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Let me introduce myself. My name is Mark Sisson. I’m 63 years young. I live and work in Malibu, California. In a past life I was a professional marathoner and triathlete. Now my life goal is to help 100 million people get healthy. I started this blog in 2006 to empower people to take full responsibility for their own health and enjoyment of life by investigating, discussing, and critically rethinking everything we’ve assumed to be true about health and wellness...

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February 13 2019

Is Keto Bad For Cholesterol?

By Mark Sisson
65 Comments

We’ve all heard the story. Maybe we’ve even been the protagonist.

Person goes full keto. They lose a bunch of weight, normalize their pre-diabetic glucose numbers, resolve their high blood pressure readings, have more energy, feel great, and have nothing but high praise for the new way of eating.

Except for one thing, everything seems perfect: their cholesterol is sky-high. It throws a wrench into the whole operation, installs a raincloud over the procession, spoils their confidence.

“Could I be killing myself?”

“Are my health improvements just a mirage?”

In other words, are the apparent benefits of keto merely superficial if your cholesterol skyrockets?

The evidence is pretty clear that for the majority of adults who go keto, their cholesterol numbers improve.

In obese adults with type 2 diabetes, a ketogenic diet improved blood lipids and boosted fat loss compared to a low-calorie diet.

In lean, healthy adults without any weight to lose (and who didn’t lose any weight during the course of the diet), total cholesterol went up from 159 to 208 mg/dL and triglycerides fell from 107 to 79 mg/dL. A lipophobic doc might freak out at the rise in TC, but given that the triglycerides dropped, I bet the change reflects a rise in HDL and an overall positive, at worst-neutral effect.

Another study of lean adults with normal cholesterol numbers found that going keto improved their lipids, reducing triglycerides, increasing HDL, and leaving LDL unchanged. Those with small pattern B LDL particles (the “bad kind”) saw their LDL particle size increase, on average. All told, keto was beneficial.

But you aren’t everyone. You aren’t the average of a population. And, given the number of readers I have and the number of people trying a ketogenic diet, there are bound to be some people whose lipid profiles go in the other direction.

I don’t give medical advice here, and I always encourage people to partner with the physicians for health solutions. That said, let me share some thoughts on the keto-cholesterol question….

I’m not just talking about high total cholesterol or high LDL-C. I’m talking about what appears to be the real, legit risk factor for a cardiac event: elevated LDL particle number. According to experts like Dr. Peter Attia and Dr. Chris Masterjohn, atherosclerosis occurs when LDL particles infiltrate the endothelial lining of our arteries. Thus, it’s not high LDL cholesterol that increases the risk of atherosclerosis—LDL-C is the cholesterol found inside the particles— it’s a high number of LDL particles in circulation. The more LDL-P, the greater the chance of them becoming oxidized and infiltrating the arterial wall. There are many factors to consider, like oxidative stress, inflammation, and fatty acid composition of the LDL particles, but all else being equal, a greater number of LDL particles seems to increase the risk of a heart attack.

What Could Be Causing LDL Elevations On Keto?

Weight Loss

I asked Dr. Cate Shanahan for her input on this topic, and she provided a beautiful explanation:

But when you stop eating so many carbs insulin politely steps aside, and your insulin levels plummet. Now your body fat can more easily and more often release its stores of fatty acids into your bloodstream.
When your body fat releases stored fatty acids, any unused fatty acids quickly get picked up by the liver and packed into VLDL lipoprotein. VLDL is a precursor to LDL. So in reducing your insulin levels and increasing your body’s use of fat, you will raise your VLDL, LDL and total cholesterol. You are simply trafficking in fat more often now. And now, because your body stabilizes fat carrying lipoproteins with cholesterol, there is a need for more cholesterol in your blood. These are not bad consequences. They are in fact happy signs your diet is doing what its supposed to be doing.

If you’re actively losing weight, you will probably experience a rise in cholesterol. This is the transient hypercholesterolemia of major weight loss, and it’s a well-known phenomenon. Once your weight stabilizes, cholesterol should normalize—although to a lesser extent than other diets, given Dr. Cate Shanahan’s explanation of increased “trafficking in fat.”

Low Thyroid Function

The thyroid is a barometer for your energy status. If you have plentiful energy to spare, thyroid function is normal. If your body perceives low energy availability, thyroid function may down-regulate. Since the thyroid plays a big role in regulation of LDL receptor activity, its downregulation can lower LDL receptor sites. Fewer LDL-receptors clear LDL particles from the blood. Folks with genetic predispositions to heart disease often have low LDL receptor activity, causing elevated LDL particles. Folks with genetic variants that increase the activity and expression of LDL receptors have lower heart disease rates. Although genes often have different effects that may affect disease risk via other pathways, that’s pretty strong evidence that LDL receptor activity regulates, at least in part, one’s LDL-P and heart disease risk.

Read this post for maintaining thyroid function on keto, and check out Elle Russ’ Paleo Thyroid Solution for an even deeper, more thorough dive into thyroid health.

Eating Too Damn Much

Some keto people pride themselves on gorging. Some are doing it for a good cause—a quest to find the fabled metabolic advantage. Some are doing it to show off and for keto cred—look how much salami I can eat! Some are using keto to deal with unresolved issues with food itself.

Everything I say about doing keto presupposes that you are eating like a normal person. You’re eating as much as you need to fuel your brain and daily activities, fitness and performance goals. You’re leaving the table satiated, not stuffed. For most people, this happens without even trying. It’s why keto is so effective for weight loss.

