A couple of things came up in emails recently. First is that I never mention that I had a chat with Ally Houston on the Paleocanteen podcast. It was fun. I think I sound like me. It's here
https://paleocanteen.co.uk/peter-dobromylskyj-hyperlipid/
Second is that karl asked if there was a general formula for working out the F:N ratio for assorted fatty acids.
Edit: cavenewt pointed out that for people unfamiliar with the FADH2:NADH ratio concept there is a reasonable introduction at Protons: FADH2:NADH ratios and MUFA. PubMed-ing Dave Speijer and CoQ makes good reading too. End edit.
There wasn't but given a few minutes and some algebra it works out like this for even-numbered, fully saturated fatty acids of carbon skeleton length n:
F/N = (n-1)/(2n-1)
So stearate (C18) is 0.486
Palmitate (C16) is 0.484
Caprylate (C8) is 0.467
For MUFA/PUFA you just subtract one FADH2 per double bond (db). This doesn't affect the NADH term.
F/N = (n-1-db)/(2n-1)
Oleate (db = 1) is 0.457
Oleate is the MUFA of stearate. Saturated fats allow us to resist insulin, MUFA allow insulin to act.
Linoleic acid, also C18 but with two double bonds, gives 0.429
This is lower than stearate or oleate. The switch for ROS generation occurs between roughly 0.486 (high physiological ROS) and 0.457 (low physiological ROS). LA is lower than oleic acid.
Glucose has an F/N ratio, from memory, of 0.2 so LA is the "glucose-like" of the common fatty acids, in Mike Eades' terminology, and so will fail to generate fatty acid appropriate ROS. Which will allow continued insulin action when it should be resisted. That will make you fat, and the loss of calories in to adipocytes will make you hungry. The exact opposite of stearic acid...
Happy New Year all.
Peter
Subscribe to:
Post Comments (Atom)
39 comments:
For those who, like me, struggle to understand these chemical details, and who, like me, could not figure out what F and N stand for in this context, this might help:
https://high-fat-nutrition.blogspot.com/2012/08/protons-fadh2nadh-ratios-and-mufa.html
Excellent - I created a spread sheet with this.
So thinking a bit - we don't generally eat a single type of fatty acid.
Foods range from about Butyric acid C3:0 at 0.419 - and range up to C18:0 0.486.
If we look at 18:2 ω-6 linoleic acid at 0.375 - imagine eating a mix - where the resulting average is in between.
I'm also wondering if it is possible that because each FA chain of C18 contains a lot more energy than the shorter ones - chain length might matter? Do we need to take an average that considers the molar difference?
I'm also thinking that it is probably a good thing that 'antioxidants' are not absorbed much. So as the ratio shifts - we get ROS - and at some point the superoxide dismutases (SOD), glutathione peroxidases (GPx), and catalase (CAT) get swamped and the signal happens? I suspect the level of some metal ions matters as well.. Zn, Cu..
So could the 'switch' might have something to do with the chain length vs SOD capacity?
Many more questions .. we need some good research that fiddles with this ( chemically defined diets)..
,.,
One more thought - reagent grade C18:0 is sort of waxy - does not mix well with my coffee.. perhaps needs a bit of ethanol solvent.. Just increased my squat weights??
.. We could use Dave Feldman testing this .. could be decades before the academic world does carefully focused science..
@karl,
Some digestive issue with reagent grade C18:0?
@karl. "One more thought - reagent grade C18:0 is sort of waxy - does not mix well with my coffee..."
I haven't tried reagent grade but I have some of the food grade stuff which I understand is about half palmitate. The melting point is something like 150° so I'm not sure, without some sort of an emulsifier, it will ever work in coffee (in my case, tea—only tried it once!) As soon as you suck it into your mouth it coats your teeth with wax.
But if you melt it in a pan about 1:5 with butter (ratio thanks to Brad/fireinabottle.net), it works for sautéing. That's how I've been doing it, mixing it with cocoa butter and butter.
Or perhaps your comment was meant jokingly ;)
"The switch for ROS generation occurs between roughly 0.486 (high physiological ROS) and 0.457 (low physiological ROS)"
That seems like a pretty large range. What factors would determine where someone is on the physiological ROS spectrum? And how much would estimating this help with optimizing one's intake to maximize insulin resistance for weight loss for example?
Love the blog!
