Thursday, June 12, 2014

Endotoxin Absorption on a High Fat Diet

Housekeeping: Endotoxin is always of some interest to an anaesthetist and the link between endotoxin uptake and high fat diets has been in my thoughts somewhat in recent months. This probably ties in to resistant starch in some way, so the next few posts will probably be random doodles around this subject. And maybe why the Protons thread is fairly well out of data to extend it and another look at brain metabolism, particularly why it doesn't run on fat (or glucose much of the time), all need posts as the time becomes available. Plus Toxic forwarded me a link on B12/folate guidelines which can be downloaded here. As she says, medics may well not read these sorts of guidelines but informed patients certainly should. OK here is the post as was planned.




Endotoxin is nasty stuff. If we want some sort of idea of how nasty it is we just have to look at this juicy quote from Hansen et al from Denmark:

“Harte et al. have reported levels of endotoxin to be between 3.3 and 14.2 EU/mL, but these concentrations are known to increase levels of tumor necrosis factor α (TNFα) in plasma and induce a massive inflammatory response in humans”.

The context of the quote is that these folks are commenting on a paper by Harte et al which described the above levels of endotoxin as being found in human volunteers, which should be nearly lethal. The victims, poor folks, had been coerced in to drinking the sort of amount of whipping cream which might be a lunchtimee snack for myself. And they survived. As do I after such an insult (so far).

What galls Hansen appears to be complete lack of any sort of an inflammatory response to this lethal chylomicron/endotoxin cocktail coursing through the bloodstream of the lipophiles (assuming they enjoyed being paid to drink the cream).

In every group studied, from normal through obese and IGT to diabetic, TNFa falls after a decent glass of whipping cream, albeit in a statistically non significant manner. Endotoxin levels go up, often dramatically and highly significantly.

It’s all in Table 2:





















Even in the deepest cesspits of nutritional research no one really expects a half a pint of cream to produce lethal endotoxaemia within a few hours of drinking it. In their response to the comment, which implies that they can’t measure endotoxin correctly, Harte are polite and point out that there is a world of difference between an iv bolus of neat endotoxin (not recommended) and the absorption of endotoxin from the gut in the presence of chylomicrons (welcome to my world).

There are a number of papers showing that apolipoprotein B containing lipid particles are markedly protective against endotoxin, albeit mostly in mouse models. Quite why an oral lipid bolus should automatically load chylomicrons with endotoxin in healthy individuals is another of those fascinating questions which may need a little thought but I think we can reliably say that it would have been eliminated if there is no benefit.

I wrote a post, several years ago, where Greve’s group demonstrated a marked protective effect of a gastric lipid gavage against the effects of haemorrhagic shock, the effects of which are largely related to loss of gut wall integrity, bacterial translocation and endotoxin uptake.

In the high fat world, endotoxin uptake is not what it seems. Lipoproteins neutralise and carry endotoxin. If you need systemic inflammation to maintain research funding you need to be a little more McDevious.


The above little exchange came to mind because Zachary mentioned (in comments on the last post) a study at his university recruiting victims to demonstrate endotoxin uptake after a high fat meal WITH inflammation. You can, of course do this. Technique: "The diet is foods such as TV dinners, meat and cheese". This may be good for getting the right result to secure subsequent funding but it obliterates the fact that a single high fat meal of unadulterated whipping cream is both anti inflammatory and might even improve insulin sensitivity, in the acute setting at least. Just skip the Egg McMuffins.

Peter

48 comments:

Nigel Kinbrum said...

I think that it's safe to say that you & I agree that a "Western" diet isn't good for us. I'm not anti-low-carbing.

RE Drinking large amounts of heavy cream or oil or melted butter: Would you like to comment on studies showing significantly increased RR for CHD with postprandial (2 to 4 hours post-meal) triglycerides?

Also, fasting serum TG's on a high-fat diet are suppressed due to suppression of endogenous TG production. However, mean serum TG's increase on a high-fat diet, due to high postprandial TG's.

