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Another potential nail in LDL's coffin ?

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librarising

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Dave Feldman, author of the Cholesterol Code website, has just published a new article
http://cholesterolcode.com/remnant-cholesterol-what-every-low-carber-should-know/

I'd never even heard of remnant cholesterol, yet he concludes
"I’m hesitant to name any single lipid marker as the “best” one to measure. But if I had to choose right now, I’d be pointing to Remnant Cholesterol (RC). As of this writing, I haven’t found a single study that includes RCs in matchups with other lipids where it isn’t the clear winner in predicting all-cause mortality."

Remnant Cholesterol (RC) is simply TC - (HDL + LDL)

His article includes a link to a calculator. Over the last 7 years my RC has gone from 1.1 to 0.5 mmol/L, and from 21.5% to 9.6%. The relevance of these are shown here :
http://cholesterolcode.com/wp-content/uploads/2018/01/remnant_vs_ldl-1.jpg

I don't fully get what he's saying in the What This Means For Low Carbers section :
"the reference range for RCs as they apply to those on a fat-based diet may actually be inflated. In other words, I’d expect RCs to actually be higher for appropriate mechanistic reasons given the higher proportion of distribution by VLDLs when LCHF/Keto"

I'm only at the beginning of this RC learning curve, so this post is a heads-up to those interested.
Geoff
 
Could sdLDL be classed as RC? That which the liver refuses to have any truck with.
 
Here in the UK, LDL is usually calulated using the Friedewald Formula
LDL = TC - HDL - TG

An actual lab essay of LDL is expensive, so it is only necessary to measure LDL in a sample where TG is high since the formula has good correlation to measured values for lower TG.

Ergo, RC in the OP post is what we in the UK call TG in the standard lipid panel.

Edit: recent understanding and research does seem to correlate TG with sLDL particles, and further correlates sLDL as being linked to CVE risk factor, This research is not yet accepted by mainstream endocrinology, but is the basic working hypothesis by the likes of Tim Noakes and Ken Sikaris et al.
 
This confuses me

It is very simply calculated: you just subtract HDL Cholesterol (HDLc) and LDL Cholesterol (LDLc) from your Total Cholesterol. (Second paragraph)

In UK measurements, subtracting the HDL and the LDL from the total leaves you with 46% of the triglycerides.
(Total cholesterol = HDL+LDL+46% trigs) So subtracting the HDL and LDL simply leaves 46% trigs.)

No idea why the remaining 54% trigs aren't included in the total.

Am I being brain dead - again?
 
Triglycerides are not a sub-division of cholesterol. Both are lipids. Trigs transport cholesterol.
 
librarising said:
Triglycerides are not a sub-division of cholesterol. Both are lipids. Trigs transport cholesterol.
Click to expand...

But to me it seems like the remnant cholesterol is 46% of the trigs (UK measurements)
Am I wrong?

No I'm not wrong. I've just done the calculation he provides and the result is exactly 46% of my trigs. So why is he making it so complicated?
 
Last edited:
Bluetit1802 said:
But to me it seems like the remnant cholesterol is 46% of the trigs (UK measurements)
Am I wrong?
Click to expand...
In the Friedewald Formula, yes. Remember 46% was only an attempt at a best fit, so LDL is always to some degree estimated. Given LDL is in the RC equation, RC has to be somewhat estimated (in opposite direction to LDL mis-estimation).
Confusing, isn't it ?
 

Sorry, I edited my last post before I saw your reply. I used his calculation tool and it comes out at exactly 46% of my trigs. So why is he making it so complicated?
 
On another point, I was reading the description about how the VLDL etc. carried fats to the cells and then was remodelled by the liver. I got the impression that it was an out-and-back process where the fat went out to the body then the carriers got remodelled when they returned to the liver.

However I checked and it seems that an individual drop of blood completes a circuit of the body in around a minute.

So if it takes 90 minutes, for example, for a variant of LDL to complete the cycle of delivering fat to the tissues, it must pass through the liver around 90 times before being remodelled.

Trying to visualise this is doing my head in at the moment.
 
Think of particles as passengers on a train. They hop off at their station then get on again after their visit.
 
librarising said:
Triglycerides are not a sub-division of cholesterol. Both are lipids. Trigs transport cholesterol.
Click to expand...
My understanding is that trigs are packets of fatty acids, which get packaged in cholesterol bubbles that transport the insoluble lipids in the watery bloodstream without harm.

https://www.health.harvard.edu/heart-health/how-its-made-cholesterol-production-in-your-body

https://en.wikipedia.org/wiki/Triglyceride

https://en.wikipedia.org/wiki/Cholesterol

http://healthyeating.sfgate.com/ldl-hdl-differ-structurally-functionally-2003.html
 
You're quite right. Being a keen Arsenal fan, I made the mistake of starting a thread before a match I was watching closely.
My fingers were racing ahead of my brain.
Geoff
 
Hi guys! I got pinged to swing by and I see I could do a little expanding here.

So for the basics on lipoproteins, I highly recommend my Simple Guide series here: http://cholesterolcode.com/a-simple-guide-to-cholesterol-on-low-carb/ -- it's super layperson friendly and can help answer the lipoproteins purpose, triglycerides and cholesterol ridesharing together, and so forth.

The Friedewald equation is for LDL Cholesterol = Total Cholesterol - HDL Cholesterol - VLDL Cholesterol*
* Estimation of VLDL Cholesterol = Trigs/5 (Trigs/2.2 for mmol/L)

(To be sure, I think my tool converts mmol/L to mg/dL first, then does the imperial version for the Friedewald that's reported as an extra at the bottom.)
 

Sorry, that is a poorly worded sentence. I should update it...

Basically, I'm saying reference ranges for low to high risk is probably different for those on a low carb diet over those on a high carb diet. A low carb diet has an appropriate reason to send out and traffick more VLDLs at any given time, given it is part of its core energy distribution. Whereas a high carb diet shouldn't be trafficking as many VLDLs given its primary energy is glucose/glycogen. Thus, it may well be a sign of trouble for the carb-centric diet at a certain RC level where it isn't for the low carber because it's routine.

Again, all of this comes back to the VLDLs themselves aren't the problem, it's the fact they are either (1) in a traffic jam (hyperinsulinemia/past fat threshold) or (2) higher quantities in order to fight disease (see Siobhan's upcoming piece). Either way, it can be a reflection of a broken system so long as one keeps the correct context in mind (how much VLDLs expected due to being fat-centric vs carb-centric).

I hope I articulated that a lot better.

tl:dr More VLDLs are appropriate on a fat-centric diet and may thus skew the RC ranges.
 
I was told, many years ago, that the Iranian equation is more accurate at estimating LDL than the Freidewald equation when trigs are low.
 
Am I understanding all this correctly? Do not not fast before a blood draw to measure Cholesterol but do fast for a Triglyceride count? As all counts are normally taken from one blood draw how should we manage this?
 
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