Peter,
Have you seen this study? Researchers at UCLA discover proton-leaking beta cells can cause hyperinsulinemia.
https://diabetes.diabetesjournals.org/content/early/2019/11/13/db19-0379
@cfmorais -- no digestive issues - nada - but I've been low-carb for years and years..
@cavenewt -
Too much trouble. I did try mixing it with a couple of ml of ethanol - then added my usual coffee and cream - seemed to work great - no floating icebergs. Might be getting absorbed better - forgot to eat the rest of the day. Try it - I didn't measure - so I could be fooling myself - only tried it once so far.
@shitmypresidentsays
That is what I've been thinking about - could be multi-factorial - amount of SOD available etc.. What I've seen in other biological control systems - almost always nested/redundant feed back loops so a single failure isn't fatal. Biology is MUCH more complex than they make it sound in the papers.
Perhaps insulin sensitivity is the coarse adjust and little swings of insulin levels is the fine adjust?
If true - what happens with a swallow of glucose? - we need to adjust insulin sensitivity if exposed.. (I think this switch is real). What is happening is LA is like a wrench in the gear box, it fools with our bodies insulin feed back loop.(excuse the analogy .. I shouldn't use analogies -- often mislead -- a bad analogy is like a leaky screwdriver...). We are not evolved to eat huge quantities of concentrated seed oils..
I'm speculating that this switch is not a typical feedback - not a level adjustment - really like a switch - a mode of operation change.
,.,
I stopped eating eggs a couple of weeks ago - so I might be confounding that with trying stearic acid - but something is happening.. I'm 64 - just increased my squats from 255 to 270 over the last week - I had been stuck at 255 for months. Just too much LA in the industrially produced eggs??..
Hi E Hosewater,
An interesting paper, I’d not linked uncoupling/uncouplers to insulin secretion. The group get Brownie Points for specifying glucose concentrations throughout and for using an oleate/palmitate mix as the FFA supply. So they are good, and interested in finding out potentially useful things. I have to agree that I think the elevated FFAs are major drivers of glucose stimulated insulin secretion and resistance but increased FFAs is a downstream phenomenon to the obesity, clearly a potentially drug-able downstream consequence. Obesity per se, to me, is systemic hyperinsulinaemia combined with the inability to resist that hyperinsulinaemia with the downstream result that FFAs leak from adipocytes due to size, not pathological insulin resistance. Linoleic acid is the primary cause of failed first insulin response necessitating sustained systemic hyperinsulinaemia (you have to do something to control the glucose which should never have made it past the liver). Stearic acid should control weight, and so limit those pathologically elevated FFAs, primarily by an appropriate and correct level insulin response to deliver calories primarily to the liver rather than the adipocytes.
But interesting about how uncoupling might elevate insulin secretion…
Haven’t read the paper well enough to see what they think about insulin secretion in a 3 day fasted human with mixed FFAs in excess of 2000micromol/l.
Peter
" Linoleic acid is the primary cause of failed first insulin response"
Can we have a giant multicoloured banner with this sentence on it towed around behind a plane, also tattooed on cardiologists and diabetologists forearms or wherever it is their heads are?
Link to the episode on Pocket Casts: https://pca.st/236vubn0
Pass,
It might be difficult getting past the anal sphincter...
Peter
I made this spreadsheet that calculates the F/N ratio for a bunch of oils: https://docs.google.com/spreadsheets/d/1kTv3Fq44m6b1lBhWmqOXKMXQvB5W5vdUmojfprzAdKM/edit?usp=sharing
Suge, that's an interesting spreadsheet. So, a 50/50 mix of butter and cocoa has the highest value (0.457). I've been mixing shea butter, cocoa butter, and butter together in a 1:1:1 ratio by weight (or by percent, 33.3:33.3:33.3, though again by weight). I've read that shea butter has the highest stearic acid content, though this likely depends on the exact butter I'm getting. And the cocoa butter and regular butter add a bit of "taste" to it, since I'm eating it "raw" right now (I put butter in a pan, heat it up until it's liquid, then add the other two over heat until they are also liquid; so these have been cooked slightly).
Have to say I've been low carb/keto for 6 years, and moving slowly toward eating all meat. I'm at about 90+ % meat. Usually eat two meals a day. Adding just cocoa butter has really had an effect on my hunger, though. I had "lunch" (first meal of the day) with cocoa butter, then was so not hungry, I did not eat again until the next day. That's the first time that has ever happened. I've tried eating one meal a day, but to do that, I have to power through the times I have hunger. With cocoa butter, I simply am not hungry -- at all.