Peter said...

Nigel, you seem lost in the concept that trigs cause cvd. Good luck.

Peter

Charles Grashow said...

http://www.trackyourplaque.com/library/fl_01-020postprandial.asp

Postprandial Lipoproteins: The storm after the quiet!
Part 1 - Fats

While excessive carbohydrate consumption leads to postprandial abnormalities in the long-term, fats are the immediate determinant of postprandial responses. The threshold for excessive fat intake in a single meal is likely in the range of 25-50 grams; more than this amount of fat in a meal and excessive postprandial phenomena develop. Non-fasting triglycerides of 85 mg/dl or less are desired.

Monounsaturated fats, such as oleic acid from olive oil, provoke the least postprandial surges, while saturated fats provoke the greatest. Cholesterol intake delays clearance of postprandial particles. Oxidized fats, principally the polyunsaturates, generate more oxidized postprandial particles that can be incorporated into atherosclerotic plaque.

Omega-3 fatty acids, EPA and DHA, but not linolenic acid (flaxseed), reduce the magnitude of postprandial lipoproteins.

Studies that use a fat challenge demonstrate higher postprandial triglycerides in normal (i.e., non-diabetic, non-alcoholic, non-obese, no lipid disorders) control subjects than observed in people eating their usual diet. The following peak postprandial triglyceride values have been observed after high-fat test meals (usually at 3-4 hours postprandial):

162.8 mg/dl—After 8 weeks of high-monounsaturated fat adaptation + 2500 mg/day EPA + DHA); fat challenge total 123 grams fat (52 g saturated, 59 g monounsaturated, 12 g polyunsaturated) (Volek 2000). Note the high quantity of total fat in the fat challenge.
150-240 mg/dl after fat test meal (1 g/kg bodyweight) in slightly overweight subjects (Park 2003).
119 mg/dl after 62 g fat test meal (Brown 1991).
74 mg/dl after 15 g fat test meal (no different than after non-fat test meal); 123 mg/dl after 30 g test meal; 133 mg/dl after 40 gram test meal; 155 mg/dl after 50 gram test meal (Dubois 1998).
150 mg/dl after 83.5% fat test meal (62.5 g fat per m2 body surface area) (Kolovou 2005). 263.3 mg/dl after same fat test meal (Patsch 1992).
142 mg/dl following test meal including 50 g fat (20 g olive oil, 30 g fish oil) (Heath 2007). Note that acute fish oil administration did not substantially modify the response, distinct from the chronic response.
89 mg/dl after 25 g fat, 75 g carbohydrate meal in normal controls with very low BMI (21.4) (Harano 2006).
169 mg/dl after 1 g fat/kg meal, mostly olive oil; BMI 24.5 (Perez-Martinez 2009).
212 mg/dl in younger (mean age 29 years), 314 mg/dl in older (mean age 66 years) subjects given 1 g/kg fat challenge (Cohn 1988).
178 mg/dl in overweight subjects (BMI 28.4) after 75 g fat meal
98 mg/dl after 50 g fat, 50 g carbohydrate challenge in mildly overweight, non-diabetic (BMI 27.9) subjects (Mohanlal 2004)

Following a high-fat diet, for example, will yield lower postprandial triglyceride levels after 8 weeks compared to the start, suggesting an accommodation process via activation of lipoprotein lipase (Volek 2000). However, once accommodation develops, it is not clear what level of fat intake can be accommodated without excessive provocation of postprandial lipoproteins to an undesirable degree. That question has not yet been answered.

Mike said...

As Volek has shown, after metabolic adaptation to a higher fat diet, it is not really an issue.

George Henderson said...

