https://cholesterolcode.

com/lmhr/

https://cholesterolcode.com/are-you-a-lean-mass-hyper-responder/

Lean Mass Hyper-responders

Generally speaking, Lean Mass Hyper-responders (LMHRs) have the following lipid profile:

 LDL of 200 mg/dL (5.17 mmol/L) or higher

 HDL of 80 mg/dL (2.07 mmol/L) or higher
 Triglycerides of 70 mg/dL (0.79 mmol/L) or lower

This pattern was first discussed in the original Are You a Lean Mass Hyper-responder articles from July of 2017.

Common Characteristics of a Lean Mass Hyper-responder

 Often lean, with low body fat (≤20% men, ≤23% women).
 Usually moderate to very fit. Many are very athletic.
 Usually very low carb (typically <25g net carbs)

Other possible commonalities:

 Often lower BHB (Blood Ketones) levels than sedentary low carbers (often 0.3-1.0 mmol/L)
 Generally higher fasting glucose, possibly through adaptive glucose sparing (often 90-105 mg/dL)
 Greater difficulty doing multi-day fasting

Why This Profile Might Make Sense

On this blog and through many articles I discuss the Lipid Energy Model. Fairly soon I’ll have a streamlined post that will
tie it together for lay people. For now, you may want to watch the linked video above as I describe it briefly.

Or for a more layperson-friendly series, check out A Simple Guide to Cholesterol on Low Carb

Also check out our FAQ as well for more information.

Is This Profile Risky

The short answer is: we don’t know.

That said, the anecdotal data looks exceptionally good so far. I’m currently working with several different people across
many disciplines to initiate studies with LMHRs in particular, as I think they may hold the answer to some very important
questions on the subject of cholesterol.

Another great article that discusses this in greater depth is Cholesterol Endgame?

Facebook Group

We also have a LMHR Facebook group that we invite everyone to join, whether you are a LMHR or just interested in the
research.

If you have further questions or thoughts on LMHRs, go ahead and post your comment at our Questions thread.
 Then there is the LMHR phenotype. Low carb, low body fat and high LDL cholesterol. Likely too low in
body fat to have a sufficient continuous supply of fat leading to low ketone levels. It is only n=1 but I
noticed for myself, also being LMHR, I had to drastically up my fat intake in order to generate
sufficient ketones and see a suppression of glucose caused by the ketones.

What does this tell us about LMHR profiles?

Putting all the sourced material together, including from the wiki, in a situation where insulin is
reduced to its minimum due to a low carb diet, it seems that the way to get very high LDL-cholesterol
exists out of the following components. The more you tick, the higher you go and the increase is not
due to an increase in production, rather due to a reduction in clearance. See the section on carnivore
further down to understand the increase plasma levels:

 Very low insulin
 High to very high glucagon
 Low free T3 (usually associated with high reverse T3)
 Low fat mass
 Very low estrogen

If you fit the LMHR profile and don’t get high ketone levels then consider the following.

You have low body fat to begin with. Reaching high ketones requires sufficient fat availability for the liver. If you
don’t get ketones in the range of >1, preferably >1.5mmol then you may not have sufficient protective effect
against skeletal muscle breakdown. I’m basing this range on the glucose suppressive effect. Only when ketones
are high enough to suppress glucose output from the liver, will it provide protection against muscle atrophy.

You should not be in a situation where you loose muscle mass or you are literally in starvation mode in my honest
opinion. If you decide to change something about this, consider a higher protein intake or higher fat intake.
Higher fat will lead to higher ketones, helping to replace the need for glucose. Higher protein will lead to more
glucose availability, also protecting against atrophy but potentially at the cost of ketones. You can also increase
both.

https://cholesterolcode.com/hyper-responder-faq/
Hyper-Responder FAQ

What is a Hyper-Responder?
The term, “hyper-responder” has been used within the ketogenic / low carb, high fat (keto/LCHF) community to
describe those who have a very dramatic increase in their cholesterol after adopting a low carb diet. This
increase can be anywhere from 50% to 100% or more of their original, pre-diet cholesterol numbers.
Typically, a keto/LCHF hyper-responder will have LDL cholesterol (LDL-C) at 170 mg/dl or higher.
How many of those practicing a keto/LCHF diet are hyper-
responders?
Because the keto/LCHF community is relatively small, the total number of hyper-responders as a percentage of
the whole is unknown. But estimates vary between 5% to 33%.