Hey Peter!
For linoleic acid, I get: (18-1-2)/(36-1) = 15/35 = 0.429
Unless I'm looking at this wrong.
Brad
Thanks Brad! calculator mis click. I've edited the corrected figure in.
Peter
I have a spreadsheet where I try to calculate all this stuff on Google Sheets. Here is the link:
http://bit.ly/2QnwPs1
@suge - I just glanced at your spreadsheet and that may be a heck of a lot simpler (better) than mine. See the tab entitled “Food composition and F-N-R” (“F-N-R” = F/N ratio) where I try to calculate the percent of ++ RET, + RET, and - RET based on the estimates from Peter, Mike Eades, and Dave Speijer (but pulled from Eades’s slide in his talk - see the top figure in the tab “Figures”).
Hopefully, anyone looking at the spreadsheet can see that most of the data is generated from my reading of Peter, Speijer, Brad Marshall on the SFA-to-USFA and stearate%, Lucas Tafur, and a lot of leaning on Wiki to be honest, as well as pulling a bunch of videos that unfortunately I haven’t done a good job of crediting on beta-oxidation, ATPs, GTPs, Succinyl CoA, etc., that would’ve sounded like not-even-Greek if I didn’t obsessively read this blog and the thoughtful comments.
I tried to highlight formulas vs manual inputs by black text and blue text, respectively.
@karl - very good points about not eating a specific fatty acid when we actually eat food. I tried to work out some sort of framework (see the message to @suge above). Granted, I only have one food listed, ribeye, at the moment, but it shows ~90% of fats coming from fatty acids that promote RET, for example.
I repeated the ethanol trick - didn't work - not sure what I thought I was seeing?? must have been a tiny amount of Stearic acid?
Here is the rub - I think if I eat a glob of solid stearic it might not get absorbed. ( Bile acids are supposed to emulsify fats - have no idea what happens with a solid?)
(There is also the question if we get a better effect if eaten as an ester or a FFA?)..
So I suppose I will have to try some different approach. My thinking is added Stearic acid could help normalize existing diseased (inflamed) adipose tissue. It does not want to be finely ground - and it forms ice sheets on the top in hot drinks.
I had cooked up a spreadsheet ( I have a column for melting points) - but I'm humbled by the ones you'all have posted. I was not expecting to see F-N ratios beyond 0.5 at http://bit.ly/2QnwPs1 ?? I'm probabbly missing something?
,.,.
Here is the bit I just don't understand - how in the world did it happen that no one has done simple mouse work with the only variable being different added fatty-acids? There is this huge sea of mouse diet papers with confounded controls - it has totally muddied the water - but most of the valuable data comes from papers that weren't looking for it.
If you took only 10% of the money spent on PSAs telling people what to eat it would have paid for chemically defined diet research that would have shown the advise was not just ungrounded - but contrary. ( I vacillate from imagining this is/was intentional disinformation or just incompetence, or degree-mill/grant money chasing? ( I knew a guy that was paid to write and publish false physics articles (never retracted) for military interests to mislead - seemed like a crime against humanity. Yes, such evil exists - people can be monsters.))..
It appears the tide is turning - personal, non-government, non institutional science may be making a resurgence due to the internet. I chose to experiment on myself. I think others are doing similar things - let the fun begin.
Karl - I have tried various ways of making ordinary beef dripping softer or spreadable. Even in an Australian climate good dripping can be intractable at room temp. I tried adding small amounts of macadamia oil to soften it first, with water but didn't like the flavour much and that is heading away from saturation.
Warmth plus water and acidity and some type of emulsifier can turn hard waxy fats into butter-like consistencies. This is how margarine is made. You gently melt the fat and add acifified aqueous solution of emulsifier (surfactant), whisking like crazy while cooling it in a water bath. This is making a water in oil emulsion. The water does the softening and the emulsifier holds tgecfat and water together.
Sunflower lecithin was successful - you only need a tiny bit but again that brings some flavour with it. I improved the taste by adding a small pinch of turmeric to give a nice earthy tang. My current favourite emulsifier is natural gum arabic. Wattle gum. Acidify a solution of that with either citric acid or lemon juice then melt fat, add solution, whisk while cooling. But it goes hard after a few days, I think the gum sets harder. Best to eat it before that happens. Oh, crushed garlic is a good emulsifer too. Can make stearic/palmitic aioli.
