One of the benefits of establishing this niche in Low Carb Cholesterol Research is that I get people sending me their labs constantly. Naturally, I obsess over possible patterns with hyper-responders.There’s one pattern that is clearly emerging that I’m calling a Lean Mass Hyper-responder. (LMHR)
General Hyper-responder vs Lean Mass Hyper-responder
I consider a hyper-responder (like myself) as anyone who sees a dramatic rise in their LDL cholesterol after adopting a low carb diet. Usually, this is 50% or more. As is typical for a low carb diet, most people see their HDL go up and their triglycerides go down.
However, a Lean Mass Hyper-responder takes this to a new level. I consider the cut points as follows:
- LDL-C 200 mg/dl (5.2 mmol/l) or higher
- HDL-C 80 mg/dl (2.1 mmol/l) or higher
- Triglycerides 70 mg/dl (0.79 mmol/l) or lower
Note these are just the starting ranges. Typically I see both LDL-C and HDL-C hit levels no one else has, while likewise having very low Triglycerides. Here are some examples:
This is only the first five I found to plug into this post. I suspect I probably have at least another half dozen or more that I’ve responded to on Twitter, email, or comments here at the site.
In fact, the very first LMHR I encountered was Nicole Recine here on the comments of a blog post. I’ve since collaborated with her quite a bit and consider her a damn awesome resource for low carb. (See her site at NicoleRecine.com) She’s sub-10% fat mass, very energetic/althletic, and much more comfortable standing than sitting. She holds at an extremely high LDL-C of 558 with an HDL-C of 140 (Total Cholesterol of 721). Yet, like me, she gets frequent checkups such as the CIMT that continue to show normal results.
Characteristics of a Lean Mass Hyper-responder
As the name suggests, LMHRs tend to be on a very low carb diet while also lean and/or athletic. Some are ultra-athletes and have taken strongly to the low carb way of life with great appreciation. And of course, all of them are shocked to see their cholesterol scores at these levels. Yet there’s clearly a mechanistic reason for this…
A Simple Theory
For me, this certainly has an Occam’s Razor-level explanation. Before reading below, be sure you at least know your basics with my Simple Guide to Cholesterol on Low Carb series.
Lean and/or athletic low carbers have three things in common:
- Lower adipose stores (less body fat energy) relative to the average peer.
- Lower glycogen stores (less incoming dietary carbs) relative to a carb-centric diet.
- Higher energy demands.
Our body seeks to keep our glycogen stores in our liver and muscles reasonably stocked, even on a low carb diet. But obviously, this is more of a challenge when you are both lowering dietary carbs and burning through it at a faster rate than most. Per Volek and Phinney, the body gets better at sparring (and I have my own data that confirms this), but the demands are still relevant for available fuel.
So think about it — (1) lower adipose fuel tank, (2) lower glycogen fuel tank, yet (3) higher energy demands. It makes perfect sense for the body to want to mobilize more fat-based energy to meet the need. And yes, that will ultimately mean more VLDL particles (VLDL-P) delivering more triglycerides to the cells, ultimately remodeling to LDL particles (LDL-P). Likewise, this means more of the cholesterol in those boats (LDL-C) being circulated along with them.
This explains why both LDL-P and LDL-C would be higher, while TGs would be remarkably low, relatively. The TGs are getting depleted from use, yet there’s no denying that more “boats” (LDL-P) are needed to provide them.
Likelihood for Children on a Low Carb Diet
This needs to get talked about as soon as possible. If this mechanism is indeed true, I’d hypothesize many children going on a low carb diet would likewise exhibit signs of a LMHR given higher metabolic rates relative to adults. Indeed, there have been three cases I’ve been made aware of in the last couple months. One privately shared via email, one in the comments of this site, and one on the forums of another. In all three cases, the child fits the pattern of an LMHR.
Naturally, this means many children could be incorrectly diagnosed as having Familial Hypercholesterolemia. Again, FH is, in fact, a genetic disease. That it often gets diagnosed on cholesterol scores alone is a modern tragedy. My fear is that this will happen more often as low carb diets become more popular and GPs don’t know enough about cholesterol and the lipid system to understand what is happening in this context.
All things considered, I hope the theory proves true given it makes a lot of sense. Before this particular pattern emerged from having lots of labs to compare to each other, I often speculated a higher mobilization of triglyceride-rich lipoproteins could be used by the body as an “alternative glycogen store”. This profile adds some weight to this possibility.[Update Nov 1, 2019: For anyone revisiting this article, I now have a great infographic that visually outlines the lipid energy model.]