Jan 20


Please consider supporting my Patreon. All funding for my research and this site come solely from individuals like you. Thank you!

  • If you know little to nothing about cholesterol->
    • And you want to learn the basics->
      • You can check out my Simple Guide to Cholesterol series. It’s full of illustrations and is written for laypeople. Enjoy!
      • Likewise, I have this video that goes over the basic markers for cholesterol while on a low carb diet. (Pictured to the right)
    • You can enter your cholesterol numbers into our Report tool to check them against many risk calculations at the same time.
  • If you’re wanting to know about my research->
    • You want an overview->
    • You want the most recent breakthroughs->
      • 1/2/2018: In this latest video, I demonstrate massive changes to my LDL Cholesterol over 5 stages in a matter of days. LDL 207 to 103 mg/dL in seven days with high carb, up again to 146 on mixed, down again to 113 on high fat. (Pictured to the right)
  • If you have seen your cholesterol rise considerably on a low-carb high-fat diet (like myself):
    • You may want to first visit the FAQ.
    • I would strongly encourage you to read through this blog and my own journey revealing the Inversion Pattern. Key moments were the Identical Diet experiment and the Extreme Cholesterol Drop experiment that I wrapped around the first presentation of my data for the Ketogains Seminar.

Jan 19

Remnant Cholesterol – What Every Low Carber Should Know

[UPDATE 1/20/18: the simple form mentioned below has been updated and can be found on the Report Page.]

I want to introduce you to something called Remnant Cholesterol. And if you’re on a #LCHF/#Keto diet, this will be especially relevant.

It is very simply calculated: you just subtract HDL Cholesterol (HDLc) and LDL Cholesterol (LDLc) from your Total Cholesterol. For example, if your Total Cholesterol were 300, your LDLc 200, and HDLc 80, then you’d have a Remnant Cholesterol (RC) of 20. That’s 300 – 200 – 80 = 20.

You can be forgiven if you thought Total Cholesterol was simply LDLc + HDLc. I thought so too before I was into keto since I was always told, “cholesterol is divided into two types, LDL and HDL…” — wrong! That little gap of cholesterol left over is very, very meaningful. When fasted, it is the cholesterol found in Very Low Density Lipoproteins (VLDL) and Intermediate Density Lipoproteins (IDL). When not fasted, it includes those two and Chylomicron Remnants.

Why This is a Problem

You see, these lipoproteins mentioned above aren’t supposed to be hanging around in the blood for very long. VLDLs pop out of the liver ready to drop off fat-based energy in the form of Triglycerides (TG) from the getgo. They bounce around your vascular system binding to tissues that need the energy and get smaller and smaller from less cargo in the process. From there they are remodeled to IDLs, which are then cleared by the liver or remodeled again to an LDL. This succession of stages to the final LDL takes under 90 minutes. So how long do LDLs hang out? 2-4 days!

This is worth reemphasizing because it’s key to understanding Cholesterol Remnants. Again:

  1. VLDL half-life is 30-60 minutes
  2. IDL half-life is less than 30 minutes
  3. LDL half-life is 2-4 days

So given this, we’d fully expect that the vast majority of lipoproteins that originated from the liver would be in that final LDL stage, even if they started out as VLDLs, right? Yes, of course!

A Simple Traffic Analogy

So imagine it this way… you have two jobs. When you leave the house in your car, you have a lot of food which you then drop off to people around the neighborhood who are hungry. This is supposed to take 1-2% of your time.

The other 98-99% of your time is spent doing the other job — patrolling the same area to help out in other ways. You might be doing citizen arrests of robbers (binding to pathogens) or helping out repairing houses that need it (non-hepatic endocytosis).

But what if there’s a problem with the roadways such as a traffic jam or you’re having a tough time finding people to take any of the food you’re offering (exceeded personal fat threshold). So now you’re spending much more time in that first job because there’s a widespread problem throughout the neighborhood that’s holding you up (and your fellow delivery drivers as well).

How They See It vs How I see It

I’ve been obsessively reading these Remnant Cholesterol papers for a while now. And this is a common opinion among them:

Remnant cholesterol, also known as remnant lipoprotein, is a very atherogenic lipoprotein composed primarily of very low-density lipoprotein (VLDL) and intermediate-density lipoprotein (IDL).

So VLDLs and IDLs themselves are “very atherogenic”?

Let me offer an entirely different viewpoint.

As many long-time readers know, I certainly see the lipids and their containing lipoproteins in our bloodstream as primarily an energy distribution system. That first tiny little stage of delivering energy as VLDLs or Chylomicrons is arguably the bulk of their “work.” Sure, it is done so quickly that it might seem like it is a small part of it. But when you see their largest payload is fatty acids (in the form of triglycerides) and their most reliable “activity” is hydrolyzing it off to the tissues that need it, you realize these guys just aren’t procrastinators, they get the biggest job done early and quickly…

… except when they don’t.

I offer two major reasons VLDLs and IDLs would be slowed down from remodeling to LDLs:

  1. VLDLs aren’t effectively distributing fat-based energy (triglycerides) and thus has longer residence time before it can move on (remodel) to its next stages.
  2. The lipid system is being employed to a higher degree in fighting or repairing a disease state. I won’t be covering this point here, but I’ll return to it in another post.