Genetic Variance

Genes aren’t destiny, but they do modify and regulate our response to a given environmental input.

Some people are dietary cholesterol hyper responders. Unlike the majority of the population, they absorb tons of dietary cholesterol and do not down-regulate their endogenous production to accommodate. The result is an increase in cholesterol synthesis and absorption, leading to a spike in blood cholesterol.

Some people are sensitive to saturated fat. In response to it, they produce elevated numbers of LDL particles. If your keto diet is high in saturated fat and you have a genetic sensitivity to it, your cholesterol will probably skyrocket.

Some people have genes that reduce the activity of their LDL receptors. This will necessarily boost LDL particle numbers.

This topic—genetic variance and how it affects keto—could be an entirely separate post, so I’ll leave it at that (and probably come back to it in the future).

Too Much Butter

Huh? Too much butter, Sisson? Is such a thing even possible?

Maybe. Subjecting cream to the butter-making process strips it of something called milk fat globule membrane (MFGM). And when you compare equal amounts of dairy fat through either cream (with MFGM intact) or butter oil (with MFGM absent), you get very different metabolic effects. Those who ate 40 grams of dairy fat through butter oil saw their lipids worsen, including ApoB, a surrogate for LDL particle number. Those who ate 40 grams of dairy fat through cream saw their lipids unchanged, and in the case of ApoB even improve.  That’s 4 tablespoons of butter compared to 4 ounces, or a half cup, of heavy cream.

Caveats apply here. The subjects weren’t eating a low-carb or ketogenic diet; they just added the butter or cream on top of their normal diet. But in keto people who are genetically susceptible, huge amounts of butter may be responsible for rising LDL-P.

I still love butter. It doesn’t affect my lipids like that. But your mileage may vary, and it’s something to think about if you’re in that situation.

For what it’s worth, whole food dairy like full-fat yogurt, kefir, and cheese do not have the same effect on lipids as butter. They also happen to be keto-friendly and more nutrient-dense.

So, What Can You Do If You See An Increase in LDL?

Start Chugging Soybean Oil

Kidding… It’s true that swapping out some of your animal fats for polyunsaturated seed oils will almost certainly lower your cholesterol levels. It does this by increasing LDL receptor activity, but, being far more unstable than other fats, omega-6 PUFAs also increase the tendency of the LDL particles to oxidize. And since oxidized LDL are the ones that end up wedging in the arterial walls and causing issues, loading up on PUFAs might not be the right path.

You know what just occurred to me? This is an aside, but maybe linoleic acid (the primary fatty acid in seed oils) up-regulates LDL-R activity because the body recognizes the inherent instability of linoleic acid-enriched LDL particles and wants to clear them out before they can cause trouble. I hope some researchers take this idea further.

Stop Being a Keto Caricature.

Half a package of cream cheese for a snack.

Dipping an entire stick of pepperoni into homemade alfredo sauce and calling it dinner.

I’m not saying cream cheese is bad. It’s great. Nor am I suggesting you never eat pepperoni, dipped in alfredo sauce or not. But the amounts are unreasonable. And turning those into regular meals is a bad idea. There’s no reason you can’t go keto while eating a hamburger patty or ribeye over a Big Ass Salad. Far more nutrients, far more micronutrients, and it tastes way better.

Eat Less

Maybe if you’re a nomadic horselord sweeping across Europe in the early Bronze Age, you need to eat an entire lamb intestine stuffed with marrow and organs, and you should wash it down with a quart of creamy mare milk. Such a meal would provide the calories you need to see your enemies driven before you and go great with the lamentations of their women. But you’re not a Yamnaya nomad. You’re you.

You probably don’t need that much food, that many calories, and that much fat—since there’s plenty of it on your body already, waiting to be liberated and converted into energy.  Therein lies the beauty of keto. That’s what this is all about: Getting better at burning your own body fat.

Balance Your Fats

The overzealous and protracted drive to demonize all sources of saturated fat as evil has led to a vociferous backlash from the other direction. But just because the supposed experts got the saturated fat issue wrong doesn’t mean the opposite is true: That all the fat we eat should be as saturated as possible.

For one thing, eating nothing but saturated fat is very hard to do using whole foods. Very few animals exist in the world, past or present, with only saturated fat. The only exception I can recall is the coconut, a curious sort of beast that spends most of its time hanging from a tree impersonating a large hairy drupe. Your average slab of beef fat runs about 50% saturated fat, 45% monounsaturated fat, and 5% PUFA. That differs from cut to cut and depending on the diet of the animal, but not by much. It’s similar for other ruminants like bison and lamb. And the most prominent saturated fatty acid in ruminant fat is stearic acid, a fat that converts to monounsaturated oleic acid in the body and has an effect on cholesterol indistinguishable from MUFA or PUFA.

Or take the fatty acid composition of game meat—the type humans encountered and consumed for our entire history.

  • African kudu (antelope family): 35% SFA, 24% MUFA, 39% PUFA
  • African impala (antelope family): 51% SFA, 15% MUFA, 33% PUFA
  • Elk: roughly 40% SFA, 30% MUFA, 30% PUFA
  • Moose: roughly 33% SFA, 33% MUFA, 33% PUFA

I could go on, but you get the idea: Humans have been consuming a wide range of fatty acids for millennia. It probably makes sense to emulate that intake.