Peter, you wisely say " Quite why an oral lipid bolus should automatically load chylomicrons with endotoxin in healthy individuals is another of those fascinating questions which may need a little thought but I think we can reliably say that it would have been eliminated if there is no benefit."
I believe the answer lies here:

http://cid.oxfordjournals.org/content/41/Supplement_7/S470.full

"The biological mechanisms underlying the recognition of, and response to, LPS are more characteristic of a hormone than of a toxin. All mammals carry endogenous stores of LPS and express dedicated carrier proteins, a cellular receptor complex, and mechanisms that specifically antagonize the response to LPS. Disruption of any component of this complex recognition system jeopardizes host defenses against infection with exogenous microorganisms."

From an evolutionary perspective, perhaps, high-fat meals originally came from scavenged carcasses. Anything that primed the immune system to deal with the possibility of infection from such a meal might be conserved. Part of this conservation might involve muting the non-adaptive inflammatory responses to LPS.

Also, egg yolks in a low-carb diet are helping to keep TNF-a low:
http://www.ncbi.nlm.nih.gov/pubmed/24079288
"Reductions in plasma tumor necrosis factor-α (P < .001) and serum amyloid A (P < .05) were seen in the EGG group only. Notably, increases in dietary cholesterol were associated with reductions in plasma tumor necrosis factor-α (r = -0.340, P = .04)."

Nigel Kinbrum said...

Peter said...
"Nigel, you seem lost in the concept that trigs cause cvd. Good luck.
Peter"
If it's just a concept, how do you explain Fig. 1 of Fasting Compared With Nonfasting Triglycerides and Risk of Cardiovascular Events in Women?
"In secondary analyses stratified by time since participants' last meal, triglyceride levels measured 2 to 4 hours postprandially had the strongest association with cardiovascular events (fully adjusted hazard ratio [95% confidence interval] for highest vs lowest tertiles of levels, 4.48 [1.98-10.15] [P less than 0.001 for trend]), and this association progressively decreased with longer periods of fasting."

George Henderson said...

Wouldn't the women with the highest PPTGs be those most sensitive to carbohydrate, eating most sugar, and so on?
To believe that study transfers to low-carb diets, you'd need a straight mechanistic reason why these TGs, in and of themselves, are damaging, and you'd need to show that VLC TGs have the same composition as these TGs.
TG in this case might means fats in VLDL, in process of becoming small, angry, and dense, whereas TG in VLC might be in IDL more and awaiting transformation to large fluffy bunnies that never hurt anyone.
At least, that's the fairy tale I've been reading.

Peter said...

George, yes. That makes a great deal of sense. It also fits perfectly well with LPS, carried by chylomicrons, being the perfect signal that a large bolus of fat is on its way and it's time to down regulate insulin signalling and concentrate on running beta oxidation.

I love stuff that makes sense.

Time to follow your links.

Peter

Peter said...

George, and the flip side is that bacterial products which come from plant derived real Foods signal their presence through their keynote derivatives, SCFAs in the colon.

That really is a nice balance.

Peter

@Nigel, go and think about it! Get beyond the "lipids are bad" focus.There is more to metabolism.

Melchior Meijer said...

I stil like Ian Spreadbury and his concept of 'dense acellular carbohydrates'.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3402009/

Nigel Kinbrum said...

Peter said...
"George, yes. That makes a great deal of sense."
It may well "make sense", but here's a straight mechanistic reason why PP-TG's correlate with increased risk for CHD. The greater the amount of fat eaten, the greater the number of chylomicron particles. Once the chylo's have given up their load, they become chylo remnants. As increasing LDL-P correlates with increasing CHD mortality (see the Kaplan-Meier survival plots in Lipidaholics Anonymous Case 291 Can losing weight worsen lipids?, why not also chylo remnant-P?

You seem lost in the concept that lipids have nothing to do with CHD.

Nige

Nigel Kinbrum said...

P.S. Chylo's & chylo remnants have Apo-B48, so they're also Apo-B lipoproteins, like LDL.

Nigel Kinbrum said...