The first point is well illustrated in many who have hypertriglyceridemia, a commonly associated CVD risk. Often they have a much higher proportion of VLDLs. Why? Not surprisingly, these are likewise associated with hyperinsulinemia and metabolic syndrome.

Broken Systems are Atherogenic, Not Lipoproteins

To put it simply, a problem arrises when the fat-based energy has few places for the VLDL to park it. Those places it does park often can’t stay there long if one is well past their personal fat threshold. The fatty acids keep spilling back out into the bloodstream, binding to albumin, and finally making their way back to the liver to… wait for it… get repackaged into a VLDL again. You see the cycle?

VLDLs, IDLs, and LDLs are not independently atherogenic, but a body that is undergoing oxidative stress, chronic inflammation, or hyperinsulinemia can be. Yes, lipoproteins participate in this process as that is one of the many “hats” they wear in trying to fight it off and/or repair it. But trying to identify a single lipoprotein to label as the bad guy misses the point of the larger perspective on what’s happening inside the body to begin with.

Remnant vs LDL Cholesterol

Here’s a couple of example RC studies:

From this study: CONCLUSIONS: Both lipoproteins [RC and LDL] were associated equally with risk of IHD and MI; however, only nonfasting remnant cholesterol concentrations were associated stepwise with increased all-cause mortality risk.” (See graphic at right from the study)

From this study: CONCLUSIONS: Increased concentrations of both calculated and measured remnant cholesterol were associated with increased all-cause mortality in patients with ischemic heart disease, which was not the case for increased concentrations of measured LDL cholesterol. This suggests that increased concentrations of remnant cholesterol explain part of the residual risk of all-cause mortality in patients with ischemic heart disease.”

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.

At a minimum, one should be looking at Remnant Cholesterol over LDL Cholesterol. That’s why I added a new tool for people to check their Remnant Cholesterol here on the site. Feel free to do yours and share the results in the comments section.

What This Means for Low Carbers

While I have read through a lot of these studies, I still consider this early in my research on it. I’m naturally thinking through the mechanics and how it applies to those who are LCHF and thus powered by fat.

Here’s a summary of my notes thus far:

  • Given the data I have so far from the followers of this site, those going LCHF/Keto will more likely to see an improvement in their RCs, even if they are a hyper-responder.
  • Ironically, 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.
  • Like triglycerides, RCs seem to be a great “cheat detector” within my own group of family and friends. Anecdotally, when they fall off the wagon and have too many carbs while still being very high fat, their RCs tend to go up.

Final Note on Fasting vs Non-Fasting Remnants

Lastly, I should warn that much of the newer research on Remnant Cholesterol compares populations who have had non-fasted lipid numbers. I suspect this will not work for those on LCHF/Keto. I’ve already found in my own data and those of others that when on a fat-centric diet, you can often have higher triglycerides relative to a carb-centric diet when taking lipids while not fasted. Hello! You are literally observing triglycerides from the food you just consumed as part of the total amount found in the blood.

Jan 08

New Report Tool in Development

I haven’t had a chance to write about Cholesterol Remnants or Atherogenic Index of Plasma, but I will at a future date. For now, I have a tool I’ve been writing and testing which will report those and other metrics for copy/paste use. You’ll find it on the new Report page.

Feel free to test it out yourself and copy/paste your report in the comments below.

Jan 05

Very Happy with the Launch, Now Time to Recover

Wow! As of this writing, it has been barely 48 hours since I posted the Capstone Experiment video and it’s definitely making the rounds.

Alas, I have made many promises to my family that once I was done with this leviathan of an experiment I’d be doing some catch-up. So I’m giving a heads up that I’ll be a little less active on social media for the next several days.

P.S. I have the most amazing wife in the world to put up with all this madness!

Jan 03

The Capstone Experiment – it’s time to #rethinkLDL

As of today, I’m declaring Phase I and II of my research complete.

  • Phase I spans December 2015 to May 2017 where I was focused primarily on the Inversion Pattern.
  • Phase II spans May 2017 to January 2018 where I was focused on Energy Status.

The Capstone Experiment combines both legs of this theory and demonstrates how fluid and agile cholesterol markers are when modifying dietary sources of energy in real time.

Naturally, there are many questions still to answer given how much there is to unpack. But for now, I want to put a white-hot spotlight on the most central and unmistakable observation of this experiment:

Cholesterol is a passenger, not a driver. Its markers are extremely agile and highly influenced by the larger energy metabolism. This runs counter to medical mainstream opinion.

Next Steps

  • Certainly, I’d like to put this into a formal study. But the process of organizing these and raising money tends to be slow, which is why I haven’t taken a lot of time pursuing it to this point. I’m an engineer, not an academic, so I’d prefer to find someone who can better navigate those waters to make this happen.
  • Falsify this! If you’re reading this and you have alternate theories or a way I can disprove this working theory, please let me know. I can’t emphasize enough that I appreciate contrarian views, so long as they are materially relevant and productive.
  • Lastly, I’ll be taking a bit more personal time in the next week to rest and catch up some time with family. Everyone has been very patient and understanding of my work through this point, chief among them being my wife. These experiments take a lot out of me, with this one being the most intensive one yet.

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