June 13, 2018

Has Your Cholesterol Skyrocketed on a Ketogenic Diet? Read This!

Has your cholesterol skyrocketed on a low carb or ketogenic diet?

Or did it start out already high, and hasn’t come down like you thought it would after cutting carbs for a while?

Is your doctor on your case to “do something” about it?  Are they pushing you to take cholesterol-lowering medication and stop that crazy high-fat diet you’ve been following?  

Or maybe your doctor’s actually pretty easygoing about it, but you are alarmed by the big jump in your cholesterol since you started low carb.  Maybe you’re wondering if all that butter, cheese, bacon, and red meat isn’t quite such a good idea after all...

People who adopt carbohydrate-restricted diets have widely varying effects on their lipid profile.  Generally speaking, triglycerides go down and HDL goes up.  This is practically a given.  Happens like clockwork.  Totally predictable.  If you were the betting kind, you could put money on it and have a virtually guaranteed return.  And this is a good thing.  More and more evidence is emerging that regardless of your total cholesterol or LDL, the triglyceride-to-HDL ratio is a strong predictor of cardiovascular risk.  

According to Drs. Phinney and Volek in their book, The Art and Science of Low Carbohydrate Living:

“The triglyceride/HDL ratio provides a broader assessment of risk, and its relationship with insulin resistance makes it far superior to LDL-C.  And how best to improve your triglyceride/HDL ratio?  The striking reductions in plasma triglycerides and consistent increases in HDL-C in response to low carbohydrate diets are unparalleled by any other lifestyle intervention, or even drug treatment, and therefore represents the most powerful method to improve this ratio.”

LDL is a different story.  In some people, LDL goes down, but in others, it goes up.  Something that happens on a low carb diet often, but not always, is a shift from LDL particles that are “small and dense” to LDL particles that are “large and fluffy.”  Even when the total LDL goes up, the pattern of the particle makeup shifts.  It’s believed—but has not been proven conclusively—that the latter pattern, called “pattern A,” is less atherogenic.  That is, when your LDL particles are predominantly the large, fluffy type, they’re less likely to “clog your arteries” (*groan*) and cause a heart attack, stroke, or other cardio/cerebrovascular disease than when your particles are predominantly small & dense, called “pattern B.”  So, on balance, even if LDL goes up on a low carb diet, it’s believed that the shift from pattern B to pattern A is a beneficial change and represents an improvement in your cardiovascular health.

But what if your total cholesterol or LDL absolutely skyrockets?  Does your particle pattern even matter then?  If your total cholesterol is 300, 400, 500, or higher, and your LDL is 200 or higher, surely—surely—all that cholesterol has to be clogging your arteries, right?  Surely your very next slice of bacon could have you staring down the barrel of cardiac arrest, right?  I mean, even if your triglycerides are low and your HDL is high, and your glucose and insulin are low, all your inflammatory markers are low, you’ve lost 60 pounds, your energy levels are through the roof, and your doctor has stopped your GERD medication, your beta-blocker, and your insulin injections, there’s no way your cholesterol could be that high and not cause trouble.


Not so fast.

Probably the single most important thing to know with regard to cholesterol is that neither the total amount of cholesterol nor the amount of LDL particles, nor even the size/pattern of your LDL particles tells you anything about the amount of calcification in your arteries—that is, how “clogged” your blood vessels are.  And yet, many doctors who aren’t up on the latest research … or, truth be told, research from decades ago … will still want to give you a prescription for a statin based on nothing but your total cholesterol.  In fact, they might even be accused of malpractice if they don’t send you away with a statin prescription for your “high” cholesterol.  (Never mind that statins come with some very serious and dangerous side-effects, including increased risk for type 2 diabetes!)

My friend Dave Feldman over at cholesterolcode.com is doing some mind-blowing research that blows the lid off everything we thought we knew about cholesterol—even those of us in the low carb and keto community, who already knew there were massive problems with the cholesterol “story.”

He’s identified a subset of low carbers he calls “lean mass hyper-responders.” These folks are, by all accounts, in extremely good health.  They’re lean, fit, highly active, have very low insulin and triglycerides, high HDL (over 100, in some cases!), and by just about all other parameters appear to be supreme specimens of human health and athletic performance.  I say “just about” all other parameters, because these people have sky-high total cholesterol and LDL.  Total cholesterol well above 300 in most cases, and LDL over 200.  (Hence the name "hyper-responder" -- meaning, when these people adopt a low carb diet, their cholesterol goes through the roof.)  Is this cause for concern?  Should they quit the coconut oil and avocados and go back to fueling their running or biking with pasta and bagels?