George Henderson said...
"Wouldn't the women with the highest PPTGs be those most sensitive to carbohydrate, eating most sugar, and so on?"
Being IR/Met-Syn and/or eating sugar would raise fasting TG's, and there was no association between fasting TG's and the RR for CHD.

raphi said...

@George & Peter

I'd gone over this excellent paper George linked to back in January & thought these points were worth mentioning:

- evolution tends to turn what we can't avoid (bacteria) into something we can't do without (germ-free human populations anyone? Didn't think so) --> "Bacterial LPSs differ in their ability to activate TLR4 signaling; thus, certain strains of LPS may serve as competitive antagonists of endotoxin activity"

- Furthermore, "LBP-knockout mice, for example, show delayed neutrophil migration and dramatically increased mortality in response to intraperitoneal challenge with S. typhimurium; however, they are resistant to intraperitoneal challenge with endotoxin" ---> our body expects a certain loads of LPSs from food & water & has a system to deal with it. Assuming that this scenario is equivalent to dealing with EXOtoxins (e.g. an arrow wound for cavemen, labs rats having endotoxins injected into a body cavities) is a mistake.

Mike said...

From recent readings, under good metabolic conditions, the chylomicrons distribute their TGs quite quickly and have a brief existence. However, in the presence of high insulin, they are unable to unload the TGs and hang around longer than designed. This causes higher and prolonged postprandial TGs as well as oxidation of the lipoproteins. So in conditions with low insulin such as HFLC this is not an issue. The end of the linked paper includes a related discussion on this.

Seems to be additional evidence that it is best to avoid a situation in which you are consuming relatively large amounts of fat in the presence of chronically elevated insulin levels (insulinemia).

George Henderson said...

Mike's explanation of the PPTG saga makes a of of sense. Reduced rate of clearance due to hyperinsulinaemia. I am suspicious of attempts to isolate one of multiple risk factor variables when they are interconnected by a common pathology.

Raphi quted "Bacterial LPSs differ in their ability to activate TLR4 signaling; thus, certain strains of LPS may serve as competitive antagonists of endotoxin activity"
Probiotic LPS or analogues being a case in point.
Lactobacillus cell wall fragments exert potent immune, gut and mood effects without the need for live bacterial cultures, by interacting with TLRs, including TLR4, in what seems to be agonist/antagonist fashion.
If anyone wants to test this, I can recommend the product ReseT advertised on this page http://www.womensmedicinebowl.com/
with what is far too little information, which I mean to make good soon on my blog.
ReseT is a cell wall extract of L. Bulgaricus in a sublingual preparation.
It demonstrates the direct action of probiotics via the LPS transport and recognition system, by eliminating competitive and biosynthetic functions of probiotic cultures. This seems to make little difference, other than to make the probiotic much more potent and the bowel less full.

George Henderson said...

"agonist/antagonist" = a weakly acting ligand occupies the receptor that can otherwise bind a potent ligand.

Nigel Kinbrum said...

Mike said...
"From recent readings..."
Got any links to support this?

Nigel Kinbrum said...

Mike said...
"However, in the presence of high insulin, they are unable to unload the TGs and hang around longer than designed. This causes higher and prolonged postprandial TGs as well as oxidation of the lipoproteins."
Sounds plausible. However, according to Insulin treatment prevents LDL from accelerated oxidation in patients with diabetes, "In conclusion, insulin therapy represses LDL oxidation even at apo B concentrations > 1,150 mg/l and should be noted for its anti-oxidation properties."

Ilaine Upton said...

Nigel, on Track Your Plaque/Cureality, various people have tried a post-prandial triglyceride test after a fat bolus using a home meter and charted their results.

Interestingly, some people's triglycerides shoot up higher and take longer to return to baseline. This may vary according to the fat, e.g. olive oil vs. butter vs. cream vs. lard vs. tallow. You have to be pretty hard core to swallow down lard or tallow. I have done it.