Once again, the folks whose cholesterol goes nuts on keto are outnumbered by those whose cholesterol improves. But if you’re one of the unlucky ones in the former category, try broadening your fatty acid intake (to, ahem, possibly include more nuts):

  • Focus on monounsaturated fats and fat from meat, rather than isolated sources of saturated fat like butter and coconut oil. You probably don’t have to eliminate those fats. Just don’t make them the centerpiece of your diet.
  • Eat more avocados, avocado oil, olives, olive oil, and mac nuts for monounsaturated fat. Salads are a great nutrient-dense way to incorporate high-MUFA foods.
  • Eat more fish. A couple portions of farmed Atlantic salmon were enough to improve LDL-P in overweight men and women. And compared to plain keto, keto + omega-3s from fish has a superior effect on inflammation and metabolic health.
  • Eat more kudu and impala (if you can get it). Sort of kidding. But really, eat them if you can.

They even have a version of keto called the Spanish ketogenic diet, which features a lot of extra virgin olive oil, olives, fish, and red wine. It works great and might be a good alternative for people whose cholesterol goes wild on saturated fat-heavy keto.

Are Traditional Lipid Markers Even Relevant for Keto Dieters?

Maybe, maybe not.

But be honest about it. You can’t oscillate between championing positive changes to blood lipids on a keto diet and pooh-poohing negative changes to blood lipids on a keto diet.

You can’t use positive changes to prove the efficacy and safety of the ketogenic diet, then turn around and claim that negative changes don’t count because keto dieters are understudied. What if those “positive” changes are actually negative in the context of a ketogenic metabolism? After all, keto dieters are largely understudied in both directions. If what’s unhealthy in a normal dieter might be healthy in a keto dieter, what’s healthy in a normal dieter may be unhealthy in a keto dieter.

I write these things as a strong proponent of spending a significant time in ketosis. As someone who frequently hangs out in a ketogenic state. As someone who wrote a book about keto and is writing another. But also as someone who insists on maintaining strict intellectual honesty and integrity.

We simply don’t know what very high cholesterol numbers mean in the subset of ketogenic dieters who experience them. I strongly suggest not being too flippant about them. 

True: There aren’t any perfect studies examining the utility of conventional cardiovascular risk factors in people eating the type of keto diets you see in the ancestral health space. Maybe your elevated LDL particle number doesn’t mean what it means in the average overweight adult eating the Standard American Diet. Maybe your inflammation is low enough that the risk of atherosclerosis and oxidative modification of LDL is low. But I wouldn’t take that risk, not until we have more data.

What do you think, folks? How did keto affect your blood lipids? Did you make any changes, and if so, did they work? Thanks for stopping in today.

Note: This information isn’t intended as and shouldn’t be considered medical advice. Always consult your doctor in the management or treatment of any health issue.

References:

Hussain TA, Mathew TC, Dashti AA, Asfar S, Al-zaid N, Dashti HM. Effect of low-calorie versus low-carbohydrate ketogenic diet in type 2 diabetes. Nutrition. 2012;28(10):1016-21.

Phinney SD, Tang AB, Waggoner CR, Tezanos-pinto RG, Davis PA. The transient hypercholesterolemia of major weight loss. Am J Clin Nutr. 1991;53(6):1404-10.

Phinney SD, Bistrian BR, Wolfe RR, Blackburn GL. The human metabolic response to chronic ketosis without caloric restriction: physical and biochemical adaptation. Metab Clin Exp. 1983;32(8):757-68.

Kleinveld HA, Naber AH, Stalenhoef AF, Demacker PN. Oxidation resistance, oxidation rate, and extent of oxidation of human low-density lipoprotein depend on the ratio of oleic acid content to linoleic acid content: studies in vitamin E deficient subjects. Free Radic Biol Med. 1993;15(3):273-80.

Rosqvist F, Smedman A, Lindmark-månsson H, et al. Potential role of milk fat globule membrane in modulating plasma lipoproteins, gene expression, and cholesterol metabolism in humans: a randomized study. Am J Clin Nutr. 2015;102(1):20-30.

Raatz SK, Johnson LK, Rosenberger TA, Picklo MJ. Twice weekly intake of farmed Atlantic salmon (Salmo salar) positively influences lipoprotein concentration and particle size in overweight men and women. Nutr Res. 2016;36(9):899-906.

De luis D, Domingo JC, Izaola O, Casanueva FF, Bellido D, Sajoux I. Effect of DHA supplementation in a very low-calorie ketogenic diet in the treatment of obesity: a randomized clinical trial. Endocrine. 2016;54(1):111-122.

Pérez-guisado J, Muñoz-serrano A. A pilot study of the Spanish Ketogenic Mediterranean Diet: an effective therapy for the metabolic syndrome. J Med Food. 2011;14(7-8):681-7.

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65 thoughts on “Is Keto Bad For Cholesterol?”

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    1. Definitely an interesting read. Thanks you for sharing the link.

  1. This is ne. NMR small particle LDL off the charts after 14 months very low carb. I am already following many of your suggestions with little improvement. My mother has hypercholesterolemia and Alzheimer’s and my father had his first heart attack at 55 and his five siblings died of heart issues. Plus, I am diabetic, hypothyroid, and have 50% blockage in one artery. I am 65. I have been resisting statins. I don’t know what else to do as keto has brought my A1C down to 5.3 and reduced my blood pressure meds by 50%. Thank you for a great article. I am tired of the flippant reaction to serious cholesterol issues and want answers.

    1. If you really want a deep dive then check out Peter Attia’s podcast The Drive where he interviews Tom Dayspring (a lipidologist) – it’s 5 podcasts each about 2 hours and lots of show notes with diagrams to help explain. He also (in a separate podcast) interviews Dave Feldman of cholesterolcode.com but in my opinion is rather rude to him and dismissive of his work.

