Ketosis And High Cholesterol According to Dr. Thomas Dayspring

Ketosis and high cholesterol and Dr. Thomas Dayspring

In my search to learn more about what the heck the relationship is between ketosis and the stratospheric increases in both Total Cholesterol and LDL that seem to occur in so many people (myself included), I came across this case presentation and write up by Dr. Thomas Dayspring, who is a renowned lipidologist.

He was one of the experts in Jimmy Moore’s Cholesterol Clarity, and has appeared in a number of Jimmy’s podcasts (two of them are here and here).

I carefully went through this paper and did my best to digest, simplify, and summarize it… mainly for myself, but I figured I might as well share it with you guys too.

It took me a couple read-throughs to process it all since things can get a bit complex.  I also didn’t realize how hard it can be to read single spaced paper like this.

Of course I encourage all of you to give it a read yourself.

Ketosis and High Cholesterol

Dr. Dayspring discusses a case in which a post-menopausal female went low carb paleo and in the span of a few months developed super high Total Cholesterol (TC) and LDL-C.

TC: 196 -> 323
LDL-C: 105 -> 230
HDL-C: 75 -> 83
Triglycerides (TG): 78 -> 49
Total LDL-P: 2643

In this 14 page, single-spaced case discussion, Dr. Dayspring explores what it means for patients who go low carb and demonstrate tremendous improvements in insulin sensitivity including loss of weight, decreased waist size, improved TG and HDL-C, and decreased inflammatory markers… BUT develop an increased TC, LDL-C, ApoB and LDL-P.

“I and other lipidologists and many patients themselves are starting to see that the above lipid response to a high fat diet as not being very rare response in people who abandon carbs and replace it with saturated fat, especially so in those doing extreme carb restriction to achieve nutritional ketosis.”

“The true incidence remains to be determined but experienced colleagues who have a lot of patients on low carb diets advise it is about 1/3 of patients

In all the literature that he’s reviewed, the most important coronary heart disease (CHD) risk factor aside from smoking and age, is having a high LDL-P.

He emphasizes that there is a lot of misinformation (according to him) on the internet saying that atherosclerosis is a disease of too-much-inflammation and not of too-much-cholesterol.

The truth (again, according to him) is that atherosclerosis is a disease of EITHER too-much-inflammation OR too-much-cholesterol.

  • People without inflammation can still have atherosclerotic plaque.
  • People with low cholesterol (TC and LDL-C) can also have atherosclerotic plaque.

Atherosclerotic plaques are composed of cholesterol that has infiltrated the arterial wall. Cholesterol enters the wall via LDL, and the amount of cholesterol that enters the wall is correlated with the LDL particle number (LDL-P) not LDL concentration (LDL-C).

The Difference Between LDL-C and LDL-P

Let’s take a moment to review the difference. I’ll begin by saying that this example is a tremendous oversimplification, and this simplification is not a part of the paper.  I included this part only to give you a better understanding of what he’s talking about (if someone has a better way of explaining this, please let me know).

LDL-C stands for the concentration of LDL cholesterol, or rather the amount of cholesterol carried by all LDL lipoprotein complexes.

LDL-P stands for the amount of LDL particles, or rather the amount of LDL lipoprotein complexes that are present.

Now let’s say there are 10 cholesterol molecules.

Let’s say these 10 cholesterol molecules are packaged into 1 LDL lipoprotein complex.

What’s the LDL-C?     10, because the CONCENTRATION is 10 cholesterol molecules.

What’s the LDL-P?     1, because there is only one LDL lipoprotein complex.

Now let’s say these 10 cholesterol molecules are packaged into 5 different LDL lipoprotein complexes, each containing 2 cholesterol molecules each.

What’s the LDL-C?      10 still, because the concentration is still the same: 10 cholesterol molecules.

What’s the LDL-P?      5, because there are now 5 separate LDL lipoprotein complexes.

Now back to the paper

Ok, getting back to the atherosclerotic plaque.  After LDL particle number, the most important factor in developing atherosclerotic plaques is the integrity of the arterial endothelium (cells lining the arterial wall).  If they are inflamed, they will develop gaps that will allow LDL to enter.

