Jul 03

Are you a Lean Mass Hyper-responder?

[12-11-2018 IMPORTANT UPDATE: We now have a great all-purpose page for Lean Mass Hyper-responders and a very rapidly growing LMHR Facebook Group.]

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:

431 147 46
226 98 52
342 110 61
263 89 55
277 102 67

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:

  1. Lower adipose stores (less body fat energy) relative to the average peer.
  2. Lower glycogen stores (less incoming dietary carbs) relative to a carb-centric diet.
  3. 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.


Final Thoughts

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 LDL-P could be used by the body as an “alternative glycogen store”. This profile adds some weight to this possibility.

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George Henderson (@puddleg)

This makes sense to me.
It’s been theorised that SGLT2 inhibitors, used in the treatment of diabetes, increase LDL by increasing fat trafficking. They don’t cause an increase in MIs and do reduce deaths from heart failure and kidney disease significantly.
“These data suggest that empagliflozin, by switching energy metabolism from carbohydrate to lipid utilization, moderately increases ketone production and LDL cholesterol levels.”


These drugs are keto diet mimics across a range of effects, including natriuresis. It’s also possible natriuresis itself contributes to LDL elevation, as low salt diets increase LDL


Interestingly cholesterol synthesis itself is via HMG-CoA reductase which is induced. by insulin and suppressed by glucagon. Hence the increase in HDL – reverse cholesterol transport may be increased to supply cholesterol for the VLDL transport of TGs. VLDL will be less TG-rich.
Low insulin can increase LDL in some because ApoCIII clearance is insulin-dependent, as is ApoB recycling in hepatocytes. FFAs elevate insulin, so there’s a neat feedback loop between adipose stores via insulin controlling LDL levels, even in low carb states, consistent with your hypothesis.


I am 43 yrs old, in low carb for one yr. But more liberal LCHF. I am 175cm, weight fluctuate 59kg to 61kg. (was 65kg before LCHF).
Last year Nov, blood test:
HDL 76 mg/dl
LDL 220 mg/dl
Tri. 54 mg/dl.


I am 50, male, did a blood test in January 2018. Weight 69kg, 175cm
HDL: 73 (2016: 61)
LDL: 175 (2016: 121)
Trig: 60 (2016: 57)

My doctor freaked out on the LDL scores. I lost 11kg over 3 years, lost 3″ in the waste and 1″ around the neck. He told me to stop my diet before he has to give me statins to control the LDL. Doctor did admit that all my other medical markers are fine, he does seem confused.

Siobhan Huggins

I went ahead and calculated your total cholesterol and then put it into our report tool

–==== CholesterolCode.com/Report v0.9.2 ====–
on – :::
Total Cholesterol: 260 mg/dL 6.72 mmol/L
LDL Cholesterol: 175 mg/dL 4.53 mmol/L
HDL Cholesterol: 73 mg/dL 1.89 mmol/L
Triglycerides: 60 mg/dL 0.68 mmol/L

Remnant Cholesterol: 12 mg/dL 0.31 mmol/L >>> Lowest Risk Quintile
Remnant Chol to HDL: 0.16 >>> Lowest Risk Quintile
Go to https://tinyurl.com/y8hokam2 for more on Cholesterol Remnants

AIP: -0.444 >>> Lowest Risk Third
Go to https://tinyurl.com/ycccmmnx for more on Atherogenic Index of Plasma

Friedewald LDL-C: 175 | Iranian LDL-C: 146
Total/HDL Ratio: 3.56
TG/HDL Ratio in mg/dL: 0.82 | in mmol/L: 0.36

Based off of the research we currently have, this lines up with lower risk categories.
Perhaps it may be beneficial for your doctor to watch Dave’s video from Low Carb Breckenridge 2017 or you could send them to the Simple Series to help explain why your LDL is higher.

Congrats on the weight loss, by the way!


Very interesting. It appears I’m a LMHR, too.

The best theories are those that simply explain the observations, are falsifiable, and make testable predictions. I was thinking about what some those tests might be.

If we have a LMHR, removing any one of the of the three pillars should decrease LDL-P

LDL-P should be decreased by:
1. Gaining 10 pounds of body fat (then readapting to LCHF). Might be possible to test with someone who’s weight fluctuates with cycles of feasting / fasting or strict LCHF / normal diet.
2. Filling the glycogen stores of the liver by carb loading. You’re N=1 experiments are consistent with this. Others appear eager to replicate to produce “ideal” lipid scores.
3. Eliminating exercise and switching to a sedentary routine. Seems unlikely many elite athletes would willingly atrophy their muscles, but injuries happen, and could be studied retrospectively.

Another prediction. Someone who is overweight and gradually losing weight should hit a tipping point as their %BF declined where LDL-P jumps up (provided they are at least moderately active). It would be extremely interesting to plot LDL-P against %BF from say 30% down to 10%.

George Henderson (@puddleg)

Also have a look at this


” Two days of fasting caused a reduction in body weight with an approximately 40% decrease in the epididymal fat depot and fat cell size. No changes in serum cholesterol were noted, but serum triglycerides fell approximately 55% with fasting. LDL receptors detected by immunoblotting decreased progressively with fasting to levels that were 95% below controls in adipocytes isolated from epididymal fat pads by 2-3 days. In contrast, hepatic LDL receptor expression was unaltered by fasting. After 2 days of fasting, the rate of synthesis of LDL receptors in isolated adipose cells was decreased approximately 35%, whereas levels of LDL receptor mRNA were diminished approximately 55%. It is concluded that the expression of LDL receptors in rat adipocytes is markedly downregulated during fasting through transcriptional and posttranscriptional mechanisms. Furthermore, LDL receptor expression is differentially regulated in adipose tissue and liver during fasting in the rat.”

So, are adipose LDL receptors downregulated by the fasting mimicking ketogenic diet?


Is the LDL conversion you give correct? I think 200 mg/dl is 5.2 mM (mmol/l).
I cycle 100 km or 200 km (up to 10 hour ride) at least once a week on an empty stomach. I closely follow a very low carb diet for two years. Anyway, my results are broadly in keeping but I’m not so lean (bmi 24).
Trig: 0.8 mM
HDL: 1.5 mM
LDL: 6.3 mM


I have your top HDL beat. None of my docs has ever seen anyone even close. Latest lipids (roughly consistent over many years):

LDL 199 (calculated)
TG 38
Fasting insulin 2 (“normal” lab range 2–14)

I eat moderate low carb, intermittent fast (no breakfast), and do very brief but extremely high intensity strength training 2x/week. Otherwise no athlete, though resting heart rate at 59 is 45. I am lean though certainly not ripped, maybe 10% body fat.

I have resisted the temptation to get an advanced lipid panel since I really don’t know what I could reasonably do with the information. And I’m unconvinced that LDL-P or anything else on such a panel has a demonstrated causal role in CVD at this time.

Another data point for you…thanks for your incredible research and thinking about all this.

George Henderson (@puddleg)

Hi Bill, you can have high HDL for genetic reasons, such as a CETP defect – and whether this is good or bad for you depends on your insulin level.
So, you are doing fine.