      1. Thanks for this Claudia. I listened to the Feldman – Attia podcast and came away with the same feeling. While I appreciate challenging and debate, Peter came across as condensending and arrogant.

        1. I kind of felt the same, even as an Attia follower, but if you notice, Feldman was completely accepting. He acted willing to be schooled to some degree. To me that shows
          1) that he acknowledges that Attia/Dayspring is/are more fully educated in the field with a bigger picture view and can see what Feldman is missing.
          2) Feldman apprears open-minded, which is encouraging.

          In spite of this and their respect for Dayspring, Feldman and Ivor Cummins do seem fairly entrenched in their view of the mechanisms as they hypothesize. Again, the issue with their approach is that being Biology outsiders while they bring novel views, they are less likely to know if there are aspects of the Biochemistry they are missing which would contradict or shoot down their hypothesis.

          I have found studied an article with Dayspring’s discussion of an exemplary “hyper-responder” case he dealt with and his interpretation of the mechanisms behind it. Summary is: drop your saturated fats down if you are the rare one. Wish I had the link…

          1. I found dropping my saturated fat did nothing, so the other side needs to be open also. We don’t know all the answers and just because someone has been schooled does not mean they know everything, we don’t know and I have defied all the general knowledge of do this or that and can say it does not work. I truly don’t believe cholesterol is the killer it has been made out to be.

    2. Also check out Ivor Cummins at the fatemperor.com who has analysed the data. He has some great YouTube videos.

    3. my guess Anita…. auto immunity……do a leaky guy protocol…..nothing else will truly normalize if intestinal permeability is putting your immune system on fire….

    4. Try what Mark suggests and cut your saturated back. Use olive, avo oils as much as possible.

    5. Anita,

      I am in the same boat as you–I have calcium deposits confirmed by a Heartsaver scan, and a family history of early deaths from heart attack. Though I eat paleo and low carb, I have also decided to take ezetimibe, low-dose atorvastatin and metformin. This comes my reading of Peter Attia and Thomas Dayspring. In my view, the hypothesis put forward by Cummins and Feldman is just a hypothesis and not worth risking my life on. They could be right, of course, but the balance of risk pushed me to take the statin.

      That said, I am not a doctor, of course, so please consult with a doctor you trust. And best of luck to you, whatever you do.

      –Hedgie

      1. Here is the RTC done on Atorvastatin (Lipitor) file:///home/chronos/u-6114ce563f8d7f12e180d3d2aaad2cf9dfa13a65/Downloads/Cholesterol/Atorvastatin%20Lipator%20Trial.pdf
        In table 3 you will see that the chance of a cardiac event went from 3% in the placebo group to 1.9% in the Lipitor group – about a 1% improvement. If you look at all cause mortality it was only improved by 0.5%.
        These small gains may be outweighed by the fact that studies have shown that statins double your chance of type 2 diabetes and can cause muscle pain, brain fog and digestive problems.

    6. Anita, is your hypothyroidism well managed? Anytime my thyroid status declines, my cholesterol shoots up.

      What is maddening is that I DON’T make TSH in response to a thyroid decline…my pituitary simply doesn’t produce it. I can be falling out of normal range with fT3 and fT4 and my TSH MAY rise to 1.0. That’s way below diagnostic threshold, but I am symptomatic and miserable, and my TC goes up to nearly 300. I have lab results and charts to document it.

      I refuse to have my TSH measured anymore. I get my own lab tests independently, and refuse the TSH or black out the result. Docs who only look at that number have under treated me, and I will not have them send me back into the Pit of Despair again.

      I tell them that I am not willing to have the CV risk that goes along with highly elevated cholesterol, and my cardiologist agrees. So they’d better treat my thyroid adequately and factor in my my under-production of TSH, or else. They don’t like it, but the CV risk part makes them want to CYA like crazy.

    7. Although not 50%, I did have a CAC score of 68 – all in my “widow maker” – which is not necessarily high, it did put me well over the 90th percentile for my age. After doing research, I came up with a protocol of significantly increasing my omega 3 intake, while cutting omega 6 as much as possible and supplementing with high dose vitamin K2 (NOT THE SAME AS K1 WHICH COMES FROM LEAFY GREENS). By high, I mean up to 2000 mcg per day. After 9 months, my CAC dropped to 52. It was done on the same machine with the same operator (who was befuddled that a score could go down). This was all done while my cholesterol continued to be very high by traditional standards (TC 266 with LDL 174). I think some of the keys were my inflammation was very low (n3:n6 ratio) and the K2 is key in moving calcium to where you want it (bones and teeth) and away from where you don’t (arteries and joints). I understand this is n=1, but it is a cheap and easy experiment to try to see if it can improve your blockage. BTW, there is no research showing statins improve existing calcification in arteries – and they have studied it repeatedly.

    8. Just take the statin. Anything to hedge your bets is good when you have so many bad metabolic markers plus a family history.

  2. For those of us whose LDL went up on keto, but also saw an improvement in HDL (up) and triglycerides (down) there is a wealth of information on Dave Feldman’s site cholesterolcode.com

  3. You left out one of the reasons KETO dieters might have skyrocketing cholesterol–not sticking to the KETO diet over time. I am the poster child of going on and off, again and again. And my cholesterol shot through the roof. Probably the worse way you could possibly eat, high fat for a few weeks then high carb for a few weeks and back and forth. I have given up on KETO because I don’t feel well on it and I can’t maintain it. Better to try for moderate carbs, moderate fat and lots of healthy veggies, for me.