Obviously the worst-case scenario is to have both high inflammation AND high LDL-P.

Dr. Dayspring cautions: “But make no mistake the driving force of atherogenesis is entry of apoB particles and that force is driven primarily by particle number not arterial wall inflammation.”

He provides a reference (which I plan on reading in the future):

Ira Tabas, Kevin Jon Williams, Jan Borén. Subendothelial Lipoprotein Retention as the Initiating Process in Atherosclerosis Update and Therapeutic Implications Circulation. 2007;116:1832-1844.

He next goes over the biochemistry and absorption of cholesterol.  I won’t go over it too much here except for some of the highlights:

“Ingestion and small intestinal absorption of saturated fatty acids in some patients can lead to a hypersynthesis of cholesterol.”

“In those on low carb diets, fewer carbohydrates are available for energy, and that energy (adenosine triphosphate or ATP) must then come from fatty acids which are broken down by an catabolic (oxidative: oxidation = burning) process.”

Basically what happens with fatty acid metabolism is that when fatty acids are metabolized for energy, they are eventually broken down by the mitochondria into a molecule called HMG-CoA, which can basically do two things: it can either be converted into cholesterol OR into ketone bodies (which occurs when not enough glucose around).

When there are too many ketone bodies around, as in nutritional ketosis, the ketone bodies can be converted BACK into HMG-CoA which is then converted to cholesterol.

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It’s through this mechanism that women with anorexia nervosa develop high cholesterol!  This was a fact that I was surprised to learn.

When the liver is hyper-synthesizing LDL, biomarkers like lathosterol and desmosterol will be high, AND because in this situation the amount of cholesterol in the liver is high, the liver will DECREASE the expression of LDL receptors, which function to clear LDL from the blood, leading to a further increase in LDL-C and LDL-P.

“The classic study of the Framingham Offspring Study done by Bill Cromwell showed clearly that risk trafficked better with LDL-P, than LDL-C. In persons with elevated or reduced LDL-C, risk was pretty much related to LDL-P, meaning there are patients with high LDL-C who had excellent survival because there LDL-P was not elevated. Also those with lower levels of LDL-C but elevated levels of LDL-P did have CV risk.

The most common response Dr. Dayspring hears about this from low carb advocates is that, “Framingham offspring is not a study of those on a low carb or paleo diet and thus does not necessarily apply to them.”

“The big question right now really is: Are there persons who do not get atherosclerosis with apoB-cholesterol/lipoprotein levels greater than the above posted concentrations who do not get atherosclerosis?”

“…It seems for a small percentage of people that is true, but using existing trial evidence (which looked at folks on no specific diets or standard AHA low fat, low cholesterol type diets) they are rare exceptions, not the rule.”


The patient was informed of all of the above and was given the option of altering the diet without returning to carbohydrates or using an LDL-P lowering medication, specifically a statin. The dietary advice was to cut back on saturated fat and use more MUFA and PUFA without increasing carbs

After doing just that for a few months the patient reports: “The only modifications I’ve made because of my high lipids are eating steel cut oats regularly, adding chia seeds to my diet, and eating apples regularly (to increase fiber levels); cutting out most dairy; and watching my saturated fat intake a little more closely–all aimed at getting my high LDL-P down.”  Weight has remained stable.

TC:     196 -> 323 -> 178
LDL-C:     105 -> 230 -> 92
HDL-C:     75 ->  83 -> 82
Triglycerides (TG):     78 -> 49 -> 21
Total LDL-P:     2643 -> 948

Cholesterol Synthesis Markers:

Lathosterol/TC:     31 (low), synthesis marker
Campesterol/TC:     217 (normal), absorption marker
Beta-sitosterol/TC:     231 (high), absorption marker

He notes that these numbers are specified as a ratio in relation to total cholesterol.

He wished the patient had these tests done prior to the intervention because he hypothesizes that in light of the elevated LDL-C and LDL-P, the patients cholesterol synthesis was probably high.