Thanks, George. I should have mentioned that, indeed, high HDL (and my lipid profile in general) does seem to run in my family even though none of them eat or exercise like I do. However, their pattern is far less exaggerated than mine. So I’d guess that, as you suggest, some of my profile is genetic, the rest resulting from some combination of low carb/intermittent fasting/high intensity strength training. I’m still not convinced anyone really knows what it all means for CVD risk (aside from various modest correlations of unknown causal significance and possibly highly context dependent). Luckily my doc knows better than to suggest a statin :-). Thanks again.


I’m so glad to have found you, Dave!

I’m a 74 year old male, but I do still fit the lean, athletic, LMHR profile.

My recent NMR results: HDL- 82, LDL- 202, Trig’s- 59, aligning about perfectly with your cut points.

I assumed my body had good reason for the out of whack numbers, but I’m relieved, thanks to you, to find they’re not uncommon.
I eliminated all grains and sugars 2 years ago, and for months now I’m all out keto.

I abused my body for 45 years with a heavily grain based vegetarian diet and ended up with a CAC score of 2300.
Got any idea’s on how I might get that number down?

Bill H
Bill H

Hi OobLaDee, just wanted to chime in here. Dr. Carolyn Dean, while not a fan of the CAC, says that calcium buildup can be dissolved by taking therapeutic doses of magnesium. https://drcarolyndean.com/2016/01/coronary-artery-calcification-increases-atrial-fibrillation/ Worth looking into, I think — I’m very curious is if there is any data on magnesium lowering CAC scores.
Bill H


Hi Dave.

Been following your work with interest.
This last post is especially germane.

I almost fit the profile, (LDL extremely high, HDL a little lower than your cut and trigs a little higher, intensive exercise). I am almost 70. When I get tested I will send my results for your database.

Logic makes a lot of sense and answers questions I have had for years.
Keep up the good work.



Hi Dave,
44-year old athletic female coming out of the woodworks 🙂 Your hypothesis makes a lot of sense to me. I lift weights, do pilates, barre, and a lot of body weight training, and kick and punch the crap out of bags. I have been low carb for a while, but recently I have been leaning toward the very low carb end of things. With 132 lbs at 5’7″ I am lean.
Had the lipid NMR done a couple of times. The last one definitely puts me in the lean mass hyper responder category (from memory):
LDL 200
HDL 115
Trigs 68
Small, dense LDL particles were below the detection limit of the NMR in both tests. I am happy to dig up and share my data with you via email.


George Henderson (@puddleg)

More evidence – huge increases in LDL cholesterol after a 7-day fast


“Fasting increased total serum cholesterol from 4.90 ± 0.23 to 6.73 ± 0.41 mmol/L (37.3 ± 5.0%; P < 0.0001) and LDL cholesterol from 2.95 ± 0.21 to 4.90 ± 0.36 mmol/L (66.1 ± 6.6%; P < 0.0001). Serum apolipoprotein B (apo B) increased from 0.84 ± 0.06 to 1.37 ± 0.11 g/L (65.0 ± 9.2%; P < 0.0001). The increases in serum cholesterol, LDL and apo B were associated with weight loss. Fasting did not affect serum concentrations of triacylglycerol and HDL cholesterol."

Even though fasting downregulates HMGCR; so the downregulation of adipocyte LDL-R might indeed be the deciding factor.
We're just not eating enough, Dave (and when you do, your LDL drops).

George Henderson (@puddleg)

And here we go – the same length fast in obese subjects lowered LDL.
So there is definitely a “lean high LDL” phenotype for some reason when burning fat.




Great information. I am a 54 yr old male. Went low carb and had the following lipid results:

LDL 304
HDL 91
TG 78

This occurred when I was initially losing weight 206 lbs to 190 lbs over an 2 month period. I am also fairly lean and Weight train ~5x week during this time which I have been doing for many years.

Become very concerned and Cut back on sat fats and added small amounts of carbs. Lipid profile change as follows two months later:

LDL 135
HDL 95
TG 59

Did not feel as good so reduce the carbs again after some research and will have a blood test later this year. Eating more red meat also.


I am 62 y/o on a low carb diet (not keto). Definitely not a hyper-responder, but my lipid profile paralells your second test. My carbs are typically from veggie sources, and eaten at 3 meals each day when I’m not doing a parital fast. Always in morning ketosis.

Hyrdorstatic tested body fat measured at 10.34%.
Blood lipids (all units mg/dl)
Total C 196
HDL 80
LDL 103
TG 45
Glucose 92

I train 5 to 7 days per week, mostly resistance training limited to <50 minutes. I time my meals and have most protein partitioned around my workouts (25g pre and two post feeding at 25 g).


I am on zero carb meat only diet since 5 months. Age 60, height 166 cm, weight stable at 55 kg. On completing 45 days (03-04-2017) on the diet my lipids were as follows.
TC: 446
TG: 205
HDL: 61
LDL: 344
On completing 90 days (17-05-2017) on the diet as follows.
TC: 673
TG: 69
HDL: 104
LDL: 555
Any comments please!
Thank you.

Mike Broadley
Mike Broadley

58yr old male.
Weight 83.5 kg – was 95kg 3 years ago. Very active 6/7 days per week. Weights and HITT.
LCHF 3years
16:8 Fast on daily basis
Blood draw done fasted.
VLCHF 6months
Cholesterol 10.1
Trig 0.8
HDL 2.5
LDL 7.2

Never felt better

Carlos Lacayo
Carlos Lacayo


Last November (before Keto) I found out I had High Cholesterol and Doctor put me on Atorvastatin. Please see Bloodwork 1.

Choleterol: 280
Tryglycerides: 64
HDL: 89
VLDL: 13

February got checked again (still before Keto) see Bloodwork 2

Cholesterol: 252
Triglycerides: 54
HDL 83
VLDL: 11
LDL: 158

At the beginning of May I discovered Keto because I had trouble loosing body fat for years. Keep in mind that I am a very active person (for the last 10 years) with weights, and cardio 4-5 a week. 2 months in Keto have changed my everyday lifestyle. My focus, my well being, my workouts have all gotten so much better. My body fat% went from 27% to 19% in just a little over 2 months and love my results. I also do Crossfit 2 times a week now because of my new discovered energy source. Also as soon as I started Keto I stopped taking the statin because I hated the way it made me feel and heard from many Keto was suppose to help me. Now Bloodwork 3 came in last week .
Bloodwork 3

Cholesterol: 360
Triglycerides: 64
HDL: 101
VLDL: 13
LDL: 246

I freaked out because all this hard work I put in has been for nothing. My doctor now wants to put me on a drug called Crestor and I want to refuse it. Can you offer some advise on what steps I cant take to lower this number? I am thinking about trying the increased in Saturated Fats like you did or possibly just cut them out and increase my carbs to about 70g a day. My macros has been consistent with 5c/25p/70f. Please let me know what you think.

Carlos Lacayo
Carlos Lacayo

I also want add that after being fat adapted for a month (beginning of June) I applied intermittent fasting 16/8. Fasting really kicked my Keto into gear especially at the gym.

Thank you for all that you’ve done and I think it’s amazing how you are helping people discover this mystery. I will definitely be donating to you buddy.