  4. We should remember cholesterol is not Bad…we will make it in our bodies, especially if we are not getting enough in our diet. Cholesterol is the backbone of the sex hormones like testosterone and estrogen. This could be one of the big reasons Statin drugs (used to lower cholesterol) cause decreased sex drive. So, just pop more Viagra to balance it all out, right? Cholesterol helps build cells and digest food. 25% of the cholesterol in our bodies is found in The Brain, what does that tell us? Cholesterol is necessary for Life! Probably one of the biggest causes of increased cholesterol is stress…it is a complex puzzle but definitely not Bad. Just 35 years ago, (before advertising meds on TV) a normal Total Cholesterol number was 250. The devil is in the details, and now we can break down the lipid numbers, just like Mark said, to see if we need to worry about an elevation in the blood lipids with dietary changes.

  5. Worries about cholesterol is such a waste of time.
    Check out Dave Feldman & Ivor Cummins if you
    want the reality of cholesterol & keto. Turns out, the more butter you eat, the lower your LDL. As long as Triglycerides are low & inflation is down, LDL is
    a non issue.

    1. My concern is that my Total LDL went down, Triglycerides went down, HDL didn’t change much (low end of good range), BUT my Small LDL particles went through the roof. Per Mark Hyman, I’m trying to supplement with Red Rice Yeast and Plant Sterols to see if I can bring particle size up or at least get small numbers down.

      I love being in Ketosis ( 16 months),but the thought of small particles building up in my arteries has this 60 year a little concerned.

    2. For some of us, the more saturated fat ( especially isolated fat like butter and coconut oil) the higher our LDL goes. And ignoring LDL levels completely is the same mistake the “all LDL is bad” crowd make, but in the opposite direction. Heart disease is nuanced, does not have one single cause factor and varies wildly from person to person.

  6. My last doctor was always on me about the LDL. However, I don’t think I was consistent enough on the diet itself. Just switched docs and here comes the blood work form.

    I don’t have that much butter – maybe 4 tbl in a day max? And that’s my bullet proof coffee and using it to cook eggs. The rest of the day I’m butter free. But I can switch to Coconut oil in the coffee and eggs. I try to Intermittent fast 2x a week as well – don’t eat until 2:00pm. Going to give it some time – a few weeks – to go to the lab and see what’s up.

    Good pointers in this – I’ve been looking for a book/article that gives this very subject an objective look.

  7. The problem is Mark, that LDL particles go up exactly like this when lean, healthy people fast for a few days.
    Does that cause heart disease?
    Obviously people fasting are not eating saturated fat. They’re not eating too many calories.
    But they are in ketosis, and their cholesterol efflux is maximised – macrophages don’t want it, adipose doesn’t want it, liver isn’t in a hurry either.
    That’s quite possibly all it means – this seems be a highly conserved adaptation, and a sign of metabolic health in many people.

  8. I have APOE3/4 and several hits for FTO snps in my genome.

    I found this when I ran my 23 and me results through the Foundmyfitness site (Rhonda Patrick) and the included recommendation after each of these high risk factor genes was to make sure my saturated fat to unsaturated was not too high. Didn’t say cut out saturated, just keep the ratio in mind. Just what Mark is saying.

    1. Yep. I’m in the exact same boat with ApoE 3/4.

      Grinds my gears how people always say “it’s no big deal that you LDL/HDL numbers have done what they did KCKO!!!”

      We are not all the same and individual genetic phenotype matters how your blood lipids (and other chemistry) will respond.

  9. Thank you Mark, for finally addressing this topic. I am a hyper responder, too. Was Keto for about six month, ldl-p shot up to over 2500. Fun fact: lean, athletic people seem to be most at risk for this type of rise.

    I actually consulted with Chris Masterjohn, and considering my predisposition to both saturated fat-related lipid increase, as well as being suspectiple to iron overload (genetics. I’m homozygous h63d), his simple solution was: eat more [good] carbs. This will increase ldl receptor activity. He said, you just don’t want that many ldl particles in your bloodstream because it’s dofficult to keep the oxidation risk low unless you really manage it well.

    I also focus on MUFA and eat more carbs like lentils, potatoes and rice. I feel better, sleep better and digestion is better. Instill drizzle the olive and avocado oil liberally, and eat full fat raw milk and cheese. Not hard livin at all!

    1. Chris, I’m also homozygous h63d with diagnosed hereditary hemochromatosis (became seriously symptomatic a few years until finally was diagnosed through a genetic blood test.) I’m 67 yrs old and I have been doing 7 days a week intermittent fasting for the last year (with a 4 hour eating window only), and a modified primal diet as well, and saw ALL my blood markers become fantastic — except — LDL=156, TC=280. Significantly raised from my pre-IF and primal eating days. I’ve been wondering if the hereditary hemochromatosis contributes. No doctors around where I live to discuss this with. I’m surrounded by statin-pushing cardiologists instead. Very frustrating. Want to believe that higher TC and LDL numbers, in the context of all my other great lab numbers are nothing to worry about, but this is all sooo complex…

  10. Thanks for acknowledging the potential contradictions here, Mark! This reader appreciates the intellectual honesty:

    “But be honest about it. You can’t oscillate between championing positive changes to blood lipids on a keto diet and pooh-poohing negative changes to blood lipids on a keto diet.”

