycaemia mimics growth factors. There is still ample scope for mitochondria to be defective in cancer and I felt the Warburg effect was a bit of a straw man. Deep understanding is needed but it is plausible that mitochondrial changes are secondary. But having acetyl-CoA dipping in to the TCA then being exported as citrate for anabolism does not mean the mitochondria are normal. Especially once you factor in cell surface oxygen consumption to facilitate anabolism.
And metformin! Argh. Metformin as a complex I blocker is just wrong. It’s an insulin signalling blocker, so this fits with his ideas nicely. Has he not asked himself why 500mg of metformin improves cycling race performance within an hour? Hint, it frees fatty acids from insulin lock-down. And why chronic metformin use extends life span (hint, insulin signalling reduction stops insulin making you die early).
Bit of a curate’s egg, good in parts.
Peter
Peter, does the last comment "chronic metformin use extends life span" mean you are now in the pro-metformin camp? I have read many of your metformin blogs and find it hard to see what position you had reached and why.
ReplyDeleteUnknown, I didn't realise there were camps on this battlefield! I want to understand. Overall it looks to be a Good Drug if you eat a diet of utterly execrable crap, say designed by a cardiologist or diabetologist. If you are ketogenic then there is minimal insulin signalling going on and the benefits seem much less tangible...
ReplyDeletePeter
Re Rosedale video and his remarks about the 1973 enucleation paper and the cybrid experiments.
ReplyDeleteSwimming in intellectual waters over my head here, but his citation of a paper about enucleation of cells doesn't seem to me to be evidence of anything – because an enucleated cell can't divide, can it? Without any DNA? So that doesn't prop up the argument *either way* about transplanting nuclei from normal cells into a cancer cell and vise versa. Without cell division, you can't tell if cancer is being propagated or not, right?
cave, I think the nuclear genomic concept is clearly wrong. I’m not sure the metabolic concept is 100% correct but interventions based on it seem to have significant effects from the few studies which have been done. I spent many months going through the early frog/tadpole experiments growing baby frogs from the nuclei of frog renal carcinoma cells. I realised, eventually, that the reason for the tumour, ie it is virus induced, could be eliminated by not transferring virus loaded cytoplasm from tumour cell to clean oocyte. Then I found that later papers said exactly this! Rules out the nuclear genotype hypothesis but I would guess the virus provided a growth signal to the cancer cell. Seyfried’s ideas continue to worry me somewhat but interventions in the LC direction almost invariably reduce signalling pathway activation, so I feel he is on the right track. I’m going to hunt for the paper which demonstrated that unadulterated hyperglycaemia activated insulin signalling w/o access to insulin. It didn’t seem that important at the time so I hope I saved it! As Seyfried claims, cell culture is undoubtedly a carcinogenic environment with copious glucose and a supply of insulin/IGF-1, which actually fits with Rosedale’s ideas rather well. It just leaves me wondering why non neoplastic cell lines can exist in these conditions… But Rosedale and Seyfried have rather more in common than the video suggested, a concept which came to me at several points later on in the video, once the straw man had been burned.
ReplyDeletePeter
"Plenty of linoleate in modern eggs."
ReplyDelete"Daily consumption of 2... standard eggs, high in omega-6, caused a 40 % increase in [oxLDL]... After eating 2 per day of the specially-composed eggs, with both high anti-oxidant and low omega-6 levels..., [oxLDL] levels were similar to the control..."
https://twitter.com/TuckerGoodrich/status/988543572948537344?s=20
"Tucker, should there be a link there?"
I think you're right, you'd have to bottle up the LA in adipocytes via insulin. Sounds like something a cardiologist would propose! LOL
I can't really see any benefit to not burning off the LA in storage, I recommend people do it as quickly and aggressively as possible, adding some form of fasted endurance exercise to speed it along.
Evidently one hopes to get it down before cancer strikes...
Justin re: chicken bones - high wheat chicken foods need to contain added phytase, to break down the high phytic acid which otherwise chelates many essential minerals : iron, calcium etc, and also to release the phosphorous but I'm not sure if anyone really thought through all the chemistry very well. Chickens that spend all their life constrained wouldn't get to, or need to develop much strength. They are omnivorous though and well capable of processing small seeds.