Tim Newton
Tim Newton

Hi Dave

Here’s another from the UK from a 66 year old marathon runner (10th fastest in UK this year!), 2 yr 6 months LCHF. I’m frequently in ketosis: 3.1 after a recent long run. Numbers in mmol:

TC: 8.05
Trig: 0.71
HDL: 2.94
LDL: 4.78
TC/HDL 2.74
Weight 9st 1lb (127 pounds)
BMI around 18/19

I had the blood test recently as part of the 5 yearly NHS healthcheck for us oldies. The GP called me in when he saw the figures and immediately opened the question of statins! I quickly disabused him, as politely as I could (not very), of the notion that I would ever contemplate that, and I would do without extra 3 days of life, thank you very much. It brought home to me with thump the grip the pharma industry has on our sacred health service. He realised I knew my stuff and backed off, saying it was fine, but I didn’t think he was convinced. I’m now thinking about finding a more sympathetic and knowledgeable GP.

Keep up the good work!

Matt Remine
Matt Remine

Hi Dave,

47M/5’5″/137lbs 14%BF Zero Carb for 3 months at time of test. 18hr daily fasts. High output daily workouts/cardio/labor in trades.

TC 471
HDL 80
Trig 88
LDL 373

Hope that helps. Thank you for all of your work.



I am a 50 years old full marathon and an ultra marathon runner.
LCHF 7~8years. Height 162 cm, weight 53~54 kg.(before LCHF weight 73kg)

LDL 261
TC 420
TG 31
Fasting insulin 2.7

Your work is very very interesting.
I also want to know what is happening?

Keep up the good work!


Hi Dave,

I’d like to add a datapoint for you. It’s my husband, they diagnosed his as FH last year purely based on his lipid profile and told him he could come back for a staton prescription or not at all. No option for further testing. Not even genetics! He didn’t go back for statins, no way he’ll ever take them! FH or CVD doesn’t run in his family at all, but unfortunately we have no tests from before our LowCarb lifestyle. We suspect he’s a LMHR but we cannot be for sure. Your work is very interesting and reassuring, because it’s hard to be comfortable with these numbers and turning down professional medical help.

Height: 178 cm
Weight: 75 kg
Waist to height ratio: 0,45
Body fat: probably below 10%
Activity: callisthenics exercises 2-3 times a week, desk job but stand desk, little walk every day
Diet: VLCHF since 2009, no IF at the time of testing
TG: 502
TG: 124
HDL: 62
LDL: 418

Hope this helps. TG little high for your LMHR profile? What could that mean? We plan on asking te retest since it’s been 2 years now. Of course we’ll happily share those numbers, also if he gets the chance for a second test. The. Hell do the Extreme Drop protocol.

Sietske (Sweden)


Last sentence scrambled up! Should be “… second test, then he’ll do the ED protocol.” Oh, and forgot to mention; 42 years old male. And its now two years ago that we got those numbers and diagnosis, not last year. Time flies!


Hi Dave,

Total cholesterol 6.4mmol/L
Ldl 4.53
HDL 1.74
Tri 0.38
Body fat around 8%
Waist size 28″
I’m 23 5’7 143lbs and would say I’m very active
Warehouse job + working out and sports
Been LCHF for 7 months with a weekly cheat day


Adding to your list:

54 years old
6′ 7″, 210 pounds
Desk job, daily fast of 10+ hours (although some heavy cream in coffee – not sure if that ruins the fast).
Mostly lift weights, some walking. Read about myocardial fibrosis in endurance athletes and dropped running.
I’m not a perfect fit for your definition, but:
Total Cholesterol: 254
Direct LDL Cholesterol: 176
HDL: 83
Triglycerides: 41
Happy to provide other data if helpful.


Hi! I wanted to offer my stats as well. I was referred to you by the Ketogenic Diet Open Discussion site on Facebook. I’ve been following a keto diet for the past year and had blood work done with these resulting numbers.

I am 52, weight is 135, height is 5’6″. I don’t consider myself a lean endurance athlete by any means, but I hike at least once a week and do HIIT on average about 3X per week. My job varies in terms of physical activity from sedentary to potentially walking several miles a day. But I would say it falls more on the less active side.

LDL-225, HDL-79, Triglycerides-154
Non HDL-256

My Triglycerides seem to be higher to qualify as a hyper-responder.


George Henderson (@puddleg)

I’ll give a little n=1 anecdote here; my chol was always a bit high, as far as I remember, despite having Hep C geno 3, which was a good thing at that time.
Clearing HCV and being low carb, it is now significantly higher, within the pattern you describe.
I’m naturally lean, exercise a bit but not intensely, practice IF to some extent.
After a very high lipid test, I decided to replace butter with olive oil, cheese with avocado, as far as possible for a month or two.
Next test, my total C and LDL were the highest they’ve ever been.
Went back to ghee and coconut oil and they went down again by the next test, at least to the point where the ratios weren’t high risk.
My conclusions?
1) high LDL in my case is probably caused by high fat/low carb intake and low insulin, not high SFA%
2) I may be a hyper-responder to plant sterols in this context.
Put this on twitter and 3 or 4 other people said they fitted type and had same reaction to high MUFA oils replacing SFA.


Hi Dave.

There is a mechanism involving triglycerides and apoB protein release and catabolism in liver that may partly explain your LMHR group.

Trigs are the prime control factor in apoB metabolic channeling. They essentially divide LDL into an atherogenic and non atherogenic pool, with a switching mechanism dependent of the trig level.

There is a U shaped curve in LDL production and catabolic rates. As trigs rise from low levels the scheme switches from non atherogenic to atherogenic LDL, with a plateau in the middle and higher values on both the lower and higher arms.

At low trigs LDL production and catabolism can be very high, this would not apply to everyone but possibly to a small group, hyperresponders may be among this group.

At the same time VLDL production can be scaled back as the liver can release a fairly broad spectrum of apoB particles directly into plasma, these would include IDL and LDL, possibly as much as 50%.

The net result could be a large presence of LDL, high production and catabolism but subdued VLDL. This would presumably be a healthy state, in spite of the high LDL since it would be group a.

Here’s the ref, check figure 5.



George Henderson (@puddleg)

Hi Tim,

I’ve been thinking along similar lines but hit a speed bump. On LCHF no TR-VLDL, less VLDL, more IDL and LDL released directly; this is also in Krauss studies.
But IDL has less TG, LDL has next to none, so how are these lipoproteins contributing to increased fat oxidation? Where does this fit in the energy demand model?

I see another aspect like this – when you don’t eat carbs you don’t need so much cholesterol. Synthesis has decreased, adipocytes are rejecting it, HDL has risen to collect it from cells, and it’s being transferred to IDL for transport to the liver for increased excretion (I suspect), making more LDL.
Also, foam cells consume 33-66% of LDL normally, according to Brown and Goldstein, with LPS attraction and oxidation as the triggers, so what if foam cells STOPPED consuming LDL in low inflammatory states? Would that make LDL pile up in serum?
All of these mechanisms would surely be temporary and at some point whole-body cholesterol stores would get low enough that LDL would start to come down, at least I think so this model predicts.


Hi George.

I think I agree but come at it from another angle.