    I’ve heard several other keto and carnivore proponents do exactly this, and it’s blatant hypocrisy.

  11. I can vouch for some people simply being hyper responders. I am one of them. While I felt and looked great while being keto… My cholesterol numbers skyrocketed to nearly uncontrollable levels. As much as I like the diet and wanted to stay on it there was no way I could justify the possible risks.

  12. Nice article Mark! There is a lot of confusion in the Keto space regarding the elevations of cholesterol. I appreciate the honesty in that we do not have a large amount of studies following cholesterol and the effects of high cholesterol with regards to cardiovascular disease in people eating ketogenic diets. I see many advocates for a ketogenic diet show their stellar lipid profiles and inflammatory markers on social media but in clinical practice we often see the opposite. We are all very unique!

  13. My total cholesterol on keto was about 285 – 300. I’m one of these people with blood pressure of 105/65, blood sugar of 93, HDL of 95, triglycerides of 69. When I went on carnivore it all stayed the same but my total cholesterol went to 395. That was a bit more than I was comfortable with. So I added berberine, broccoli, salads, asparagus and green beans back in. I felt fabulous on carnivore and my skin was great, mood great. I don’t feel and look quite as good, but until they start studying this (and I ate grass fed beef and organic only), I want that total cholesterol under 300 since I don’t want to take statin drugs. I do have Hashimoto’s thyroid problem and that may affect my cholesterol. That is the only pill I take. Levothyroxine, berberine and a homocysteine plus supplement. I also have very low c-reactive protein, but slightly elevated homocysteine. I wish this was studied more. I was drinking a little butter in my coffee and stopped that. Sticking to a bit of heavy cream now and then. I do eat eggs, a bit of cheese. Very little fruit.

  14. I am one of those lean mass hyper responders due to a keto diet. Trigs were always low, HDL always elevated, but it was my LDL that almost doubled about about 5 years ago when going Wahls AIP keto. Don’t overeat, no dairy/butter, can’t tolerate avocado, but I did use coconut oil and milk. About 3- years ago my LDL continued increasing so I shifted to mostly mackeral and sardines for protein, kept weekly organ meat, and only olive oil for fadded fats. The effect was slightly lower HDL and even higher LDL. Trig/HDL/total ratios are all still in good and healthy range but new PCP is freaked. So adding a little coconut milk back and hoping for lightly lower LDL and higher HDL. ??

    1. Check you TSH numbers. You may have undiagnosed hypothyroidism.

  15. Thanks, Mark, for this addressing this issue in detail. I have been primal for a few years now, and just recently started the Keto Reset last January. I took a blood test early on when going keto as a baseline. All was good, with the exception of cholesterol which was significantly high (and “out of range”) compared to my “normal” blood test 3 years ago. The rest of my lipid profile was within “normal range”, however.

    You made insightful points on how to interpret such results in the context of what we already know and what they could mean specifically for keto dieters. I guess I’ll try some dietary shifts with less coconut oil/butter and more olives, nuts, and avocado and hope for the best. Otherwise, I feel and look great and am enjoying the keto diet. Great food for thought (pun intended)!

  16. This article is very informative. I plan to quote it on the page dealing with the ketogenic diet on my site. I am also doing regular periods of keto in alternance with a low-carb diet plus exercise following your and Phil Maffetone’s advice…
    A point deserving a more critical evaluation is the presumed causal link between “high cholesterol” (more specifically LDL-C) and the risk of cardiovascular disease. After an acute coronary syndrome which was treated by the implant of 4 stents I did a detailed documentary research on this subject summarized on this page: https://lebonheurestpossible.org/pourquoi-diminuer-le-cholesterol/
    (Automatic translation will render it in English.)
    As suggested by your paper, cholesterol figures have not proved causally associated with cardiovascular events. High cholesterol is even associated with a longer life for aged persons… Indeed all these biological markers follow a U-curve in terms of risk: too high and too low are equally detrimental. Still, this does not prove a causal effect: we could imagine a reverse causal scenario by which a person’s cholesterol goes high as a protection against a pathological state…
    Finally it may also be pointed out that dietary cholesterol only takes part in about 20% of the cholesterol circulating in blood. Therefore dieting to reduce LDL is illusory.
    I also spent months documenting statins and anti-cholesterol medications on page:
    https://lebonheurestpossible.org/statines-et-medicaments-anticholesterol/

  17. Hi, we are all different, what could be good for me is not for you, but just to be clear, I’d like to share the results of my blood test from last week, and also I’d like to share that I’m in a Keto diet together with OMAD since one year ago.
    Total Cholesterol = 165
    LDL = 83
    HDL = 75
    Triglycerides = 33
    I hope this will help and prove that a Keto diet it’s the best thing that you can do with your body.
    I forget to say I do exercise everyday and I’m a long runner.

  18. My total cholesterol was 220 a short while ago…..LDL the same as pre Keto, HDL higher….all my dr had to say on the matter was “whichever way you look at it high cholesterol causes heart disease”………this is what we are up against, and at the back of my mind is a niggling question as to what we are doing to our bodies long term by following this way of life……..

  19. After being on a pretty strict keto diet for over a year and losing 50 lbs. of body fat (now 6′ tall and weigh 170), I was interested to see what my cholesterol numbers were when I went to my last cardiologist visit. They were pretty bad:

    Total: 380
    LDL: 319
    HDL: 22
    Trigl: 193

    All my numbers went south. I don’t have any symptoms of cardiovascular disease, but my CAC calcium scan score is over 600, and that’s why I regularly see a cardiologist. Like another person commented here, I’m not willing to gamble my life on whether or not cholesterol is good or bad for my health. My doctor has prescribed atorvastatin, ezetimibe, and baby aspirin. The monetary cost of these drugs is low, and so far I don’t have any side effects. So I’m going to follow his advice and take them.