Personally, I clear triglycerides from a fat bolus pretty fast. The type of fat doesn't seem to matter. What elevates my triglycerides and keeps them elevated is carbohydrates. Which isn't surprising, in fact, it's normal. The body converts excess glucose to triglycerides.

George Henderson said...

One difference between hyperinsulinaemia and insulin therapy is the relative glucose concentration.
That paper says that insulin therapy reduces TG, VLDL TG, and small dense LDL, but leaves LDL-c unchanged.
Sounds like LCHF.

Nigel Kinbrum said...

Ilaine Upton said...
"Nigel, on Track Your Plaque/Cureality, various people have tried a post-prandial triglyceride test after a fat bolus using a home meter and charted their results.

Interestingly, some people's triglycerides shoot up higher and take longer to return to baseline. This may vary according to the fat, e.g. olive oil vs. butter vs. cream vs. lard vs. tallow. You have to be pretty hard core to swallow down lard or tallow. I have done it.

Personally, I clear triglycerides from a fat bolus pretty fast. The type of fat doesn't seem to matter. What elevates my triglycerides and keeps them elevated is carbohydrates. Which isn't surprising, in fact, it's normal. The body converts excess glucose to triglycerides."
Hi Ilaine. The fact still remains that it's 2 to 4 hour post-meal TG's that correlate with RR for CHD, not fasting TG's. Have you read the studies in Ultra-high-fat (~80%) diets: The good, the bad and the ugly.?

Nigel Kinbrum said...

George Henderson said...
"One difference between hyperinsulinaemia and insulin therapy is the relative glucose concentration.
That paper says that insulin therapy reduces TG, VLDL TG, and small dense LDL, but leaves LDL-c unchanged.
Sounds like LCHF."
I posted that study as it contradicts Mike's assertion that insulin increases lipoprotein oxidation.

Are you now asserting that it's blood glucose, not insulin that's the problem? Because mixed meals don't produce much of a glucose response, unlike 100g of neat glucose.

Nigel Kinbrum said...

And finally, folks...

I know that Peter has a low CAC score, as he's mentioned it in the past. The bad news is that Stenosis Can Still Exist in Absence of Coronary Calcium.

Peter said...

"And finally, folks..."

Phew, is that a promise?

Peter

raphi said...

@Nigel Kinbrum,

1) 'mis-placed calcium' certainly plays a role in CVD disease but taking that to mean it is a cornerstone of stenosis ignores how bad we still are at predicting CVD outcomes based on tissue assessment (whether through scans or biopsies). Thus, stenosis being possible despite a 'great CAC score' shouldn't surprise the breaches off you!

2) How does this support (or oppose) your argument that fats are the bigger evil when it come to post-prandial circulating TGs? If anything, it suggests that CVD outcomes aren't as closely causally tied to 'conventional' markers (CAC & cholesterol) as many have argued...in vain. ---> the hint here is to look at cellular metabolism in addition to endocrine patterns.

George Henderson said...

You'd probably die if you had zero oxLDL, and you'll live longer if you can run a CAC score when you need to. Nothing is wasted; like LPS, unavoidable hazards serve a purpose.
On the other hand, a lot of diseases are out of control repair jobs.

raphi said...

I thought this was an interesting data point:

Recently, I saw my apoB numbers come down slightly concomitant to an increase in oxLDL, from a previous lab test indicating higher apoB & lower oxLDL levels.

If one believes that > apoB MUST = > oxLDL levels then, either; my testing messed up; i'm an alien; or our current understanding fails to explain such apparent contradictions (hence, back to the drawing board).

Seems to me like banking on oxLDL & apoB levels as < is always better, is quite short cited. Context context context...

Nigel Kinbrum said...

Peter said...
""And finally, folks..."

Phew, is that a promise?

Peter"
That was for last night!

Have you had LDL-P or CIMT tests done?

Nigel Kinbrum said...

raphi said...
"@Nigel Kinbrum,
1) Thus, stenosis being possible despite a 'great CAC score' shouldn't surprise the breaches off you!"
I mentioned it in case people were unaware of that fact.