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After the patient reduced her saturated fat intake, this normalized her cholesterol synthesis and thus her elevated LDL-P.

With regard to these markers, he cautions that:

“Another key point regarding absorption synthesis markers is that these change in response to nutrition, drugs, aging, other morbidities and they are not ever too be used as a onetime assessment. In at risk persons, like lipid and lipoprotein and other biomarkers, they need to be repeated with each and every blood draw.”

For people who want to control their LDL-P while at the same time remaining in ketosis, Dr. Dayspring proposes three options:

  1. Do nothing and hope for the best.
  2. Decrease intake of saturated fat
  3. Start a statin and/or ezetimibe (depending on absorption/synthesis markers).

He also says that sometimes the combination of 2 and 3 need to be employed.






28 Responses to Ketosis And High Cholesterol According to Dr. Thomas Dayspring

  1. Albert says:

    Great post, as always! In my various N=1 with ketosis, LCHF, and all combinations you can imagine (right now with CBL 3xWeek) my experience tells me that, in the end, it might be better to reduce overall fat intake, specially when it comes to saturated fat.

    Two months ago I reached 8% BF for the first time ever with a lot of walking and short strength training sessions paired with a very low calorie diet, first something similar to DiPasquale Radical Diet with 1 day all-in and 6 VLC (900 to 1300 kcal/day) with 2 meals + snack (whey), got great results. Then after some weeks I tried a Bodyduilding style 5x very small meals a day very low fat, just protein, rest carbs (sugar!)… got even better!

    Well that is only some context to show where I was when I finished the cutting phase and was happy with the results, because I thought it would be perfect timing to try an epic N=1: ‘ketogenic’ ad-libitum hipercaloric diet. Something similar to what Sam F. has tried to prove LCHF is better, but I did not using nuts… but a lot of olive and coconut oil, cheese, butter, pork and ghee, most of what the paleo comunity would consider ‘healty saturated fats’.

    In two months, eating 2700 to 3600 kcal/day OF NO CARBS other than leafy greens and salads I went from 61kg to 67kg, 8% bf to 15%!… so you see, in the end, fat somehow CAN make you fat and calories still matter a little bit 😉

    To be fair I think I gained some muscle mass in the N=1 along with the bodyfat (was the 2nd goal to the N=1, to see if one can put mass on low-carb) based on anthropometric measures and strength gains against the irons, but to be honest I’m quite SURE there was a lot more fat than muscle… granted.

    Not only that, but I also felt a little bit bad overall and observed some steatorrhea as well… which I guess would be normal eating 250gr of fat a day to reach my 70% fat considering I would not sacrifice my 2gr per kg of protein to put mass. I know you follow Kiefer’s stuff so I’m pretty sure you noticed the study cited in CBL that saturated fat alters the cell medium so that it makes cell walls thicker, while PUFA make them more permeable to nutrients.

    Right now I’m in full reversal mode with CBL and feeling a lot better with just sticking to the saturated fat that comes naturally in food which IMHO is probably the quantity we should aim to, plus keeping an eye with hard cheese consumption. Rest is seafood for DHA/EPA and some olive oil, nuts and avocados trying to get a nice SFA/MUFA/PUFA ratio and not more than 1.5gr per my body weight of fat intake… that means that in order to be ketotic and achieve at least a 2:1 ratio with carbs+protein probably one would need to lower protein intake pretty much ad be slightly hypocaloric which in the end I think is what really suits ketosis (not so much a fat binge) so in the end maybe not the best of the ideas if you want to put on muscle mass. For the sedentary people? probably ok. If you want the cognitive super-powers and purposed longevity, then I guess it’s ok if not afraid by the microbiome assault some think it may be, etc etc…

    For me, I think that a cycling approach such that I cut on fat the days I go high carb and viceversa might be where I could stick to in the future and if not, well then maybe I’d just get rid of the ketogenic/VLC idea and just eat a balanced diet rich in vegetables and more or less lean meats and a lot of seafood with some fruit and that’s all.