ReplyDeleteI just yesterday received a massage from one of keto-followers/ She was obsessed about loosing weight and spent 3 years on a low-carbs low-calories diet under 1500 calories and lost from 185 to 132 lbs living some days on a coffee with batter. Normally, I disapprove of such poor diet, but it worked for her as she has found out. Two days ago, she was hospitalized with peritonitis. During the operation, a large disintegrating tumor of the rectum was found. No metastasis. No histology results yet. It looks like her tumor disintegrated due to malnutrition. Doctors told her they never saw such a thing.
ReplyDeleteVery interesting Galina. Deep ketosis much of the time combined with malnutrition. I've heard the Gerson diet in its modern form is relatively ineffective due to present day folks refusing to accept the caloric restriction required... No backup to the statement. But perhaps hypocaloric malnutrition is something organisms might survive better than cancer cells might?
ReplyDeletePeter
Morning Peter,
ReplyDeleteis this paper of any use for your mitochondrial LA-theory? I can't tell...
https://www.physiology.org/doi/pdf/10.1152/ajpendo.00032.2014
This is an interesting conversation with Dr. Bill Schindler, who is Associate Professor of Anthropology and Archaeology at Washington College in Chestertown, Maryland.
ReplyDeletehttps://humanperformanceoutliers.libsyn.com/episode-165-dr-bill-schindler
At one point, he discusses going to visit a hunter gatherer tribe to make what he thinks will be jerky. Instead, what they did was kill an animal (lamb?), take the parts off that had to be eaten, then basically "unwind" the animal into thin meat strips. They dried these. They also crushed the bones, and dried these. But instead of making "jerky", they made soup. The dried meat would reconstitute, and the bones added flavor and nutrition to the soup. They then ate/drank the soup.
I thought this was brilliant and unexpected. I was expecting tallow, pemmican, jerky, etc. Instead, soup.
Alex, yes, it is very supportive in some ways. Obviously the mice were calorie restricted. If you do this LA looks very good. Unfortunately they are also hungry, in humans this means they eat more. Not the case for the mice, they have no extra food in the fridge. It's nice the ALA seems to be a disaster area, generally it comes out very well but omega 3s are the darling of modern nutrition. Have to look at the details there...
ReplyDeleteUnder LA adipocytes stay insulin sensitive until they are so big they leak FFAs and make the rest of the body insulin resistance by that route without becoming IR themselves. They can become insulin resistant but that is probably insulin exposure triggered and is independent of size. I have a nice paper on that waiting for posting for years.
Peter
Those were also Zucker obese mice, purchased as obese at the start of the experiment. No notes on what they were fed prior to being purchased.
ReplyDeleteThey lack leptin receptors.
To Peter's point, this is may be a classic example of an experiment where calorie restriction is an intervention, not a control.
Is there any end to the damage done by the lipid hypothesis?
ReplyDeleteIt seems not. Here's a government-mandated change in oils, because Keys, affecting a captive population.
It looks like this did not go as well over the longer term as the 7 Countries and WHO experts overseeing it here expected.
https://www.bmj.com/content/313/7064/1044.long
This 2015 report states "54.2% of the participants were overweight or obese - The prevalence of type 2 diabetes in the Mauritian population aged 20-74 years was
20.5%: 19.6% in men and 21.3% in women -
for the first time in 30 years diabetes prevalence is not increasing and in the 2015, some six years since it was last measured, diabetes prevalence appears to have stabilised."
28 years since the sudden increase in omega 6 - this population has now reached saturation for its obesity and diabetes potential.
https://health.govmu.org/English/Statistics/Documents/Mauritius%20NCD%20Survey%202015%20Report.pdf
Puddleg, I'm sure they will find a way to make it worse! Do we know what has happened to lifespan? Can't see it in the index or a few searched on longevity, mortality etc...
ReplyDeletePeter
@Peter,
ReplyDeleteI think mortality has started to drop slightly in recent years, what with all the health-care expertise the island has had to import, but there is some interesting data here: when coding for vascular mortality and diabetes mortality was updated, the 2 conditions switched places!
See fig 2 - I can't think of a better illustration of Kraft's thesis that CVD is "diabetes in situ".
bmcpublichealth.biomedcentral.com/articles/10.1186/s12889-019-6748-7
I spent some time a while back trying to find any paper on the LA/PUFA contents of chicken eggs that were NOT fed chicken feed - I didn't find the data.