"2) How does this support (or oppose) your argument that fats are the bigger evil when it come to post-prandial circulating TGs?"
I gave a mechanism above. Did you see it? Dietary fats are carried in chylo's. More fats = more chylo' particles = more remnants = more ox-remnants = more atherogenesis.

LeenaS said...

Nigel, I think that you KNOW that in the INTERHEART study they monitored Apo-B100 only, without Apo-B48s?

If not, maybe you should get into that Lancet 2004 paper again? But then again, lipophobes do not really like that kind of stuff. They should, since it was actually a follow-up of The MONICA which was a follow-up of The North Carelian Project, which was a success to the lipid paradigm. Too bad none of the other sutdies (better controlled, larger and definitely without the elaidic acid transfat of the sixties; and oh yes, we had plenty of those at the time although you have to dig a bit to find it...) could never repeat the results, in spite of much clever trying...

Cheers,
LeenaS

raphi said...

@ Nigel

1) hhhmm…OK?

2) Yes, I saw your mechanism & understand the rationale.
However, if one follows through without a double-standard it becomes apparent that the best way to control unwanted TG excursions (fasting, pre or post-prandial) remains carbohydrate moderation in modern populations. Your statements regarding fat bolus’ disregard this.
Yes - there is significant variance in the necessary levels of carbohydrate restriction. Apparently biology doesn’t care for neat theories!

Your mechanism also ignores the different ‘milieu’ in which those TGs circulate. Again, modern populations on higher-carb diets tend to display worse inflammatory profiles & higher BG levels than those on HF diets (on average). I don’t see how one can discount these important variables without being led into tons of paradoxes, contradictions & half-truths…

Ilaine Upton said...

Nigel, man, it's very easy to prove that restricting carbohydrates lowers your triglycerides ALL the time. Just get a meter and test it for yourself.

Ilaine Upton said...

Nigel, yes, you have have stenosis even with a zero or low calcium score. But it's not likely. Calcium scoring is easy, fast, and cheap, but most important, very low radiation.

Testing for stenosis in the absence of symptoms doesn't make sense, really, because it's a massive dose of radiation, and for what?

Calcium scanning is statistically an excellent proxy, as is CIMT, which is zero radiation. Also fast, easy and cheap.

Nigel Kinbrum said...

Ilaine Upton said...
"Nigel, man, it's very easy to prove that restricting carbohydrates lowers your triglycerides ALL the time. Just get a meter and test it for yourself."
If that's the case, would you like to explain the OFTT (40g of fat as cream) results in Figure 3B? Fig. 3A shows that an OGTT (100g of glucose) makes no significant different to plasma TG's over a 6 hour period.

Nigel Kinbrum said...

Ilaine Upton said...
"Nigel, yes, you have have stenosis even with a zero or low calcium score. But it's not likely."
The younger the subject, the less calcification there is. The higher the vitamin K2 intake, the less calcification there is.

Nigel Kinbrum said...

LeenaS said...
"Nigel, I think that you KNOW that in the INTERHEART study they monitored Apo-B100 only, without Apo-B48s?"
All I can find is INTERHEART: A Global Case-Control Study of Risk Factors for Acute Myocardial Infarction. How does this contradict what I'm saying?

Nigel Kinbrum said...

I found the Lancet study Effect of potentially modifiable risk factors associated with myocardial infarction in 52 countries (the INTERHEART study): case-control study. I still don't see how that contradicts what I wrote. Please explain.

LeenaS said...

You were calling Apo B-48's in chylos as a problem. As far as I know, these were not taken into the Apo count in Interheart. I see no problem in them.

Nigel Kinbrum said...