    Sorry no very well elaborated but wouls take much time hehe, maybe you can get some insight from my N=1’s as I get from yours!

    • BJJ Caveman says:

      Wow! 8% to 15% is quite a bit! I imagine your clothes must’ve felt uncomfortable, especially with an almost doubling of body fat percentage!

      I wonder what the difference is between you and Sam Feltham… maybe gut biome related? But yeah, what a stark difference.

      I’m starting to lean towards your same conclusion as well. I think it’ll probably be better just to get my fat from food… and cut back on the amount of MCTs and Heavy Cream I’ve been taking… with a carb up day every 10-14 days.

      I really appreciate you sharing your N=1… it really did provide a good deal of insight..

      still shocked at the 8%-15% thing!

      • Albert says:

        Well, I still use the same clothes, the belt can handle the difference pretty well! hehe. In fact it is not very noticeable while I’m wearing clothes, I mean, I’m still overall fit, but it makes the the difference if I get naked, between having good vascularity, six pack and muscle separations or looking pretty fluffy, hidden abs and puffy nipples and love handles. It certainly sucks hehe.

        I think the difference between Sam and I is that I once was a fat kid with man boobs caused by everyday abuse of donuts and cheerios and thus I developed a great fat count that now is pretty difficult to handle. I’ve to eat very strictly 24/7 if I want to stay lean. If not, the worse areas like the fat around the nipples and the low handles ruin everything very easily, even at 12%BF.

        Someone that is naturally lean and has never been obese surely will have some easier time getting rid of the extra calories via uncoupling mechanisms since they might burn them as heat, I think better leptin/insulin sensitivity due to lowered fat cell count. Most people in the paleo sphere claim that T2DM can be “reversed” but if you think about it it’s more like that it can be somehow halted, but proof that it’s not really reversed is that you eat bad and you regain the weight again pretty fast… that does not happen to naturally lean people who don’t vary their weight too much by changing the way they eat.

        I must say that the N=1 was pretty hard on the low-carb diet because I started it being very far away from my comfort weight (I like to apply statistics in these cases, think about a gauss curve, if I tend to fall at naturally to 63 kg and 12.5% BF, getting to 61kg and 8% needs a lot of effort from my side, so anything that I do after that will push me again to the center very easily, typical yo-yo). But I did it on purpose because if the low-carb diet is so superior as many claim that you can eat all the fat you want with no carbs and don’t get fat, it should have worked in these case too. It clearly did not. I guess people that is all over the insulin hypothesis has overlooked some other agents like the ASP which will rise triglyceride storage even in the absence of sugar.

        Considering that in the past I eat a lot and mixed fat+carbs with even worse results, and that I could also get lean by cutting calories a lot both on a ketogenic and low-carb template as well as a high-carb (not that high in reality if you stay hypocaloric but still 60% of the macros, that’s why I prefer to refer to grams per bodyweight of something than just %’s, it can get very misleading) that seals the deal for me. It might not sound cool but in the end calories “somehow matter”. Do I think meal timing and other black magic can make a difference? Yes I do but not to such an extend that you can just forget of calories, at least if forgetting means getting to high.

        Well, no problem in the end. At least the paleo template allows to get all the essential nutrients packed in a reasonable amount of food so you can cut some calories without starving too much. So if you stay the rest of your life on track you can still do pretty well over time heheh.

        • BJJ Caveman says:

          Can you explain to me what ASP is and how it increases storage of triglycerides in the absence of sugar? It isn’t something I’ve run across before and would love to learn more about.

          I know what you mean about people that are naturally fat. I’m one of those people… when I lose weight… it’s soooo easy to put it back on, whether low carb or not.

          The BJJ Cavewife on the otherhand is one of those naturally lean people. Very hard for her to gain weight… and when she does put on some weight.. it just falls right off with minimal effort. I do envy her.