Of course I call this my Animal Margarine. Aka: I can't believe it's not marg.
Btw stearic triglyceride or stearic and/or stearic and/or palmitic and/or etc triglyceride have much lower melting points than the unreacted fatty acids. Perhaps more easily digested?
@karl - re: F/N ratios greater than 0.5:
Yes, Speijer mentions it in one of his papers (Being right on Q) that the breakdown of very-long-chain SFAs occur in the peroxisomes (Peter has noted it as well), so the F/N ratios can be misleading.
Speijer (from the reference above): “If mitochondria would perform the breakdown of very-long-chain saturated FAs (e.g. cerotic acid, having 26 C atoms), this would give an F/N ratio (25/51) of ∼0.49. Cerotic acid breakdown via peroxisomes (with breakdown presumably proceeding to ∼C-8 before allowing mt β-oxidation; see also below) results in a reduced F/N ratio (16/51) of ∼0.31. This set-up thus lowers F/N ratios and buffers against large ratio variations over time, probably to efficiently suppress ROS formation. Both the creation of H2O2 and the loss in ATP generation underscore that getting rid of the FADH2 formed during VLCFA oxidation is crucial. Indeed, the so-called PPAR transcription factors strongly induce peroxisomes upon high-fat diets. Under such circumstances, peroxisomal FA breakdown without concomitant FADH2 generation in mitochondria can make a much larger contribution to overall fatty acid breakdown, lowering F/N ratios [55].”
First, it occurred to me that Wikipeidia desperately needs a F:N page with Bob's graph and more..
@bob
Interesting - I just looked up the upper fatty acids - they seem to share having an "unpleasant order" - which could be an evolutionary feature. (The smell of rotting oil is pretty much universally repulsive - probably for our protection? I remember having to help dump a barrel of grease - the smell was overwhelming - primal in being repulsive. )
What caught my eye - Pentadecanoic acid - found in durian. (Durian is hard to explain - The first time I tried it - I was sure it would be the last - not sure why I tried it the second time - but after the third time - I was hooked. The smell is sulfury - think of a leaking gas pipe.) ( it also has some Arachidic acid in it) There are all sorts of health claims made about durian - from being an aphrodisiac to being a cure of fever, swelling, high blood pressure, jaundice, malaria, parasites -- ( I would assume this is 99% BS)..
https://pubs.acs.org/doi/abs/10.1021/jf303881k?prevSearch=durian&searchHistoryKey=
https://moscow.sci-hub.tw/304/9b58042710821a28232656583161013a/maninang2009.pdf#view=FitH
Psyllic acid - has been sold as a health tonic in the form of wolfberry seed oil..
Valeric acid - I think give some cheeses their odor..
@Passthecream
I'm going to try melting Stearic acid with Butter 1:2 ratio - see what I get...
Karl, butter has some emulsification properties too because it is a type of emulsion and already contains some water. Try adding a little extra water and whisking the hell out if it if your first try isn't soft enough.
@karl
I live in the middle of nowhere, but recently spent a month in Salt Lake City and enjoyed some of the cultural benefits. There is one large oriental market where I admired a number of mysterious vegetables, one of which was the durion fruit. I have to go back in a couple of months and will make it a point to pick up a couple to try.
Could somebody tell me if supplementing with NAD precursors would alter the effects of eating to affect RET and ROS generation?
Hi Suge and Bob, nice spreadsheets!
Karl, I would expect odd chain (and probably branched chain) fatty acids to give an F/N ratio greater than 0.5 as they generate proprionyl-CoA rather than acetyl-CoA as one of the steps of beta oxidation. Instead of acetyl-CoA’s 3 NADH + 1 FADH2, the propionyl-CoA will enter the TCA as succinate w/o the generation the two earlier NADHs. So odd chains lose 2 NADHs on their final TCA cycle which will allow the ratio to increase above 0.5.
Interestingly someone messaged me about the hypothesis that propionate as a food additive might drive insulin resistance which would be fully compatible with an F/N ratio greater than 0.5, occurring in the mitochondria. It’s possible that branched chain amino acids do something similar, generating reduced electron transporting flavoprotein, much as step one on beta oxidation does.