ReplyDeleteMy hunch is if someone tested eggs - say from the Caribbean (where chickens are anywhere where they can get some fresh water - they eat the lizards and bugs) - the PUFA content would be much different.
This paper seems to be saturated with the lipid hypothesis and the authors need to read the Cunnane paper for guidance I think. But?
ReplyDeletehttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4487977/
This one about wild ducks is more interesting, I can't copy the link but easy to Google
Fatty acid profles of yolk lipids of five species of wild ducks
(Anatidae) differing in dietary preference
J. Zool., Lond. (2002) 257, 533±538
Lipids, waxes etc may also vary with climate.
https://www.sciencedirect.com/science/article/pii/S1319562X13000855
Puddleg, nice. I have the greatest respect for diabetes in-situ as a concept. Kraft wasn't so much ahead of his time, more like the cardiologist are still lost in lipids!
ReplyDeletekarl and Pass, I was wondering what wild birds might be like. Next is what non aquatic species might have as their egg lipid profiles...
Peter
I'm half tempted to dig up the methods used to analyze the fatty acid profiles of egg yolks and gather my own data. I don't have a gc-ms at work, but I have a couple 5890 gc's and a bunch of different columns and plenty of solvents. I wonder if I could make up calibration samples of pure fatty acids
ReplyDeleteAt different concentrations and then use AUC to quantify each component in the mixture extracted from the egg yolks? Would love to do a controlled experiment with my birds and feed them lots of coconut meat and just let forage for the rest. Would have to do it during a nice wet spring.
Clarified fat from completely free ranging geese is like thick olive oil at room temps. Domestic breeds but left to their own devices.
ReplyDeletehttps://www.ncbi.nlm.nih.gov/pubmed/11517448/
ReplyDeletekarl—
ReplyDelete"My hunch is if someone tested eggs - say from the Caribbean (where chickens are anywhere where they can get some fresh water - they eat the lizards and bugs) - the PUFA content would be much different."
I'm still very interested in the question of which came first, the PUFA or the egg?
Since nobody seems to have looked at true free range eggs*, could one assume that the yolk, which is essentially a pre-embryonic chicken, would have a similar lipid profile to the adult bird which produced it? Are there any parallels with other types of animals that might be helpful?
* not the pale simulacra that pass for "free range" commercially in the United States.
Peter:
ReplyDeleteSomeone posted this on Reddit ketoscience:
https://www.sciencedirect.com/science/article/pii/S0005273612000156
Have you discussed it?
Regarding the duck eggs - if wild ducks can get a decent 3/6 ratio whatever they eat, and domesticated ducks don't, then how likely is it that when we breed animals to fatten easily we are really selecting for alleles that increase arachidonic acid and endocannabinoids over DHA and EPA?
ReplyDeleteBecause that would really help...
I always tell people chickens are omnivores with a carnivorous slant. Lol!
ReplyDeletehttps://youtu.be/LRn0puwK_f0
Passthecream, I can't wait to deal dive into the methods on those papers! Thanks for posting!
ReplyDeleteI'm a big fan of guineafowl but there are none living near me atm and I know nothing about the lipid profile. I will enquire.
ReplyDeleteJustin—
ReplyDeleteSomewhere I have a video of one of my chickens fighting the cat for the remains of a squirrel the cat was eating. Chook acquired the tail, which she slurped down like a cartoon spaghetti noodle.
Cavenewt-
ReplyDeleteThat's crazy! I've seen them do the snake slurp thing many times in the spring. They once killed a giant copperhead and fed on it for a couple of days until just the bones were left.
Justin, you are probably the one to ask - I have been thinking about methods of separating fatty acids. Thermal methods would seem to be better than centrifuging since there is not a huge density variation from linoleic through to stearic acids. Frozen olive oil is a well known gourmet treat as a butter alternative but that is all triglycerides. If you put a cup of oil in a freezer, the higher freezing point tags do go viscid more quickly around the edges of the container but not as big a melying point range between eg stearic-stearic-oleic triglyceride and oleic-la-la as between stearic acid and linoleic acid. There seems to be a lot of thermal inertia too ie between freezing back to melting, hysteresis.
ReplyDeleteThen there is the question of how to extract the fatty acids from the triglycerides - saponification? Maybe with super-fatting in saline alkali and excess water, harvest the scum from on top? The only alternative seems to be fats in water in a pressure vessel to 280c to separate the fatty acids. Bit risky!!!