My take is that in healthy individuals at extremely low trigs LDL levels tend to be very low but production and catabolism very high so the hepatic LDLR activity is high. Here after a low carb/high fat meal LDLRs are available for catabolism of chylomicron remnants but tissue, adipose and muscle is fat replete and properly sized so the small amount of remnant fat gets recycled rapidly into IDL/LDL but catabolized very quickly so levels of LDL remain low but particles are large (with large lipid and cholesterol loads), and consist almost exclusively of LDL I/II, ie non atherogenic, VLDL is almost all VLDL2 so small and again non atherogenic. There is little to no cholesterol esterase going on so not much lipidation of VLDL, the action is mainly in LDL. The system buffers the high fat meal in muscle and adipose and meters it out later from adipose. I”m not sure how you can get high cholesterol in such a system except as a mismatch between production/catabolism, but even a small mismatch could see outsize levels as the rates are high, I suspect this would be rare.

As trigs rise CETP (cholesterol ester transfer protein) gets turned on and cholesterol transfer from LDL/HDL to VLDL starts. This shifts part of the cholesterol load to VLDL from LDL/HDL and lipid is given in exchange. Subsequently HL and LPL delipidate both LDL and HDL so you are left with small/dense LDL and small HDL. The HDL particle is unable to retain the apoA1 protein and sheds it and it is cleared from circulation. In this system you would have higher but not necessarily super high trigs, low/normal LDL and low HDL. The LDL would be small and dense and reside in circulation much longer because the LDLR has less affinity for it. LDL, being in circulation longer has more oxidation and accumulates more sugar labels. As trigs rise further the situation would get progressively, but slowly worse. Your foam cells would start to accumulate as inflammation/oxidation would rise.

The dynamic action as this system progresses is in the LDL pool size and character as trigs move up. LDL pool size increases as catabolism rates decline and the spread between high and low increases so you can get high LDL at moderate but still relatively low trigs. The non atherogenic pool starts to decrease and the atherogenic (small/dense) starts to increase and HDL starts to drop. Later as trigs rise further you get increasing catabolic rates again and LDL pool size starts to drop but the character has changed to atherogenic. This I think is why cardiac admits have low/normal LDL.

So highest LDL is seen when trigs are somewhat higher but still on the low/normal side. Also you see the biggest spread between low/high. I think this is where the hyperresponders fit. If you look at the chart (Figure 5) the densest cluster of high LDL is in this area.

So how does this make sense in energy transport? Good question. On LCHF you eat less and lose weight at least initially so some of the LDL will be coming from adipose, as adipose distributes lipid and shrinks it cannot at some point hold onto the stored cholesterol so it comes into plasma. You could also, be getting additional from ectopic storage via reverse transfer from higher HDL and with lower inflammation perhaps foam cell discharge (this pool size could be large). This discharge could be quite large and sustained. I believe that cholesterol does eventually normalize for most individuals on LCHF but this can be a long time. If you were getting substantial flow from storage AND trigs were at the right levels the two streams (anabolic and catabolic) would add so you could in theory get very high LDL, perhaps this is the explanation as you say.

Don’t know. I think you’re right, that cholesterol levels would eventually return to sanity and the mechanisms involved seem plausible so maybe. If this is right then the base levels of LDL may fit and Dave’s results would be a shorter term modulation of them.



Some more data.
First, I’m not 100% “LC”,
Mornings are MCT and heavy cream coffee.

Lunch Salad with some sort of protein (sardines, salmon, beef jerky…)
Diet Coke, almonds and some 70% dark chocolate.

Dinner is as LC as I can make it. (I eat with the family and don’t want to rock the boat).
ice cream later at night

Started in in Jan-2017 and dropped from 172 to 164 ish
Run 4 miles 4 times a week (8:45 min miles)
OR bike to work (30 to 45 miles total) 16->18 MPH average
I consider myself reasonably athletic (compared to the general population)

6’2″ (188cm)
164 lbs (74.4kg)

Blood work from last year (June 2016) when I wasn’t low carb:
Total Chol: 204
Trigs: 74
LDL 126
HDL 63

Last month (June 2017) on the quirky low carb:
Total Chol: 241 (up 37)
Trigs: 61 (Down 13)
VLDL 12 (down 2)
LDL 149 (up 23)
HDL 80 (up 17)
A1c 5.5 (I don’t have a number from last year)

I’lll get a physical in Sept and see what the Dr. has to say about these numbers.
BTW, the 2017 data was from Walk In Labs, it was a $46 test, seems reasonable to me.

I feel like I’m hovering around ketosis. On mornings with it’s a 35 miles ride in, I feel fine. However the 15 mile ride home is sluggish on the border of bonking. Then sometimes it’s another slice of seedy bread w/ PB. Eventually would like to go full keto and see if that goes away or gets different. I’m impressed by people that do sub 4 hour marathons in ketosis. Is it genetics, the ketosis or something else?

One last bit, if you forget to enter the CAPTCHA code the post text gets deleted : (


Hi George/Dave.

Further thoughts on the mobilization of cholesterol to/from plaque and fatty streaks and ectopic locations, this is a minor wrinkle on circulating LDL levels but may be important in some cases..

The major holder of cholesterol in plaque is macrophages that aggregate into foam cells. Cholesterol entering these structures is damaged or altered in some form, ie it is not the native cholesterol from pool a. The mechanism of entry is receptor mediated endocytosis, ie receptors are concentrated in coated pits and bind lipoproteins like damaged LDL by invaginating and passing the contained material to lysosomes to seperate the cholesterol and other constituents for degredation. This is because macrophages do not have many receptors for native LDL but have numerous receptors for chemically altered LDL, so macrophages scavenge this damaged LDL as a way of reducing its presence in plasma. Once in the cholesterol is esterified in droplets but enters a futile esterification cycle where it is repeatedly re-esterified and returned to free cholesterol and is essentially trapped as the plaque builds. For exit from the vascular wall the membrane macrophage must find a cholesterol acceptor since free cholesterol is aquaphobic. Once there is a minimum of acceptors the interior foam cells can pass cholesterol to the membrane macrophages as there is an exit from the esterification cycle where free cholesterol can pass out of the cell.

The main acceptor candidate is HDL although there are other known acceptors HDL seems to be the prime one.
Once in HDL, cholesterol can be delivered to the liver, or if CETP is active it can be transferred to VLDL.

To sum up the above several comments there seem to be the following things happening.

1. At low trigs native LDL is predominant so there is little LDL traffic into the vascular wall and consequently not much out apart from that required for cholesterol homeostasis with the cell constituents of the wall itself, which is not that much compared to the deranged accumulation seen in atherosclerosis.

2. At higher trigs poolb becomes dominant this pool contains far more damaged LDL so macrophage accumulation of cholesterol becomes important. This is compounded by lower levels of HDL accompanying the CETP activation.

3. With LCHF the increase in HDL becomes important as does the drop in inflammation and the large drop in triglycerides. This seems to accomplish several things. The increase in HDL increases the cholesterol acceptor capability at the vascular wall which starts the plaque mobilization of cholesterol into plasma. This in itself may or may not be sufficient to stop plaque accumulation but for sure it will at least slow it down. The drop in triglycerides moves the system from accumulating small/dense LDL towards a more balanced structure with poola being restored somewhat and poolb degraded by less addition and continued, albeit somewhat slower catabolism and somewhat larger LDL total pool size, so balance gets restored to some degree between the atherogenic and non atherogenic pools. I suspect the combination does indeed stop further plaque build but the reversal and diminution of the plaque may be very slow, I suspect that it is. One reason may be that in parts of the plaque the cholesterol becomes crystalized and harder to mobilize.