Personally my plan is to resist insulin. Seems like a good idea, if you don’t plan to make yourself hyperglycaemic.
Hap, Hoffer tried this decades ago in people, https://high-fat-nutrition.blogspot.com/2013/02/complex-i-hoffer-and-b3.html. Might have had an effect but there are a lot of confounding factors in his observations. I would just say that eating fat appears to do this automatically. Beta oxidation is cytoplasmic NAD+ neutral, as is glycolysis to lactate, NAD+ depletion being induced by insulin diverting pyruvate to mitochondria by activating PDH. So insulin depletes NAD+. No surprise there then.
Peter
Hap, I didn't quite read the question correctly, mea culpa. Adding extra NAD+ should increase the NAD+/NADH ratio, making it easier to put an electron back through complex I without transferring it to oxygen, it just regenerates NADH. ROS generation occurs during RET when the NAD+/NADH ratio is low. Whether this is a good or a bad thing depends on how you view ROS and how pathological a person's core food choices have been. Certainly niacin is also a ketone mimetic and a FFA release inhibitor so there is a lot going on with this particular precursor.
Peter
@Suge
I hope you add beef and other meats to your spreadsheet.. possible corrections using the numbers from Bob's spreadsheet..
,.,.
Thinking about this more -- I have a hunch - that the sweet spot is an F:N of about .5 - could be that going above 0.5 could start 'bad-things'(tm)' happening..
Propionate awaits proper dietary research along with a long line of other fatty-acids.
,.,
A Speculative trail here (gets back to F:N at the end): I also started thinking some more about this in terms of evolution. I think our intelligence and loss of hair appear to have happened about the same time - amazingly it appears no one has systematically researched photo chemicals of our skin. There are various hints of trails that melanin - vit-D might be involved in what makes our brains special. The idea that we are just another ape nutritionally I think is wrong. Our brains require a lot of fat - for the insulation of nerve fibers. Also - the amount of calories burned by the brain is serious. The explosion in technology is very recent evolutionary.. My take is there was a genetic change that triggered it - and it changed our nutritional requirements.
There is a narrative that our teeth mean we are not meat eaters - there are a couple of problems with that - our teeth don't like a high carb diet. Also, the change in humans in my opinion is more recent - just 10s of thousands of years - for our teeth to adapt to our vastly improved hunting skills - and not under high pressure any more due to cooking and cutting tools.
I wonder if the key to gaining improved intelligence had to do with photo-chemicals produced in our naked skin - it reminds me that part of the photo reaction is ROS generation. This is limited to the skin - no sun shining in our fat deposits. If sunshine makes our skin more insulin resistant - changes mitochondrial numbers - what does that mean for the rest of our bodies? Particularly the brain? Lots of basic research waiting for some one to work on..
There may be a "hitch in the giddyap". Individual beta cells "leaks" insulin without without presence of glucose????
http://newsroom.ucla.edu/releases/researchers-discover-process-that-may-explain-how-type-2-diabetes-develops
Hi Peter,
I've been reading your blog for a few months now. I've found it after watching the talk "A New Hypothesis of Obesity" by Dr. Michael Eades.
I'm by no means a biologist, but your posts makes a lot of sense. Especially the ones in plain English, because I understand those best :) So thank you for that, I find it all very interesting.
It might not be really related to this post, but I have to ask, what is your opinion on fried fish?
I (used to) eat once or twice a week fried fish, bought at a fish stall. And obviously this is fried in seed oils. Other than that, I'm trying to avoid seed oils as much as possible and I do eat a fair amount of butter and beef tallow.
Does the fish balance out the oil? I'm lean and healthy and I like to keep it that way. Is this amount of PUFA/omega 6 safe or not? Historically we've always eaten very little omega 6 if I'm correct, although not fried making it more prone to oxidation. I'm in doubt whether or not to continue eating this.
Stefan
Stefan, I eat fried fish at home occasionally but fried in beef dripping, very occasionally in butter. Overall I am the first to admit that I am far from a perfectionist and you have to trade off the reasons for a fish supper from a takeaway with ingesting small amounts of oxidised omega 6s. I doubt the total PUFA on a background of a beef fat based diet would matter much… You pays your money and takes your choice!