It would be fun to isolate some stearic acid via bucket chem.
Any thoughts?
Passthecream
ReplyDeleteWe've done a fair amount of separations over the years at work. Without thinking about it too much, distillation is the first thing that comes to mind. I feel like it would have to be a multipass kind of thing with the correct condenser geometry to get the purity you want. Definitely expensive unless you have good fab skills and some material/hardware laying around. I'll ask my boss about it and see what he says. Need to look up the boiling points of each fatty acid when I have a chance.
Separations chemistry is actually pretty cool stuff. I will use dirty nylon fibers as an example. Dissolve the nylon in formic acid. Run the liquid through the appropriate micron rated filter to get the contaminates out. Then load the formic acid/nylon solution into a blender and slowly pour in water. The formic acid is miscible with the water but the nylon isn't. You will crash out the nylon and then all you have to do is pour off the aqueous formic acid solution and rinse the nylon a few times with water. I used to do this in big SS party blenders. Fun stuff!
ReplyDeleteHere is one possible small scale way of separating. Better hope you have deep pockets though. Gotta pay to play. Lol!
ReplyDeletehttps://www.brinstrument.com/fractional-distillation/spinning-band-distillation.html
Justin, I think I'd get a knock on the door from the p.i.c. if I built one of those.
ReplyDeleteM.P. differences of the isolated fatty acids are huge:
69C for stearic vs 25c for oleic and -7c for linoleic so a simple refrigerative technique should work. Cooled spinning disk?
If chickens are anything at all like mammals I imagine you'd find the most saturated FAs not in the more exterior parts you'd normally get from the BBQ chicken shop but around the organs and within your 'inner chicken'.
ReplyDeleteA deep philosophical construct for some, I'm sure.
Passthecream-
ReplyDeleteI evaluated solid at room temp fats/oils years ago as potential phase change materials to soak up heat in an oxygen generator I was building. In mixtures you don't really have discrete melting points of each constituant. The mp is basically dictated by the ratios and in the case of cocoa butter the crystals that are formed during the original melting/quenching cycle. Chocolate bar manufacturing is cool stuff because of this. Allows you to handle the chocolate without it making a huge mess in your hand. A lot like metallurgy. I have a dsc at work and can see this in the traces. An easy test to find the actual melting point is to poke the fat with a small glass capillary tube and place it in a glass beaker full of water. You slowly raise the temp on the water bath until the solid goes from a crystalline form to a clear transparent liquid. All while watching the water temp. You can't be messing around and get distracted. I found using a nice HD video camera with a higher framerate worked awesome so I could continue to multitask. Lol!
Btw, I found a cool paper that evaluates the different methods for analyzing fatty acid profiles. Hard shoot fatty acids and get good data on the GC since they are already somewhat oxidized? The FID might have a problem because of that. HPLC is probably the way to go. You can methylate them with methanol and then they are much more volatile? Then you can get good differentiation on the gc. Then you just use a reference methylated fatty acid at known concentrations that wouldn't be in the normal makeup and ratio that in to the mix, then you should be able to quantify. I'll post up the link to the paper when I get to work.
https://www.hindawi.com/journals/jfq/2017/9698107/
ReplyDeletehttps://cen.acs.org/articles/91/i6/Splitting-Fatty-Acids.html
http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0103-50532006000100013
OK - "On average, therefore, the yolk ω-6:ω-3 ratio is some 10 times greater in captivity than in the wild. In this light, the fortification of table eggs with ω-3 PUFAs to enhance human health can simply be seen as a return to the natural situation."
ReplyDeletehttps://link.springer.com/chapter/10.1007/978-1-59745-330-1_10
Big Ag - "industrialized food" is not human food..
karl,
ReplyDeleteThis makes me happy I've spent the money for pasture-raised eggs for awhile now.
One thing about such eggs is that the raw yolks seem more susceptible to breaking as the white runs off. It's like a more viscous white adheres more tightly to the yolk.
A friend once cooked a Thanksgiving turkey noting it was "vegetarian fed". He thought it was a feature.