LeenaS said...
"You were calling Apo B-48's in chylos as a problem. As far as I know, these were not taken into the Apo count in Interheart. I see no problem in them."
If Apo-B48 or TG's weren't measured postprandially, there's no data on postprandial TG's in that trial. Absence of evidence =/= Evidence of absence. Therefore, that trial is irrelevant to my assertion. I understand that you see no problem in them. Have you read my blog post Ultra-high-fat (~80%) diets: The good, the bad and the ugly? There's evidence there to support my assertion that there is a problem.

LC/VLC diets don't guarantee freedom from atherosclerosis & CHD. What about Barry Groves, Robert Su and Seth Roberts?

George Henderson said...

There are many things that influence atherosclerosis independently of diet. Air pollution, smoking (Barry Groves seems to have been a tobacco sceptic), heavy metals. And stress. For some people, being a contrarian pioneer is probably quite stressful.
There is an interesting bit in Samuel Elliot Morison's History of U.S. Naval Operations in World War 2, volume 14 (but read the whole thing, seriously the best history book ever) where he sums up Dragnet-style the post war careers of his heroes.
Most of the carrier admirals die a few years after the war of CVD-type ailments without getting to enjoy retirement. Few jobs would be as stressful as carrier admiral in a wartime navy.
It's possible to be sceptical or gullible about things other than the essentiality of carbohydrate or the harms of saturated fats, and some of that scepticism or gullibility might always be misplaced.

LeenaS said...

Oh dear Nigel. LCHF does not guarantee eternal life. Nothing does and nothing ever will.

Yet, according to anecdotal evidence, even a medic here doing autopsies (long time ago, of course) had a clear vision claim what keeps arteries clean. He praised cream.

And, in addition to Peter's mitochondrial musings, epidemiological studies like Interheart and my personal experiences, quite a bit of practical evidence (for more than a decade in our LC community) gives only more and more ground for such a vision.

I seem to be the only one in my kin without medication at this age. And it feels good to wake up morning after morning, feeling well and refreshed. I'm not expected to live as long as Barry Groves did, but should I do that and then die of a gentle heart attack (instead of the wasting diseases seen in the family)... it would be a gift indeed.

Cheers,
LeenaS

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JS said...

All:

It's unfortunate that Nigel is still banging on about post-prandial TG (via Bansal et.al.) when the following has been clearly explained to him, over two years ago:

1. Post-prandial TG/TAG doesn’t co-vary with HDL
2. Why that’s not important
3. Why fasting TG is important even though it tends to co-vary inversely with HDL.

To that we can add the elementary statistical truth that "adjusting" for a strong covariate can get you any result you want.

See this link for the conclusion. (Scroll up if you wish to see the humorous context, in which Nigel flies into an incoherent rage…and has since apparently doubled down on his basic errors, on the theory that if you repeat something often enough it becomes true.)

JS

Ilaine Upton said...

Nigel, if you have a link to the cause of death for Dr. Su, please post it. I looked for it and never found it.

Ilaine Upton said...

Nigel, I am going to post a link to the Cardiochek portable blood test machine, you can buy it on Amazon, it's quite reasonable. If you buy the strips, make sure they are not out of date, they expire. Test yourself, report back. We are all N=1. If you clear triglycerides from carbs, that's just you.

I know I clear fat quickly, but carbs elevate my triglycerides. Same for my husband. We are both insulin resistant. That's just us.
http://www.amazon.com/CardioChek-Portable-Blood-Test-System/dp/B000BN9HR8/ref=sr_1_2?ie=UTF8&qid=1402858728&sr=8-2&keywords=cardiochek

raphi said...

@JS

Thanks! That was just the link to end a fruitless back n' forth.

PS: did you follow Guyenet's response to your interpretation of satiation/satiety/hunger/motivation/reward in terms of Berridge's work?
I think it hit a nerve, seeing as how he went all "credentials" & "ad hominem" up in this b*tch. It's funny to see people scramble when they realise 'their' references may reveal another story. I think this is where you see the science sausage get made.

PS2: When are you posting again?

Purposelessness said...

Thank you JS, very nice. Won't change Nigel but comments such as yours are a gift to interested bystanders.