I don't do twitter or facebook (If you are a metabolic person and have friend-requested me and I've ignored it please don't take it personally, it's just not what I do with faceache) to any extent and almost never use them for metabolic subjects. By an accident of twittard I picked up this tweet by Chris Masterjohn (via raphi and Mike Eades). It made me laugh out loud and still has me giggling occasionally:
"No! Carbohydrate restriction is the stupidest approach to fatty liver ever devised. If it “works” in any case it is almost certainly by supplying more methionine and choline, not by lowering carbs. It is impossible to make more fat from carb than you get by eating fat"
I can't help but think "chylomicron", "thoracic duct" and "physiology".
Then I giggle some more.
Peter
I guess it ranks along side of "Masterjohn", "Martha" and "RQ 0.454".
Edit on 27th Feb: Published 2 days ago, very post hoc. This is what happens to surrogates for NAFLD when people apply the “stupidest approach to fatty liver ever devised”.
Post hoc analyses of surrogate markers of non-alcoholic fatty liver disease (NAFLD) and liver fibrosis in patients with type 2 diabetes in a digitally supported continuous care intervention: an open-label, non-randomised controlled study
End edit.
ok, tweet is mostly stupid.
ReplyDeletebut how much TG does the liver make out of carbs? what is the maximum? How many carbs would a 70kg person need to eat to get, say, 180g of fat? what is the convertion rate?
I remember the liver does make some 125g or so of TG but don't remember whether that is the limit or no.
any idea?
best regards
Alex
He did end up apologizing for the original tweet. He apparent did his thesis on NAFLD. So, it kept coming back to normal low carb being pretty good, since it does provide choline, protein, and whatever else it was he was concerned about- primary issue seemed to be lose weight.
ReplyDeleteMaybe the mythical keto vegans are in trouble (there was one girl on youtube trying this, I haven't check to see if she's given up or is dead yet).
Hi Alex, I don’t think DNL matters, my own suspicion is that low insulin will stop the liver storing fat just as it stops adipocytes storing fat. That will coincidentally be a low carb effect. The rodent ketogenic F3666 does cause fatty liver but it is manufactured specifically choline deficient to do this as choline deficiency maximises ketosis, at the cost of NASH. I sort of thought about a series of posts around F3666 and choline replete versions but never got round to it. Chris M makes me laugh because he is an impartial scientist with his biases nailed to his forehead. Anyone can see them except himself.
ReplyDeleteAs an aside, I think a lot of the fat in fatty liver comes from adipocytes releasing lipid inappropriately, in the face of elevated insulin. That would be from drugs such as alcohol, sugars such as fructose and fats such as trans fatty acids. You can get there if your adipocytes exceed their lipid storage ability too but ability to store lipids before leakage goes up with PUFA ingestion.
August, fascinating, a lot of time wasted there then. Of course all that is needed is weight stable LC eating to see if weight loss per se is what matters for fatty liver resolution (it won’t matter, just as weight loss doesn’t matter for improving lipid surrogates like HDL and trigs etc). But getting people to avoid weight loss under study conditions of strict LC eating is not easy!
re keto veg*ns: I guess there are plenty of vegan sources of choline and protein, but then I suspect that all veg*ns are in trouble anyway!
I think Chris is barking up a lot of random or outright misplaced trees these days. His newsletter emails also keep getting more commercial, and I think he is starting to cover a lot of fringe themes, maybe in an effort to sell more special counselling.
ReplyDeleteBack no NAFLD, according to Dr. Lustig (fructose talk), its all fructose or alcohol. I don't remember his special version of the Krebs cycle in detail, but there seems to be one pathway for fructose and ethanol metabolism that puts the fat straight in the liver without a detour through the blood stream ansd adipocytes.
Eric, yes, there is doubt about DNL from fructose and alcohol being automatic. I have no problem with this. But both of them (and transfatty acids) do trigger lipolysis in adipocytes. To me the question is how important this excess FFAs becomes. I think I may have papers somewhere about suppression of this lipolytic effect ameliorating NAFLD but it would take some hunting to track them down. Unfortunately I've just stumbled on this gem "Structure of an Ancient Respiratory System", of no interest to anyone but myself (it looks really cool, two proton pores plus a sodium ion pore, oh boy, just what I've been looking for. And one of the proton pores is upside down in the membrane, yes!). But then, I have no choice in what interests me!!!!
ReplyDeletePeter
What is interesting, is those pushing ungrounded narratives are having a harder time these days.
ReplyDelete" impartial scientist with his biases nailed to his forehead. Anyone can see them except himself." LOL
His first paragraph here is interesting:
https://www.westonaprice.org/health-topics/vegetarianism-and-plant-foods/vegetarianism-and-nutrient-deficiencies/
I think he still wants to be a vegan - reminds me of this paper:
http://www.plosone.org/article/fetchObject.action?uri=info:doi/10.1371/journal.pone.0088278&representation=PDF
I realize that it is not a great paper - correlations are not causation - but I do wonder if the mental illness bit is true - which way is the arrow of causation? Permanent effects?
karl, Yep, if you consider veg*nism to be a mental illness in its own right then I guess it should come as no surprise that it clusters with other mental illnesses, confounding the arrow of causation. I hadn't realised that there might be a financial conflict of interest there too.
