"In fact, traditional CV [cardiovascular] risk factors, such as hypercholesterolemia and obesity, have not been found to be reliable predictors of mortality risk in these patients..."
"... as previous studies have shown these factors are paradoxically associated with better survival in the hemodialysis population."
"More recent studies have found that combination of high TG and low HDL-C in the form of a ratio, and its use as a single marker has greater predictive value for detecting the risk of CV disease when compared with each of those individual markers alone."
"Moreover, serum triglyceride/HDL cholesterol (TG/HDL-C) ratio can be a good predictor of risk for the occurrence of nonfatal CV events (14–16), CV death (17,18), and all-cause mortality (19,20) among healthy individuals and those with a wide range of CV risk factors."
Uh oh... "However, there is a growing body of evidence indicating that postprandial TG levels are important predictors of CV disease and mortality (23-25)"
Okay, so I have to pause to emphasize to everyone on low carb why this is problematic...
This metric at looking to postprandial triglyceride levels are going to apply to us differently when compared to a typical mixed-diet population. Exactly how much and in what ways are going to take some time to study and understand....
... But I can confidently say the physiology where fat adapted is going to be different -- and probably in substantial ways given we're consuming less carbs, thus potentially less bolus insulin response (on net), and literally installing more TG via intestine-dev Chylomicrons...
... This would be like looking at super low insulin levels of a LMHR and concluding they have Type 1 Diabetes in spite of excellent glucose homeostasis. For some limited data on this, particularly with even overnight-into-morning levels, see cholesterolcode.com/triglyceride-c…
Interesting 👉"We have previously shown that the association of serum TG and HDL-C levels with outcomes in patients on maintenance hemodialysis (MHD) does not follow the pattern observed in the general population, and in a subset of patients can be paradoxic to what is expected."
"In contrast to the association between TG/HDL-C ratio and mortality that is seen in the general population, higher TG/HDL-C ratio was associated with better survival in patients on incident hemodialysis."
Discussion section gets interesting in exploring many possibilites.. "In fact, a study in a cohort of Japanese patients on MHD found that higher HDL-C concentrations were associated with higher levels of oxidized HDL-C, which were also associated with increased CV mortality (49)"
"The same concept can be applied to TG and TG-rich lipoproteins because serum TG levels do not reflect the qualitative characteristics of the TG-carrying lipoproteins..."
"... Therefore, it is possible that the make-up or nature of a particular lipoprotein is much more important than its quantity in determining its effect on CV disease and mortality."
I'm sure we all know where I stand on this, of course. ;)
Incredibly happy to be reading these words.
"... it is also possible that lower TG/HDL-C ratio is not a cause but a consequence of underlying conditions.."
Yes yes yes!
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1/ There really has been a sea change I've noticed lately with regard to both the #LipidTriad and the #LMHR phenotype.
I'm not going to call anyone out, but I will say there are many who I had several spirited discussions in the past few years...
2/ ...who considered high LDL = "high" risk, full stop...
... but are now expressing #LMHRs may actually be at "low" risk of cardiovascular disease (in spite of having LDL in the 95% of the pop), just that they "could be better" if they have these LDL levels lower than they are.
3/ It's worth emphasizing their position hasn't changed with regard to higher LDL = *more risk* of CVD. Thus, it would still be better for #LMHRs to have lower LDL, all else being equal.
But the magnitude of difference in the assumed risk has changed for many.
Had to run minute 23 Tucker brings up that there are some amount of these PUFAs that are necessary and obligate to the body, but the quantity is typically much higher in the modern diet due to heavy use of seed oils...
... I bring this up because I do think @TuckerGoodrich is often portrayed by others as though he’s against any amount of PUFA in the diet. As always, I’m #ProNuance. ;)
“... the brain is not efficient at using fat as a source of ATP.”
“... nevertheless when the brain goes through crises and cannot utilize glucose, we have a mechanism to extract ATP from fat. But the result is a price tag, the result is oxidative stress.”
Please visit this around minute 24 to get the full context.
1/ So I did my 3D body scan this morning (and no, not posting pictures or sharing absolute numbers).
This will have been 5 days since isocaloric carb swapping in low-ish carb for keto.
Waist +0.9"
Stomach +1.2"
Hip +0.4"
Wow... in 5 days? This was pretty unexpected...
2/ Just a reminder-- this is the most controlled experiment between phases I've had to date. Replicated sleep and exercise timing and patterns, even water quantity and consumption window.
Given this shorter time span for the phase, I wasn't expecting much difference to emerge...
3/ Although, to be sure, both my wife and I noticed I was putting on more weight in the midsection even before the scan. I'm holding at around 199.6 for two days in a row, so while I gained around 2.5lbs initially, it seems to have leveled off.
I'm gaining weight on my "bonus" carb-swap phase in spite of it being isocaloric and everything else being nearly identical (exercise, sleep, supplements, even liquid consumption) w/ prior keto phases.
And I'm gaining it pretty fast, actually...
2/ And actually, the "low carb" phase is technically slightly lower in calories than the keto phase.
And this experiment is as controlled as I get
- Fixed eating times with fixed meals (9am/2pm/7pm)
- Fixed exercise (walking) with same route and time (~3pm)
- Comparable sleep
3/ Sure -- like many reading this, I'd assume this is in large part glycogen and water gain. But I'll concede this is impressively fast given I'm at maintenance level of calories -- which was literally just demonstrated in the run-up phases before this one.
This paper by @zinocker, @kariannesve, @simondankel is proving an interesting read. Before I get too much further, I'm going to turn it into a "reading thread" and post some of these quotes as I go...
2/ "In this paper we propose a novel model, the homeoviscous adaptation to dietary lipids (HADL) model, which explains changes in lipoprotein cholesterol as adaptive homeostatic adjustments that serve to maintain cell membrane fluidity and hence optimal cell function."
3/ Later in the abstract: "Hence, circulating levels of LDL cholesterol may change for nonpathological reasons. Accordingly, an SFA-induced raise in LDL cholesterol in healthy individuals could represent a normal rather than a pathologic response."