4. This stream of cholesterol may or may not be important compared to issue from adipose depending on circumstances and I have no idea what magnitude it may compose of circulating LDL cholesterol.

5. Hyperresponders may be largely immune from plaque build because trigs are low enough to ensure predominance of poola relative to atherogenic poolb.

6. Hyperresponders are a small group of LCHF, somewhere between 5-20% or so according to Sarah Hallberg and others so it seems a combination of circumstances may be required to produce one.

Still puzzled.



65 Y/O female LMHR here who already has plaque in LAD and exercise-induced angina. Reading this, and the papers you cite with great interest, been hacking the problem from every angle I can. Tim, please, you mentioned that HDL is the main acceptor candidate “although there are others” Can you point me to what they are?

George Henderson (@puddleg)

Hi Tim,

Sarah Hallberg’s experience is with weight loss and I’d expect the lowest rate of hyper-responders in that population based on the fasting studies (and my own impressions based on feedback for the What The Fat diet book).
I’m thinking if there was a large reduction in whole-body cholesterol as we’re discussing, this would take time because I don’t think fecal cholesterol reabsorption/excretion can be regulated by the LDL pool.
In low insulin states foam cells make cholesterol directly from glucose and don’t take in LDL, insulin switches this off. This is the opposite of liver, where insulin stimulates HMG-CoAR


Hi Dave,

Thanks for your passion in studying this topic!
I feel a bit puzzled because I almost fit your profile (lean,very active,with LDL going way up on low carb),however in my case hdl goes down and trigs up on low carb+intermittent fasting (never went full keto).Here are my values (all in mg/dl):

On low carb:
ldl 250
hdl 54
trigs 105

After 3 weeks of higher carb and lower fat:
ldl 141
hdl 60
trigs 41

I wonder if you have any insights into what might be the mechanism behind this pattern…

Thank you,


Hi Dave,

I conducted the Ketofest experiment at home in Florida (I’m saving my photo food logs for your Google Drive folder) and received my Friday morning lab results a few minutes ago (I fasted TWR except for supplements, coffee with HWC, water, salt). Here are some of the results:

LDL-P: 2083
LDL-C: 185
HDL-C: 52
TG: 71
Total Cholesterol: 251
HDL-P: 24
Small LDL-P: 544
LDL Size: 21.5
C-Reactive Protein: 3.43

I’m a 52-year-old woman and I’ve lost about 30 pounds so far in 2017–currently 172–on a ketogenic diet with some fasting. I weight-train approximately four days/week (including last week WRF while fasting).

I really appreciate all your analysis. Had my second round of blood work this morning after three days of feasting. Looking forward to those results, too.



Hi Dave,

We’ve talked before on the apoe4.info forum. Very interesting stuff here! Here’s my lab numbers as I progressed from a 50% carb diet to ketosis. I am 72 yrs, 10% body fat, moderately active, apoE: e3/e4. Although you can’t see it here because I keep my SFA down, thanks to my e4, I am a hyper responder to SFA.


Although I don’t take pictures, I’ve weighed and recorded my food intake for years as well as tracking other variables.

– Dan


Any data on long lived people with healthy arteries & also have the LMHR profile?


Another person with results for you. I’m a 48 yo female, keto diet for a 3 months–fairly active with swimming,
rowing, and yoga. Recent labs: Triglyceride 56, Total cholesterol 215,
LDL 132, HDL 72, Vldl 11, Chol/Hdl ratio 3

David Mitchell
David Mitchell

Hey Dave, Few questions…

– We hear that its not the cholesterol but the particle count where the risk is. However in all probability if your cholesterol is high, isn’t it likely LDL-p will be high too? Have you come across a major discordance between LDL-p and cholesterol numbers, like someone having cholesterol of > 350 but a LDL-p of 1500?

– So i recently had a CIMT done [Right=0.87mm, Left=0.92mm] which definitely seems fine. In any-case, even the technician agreed that calcium score trumps CIMT when it comes to heart disease risk. My calcium score did increase on a low carb diet!

I have (briefly) been on statins and heard that they can lead to an increase in calcium score. Have you heard of the same?

– For folks who get calcium scores of 0, any thoughts on maybe they being genetic predisposed towards minimal plaque build-up in the first place. I mean, don’t we expect some plaque build up in all individuals post 30. Also, if someone had a calcium score of 0 before (or shortly after) starting a diet maybe his previous diet was working too?

– I was on a low fat whole foods plant based diet (~0-10g fat, 0g saturated fat) which resulted in probably one of the (conventionally regarded) best blood reports (LDL-p 1150, LDL-C 105, HDL-C 46, trigs – 37, Small LDL-p 159, H1ac 4.9, Insulin 3.9), (I must add here that i felt way better on a ketogenic/low-carb diet).

Does the cholesterol experiment work only if you are ingesting a certain amount of fat? If not, I would imagine anyone who has no fat in his diet, his cholesterol would be highest (which doesn’t seem to be true in my case). Whats the trigger for the inversion pattern to take effect?

– I believe above post “Are you a Lean Mass Hyper-responder?” implies that the ones who see a higher cholesterol are usually athletic and with a low fat %. Again, my example could be an outlier. I’ve had sky high cholesterol level despite not being super lean (maybe ~23% at my leanest) or doing a lot of workouts.




LDL-C and LDL-P sometimes are sometimes discordant, meaning one is high when the other is low. If you account for LDL-P, LDL-C has almost no value as a risk factor. Here’s a good article on the topic:

I expect both nature and nurture factors would contribute to a calcium score in middle age. However, I would think that there are traditional lifestyles where most elderly individuals have 0 scores (just based on very low incidence of CVD in almost all pre-agricultural societies). Steady accumulation of plaque seems to be a modern affliction.

Relating to diet changes, if you were on diet A for 40 years and diet B for 3 months, you’re calcium score will be more a reflection of diet A. This is exactly my case. It will only be a retest in a couple years that I’ll know if diet B is any better.

The experiment tested the inversion pattern (using the Feldman protocol) for long-term LCHF individuals. Fat-adapted individuals use a higher percentage of fat for their energy, so their LDL may change more in response to short-term fat intake. For individuals who get very little of their energy from fat (e.g., those that eat a sugar snack every 2 hours for 18 hours each day), other factors may drive their LDL levels (fructose clearance, metabolic syndrome, etc.). We don’t have a much data and and there is a lot still to learn.



Thanks Craig


Hi Dave,

Thanks for your blog. I’m 39 years old woman, 49-50 kg, 162 cm. I go to gym 2-3 a week and I do yoga. I’m on keto since 2 years and I eat 8/16 or 6/18. 18-20% fat mass.