    My doctor also thinks I might be a hyper responder to saturated fats, so I’m cutting those back. I’m sort of keto now…I eat mainly fish, greens, and nuts, but instead of butter and cheese, I focus on olive oil as a fat source. And no seed oils, no sugar, no alcohol, no dairy, no grains, no fruit.

    I’m pretty confident that this “pescetarian” diet, along with statin and aspirin therapy, will bring these cholesterol numbers down. Whether or not that actually matters to my health remains to be seen over time, I suppose.

    This is a great and very timely article. Thank you!

    1. Smart move because you are not the typical hyper-responder profile. You HDL is super low and TG really high, which is opposite of what happens to typical hyper-responders like myself. I would had done the same thing in a heartbeat.

  20. I’m one of those lean, athletic hyper-responders as well, with a family history of bad cholesterol. LDL-P shot up, other numbers great, even a zero calcium score.

    I saw a passage in Wolf’s Wired to Eat book about this, that we just don’t respond well to ketosis. The suggested solution was to eat more carbs, so I’m increasing vegetable portions and avoiding ketosis/fasting as a first attempt at lowering LDL-P.

    That being a simpler solution, I’m trying that first, but I appreciate all the info and suggestions in this article and the comments.

  21. Thank you Mark for posting this controversial subject: even though we have so many questions the only way to get some of these answers is to keep asking questions. This is the nature of science and progress.

  22. Dr Eades at proteinpower believes that cholesterol is very dynamic and “there are some old studies out there kicking around showing that people who fast actually drive their cholesterol levels up” so he suggests increasing the amount of fat in your diet for three days before testing. I haven’t tested this theory yet on myself.

  23. Great article, Mark. I was on Keto for only a few weeks and my cholesterol jumped 57 points to 258. I was eating a lot of goat cheese and butter so I’ve backed off those and will concentrate more on fish and olive oil.

  24. “For the majority of adults who go keto their cholesterol numbers improve…”

    Really? Who’s testing every adult who goes keto? Of EVERY adult who goes keto, how many are actually getting their blood work done?

    Lets realize that the number of adults who go keto is amazingly small, and those getting regular blood work even smaller – so drawing broad conclusions for the general public is the epitomy of poor reporting and simply unscientific.

    There is not enough rigidly performed scientific studies on truly large population/sample size done to draw such broad general population related conclusions.

    The confirmation bias here is astounding. For profit confirmation bias.

  25. Thanks for the article! Very well represented perspective. I took both Keto Reset course and Robb Wolf’s Keto Masterclass, in process of Primal Blueprint coaching certificate. Randomly measured ketones between 2.5-3.5 mmol for 90 days, side note 6’2” 175 lbs. Then did a particle lipid panel via TrueHealth, sky rockets in flight. All of the sudden I was extreme risk cardiovascular profile. Sooo, elimated bacon, butter and coconut oil (except for Primal kitchen collagen bars) and switched to lots of greens, nuts, fish and almost drinking olive oil. Outcome, tbd but ketones still remain at nutritional ketosis levels. I think the most important thing is to take personal ownership in your progress, be open to outside perspectives and work towards metabolic flexibility as low carb as you can. Also, working in the cardiology field, Peter Attia has a 4-5 series podcast with a lipidologist that is definitely worth the investment of your ears.

    1. Nick, let us know when you find out if your changes affect your lipid levels.
      Thanks for your post!

  26. After spending quite a few years in a Ketogenic state, from Atkins to more recent incarnations, I found that I must be one of those hyper-resonders mentioned above. Many blood tests later, I found that egg yolks, a bit of butter, cheese, or macadamia nuts all have the same (quick) effect of dramatically raising my LDL and not only that, but fasting glucose AND fasting insulin levels became scary high. I kept trying, thinking maybe time would straighten things out, but when I stopped losing weight (never lost much anyway) and my total cholesterol was almost 400, and blood pressure was getting stubbornly high, I gave up and finally admitted that my body is very different. Ketosis sounds great to me, except…….it doesn’t work at all….for me. I have been almost completely vegan for the past year now, and I feel great. My fasting glucose went back down into the 78ish range, cholesterol down to the 250 range where it has always hung out, and blood pressure, thank god, back down in the 110/60 range. I’m so glad that my health was permanently damaged by going Keto. I follow a pretty high complex carb/lowish fat eating style and eat as much as I want which can be quite a bit, but my weight is lower an easier to control than ever. I know people, such as my husband, who seem to function better with more protein and fat but some of us do better with lower fat and more fiber/complex starches. Its all very interesting but I like that Mark is pointing out how important it is to pay attention to what goes on with our own unique physiology. Just because something works for most people doesn’t mean it works for everyone. Thanks to all who post here.