Or, might there be some other way of assessing actual cardiovascular disease risk without using surrogate markers, like cholesterol?  Because that’s the thing, dear readers: cholesterol is a measurement, not a disease.  “High cholesterol” is not an illness.  (Despite your doctor possibly being able to code for that and bill your insurance company.)

Once more, for emphasis: the amount of cholesterol and the number of LDL particles carrying it in your bloodstream tell you nothing about the presence or absence of damage or disease in your blood vessels or heart muscle. 

This being the case, it would nice if there was some method of detecting actual cardiovascular disease.  Actual buildup of plaque in the blood vessels, rather than a measurement of a substance contained in the blood traveling through those vessels.  Ya’ll with me so far?    

Okay.  The good news is, THERE IS SUCH A METHOD!  It’s called the coronary artery calcium scan, or CAC test for short.  I wrote a detailed post about it for Heads Up Health.  It is probably one of the most important things I’ve ever written—for just about everybody concerned with their health, but most especially for low carbers and keto folks whose total cholesterol and/or LDL are in the stratosphere and they’ve got some nagging doubts about what this might mean for them.

I didn’t want to rewrite it just to post it on my own blog, so here’s the link, and I give it to you along with my strongest encouragement to give it a read.  It might be very educational for you, even if you already kinda-sorta “know” the whole cholesterol deal is bogus.

I could say more about the CAC test here, but honestly, it’s all in that post, so hop on over to Heads Up Health and check it out.  The one thing I will say is that some of Dave's lean mass hyper-responders have done CAC tests, and most of these folks -- who have astronomically high LDL -- had zero -- zero arterial calcification.  Zero evidence of cardiovascular disease.  So much for cholesterol clogging the ol' arteries, eh?

If you’d like to learn more about just how far off the mark conventional thinking is on cholesterol, here are my top book recommendations, all of which are quick and easy reads, intended for a lay audience. There’s just enough science to get your learnin’ on, but not so much that your eyes will glaze over and you’ll feel overwhelmed: 

I also recommend just about any video Dave Feldman has done on his cholesterol research, many of which can be found here.

Additionally, I did a podcast with Dave Korsunsky from Heads Up Health not long ago.  We talked about interpreting labwork in the context of low carb/keto, and how some of the reference ranges aren’t what they’re cracked up to be.  You can find that here.

P.S.  I know I’ve been slacking on the blog lately.  My apologies.  I have a couple of very big, very important posts coming up on insulin, obesity, and type-2 diabetes.  Lots of really fascinating stuff that I think will be new for many of you.  (It was to me!)  Unfortunately, because they’re big and important, they’re taking a long time to write.  When I’m writing about things that really matter, I want to make sure I do the material justice, and that means the posts take extra long to write.  (And my gold medal level of procrastination doesn’t help.)  Anyway, I know you’re probably wishing I’d get back to writing “real” posts, and I will, soon.  Thanks for your patience!  In the meantime, the CAC post really is a doozy.



  1. You're a real warrior...keep it up, girl.

  2. I think that all of your posts “really matter” and are done very well.

  3. Hi Amy.

    I have been looking at this for a long time now and have a couple of things to offer.

    1. With Dave's LMHRs there seems to be a universal response of very low trigs. This can raise LDL-C in a couple of ways. First with low carb the fat build in the liver declines as there is no. or essentially no, glucose over oxidation requirements to convert to lipid so the carb lipid build dimished to zero. Secondly the fat adaptation in LCHF means that lipid oxidation in the liver increases to a very large amount (Randle Cycle). Both these effects typically reduce the liver output triglyceride stream by about 50% (Volek/Phinney).

    2. The drop in trigs moves the liver secretion profile from large VLDL1 to smaller VLDL2 and to direct IDL and even LDL secretion by the liver. These particles have higher cholesterol to lipid ratios and as the lipoprotein system is a lipid delivery system first and foremost for the same lipid you will get more cholesterol.

    3. In addition most LCHF eat more saturated fat. Saturated fat raises LDL cholesterol. This is a theoretical puzzle but a practical fact and goes back to Ancel Keys but has been varified by Hegsted, Grundy, Mattson, KC Hayes, Reaven and many others.

    I think these factors plus insulin and dietary cholesterol also play a part, however the influence of triglycerides is the key.


    1. Thanks, Tim. If Dave's work is showing us anything, it's that we know far less about all this than we thought. It's quite unsettling, as I feel that millions of people are being medicated for something that is not an illness, and the medications are not benign in the slightest, but rather, come with vert alarming and dangerous effects. (Not "side" effects, *effects.*)

      Thanks for your insights. Lipid dynamics is not my area of expertise. I can barely keep up with what Dave and Siobhan Huggins are sharing. At this point, all I'm trying to do is share information, because even after all these years of people feeling much better and having markedly improved health on low carb diets, LDL is still some kind of bogeyman that scares people (and their doctors). People are discouraged from following a diet that is, in my opinion, without exaggeration, lifesaving.