Since turkeys eat bugs, I'd consider a vegetarian-fed turkey a bug, not a feature.
karl, good find. I scanned the references and checked the two that looked promising to see what the "domestic" birds might've been fed. Grain, of course, in the one reference that mentioned anything at all. https://www.sciencedirect.com/science/article/pii/S030504919900108X
ReplyDeleteHere in the US we can pay an exorbitant amount for commercial "omega-3 eggs". I suppose they've been fed less grain, or perhaps, per another one of those references, their feed has been supplemented with something like fish oil which does raise O-3s – I'll try to find out. But still, anything commercial in a grocery store I would suspect is a lot less beneficial than buying eggs from a neighbor whose hens spend most of the day out in a big pasture, though I'm sure they have access to corn-based supplemental feed. When I had chickens and they were foraging every day, they ate very little commercial feed. They vastly preferred squirrel tails.
https://academic.oup.com/ps/article/79/1/51/1548774
"The amount of the different n-3 long-chain PUFA was lower (P < 0.001) when FO [fish oil] was present in lesser proportions in the diet."
Is this statement paradoxical? "Replacing FO with LO [linseed oil] resulted in the lowest decline of its derivatives by elongation and desaturation and an increase in the total n-3 FA in the form of linolenic acid (LNA)." I can't recall if we like linolenic acid or not...
@cavenet
ReplyDeleteOnly one problem - O-3s are not one thing. The O-3s in fish oil that might matter are the long-chain ones. "omega-3 eggs" I suspect is pure marketing crap - they don't list the eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) content. The other O-3s could even be a bad thing. The O-3 in eggs is probably from feeding them flax-seed oil which is about 1/2 Linoleic acid.
And - there is correlative evidence that these LC-O-3 may have benefits - a so-so blood thinner - connection with less mental illness. I don't think we 'know' anything close to the narratives preached about fish-oil say.
I would want eggs from chickens eating bugs and lizards and grass..
karl
ReplyDeleteThanks for the details. I was skeptical of "Omega-3 eggs" anyway. I'll stick with the bugs and squirrel tails.
@Karl @Cavenewt,
ReplyDeleteEven in the absence of high LA intake, high ALA intake can suppress long-chain omega 3 content of circulating lipids.
The best outcome for EPA and DHA seems to be with higher SFA and lower LA and ALA - dig up the Gibson paper for a cool 3D graph of this.
From these papers, if you had no meat or fish so had to use mustardseed, canola or flaxseed oil to get your omega 3, you'd keep the dose very low and add plenty of butter.
As vegetarian Indians used to do, before their diabesity epidemic, by adding a little mustardseed oil to ghee.
1] Gibson, Robert A. Musings about the role dietary fats after 40 years of fatty acid research. Prostaglandins, Leukotrienes and Essential Fatty Acids, Volume 131, 1 – 5
2] Garg ML, Thomson ABR, and Clandinin M T. Interactions of saturated, n-6 and n-3 polyunsaturated fatty acids to modulate arachidonic acid metabolism.
February 1990 The Journal of Lipid Research, 31, 271-277.
3] Dabadie H, Motta C, Peuchant E, LeRuyet P, Mendy F. Variations in daily intakes of myristic and alpha-linolenic acids in sn-2 position modify lipid profile and red blood cell membrane fluidity. Br J Nutr. 2006 Aug;96(2):283-9.
4] Dias Cintia B, Wood LG, and Garg Manohar L. Effects of dietary saturated and n-6 polyunsaturated fatty acids on the incorporation of long-chain n-3 polyunsaturated fatty acids into blood lipids. European Journal of Clinical Nutrition. 2016; 70: 812-818
Puddleg, thanks.
ReplyDeletehttps://www.sciencedirect.com/science/article/abs/pii/S0952327818300140
I have the whole thing if anyone wants it. Haven't perused yet.
It's good stuff - interesting case study in there of woman able to have successful pregnancy with no "essential" fatty acids (or fats at all) in diet!
ReplyDeleteThe mechanism for SFA raising serum omega-3s is described elsewhere as follows:
Long chain omega 3s and myristic acid (C:14) both reduce triglycerides by triggering removal and catabolism of TGs from ApoB within the liver. (The omegas also cause the ApoB to be catabolised and the C:14 doesn't). So if C:14 is present with omega-3s it is sacrificed instead of some of the EPA or DHA, sparing more into circulation.
That effect is independent of other benefits from SFA as a replacement for LA, which will also improve 3/6 ratio.