  27. correction: “Glad my health WASN’T permanently damaged by Keto (as far as I know). May be more typos in that post, haven’t proofed all of it yet

  28. HI! So…my ldl-c is 4 times the normal high, with high TG,
    and i am positive for Apo-b. I qualified for the newer injection drugs but take no medication …per the following story :

    No meds as the good news is that although my body in 65, my arteries per scans are age 30 !
    . no plaque, no calcifications, so apparently no inflammatory response.
    And so the arteries are perfectly clean (per a functional CT scan, and MIBI .. all is good !
    NOW why am I okay? My family who are not keto and not athletic,do have arterial plaque.
    THE ANSWER? The good specialist (sport medicine who I was seeing for A_fib, us rowers who over race get this at my age and need to detrain ) said probably as I have always been low carb that I had no inflammation. (Low carb as at age 30 carbs were found to be my migraine trigger due to insulin…. )
    However this specialist more importantly said importantly, that maybe as I always sprinted that I just “blew” out the plaque. ( I am a happy to be Medium-level athlete, love movement . and actually I have never done long distance sports, only 45 minutes of activity 4 days per week, with sprinting intensely for 30 seconds a few times a few days per week. Never same sport 2 days in a row. Never sprints 2 times in same sport in a week.. 36 hours per week no sports except walking. Ran,biked, rowed, wt lifted . weights were heavy and brief 2 times per week.
    could not drink re migraines…
    Just saying …as maybe someone may want considering adding in sprinting up a short hill 2 times per week, one bike, one run, as could be helpful for some ? if their doctor agrees?
    Hmm, so looking back on a lifetime of migraines…I am actually lucky to have had to be carb free ….interesting, yes?
    Anyway, hoping to help….. best, good luck! Carol

    1. Not so sure about sprinting ‘blowing out” your plaque. However, when my grandfather had a heart attack, which he though was just feeling tired that day, his doctors noted that his body had created it’s own bypass over the years by building additional feeder arteries. Enough to turn a fatal heart attack into a flu like experience. My grandfather had been an athlete his whole life. They speculated that because he always worked out, his body needed to keep his heart beating at capacity and took the necessary steps to do that. Sounds right.

  29. Perhaps if one consume soluble fiber such as psyllium seed husk, it would feed your native population of akkermansia municiphila. This species of microflora helps to break down saturated fats into healthy compounds.

  30. Lean Mass Hyper-responder myself. Senisitive to saturated fat but LCHF diets jack up my numbers big time.

    Total Cholesterol:327, HDL 138, LDL 176 (pattern A), TG: 43 VLDL (remnant cholesterol) 13
    Also: Low blood pressure, low C reactive protein and good insulin sensitivity

    Objectively, very good metabolic markers.

    Trouble is, I’ve never felt better. Faster recovery time. Better endurance. More resilient to stress. Easy to stay lean.

    Fortunately my doctor and his cardiologist partner gave me the honest answer. We don’t know what these numbers mean because they don’t makes studies on people like you. If you were in a study, they’d let you go because you’re an outlier. So there are no data points.

    I also have hypothyroidism which I’m treating and this condition preexisted LCHF. So no correlation.

    Other than the high LDL, my numbers are the stuff of legend. There also seems to be no data that show pattern A LDL is an issue when isolated from elevated TG, low HDL, diabetes, obesity, hypertension and high C reactive protein levels.

    So far I’m staying the course and making sure my carbs don’t go too low. But I have a hard time believing that every other marker can be exceptional, and show very good metabolic conditions, but the elevated LDL is going to render it all moot.

    It doesn’t make sense in the big picture.

    And if we didn’t have stains, I’m not sure we’d really even be focused on LDL. I have yet to see a doctor freak out over high TG, even though that is undisputed as being bad in all studies. But, we don’t have a drug for it either. So a doctor would need to know that sugar raises triglycerides AND get their patient to stop eating sugar. Good luck with that one!

    Much easier to go with a drug, that works as intended (reduce LDL), regardless of the patients lifestyle. Safer too, legally, as that is a well established option for elevated LDL. No one will blame you for prescribing a statin.

  31. Thanks for the tip about Spanish keto…as someone with high familial hyperlipidaemia, have to care be full : )Just read some of the papers, perfect! Big warms from UK….

  32. My problem was eating too much butter. My lipids became terrible.

    LDL direct: 302 mg/dL
    Cholesterol: 464 mg/dL
    Triglycerides: 533 mg/dL
    HDL: 96 mg/dL

    Dave Feldman did say that butter and isolated forms of fat can increase triglycerides, and you can see this onbmy blood test.

    I am glad I found out about the damage I was subjecting my heart to and how Mark was willing to correct his stance on what he said about saturated fat in 2009:

    “To begin with, man has a taste for fat. It’s delicious, and that’s no mistake. Given the choice between a lean chicken breast and a fatty, crispy thigh, most people instinctively go for the thigh. Social anti-fat conditioning might direct a few of us toward the dry breast, but fatty cuts just taste better. I think even Cordain would agree that Grok would opt for the fatty cuts first; where we differ is in our opinion of Grok’s access to such fatty cuts. Cordain believes the fatty acid composition of ancient game was mostly monounsaturated, while I doubt it was so clear cut. According to the WAPF’s Mary Enig and Sally Fallon, the fatty acid composition of wild game available to native Americans varied, with the most prized sources of fat (kidneys) being primarily saturated. In fact, Vilhjalmur Stefansson, hallowed purveyor of pemmican and admirer of the high-fat Inuit diet, spent considerable time with the northern native Americans and noted that they seemed to “hunt animals selectively.” They would specifically pass on the tender calves and go for the older caribou, the ones with huge slabs of back fat that could be rendered and stored. This caribou fat was about 50% saturated. These are more modern animals, but they’re still wild, and I don’t see how the large animals being consumed by Grok would have inexplicably been low in saturated fat.”

    https://www.marksdailyapple.com/saturated-fat-healthy/