          • Hemming says:

            On the flipside of the resistance to weight gain is also (to me at least) a resistance to gain muscle and get stronger.
            I’ve never had a problem with weight or leaning out but I can’t gain 1kg/month (fat or muscle). One year ago I was 58kg (5’9″), today I’m 63kg and I would say it has required a very conscious effort from my side to get to here.
            When people at the gym tell me I should be 90kg due to my height I’m thinking it will take me a decade 🙂

          • BJJ Caveman says:

            I guess the grass is always greener… you, like my wife have trouble gaining weight… wish we could trade problem at least for a few months.

            If you had my metabolism.. you’d get chunky in no time!

          • Albert says:

            Sure! ASP stands for acylation stimulating protein and seems mimic what insulin does with glucose but with fats. I’m by no means an expert here, just your average biohacker hehe, but if I understood correctly it would be something like that.

            Here you have two free access papers I found on the subject if you want to have a look.

            This one is an oldie:

            Heck, I remember a very cool one describing all factors implicated in hunger and fat storage but I cannot find it, this other one has some more info:


            I try to keep track of all these articles on my blog database:

          • BJJ Caveman says:

            Excellent, I’ve saved these to my to-read list.. which is growing by the second! Too much to read! Not enough time!!

          • Hemming says:

            Oh yeah, don’t get me wrong. I would rather keep my metabolism.
            Its just interesting to see my dad, who does live a pretty healthy live I would say, but on the other never shies away from everything stays so lean and fit compared to so many his age.

  2. Hemming says:

    Good post, interesting points about the fatty acids metabolism. Do you know if any factors will affect the production of ketones vs. cholesterol (except ketones already present). Btw, you don’t need to be a women with anorexia to have your cholesterol go up – I experienced exactly that when I lost a lot of weight due to anorexia.

    • BJJ Caveman says:

      I’m not sure yet about the factors affecting production of ketones vs cholesterol. Reading this piece by Dr. Dayspring was my first introduction to that concept, so it’s something I definitely need to look into more deeply.

      It really is an interesting concept though…

      • Hemming says:

        Please share it if you find some references on how this works.

        One of the doctors who went over my tests during my anorexia wasn’t surprised to see my LDL go up to 155. Weight loss seems to be a factor (like Jimmy Moore experienced). The fun thing is that my brother who strength trains a lot also high LDL (not quite as high as me) and he was told by his doctor that its normal when training that much and gaining a little weight. My dad has always had even higher LDL so I think its more about familiar hypercholesteremia. I would be really curious to see my LDL after I’ve gained around 5kg since my last test.

        • BJJ Caveman says:

          Will do. It’s something I’m very curious about, so I plan to look into it more. Hopefully I’ll be able to find something of substance.

          It makes sense that weight loss would be associated with an increase in LDL… but what about when you’re not losing weight? Like in my case. Puzzling.

          It sounds like in your case there is a genetic component to it… however, was there ever a time in your life when it was very normal? Like when you were pre-keto?

          • Hemming says:

            Four years ago when I was (literally) running on carbs (real food though) my LDL was 125, if I remember correctly. Already back then I was told it was too high. My HDL was 65 and that has now increased to 96.

            I also think it runs in the family. Dad has tried various things to lower it including statins which he quickly stopped doing because it didn’t do him any good. His doctor has told him not to worry about it as he might not be able to lower it in any way and that it might not be harmful (I would like to see his trigs a little lower though).

            I would also like to see my LDL after I’ve gained weight (stupid expensive tests in Denmark). Have you heard Dr. Gundry’s ideas on genes and how different fats affect cholesterol?

            I really appreciate you post all this information on both your own experiments and the science. Its not many people who shares that much data.

          • BJJ Caveman says:

            Dr. Gundry spoke about it on the Body IO podcast, that I summarized here:


            The take home was that he recommends removal of dairy in some patients with high cholesterol and has seen it be effective.

          • Hemming says:

            Yeah, he has some interesting points. But regarding dairy he said its about what type of casein they carry. In Europe its mainly A2 which should be less of a problem. Additionally, I do eat dairy but not on a daily basis and not that much of it.