Before ketogenic diet my results are:
TC: 7,1 mmol/l (273 mg/dl)
TG: 0,79 mmol/l
HDL: 2,48 mmol/l
LDL: 4,24 mmol/l
Glucose: 5,1 mmol/l
H1A1c: 5,5%
TSH: 2,65 uIU/ml

…and with keto:
TC: 17-20 mmol/l (660-769 mg/dl)
TG: 0,89 mmol/l
HDL: 3,82 mmol/l
LDL: 15,78 mmol/l
Glucose: 3,8-4,4 mmol/l
H1A1c: 4,8-5,0%
TSH: 1,8 uIU/ml
Apolipoprotein A1: 269,0 mg/dl (ref: 125,0-215,0)
Apolipoprotein B: 304,0 mg/dl (ref: 55,0-140,0)
Lp(a): <30 mg/L (ref: <300)

My blood pressure from 90/60 to 100/70 and I haven't heart problem.
My liver result are fine and my Doppler test on my neck was normal. The NMR measurement not available in Hungary.
I'm ApoE3. I have alpha-1 antitrypsin deficiency (PiSZ phenotype).
My husband is on keto too, we eat same food but his cholesterol levels are not so extreme like as my results.
I would like to continue the low carb lifestyle and 2 weeks ago I started the zero carb diet. I' m curious about my new cholesterol level.


George Henderson (@puddleg)

Hi Dave and Tim,

I found this paper on high cholesterol in the diabetic (near zero insulin) rabbit.
it says
When cholesterol influx into arteries is reduced, in spite of high plasma chol levels, atherogenesis is prevented.

They’ve used alloxan to drastically reduce beta cell function. The lack of insulin plus the high dietary cholesterol load results in large particles, and these aren’t being taken up.
Now, these lipoproteins are full of TGs, and the rabbit has no CETP, so there are differences from our human models. But, in principle, LDL and other particles can be rejected by arteries when insulin is low, even when plasma cholesterol is high, and particle size is part of the equation.


Hi George
Here are two more articles on diabetic rabbits with hypercholesterolemia:
And here is a one with a diabetic dog where insulin administration caused atherosclerosis:

In response to your earlier question “so what if foam cells STOPPED consuming LDL in low inflammatory states? Would that make LDL pile up in serum?” – Here are two in vitro studies on the effect of insulin on the monocyte LDL receptor

The LDL receptor seems “linked” with the insulin receptor as both a properly functioning insulin receptor as well as a small amount of insulin are needed for the LDL receptor to function:

Additionally, insulin also affects the production of LDL receptor. Low insulin levels both decrease LDL receptor mRNA synthesis as well as decrease PSCK9, so there are less LDL receptor and less receptor degradation. Presumably, this has no net effect, but it would be interesting to test it.
Tim, what are your thoughts on this? It seems to against your idea that LDL catabolism and LDL receptor activity are high. Although, I do agree that the size of LDL will be as you stated.

Low insulin levels can also cause an increase in ApoB secretion, but I could not find the numbers for the insulin levels so it may or may not be relevant physiologically

Dave I think you’re going to like this one if you haven’t already seen it, infusion of fatty acids caused differing effects on the liver based on whether or not they were bound to albumin. Specifically, the conclusions are “1) increased FA delivery to the liver in vivo increases secretion of apoB-lipoproteins via post-transcriptional mechanisms, 2) OA-induced apoB-lipoprotein secretion occurred at least in part via mechanisms other than by providing substrate for TG synthesis, and 3) the route of delivery of FA is important for its effects on apoB secretion.”

Finally, this discussion is fascinating, but may also end up being irrelevant if cholesterol does not enter from the luminal side of the artery as this article would suggest: http://www.sciencedirect.com/science/article/pii/S1359644616301921

George Henderson (@puddleg)

” A suppression of LDL-receptor activity resulting from deficiency of insulin and elevated plasma catecholamine concentrations in uncontrolled insulin-dependent diabetic patients may contribute to the increased levels of LDL cholesterol observed in these patients.”
All good stuff and I think there is a shut-down of LDL-R simply due to less cholesterol being needed by all sorts of cells in the pseudo-unfed state, combined with a dumping of the excess cholesterol from shrinking cells like adipocytes and possibly reversing plaques.
Looking at epidemiology, merely to create a narrative around this, I’ve found populations – Malmo is the best example – where cholesterol is associated with CHD mortality and yet a higher total fat % of the diet is protective against it (in men, who have most CVD deaths) and saturated fat is benignly neutral.
Presumably these protected cases also have higher LDL (i.e. compared with equally healthy people not eating high fat), but in any case it shows that the contribution of increased fat oxidation to raised cholesterol is not the cause of population associations, is instead protective, and neither is the effect of higher SFA.
Something that raises LDL – probably genes – does increase CVD risk but it’s not the effect on LDL of eating more fat, which is probably protective.
If we consider total mortality instead, higher LDL seems to be protective in high-fat, high-SFA populations, but not necessarily in low fat ones (but it’s not clear what total mortalty was in the Iran paper)


Those are good narratives. I particularly like the Denmark paper, although I wish they had stratified by statin usage instead of adjusting for it. I think aging to 50+ without developing diabetes or CVD likely means the participants are relatively normo-insulinemic, which explains the following: “However, we did exclude all those with a diagnosis of CVD or diabetes at baseline. These subjects could be the vulnerable subjects, leaving a population resistant to the harmful effects of high LDL-C or TC levels.”

George Henderson (@puddleg)

The Demark paper is consistent with healthy high LDL being a side-effect of HDL efficiency in a high-fat population, while unhealthy high LDL (or any LDL) will associate with poor HDL function.
Many people are diagnosed with CVD or T2DM over the age of 50, probably most are, there’s a bit of discussion around this in the paper. And the lowest LDL category, <2.5 mmol/L, includes the healthy recommendation – it's not some freakishly low "occult disease" group.
As the statin use was voluntary not randomised it's hard to say what effect it had.


Hi Dave.
This caught me at perfect timing! I was just sent by my doctor to a lipidologist because my LDL is too high.
I am not LCHF, but a strict Paleo for years, and beacuse I’m very lean and active I live on around 150-200 gr of carbs daily, usually much more. My LDL and HDL rose significantly on this diet, while my trigs are very low.
Can your protocol work on this type of diet?
If so, can I up my calories intake by upping only the fat?
What type of fat do you recommend (I understand not coconut oil)? Can it also be MUFAs or just SF?
Can’t wait to test your theory! (to get the doc of my back)




So far, we have had mostly LCHF’s do the protocol, so I’d be awesome to get some more data on other types of diets. At 150-200g of carbs, you might be closer to the carb-swap experiment that Dave did. Exercise also has an impact.

The interaction between gut-based and liver-based delivery of fat energy is the most likely driver of the inversion pattern. All other things being equal, eating more fat in the 3-days prior to a test should drive down LDL. In the ketofest experiment, there was no guidance on type of fat, just proportions of macros. I would advise you to not increase your intake of carbs, though, especially sugar and alcohol.



Hi Dave, so I’m basically a 29-year-old female I weigh 150 lbs , and I’m 5’6 y’all. I started the keto genic diet about 3 1/2 weeks ago, and I felt 100% better on it and I’ve even lost 8 pounds . I went in for some bloodwork, and when my total cholesterol came back it came back at 393!! My doctor wanted to put me on a Statin. And do another blood test in a month.i’m afraid that I might be a hyper responder, and I’m afraid that I won’t be able to continue at this rate I don’t care myself. Is there something I can do to bring to my cholesterol down?? I really want to continue on keto. The rest of my results were triglycerides 88 mg/dl, HDL is 57 LDLC is at 318, any ideas or help would be really appreciated thank you!!