    2. Let me posit this question: If saturated fat raises LDL, then why does Dave Feldman, who goes from 3 days of a very low calorie or fasting diet, to 3 days of eating a very high calorie, high fat (including high saturated fat) diet, experience a dramatic drop in LDL? Saturated fat went (way) up but LDL went down (dramatically).

      Can you create a test where "adding" "saturated fat" to your diet/"increasing" "saturated fat" intake causes LDL to go up? Sure, as shown by certain studies. But that has to be interpreted in light of what Dave is showing, which has been verified by something like 100 people now. I was at ketofest last year, when Dave and a bunch of others did the same test and Dave presented the results, and one woman complained that the test results better go well, because she had to chug a cup of cream to meet her fat goal. That's a lot of saturated fat. (And the test results were inline with what his results were.)

      That's the whole issue with this area: Everyone believed something (sat fat = bad; polyunsaturated fat = good), without proof (or proof that was very poor or poorly controlled), and then went out to prove it to be true. One can construct "proof" that saturated fat = higher LDL, but what does that "proof" signify?

    3. The idea that saturated fat raises cholesterol and LDL is a theoretical puzzle (no one seems to be able to pinpoint the mechanism) but a practical reality, at least according to the research going back to Ancel Keys. Keys produced a set of linear equations for predicting this which he claimed gave very good agreement with measured results. These equations were improved upon by Hegsted, KC Hayes, Grundy, Mattson and others.Even Reaven agrees with this aspect of saturated fat intake. However the intricacies are quite pronounced and KC Hayes showed that polyunsaturated fat intake, particularly Linoleic acid has a a profound influence on LDL levels at very low inputs. Dave's results while striking don't get to the heart of this matter because he doesn't partition the fats. Also the highest LDL levels in his results come from very active adoptees of LCHF. Another question then is why do these LDL levels go so high when they move from a low fat to a high fat diet. The question is not simple.

    4. Sorry left out a response to your last point.....


      Exactly nothing in my opinion. The cholesterol "scare" is just exactly that. Even if you can construct a case for high cholesterol being "dangerous" which is hard to do the resulting risk is way down the list after insulin resistance, hypertension, low HDL, BMI etc etc. The crusade against cholesterol is and always was about money.

      My interest has been to indicate to people that high cholesterol is not a concern, or at least a low priority one, and Dave has added some points to that argument but there are many aspects to it.

  4. Well my numbers went sky high for Ldl when I did KETO. Being diabetic, I did low carb for years. Then something odd happened when I actually took all animal products out of my diet, and INCREASED my carbohydrates by including more fruit and grains in my diet than before. Within 6 weeks my cholesterol LDL dropped 57% by doing all this. My blood sugars and blood pressures normalized. By week 10 I was taken off two medications, lost 40 lbs and dropped almost more than 3 dress sizes. I've also seen people develop health scares in their bodies by doing KETO for too long. I am not a fan of KETO.

    1. I support whatever works! Glad you found something that's right for you. :)

    2. I've experienced the exact opposite situation. I was on very low fat (<10% fat by cals) for years, with few to no animal products (eg, egg whites, chicken breast, no skin, etc.). I had massive mood swings, depression, IBS, you name it. Switching to low carb then adding intermittent fasting, then concentrating on keto, I've lost 50+ pounds and improved everything. As for LDL, I've never had "high" cholesterol levels and don't know, but as Dave is showing, and as I've found out, my cholesterol levels change all the time. If I fast for multiple days, TC, LDL, trigs go up, HDL goes down. These vary widely, within + or - 20% at least.

      Also, what does one mean by "keto"? I pretty much eat meat now, with some selected veggies at times, but I'm 90% meat. I eat some dairy, but not much and intermittently. I don't avoid eggs, but only eat them intermittently. I also concentrate on -- gasp! -- red meat and seafood, and avoid eating chicken (main reason: after years of chicken breast w/o the skin, I hate chicken). One could easily eat "keto" with a high Omega 6 content (eg, chicken, veggie oils) and that would not be a good version of keto. But you can't say "I ate keto" and denigrate it without saying what you mean by "keto".

      I don't espouse keto for everyone, but for those of us who have been harmed by a high carb diet, it can be a lifesaver.

      Also, it's very difficult for some of us to be ketogenic, even eating a keto diet. I always have low levels (<1.0) of BHB, and if I eat too much of a keto meal (say, with cabbage), I'll get <0.5 on my meter. And that's from eating too many veggies. If we make a sauce to go with meat, and I eat more than a few spoonfuls of sauce, I'm out of ketosis (if ketosis = BHB >= 0.5). Even though I try to maintain ketosis, I go in and out all the time. Relatively minor amounts of veggies or sauce or too many olives, etc., all kick me out. I don't mind this (I learned I can't chase numbers, as I'm not sure what they mean anyway), but am I on a "keto" diet or not, if I get kicked out regularly?