Is having high LDL cholesterol (LDL-C) on a keto/LCHF diet

dangerous?
This is the important question, of course. The short answer is – we don’t know.
As of this writing, I have much more confidence there are good reasons LDL-C could be high and bad
reasons LDL-C could be high. And these reasons aren’t mutually exclusive.
Possible good reasons:
 The body is transporting more fat for energy to your cells due to being on a high-fat diet. Since
cholesterol “ride shares” with these fatty acids in lipoprotein “boats”, it shows up in higher quantities in a
blood test. This is typically shown in a blood test where there are low triglycerides (the cargo is distributed
easily). For more on this hypothesis, see CholesterolCode.com/model
 The body is healing from a temporary injury. (You probably want that)
 The body is recovering from a temporary infection. (You probably want that too)

Possible bad reasons:

 The body is attempting to provide energy to your tissues with triglycerides via lipoproteins, but cells are
insulin resistant or they are overloaded, and thus unwilling to take in more. This leads to more residence
time of VLDLs (the precursor to LDLs) in a “traffic jam” of the bloodstream. This is typically shown in a
blood test where there are high triglycerides (the energy “cargo” is difficult to distribute). Often, this
suggests a particular profile with the LDL particles which — when combined with low HDL-C — is known
as Atherogenic Dyslipidemia.
 The body is trying to heal from a chronic condition, yet failing. This leads to chronically elevated LDL.
 (More will be added to this section soon, but the above two cover the largest categories…)

Is having a high LDL particle count (LDL-P) on a keto/LCHF diet

dangerous?
In my personal research, I find most lipidologists are confident that high levels of LDL-P (total LDL particles) are
strongly correlated with a higher risk of atherosclerosis (buildup of plaque in the arteries) and can point to several
modern studies that suggest this. It’s also worth noting that prominent voices in the field of cholesterol, such as
Dr. Peter Attia and Dr. Thomas Dayspring, likewise consider high LDL-P as a potential risk factor for
atherosclerosis.
However, those who argue against this will point out that these studies did not include people practicing a low
carb diet. It is commonly asserted—but has yet to be determined with absolute certainty—that the presence of
higher LDL-P is inconsequential if it isn’t coupled with the inflammation that is commonly remedied through
following a keto/LCHF diet. Ivor Cummins is one such voice and regularly provides counter-analysis in articles
and videos (such as Cholesterol Conundrum).

Are there any factors that might predispose one to be a hyper-

responder?
 In my research to date, I believe the largest influence of one being a hyper-responder is how lean
and/or fit they are while likewise following a keto/LCHF diet. While unintuitive, those who are lean
and/or fit often exhibit the highest LDL-C and LDL-P numbers we see (along with impressively high HDL
and incredibly low triglycerides). At the furthest end of this spectrum is a profile I call “Lean Mass Hyper-
responder” and detail it here. [Geeky technical explanation: This makes perfect sense mechanistically, as
the body is both fueled by fat while likewise working with adipose tissue (body fat) mass for “staging”, thus
theoretically, there is the likely greater need for “global distribution” of fat-based energy via VLDL turnover
than “local distribution” via adipocytes. more on that in an upcoming post.]
These are the four other most commonly referenced factors to becoming a hyper-responder:
 Familial hypercholesterolemia (FH) – A genetic disorder that presents early with higher cholesterol, and
in particular, high LDL. However, this is less likely if the hyper-responder had “normal” ranges of cholesterol
 before starting the low carb diet given FH would have likely shown beforehand as well. (See here for more
information.)
 One or two copies of the ApoE4 gene – this gene has long been identified with higher risk for
elevated cholesterol. Anecdotally, many hyper-responders find they have one or two copies of the ApoE4
gene; 3/4 or 4/4 pattern. (I myself have the 3/4 pattern, which I found through my test with 23andMe. See
here for more information.)
 Hypothyroidism – when the body’s thyroid slows down, it leads to a slow down in the production of LDL
receptors. These receptors are important for usage, and, ultimately, clearance of LDL from the
bloodstream. (See here for more information.)
 Hyper-synthesizer. Generally in reference to someone with insulin resistance who experiences an
abnormally high production of cholesterol. (See BJJ Caveman’s lecture notes for more information.)