BigWhiskey, as a total random aside I'm reading about the cross talk between the ETC and the NADPH oxidases, both of which provide superoxide/H2O2 for insulin signalling/resistance. One system for facilitating transmitting ROS from mitochondria to NADPHs (to activate them) is, surprise surprise, Cyclophillin D… It’s in here but it’s not light reading! https://www.sciencedirect.com/science/article/pii/S0005272810000435?via%3Dihub
Peter
@Karl, Brad from Fire in a Bottle said that his limit is about 30% stearic acid to butter, and he likes 20% better. I think if it's 30%, it begins to get too much like wax. So, 1:4 ratio by weight. He was using the "regular" stearic acid, which is supposedly really 50/50 stearic acid and palmitic acid. I've ordered his higher percentage (90%) stearic acid and will try to make my own "fortified" butter when it gets here.
Anyone looked into GIP signaling for this? For instance, this says stearic acid results in higher GIP signaling (in mice, of course):
https://www.ncbi.nlm.nih.gov/pubmed/4063474
But the Wikipedia page doesn't really say whether that's good or bad:
https://en.wikipedia.org/wiki/Gastric_inhibitory_polypeptide
Gabor Erdosi implies that higher GIP is worse, but I haven't figured out why.
I can't see it (higher GIP) being that bad, as stearic acid seems to cause a marked decrease in hunger for me. (Though I'm trying cocoa butter and other higher stearic acid fats, which I know have many different fatty acids in them.)
Peter, Thanks for your persistence in tracking down these odds and ends. I thought, for sure, this protein, CypD, is the Angel of Death, "Further, obese mice who lacked the gene for CypD did not secrete excess insulin. The team confirmed the same process was taking place in isolated human pancreas cells: In the presence of fatty acids at levels that would be typical in obese humans, the cells secreted insulin in the absence of elevated glucose.".
I felt a chill from a strange unseen source....sure dropped whatever glucose I had in me.
Hi Peter, I thought you might find this study on fatty liver interesting.
https://www.hopkinsmedicine.org/news/media/releases/researchers_surprised_to_find_fatty_liver_disease_poses_no_excess_risk_for_death
“Non-alcoholic fatty liver disease (NAFLD) is a common condition associated with obesity and heart disease long thought to undermine health and longevity. But a new study by Johns Hopkins researchers suggests the condition does not affect survival.
A report on the study was published online last week in BMJ, the British medical journal.
“Physicians have considered fatty liver disease a really worrisome risk factor for cardiovascular disease,” says study leader Mariana Lazo, M.D., Ph.D., a postdoctoral fellow at the Johns Hopkins University School of Medicine’s Welch Center for Prevention, Epidemiology, and Clinical Research. “Our data analysis shows this doesn’t appear to be the case. We were surprised to say the least because we expected to learn by how much non-alcoholic fatty liver disease increased the risk of death and instead found the answer was not at all.””
One to think about!
Peter
this could be useful:
https://www.mdpi.com/1099-4300/21/8/746
Hi peko,
Bit of a brain bender, that one!
Peter
Hi Peter,
yes definitely, but many good references inside. Quite in-depth and extensive coverage of mitochondria energy efficiency knowledge.
Hi Peter,
Any idea why such a small change in F/N can cause such a large change in ROS? I went through a few of David Speijer's articles, and only saw him compare F/N for glucose with a long chain SFA, where the shift in F/N is large. Do you have a proposed mechanism for ROS production being triggered at F/N of 0.49 but not so much at 0.46? Thanks, John
Hi John, sorry not to reply to your previous query, it was on the to-do list but never got done. I can't see any way of working this out empirically but the data from treating cells with palmitate vs oleate or even vs palmitate plus a little oleate suggest that unadulterated palmitate (never seen in vivo outside a SCD1 k/o mouse on a low fat diet) produces markedly more ROS than oleate and that oleate rescues cells in culture from palmitate "toxicity". Usually working with 25mmol/l glucose of course, though not always.
I have to say that the front end of the ETC, complexes I, II and ETFdh look remarkably like a sophisticated transistor/solid state switching device. Reminiscent of a field effect transistor but not quite. Given a couple of billion years this could be made very specific and tailored to a switching purpose...
One problem experimentally is that you can't supply "FADH2" alone or as ETF to mitochondrial preps, it has to be as the carnityl or CoA derivative of a fatty acid and theses are highly biologically active in their own right as regulators of the ETC. It's tricky but I believe people may be thinking about experiments.
Peter
Post a Comment