If you feel great and look great on keto, that’s 2 very strong reasons to KCKO (keep calm, keto on). If you are also happy with your lifting and HIIT performance, you’d need to hear a very strong argument to change back to your old diet. (although 3 1/2 weeks is barely enough time to become athletically fat-adapted) I’m not convinced high LDL-C alone is enough evidence for any change, either to add back the carbs or start taking a Statin.

If you just want to lower LDL-C for your doctor, follow Dave’s protocol for 3 days before your next test.

If you want to get a better risk assessment for your own peace of mind, you can instead ask to broaden the set of tests to do next time, e.g. do NMR Lipoprofile instead of just LDL-C. Dave has a whole list he gets to “debug” his metabolism that I’m looking to writeup sometime soon.


Hi Dave, so I’m basically a 29-year-old female I weigh 150 lbs , and I’m 5’6 y’all. I started the keto genic diet about 3 1/2 weeks ago, and I felt 100% better on it and I’ve even lost 8 pounds . I went in for some bloodwork, and when my total cholesterol came back it came back at 393!! My doctor wanted to put me on a Statin. And do another blood test in a month.i’m afraid that I might be a hyper responder, and I’m afraid that I won’t be able to continue at this rate I don’t care myself. Is there something I can do to bring to my cholesterol down?? I really want to continue on keto. The rest of my results were triglycerides 88 mg/dl, HDL is 57 LDLC is at 318, any ideas or help would be really appreciated thank you!! I also forgot to mention that I’m very active , I wait lift and do hit workouts

Kevin Fansler
Kevin Fansler

I am a hyper-responder who is now 79 years old. My total cholesterol was around 200 with a healthy conventional diet 15 years ago. My triglycerides were nearing 400. My testosterone level was 289 ng/dL and I started taking testosterone supplements. My doctor later prescribed Lopid to lower the triglycerides. I decided to go on an LCHF diet instead. This approach brought my TG down near 100, but my TC went up to around 350. I was on this regime for around 12 years when I decided to go off my testosterone supplement. The resulting testosterone level was a perfectly normal result of almost 700, which is quite a bit higher than President Trump’s 4xx. What to make of these results? I think the LCHF diet was what I needed to improve my general metabolism, statins be-damned. By the way, I fired a GP who tried to bully me into taking statins and found a more compliant physician.

Kevin Fansler
Kevin Fansler

I am a hyper-responder who is now 79 years old. My total cholesterol was around 200 with a healthy conventional diet 15 years ago. My triglycerides were nearing 400. My testosterone level was 289 ng/dL and I started taking testosterone supplements. My doctor later prescribed Lopid to lower the triglycerides. I decided to go on an LCHF diet instead. This approach brought my TG down near 100, but my TC went up to around 350. I was on this regime for around 12 years when I decided to go off my testosterone supplement. The resulting testosterone level was a perfectly normal result of almost 700, which is quite a bit higher than President Trump’s 4xx. What to make of these results? I think the LCHF diet was what I needed to improve my general metabolism, statins be-damned. By the way, I fired a GP who tried to bully me into taking statins and found a more compliant physician.
I wanted to clarify my too-brief remarks above. I did not explain why I stopped taking testosterone supplements. I found a research article concerned with the testosterone levels of men with metabolic syndrome. These men presented with lower than average levels of testosterone. I did not have all the symptoms of metabolic syndrome, but my three siblings all developed diabetes. Because I had become normalized with the LCHF diet, I thought that my testosterone levels would also have become normalized. I was proved right. Low testosterone levels are often a sign that something has adversely affected the metabolic processes. Taking testosterone supplements will most likely not improve your metabolic processes. Likewise, taking a statin will most likely not improve your metabolic processes, even though you may then attain the cholesterol levels of your youth.


Great story, Kevin. Sounds like you took control of your own health and got to a great place that wouldn’t have been possibly blindly following the advise you were given.

Vijay Iyer
Vijay Iyer

My report after 3 month of keto

BLOOD KETONE (D3HB) – 5.5 mg/dL

Cholesterol Test



LDL CHOLESTEROL – > 300 mg/dl






Diabetes Test

Fasting INSULIN – 2.12

HbA1c – 5.4

FASTING BLOOD sugar – 92


Thanks for sharing, Vijay. Did you happen to have your pre-keto numbers to compare against? I assume you are feeling great, otherwise you’d have switched back.


I don’t quite fit.
Here is my Nov. 14 2016 lab report:

LDL-P 2943
LDL-C 305
HDL-C 61
TG 76
TC 381
HDL-P 29.0
Small LDL-P 692
LDL Size 21.8

An April 12, 2016 DEXA body scan had me at 17.8% fat.

That seems not very lean yet for my age at the time of 60.4 years that put me in the 1st percentile. I.e., 99% of people my age had higher total body fat percentages.

George Henderson (@puddleg)

Hi Mike,

I’m probably not super-lean either but I think leanness might be a genetic category here, with most people in it being lean, and same with activity, being a born fidget at any lean mass might be similar to being an athlete.
Or another way of looking at this, the level of fat mass at which your metabolism decides you’re lean enough can vary.


Sorry for the second post but I just found an Oct. 24 2015 NMR. Feel free to combine this with my previous post.

LDL-P 1831
LDL-C 232
HDL-C 72
TG 70
TC 317
HDL-P 33.4
Small LDL-P 213
LDL Size 21.9

From Cronometer, here are my macros for the five days preceding the blood draw:

11/9/16-11/13/16 2415 kcal; 100 g PRO; 22 g CHO; 218 g fat

10/19/15-10/23/15 3440 kcal; 96 g PRO; 24 g CHO; 335 g fat

Basically an increase of 50% in fat brought LDL-P down more than 1,000 nmol/L, LDL down more than 70 mg/dl, and Small LDL-P more than 2/3.

Living in NY or NJ makes getting testing hard. Requestatest recently called me up and cancelled an order. But I think I found a workaround so that I can test again next weekend.


Mike, thanks for sharing your data! Another solid example of the Inversion Pattern in action.

You’re reminding me I should go eat some more to improve my numbers for tomorrow. It’ll be my first NMR Lipoprofile.

George Henderson (@puddleg)

Assuming that CETP is accelerated in the LMHR phenotype,

Transfer of CE from HDL directly to LDL by CETP could also be antiatherogenic if the LDL is cleared by the liver LDL receptor. This role of RCT is especially important if the original source of cholesterol is from plaque (4). As this process is potentially antiatherogenic, inhibition could be disadvantageous.

An additional concern is that excessive CETP inhibition increases HDL-C to supra physiological levels (>70 mg/dl), which appear to result in paradoxically high rates of cardiovascular disease (CVD), as shown in several epidemiological studies (13, 14) and in one CETP inhibitor interventional trial (15) but not in another (dal-OUTCOMES). The dal-OUTCOMES trial was terminated for lack of efficacy, and the details of this study were not available at the time of this review. Regarding the former study, increased CVD was attributed to hypertension, and an unusual number of patients had fatal sepsis; HDL is known to be crucial for innate immunity, e.g., lipopolysaccharide sequestration (16). High levels of circulating HDL-C may also be associated with dysfunctional HDL species in some studies (17). Finally, as CETP activity decreases in the general population, increased rates of CVD are observed (18). From the entire pro- and antiatherogenic concepts of CETP inhibition and clinical intervention trial results, no clear conclusions are apparent.