ReplyDeletePeter
Aren't Weston Price folks and vegans like fire and water? Chris keeps promoting pastures meat and offal, so he hasn't converted.
ReplyDeleteEric, Masterjohn is a recovered veg*n. His current illness is LC denialism. Perhaps he will recover from this too one day... One can but hope.
ReplyDeletePeter
Hi Peter
ReplyDeleteLiver and PUFA. I translated your "butter makes you fatty liver -again" post to finnish site, linked back here to the original and included Dr. Eades´ video presentation of Protons. Hope you are fine with this. http://turpaduunari.fi/piiloutuneen-pufan-jaljilla-jos-se-ei-kerry-maksaan-niin-mihin-sitten/
I analysed earlier on a meta-analysis of this same professor on liver fat, and you guessed it, it was filled with omissions, cherry picking, logic error and 180 opposing view of her reference. Not to mention religious stupidity, all clear enough for a layman. So, after this, I used your article to explain the destiny of PUFA, why it does not appear in the liver, and why...
The funny thing was goose feeding with figs, I "helped" my friend and the goose liked it (and carps in the pool, too. The fast ones eat the slow ones). The friend did not, so I tried to find out if it is appropriate. Well, surprise, the whole Latin Mediterranean world uses "Fig" as root for liver,e.g. "Figado" in Portuguese, since the roman times. The reason is, they fed goose with figs in order to get fatty liver. The Romans contemplated doing the same with pigs...
Funny, Romans did not know, that glucose and fructose made their fig, they just knew it makes large "figado". The professor knows these elements, but as you say, there is little understanding of what makes the fatty liver.
So, I am still musing at watching carps and goose competing for the figs... and wondering how these professors can spread their garbage.
rgds JR
Hi JR, no problem. Of course the other question to ask is "How do they sleep at night?"!
ReplyDeletePeter
My favorite aspect of this was when Dr Jim Johnson spanked him in public, totally disregarded his phd and referred to him as an internet consult selling abs man, who doesnt know insulin is directly involved in the pathophysiology of fatty liver. I admit i cheered him on, to which he DMed me to apologize he had been drinking.
ReplyDeleteApologize for NOTHING, spectacular own sir, of a very arrogant+ignorant person who couldn't deserve it more.
Hi Woo, good to hear you! Being a Twittard Dullard I've not seen (or worked out how to view) the full thread but that sounds perfectly reasonable to me!
ReplyDeleteWhen I was a noobie to LC I spent a lot of time on Dr Bernstein's forum. I remember Anthony Colpo posting a pic of his (wow!) abs. Best response from the largely female respondents was "disturbing". LMAO.
Peter
Hi Peter
ReplyDeleteJust for fun, you seem to like giggles
First excerpt from "Nutritional modulation of NAFL..." a solo meta-analysis.
Isocalorific comparisons, of course anything below 40% is lowcarb. The last sentence is nice...
In three of the studies shown in Table 1, a low fat (16%–23% of total calories)–high carbohydrate (57%–65%) diet was compared to a low carbohydrate (31%–38%)–high fat (43%–56%) diet. Quite consistently, liver fat content decreased during the low fat-high carbohydrate diet and increased during the high fat-low carbohydrate diet (Figure 2). The high fat rather than the low carbohydrate component in the diet is the likely cause of the increase in liver fat since low carbohydrate diets seem particularly effective in reducing liver fat (vide infra).
The second is professor level causality lesson, actually from the paper you analysed for "butter gives you fatty liver. Again"
”The rapid increase in the prevalence of obesity has led to a co-epidemic of nonalcoholic fatty liver disease (NAFLD) (1). NAFLD is strongly associated with insulin resistance (IR) and predicts the development of type 2 diabetes and cardiovascular disease (1). Although obesity is its primary acquired cause, some subjects who gain weight do not develop NAFLD(1,2). As weight loss rapidly reverses both NAFLD and hepatic insulin resistance, it seems that obesity is a true cause of both.”
holy bias !
Rgds JR
I made the following response to that tweet, and Mr. Masterjohn replied:
ReplyDeleteChris Masterjohn
@ChrisMasterjohn
Feb 18
Matthew
Replying to @DrEades
@ChrisMasterjohn almost universally triglycerides (blood fat) drops dramatically with a low carb diet. Mine went from 185 to 67, even though I'm having a package of bacon for dinner once or twice a week. Carbs produce 3 times more blood fat, at least in my body, than fat does.
Chris Masterjohn Retweeted Matthew
You are correct, and this is mainly true in insulin resistant people. However, your blood concentration does NOT tell you anything about how much fat is synethesized from carbs and this only accounts for 14% of the flux of triglycerides in the liver of people with NAFLD.
Hi Matthew,
ReplyDeleteI’ve not followed this conversation in detail, none of it really matters. As I recall the only interesting point is that Dr Masterjohn tweeted that “Carbohydrate restriction is the stupidest approach to fatty liver ever devised”.
This tells us huge amounts about Dr Masterjohn.
He’s not someone I would consult about fatty liver…
Peter