@cavenewt @Puddleg
ReplyDeleteFirst, the 'Mediteranian diet' was actually a marketing campaign. (read :'The Big Fat Surprise: Why Butter, Meat and Cheese Belong in a Healthy Diet' for the details).
What I would also say is all of the "concentrated seed oils (aka PUFA) belong in your diet" narrative is marketing - not science.
If you pay for lunch for the right people you can get the results you want.
Most of the fatty-acid nonsense is based on junk-science/weak-correlative-evidence and ego powered narratives. Be very careful what you believe.
One line of the paper jumped out "Omega 3 fats as a component of a healthy diet have been extensively studied and there are now recommended intakes from a number of organisations[sic] ."
Yes, it has been studied - Most of the papers are junk though - yet the narratives are 'all-knowing'. Most everything I 'knew' about diet 25-years ago turned out to be wrong - I suspect many bits of what I think I now 'know' is wrong as well. Be very careful about what you believe.
One has to realize that adding seed oil to the diet is a second round of the Malthusian theory - the first was farming - big population spike. Would there be enough food if they were not pushing seed oils? I think it is 'junk food' - but think of how many people get the most of their calories from eating sugar-drinks and oil-covered carbs(CIAB).
I don't think there is real science behind the 'essential fatty acid' narratives - they had confounding uncontrolled variables. Could be a long wait for someone to do a proper follow-up study; why do a study when everyone 'knows' the results?
Some of the problem is understanding not only if the results are 'significant' in the science - as well as 'significant' in the common understanding of the word. Humans are very bad at judging relative risks..
@Karl,
ReplyDeleteand here we find that EPA and DHA do not improve macrophage cholesterol efflux in vitro.
Thanks to Peter's lessons, I now know to look at the culture medium.
2000 mg/dL glucose?
So I take it that this is what we might see during a post-prandial glucose spike in someone with impaired glycaemic control.
Who knows what will happen in a healthy individual, or in the fasting state.
https://www.sciencedirect.com/science/article/pii/S1388198119301878?via%3Dihub
@ Puddleg
ReplyDeleteAfter looking at that paper, I feel like I'm living in the future.. "Volume 1865, Issue 2, February 2020, 158536" (false like other published things)..
But let's take the very first sentence of the paper: "A high consumption of polyunsaturated fatty acids (PUFAs), particularly n-3 PUFAs, is atheroprotective."
Notice how this is stated as FACT even though PUFAs are not a thing - they are a class of things, and some appear to have bad effects. I don't think I believe they 'know' this 'fact'.
The reason they say they "know" or are willing to state this as fact is from correlative papers that don't show causation.
"Since the 1970s, most of the epidemiological data highlighted the cardioprotective attributes of a high consumption of polyunsaturated fatty acids ..."
Once they finished spewing the grant seeking mantra - the paper is about macrophage uptake - not cardiovascular disease ( unless you accept another series of ungrounded narratives).
This does not show LDL entering the intima wall - it is about it entering macrophages.. If you follow this story close enough it is important to try to see what they are NOT talking about.
Their narrative is that PUFA's lower LDL and because everyone 'knows' that LDL is the 'cause' eating concentrated seed oil is 'cardio-protective'. BS -- I don't think macrophages appear until after the damage occurs - I don't think they can show LDL (no matter what size or color of the stripes) entering the intima wall because it probably doesn't.
My hunch is that eating PUFA lowers LDL by causing inappropriate storage of lipids - making people fat and miserable. Big ag pushed this to the max - selling seed-oils as some sort of health elixir - yet the Keys' data was hidden as the death rate went in the wrong direction - much easier to treat blood-test levels than the pesky death statistic.
@karl, @puddleg
ReplyDelete"Thanks to Peter's lessons, I now know to look at the culture medium." Follow the DMEM! I mean, I knew to look at in vitro experiments with a grain of salt anyway, but once Peter put up that post about Dulbecco's modified Eagle's medium, in vitro deserves even more of an askance glance. Apparently the stuff comes in both high-glucose and low-glucose versions, but still.
As for EFAs, speaking from the perspective of someone who struggles to understand the ins and outs of the subject, I've decided that simply sticking to real food, or as close to it as we can get it in today's world, will probably be just fine in terms of evolutionarily appropriate ratios. It just doesn't make sense to have to measure and calculate every bit of food one puts in one's mouth. I try to let evolution be my guide. Even so — "Be very careful about what you believe" seems to be pretty good advice.