From this review, it appears likely that CETP action is pro-atherogenic when TGs are high (when VLDL-1 and sdLDL are major players) and anti-atherogenic when they are low.



Hi, Dave.

I’ve been reading through with interest.
I’m T2 on LCHF with normal weight, normal BG but high lipids.

I will post my numbers when I can dig them out, but I’m intrigued by your theory that lean athletic people eating low carb tend to run higher blood fat levels.

A simple take on this could be that the body is learning that it is more efficient to store fat in the blood than in fat cells because the fat is always being burned off at a high rate.

I would be interested in the mechanism the body uses to achieve this.
Fat storage usually involves insulin so the usual suspects would be lower insulin production or insulin resistance in the fat cells.

George Henderson (@puddleg)

Here’s an idea;
keto is a pseudofasting state. Fasting elevates LDL. So, does already being in a pseudofasting state predispose us to a more rapid effect of fasting itself, so that the short fast before a lipid test is enough to push up lipids?
That is, does a lean, healthy, active ketogenic dieter experience a rapid transition to fasting state lipids?
This would be consistent with your hypercaloric feeding experiments – the extra energy and insulin response to that slows the transition to the fasting state afterwards.
Does anyone have non-fasting results? And wouldn’t these be bollixed anyway because chylomicrons can end up in the LDL fraction?


Funny enough, I actually got a blood lipid test in a non-fasted state by accident. I thought they would defer my test to the next day because of that, but they just said “they’ll adjust for it” (ha!).

Test1 is 2 hours after a hearty bacon & eggs breakfast, but 36 hour fast before that breakfast. 2-months later, test2 is 3-day low-calorie, test3 is 3-day high-calorie.

TC 342 360 367 333
TRIG 176 80 68 51
HDL 98 113 115 114
LDL 209 232 238 209

Just a few data points, but take it for what you will.

UPDATE: Added test4. Average calorie keto, massive run 48 hours prior.

George Henderson (@puddleg)

This paper finds that even in the normal diet non-fasting lipid test has lower LDL and higher TGs, same HDL.

So it’s not a stretch that a pseudofasting diet can push this relationship further in the opposite direction

George Henderson (@puddleg)

So not as much difference between low and high calorie, as between fasting and non-fasting.
And non-fasting really skews the TG/HDL ratio – but does lower LDL and total C. So the chylomicrons in your case seem to be in the TG fraction, and it’s likely that a better separation that removed chylomicron cholesterol from the equation would see LDL even lower.
As far as we can tell from 3 tests anyway!


Now 4. 🙂 I think my body was eating up those LDL-C’s to rebuild my sore muscles.

George Henderson (@puddleg)

FYI, here’s an animation of the cholesterol transport system that has most of the working parts, including the role of the various lipase enzymes

George Henderson (@puddleg)

To support my “Reverse Cholesterol Transport on Steroids” model, this paper studying the kinetics of hypercholesterol feeding in the guinea pig model.
Guinea pig is a good human-equivalent lipoprotein model, and Fernandez works with Jeff Volek now.

Guinea pigs were fed
15% (w/w) .fat diets (lard, olive oil, or corn oil) with cholesterol
levels corresponding to absorbed intakes of 6 (basal), 50, 100, or
200% endogenous cholesterol synthesis. Guinea pigs maintained
stable plasma cholesterol levels until cholesterol intake
equaled or exceeded endogenous synthesis (P corn oil, with olive oil being intermediate
(P < 0.05). Hepatic membrane apoB/E receptor number (Bmu)
decreased as dietary cholesterol increased (P < 0.001) without
an independent effect of dietary fat saturation. B,,, values were
significantly correlated with plasma LDL cholesterol levels
(r = -0.632), and with hepatic free (7 = 0.527) and esterified
cholesterol (Y = -0.512) concentrations, which were both increased
with dietary cholesterol (P < 0.001). significant interactions
between dietary fat type and cholesterol mediated the extent
of hepatic free and esterified cholesterol accumulation.
Dietary fat and cholesterol interactions also contributed to
changes in LDL particle composition and peak density. a The
results of these studies do not support the thesis that dietary
cholesterol-mediated suppression of apoB/E receptor expression
is ameliorated by intake of polyunsaturated fatty acids. Dietary
fat type and cholesterol amount interactively affect hepatic
cholesterol concentrations and LDL composition and size,
which in part determine plasma LDL cholesterol levels.-
Lin ECK, Fernandez ML, Tosca MA,
McNamara DJ. Regulation of hepatic LDL metabolism in the
guinea pig by dietary fat and cholesterol. J Lipid Res. 1994. 35:

If reverse cholesterol transport saturates the hepatic cholesterol pool LDL receptors will be downregulated.

Evidence from the cholesterol-fed, hypercholesterolemic, guinea pig model (which produces huge elevations in LDL) that cholesterol accumulation in aorta is prevented by a 10% carb diet.

Twenty guinea pigs were fed either a LCD or a low-fat diet (LFD) in combination with high-cholesterol (0.25 g/100 g) for 12 weeks. The percentage energy of macronutrient distribution was 10:65:25 for carbohydrate:fat:protein for the LCD, and 55:20:25 for the LFD. Plasma lipids were measured using colorimetric assays. Plasma and aortic oxidized (oxLDL) were quantified using ELISA methods. Inflammatory cytokines were measured in aortic homogenates using an immunoassay. H&E stained sections of aortic sinus and Schultz stained sections of carotid arteries were examined.

LDL cholesterol was lower in the LCD compared to the LFD group (71.9 ± 34.8 vs. 81.7 ± 26.9 mg/dL; p = 0.039). Aortic cholesterol was also lower in the LCD (4.98 ± 1.3 mg/g) compared to the LFD group (6.68 ± 2.0 mg/g); p < 0.05. The Schultz staining method confirmed less aortic cholesterol accumulation in the LCD group. Plasma oxLDL did not differ between groups, however, aortic oxLDL was 61% lower in the LCD compared to the LFD group (p = 0.045). There was a positive correlation (r = 0.63, p = 0.03) between oxLDL and cholesterol concentration in the aorta of LFD group, which was not observed in LCD group (r = −0.05, p = 0.96). Inflammatory markers were reduced in guinea pigs from the LCD group (p < 0.05) and they were correlated with the decreases in oxLDL in aorta.

These results suggest that LCD not only decreases lipid deposition, but also prevents the accumulation of oxLDL and reduces inflammatory cytokines within the arterial wall and may prevent atherosclerosis.


We're not under as much stress as the cholesterol-fed guinea pig. Fernandez points out here that RCT is the protective feature of HDL and is actually unaffected or improved by HDL catabolism.

This all fits with LMHR being a side effect of increased RCT in people in whom it was already ideal, driven by increased fat oxidation and/or ketosis, i.e. the TAG breakdown driven by HDL.


Hi Dave,
Could you please give me your E-mail address for sending you my CIMT and Calcium Scan test reports? I have done them as you had suggested.