    3. Why are you measuring your ketones so often? What are you trying to accomplish? Are you worried for some reason when your ketones are below 0.5? Have you read my posts on ketogenesis and measuring ketones? I think they will lay to rest any fears and worries you have over maintaining a constant state of ketosis, which, for many people, is not necessary.

  5. I'm a cholesterol hyper responder. The more I stayed at my normal BMI (6+ years) after 40 years of obesity, the higher my total and LDL went. When I started 18:6 fasting daily, my values went even higher.

    I've gotten a Cardio IQ lipid panel (it's like NMR), a CAC (0%) and asked the Low Carb Cardiologist (Dr. Bret Scher) what else I should do- and yes, he recommended a CIMT to get a baseline at the age of 52 then monitor carotid thickness yearly.

    I discussed this very topic with Dave Korsunsky on a recent podcast and he reminded me you had discussed this topic before on the Heads Up Health podcast.

    Thank you, Amy. Really the only thing keeping me in long term weight maintenance is LCHF and Fasting 18:6 most days. If I had freaked out about my high cholesterol, I would be obese again with a "normal" lipid panel and miserable.

    Keep up the great work! Karen P

    1. Thanks for the great comment, Karen! I'm glad you've stuck to your guns and followed your own instincts. (Funny how those don't usually steer us wrong!) You are such a great example of someone who has maintained a significant weight loss for several years -- and even more heartening for a lot of people out there -- a "woman of a certain age" who's proven it CAN Be done. You give me hope for myself, to be honest, because I'm going to be 40 this summer, and I know weight management certainly isn't going to get any *easier* as I age, and it's sure no picnic *now* as it is! ;-)

    2. You are 100% correct Amy! Carry on! I think our friend Dave over at Cholesterol Code is doing a blog post on my case very soon.

  6. This is a great synopsis to alleviate the worry around cholesterol on a high fat diet.

    I think it might be helpful for people to known that cholesterol is carried in the body by lipoproteins. These same lipoproteins also carry triglycerides - fats to be delivered to cells for energy.

    Someone on a high fat diet and is using fat as their primary energy source often needs more lipoproteins to carry this energy to cells = increase in cholesterol.

    It's not a bad thing, it's a totally natural mechanism of metabolism.

    1. And thereby I suspect hangs the tail. If you have high LDL because you are transporting fat - dietary or body fat - to be metabolised this is good. If you have high LDL because you are NOT metabolising fat so all the lipoproteins stack up in the blood not being unloaded, this is bad. Same test result, completely different mechanism.

  7. Keep the posts coming, Amy, you're brilliant. And don't worry about the delays... just gives us keen followers more anticipation time. Looking forward to listening to your Heads Up Health podcast reading the CAC post. Thanks for all of your research and writing... keep up the great work!

  8. I have always had ideal lipids, no matter what I ate. Even on keto in 2017, and eating about 80% calories from fat, my LDL was around 50; total under 150; and triglycerides around 70. I do not consider low cholesterol to be a risk factor, as many confounded studies suggest. Sick people who are eating too little food due to illness can have low cholesterol, and obviously won't fare too well due to the underlying disease that is dropping their appetite, or causing absorption problems. In my case, I am heterozygous APOE E2/E2 which can cause rare familial dysbetalipidemia, but low cholesterol in the majority of people with this genetic marker.

  9. As I understand it cholesterol tests are pretty meaningless, as, like blood pressure - they vary greatly during the course of the day, depending on what you're doing, how tired you are etc etc a miriad of influences. So how can one measurement be meaningful?

  10. I don't know what you're planning to write on insulin and T2D, but I really hope it involves Keith Frayn atricle and the idea that "adipose tissue falls first". I've listened to talks by Ivor and Ted many times, and still I'm not quite sure that I get it.

    1. YES! Actually, I *am* going to write about the personal fat threshold theory. Huge Frayn fan here. :-) His papers on this are excellent. i’ll be writing some other stuff about insulin to, but will definitely be including the person off at threshold. It’s a fascinating idea, and seems to explain a lot of disparate and/or “paradoxical” things.

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  12. So, what to do if your calcium scan shows blockage and one is eating LCHF?

  13. Just got my lipid panel my triglycerides were normal they weren’t before keto. My total cholesterol 345 very high for me and ldl 245. Lost 20 pounds on keto and my blood pressure has normalized and I’m off my blood pressure pills and take my blood pressure daily it’s usually 110/70 I’m 51 year old female.