  3. Chris says:

    Does this accord with your own personal experience? From what I recall, the cholesterol seemed to be more a factor of being in ketosis rather than saturated fat intake, per se – although I could see it being different for different individuals. The thing is, it seems more likely to me that upping carbs is the healthier strategy to upping PUFAs, but I could be wrong.

    • BJJ Caveman says:

      I did to a trial before where I tried to cut back on my saturated fat intake (removing butter and coconut oil), despite remaining in ketosis, and it didn’t really have any effect on my LDL…

      But maybe it’s because I didn’t do it long enough? It was only for 3 weeks:

      In this article the woman did it for 6 months… so it may require a longer interval.

      I’m not sure what I’m going to do next.. but this article certainly did raise interesting questions.

  4. pillu says:

    Dear bjj i had exactly similiar prob as far as cholosterol is considered
    my reading one week before were TC 312 HDl 52 LDL 242 TG 82
    i was eating VLC and almost 120 gms saturated fat daily.
    Another observation is when this started my body has started Dawn phenomenon also
    earlier it was not there.
    So my question to u is What do i do now and how to tackle this prob
    shall i leave VLC and start normal diet

    • BJJ Caveman says:

      I’m afraid I’m not sure how to advise you since I don’t know what the heck I’m going to do with my own situation.

      Overall I still think eating low carb is good.

      The answer may lie in upping the carbs a bit… maybe in the 50-100 gm range. Low enough so that you’re only briefly entering ketosis here and there when exercise, or skip a meal here and there… but not low enough that you’re in deep ketosis all the time.


      cutting back saturated fats, and replacing those with polyunsaturated fats like olive oil…


      Statins (although I would probably consider this as a last option)


      Some other solution that we just haven’t come across yet. I have one other area that I plan to write a post about that may provide some answers…

      But yeah, I wish I had something concrete to recommend to you… but as I wrote in my review of Jimmy Moore’s Keto Clarity, there are a lot of people who go keto and experience this and get freaked out… and no one knows what the heck to make of it.

      We’re in uncharted territory. Most of Jimmy’s experts think that it’s probably not too worrisome if all the other inflammatory markers are good… but this article by Dr. Dayspring really calls that into question. So… who do we believe??

      • pillu says:

        I had very good explaination only at your blog
        lot of thanks for keeping us informed
        In my case CRP is negative reading i do not know what is that
        Some low carb advocates do not warn the people about consequences
        before low carb my thyroid was in range recently i did not check
        I think i will also up carbs along with olive oil & stop eating sat fat
        I was also in deep ketosis for almost two months
        pl help me in comimg out of this mess
        i think i would not entered into this low carb gamble and ketosis
        Art & science of low carb living not at all talking about this
        i have gone through it

        • BJJ Caveman says:

          CRP is an inflammatory marker. If it is elevated, that means you have an underlying systemic inflammatory reaction going on. So the lower the better.

          I agree that low carb advocates need to do a better job about warning people about these potential side effects rather than letting people get alarmed all on their own.

          I think it would be worthwhile to try upping the carbs for a month or so and then re-checking your cholesterol numbers just to see if that helps.

          You are correct, neither the art & science nor Jimmy’s books provide much information about this… but that’s because there isn’t much information out there… we’re on the cutting edge here.

          Best of luck.

      • Robert S says:

        I have a hard time with Dr. Dayspring because he works for pharmaceutical companies that make and sell statins and I believe that has an effect on what he says. It’s a shame because I do believe he’s the foremost expert on lipidology and such, but I find it hard to interpret his message due to what I perceive to be a conflict of interest. This is disclosed in Moore’s previous book, Cholesterol Clarity.

        • BJJ Caveman says:

          I can see where you are coming from… but at least for me it doesn’t take away from the fact that the information he provides MAY be helpful. I’m not ready to accept it as gospel yet, but I feel that it does give me a bit of direction as to where to look.

          I might try cutting back saturated fat intake more rigorously as the lady in the case did.. and recheck after a few months. I feel like this is a reasonable option.

          But at this point, I’m just trying to gather more information… and I do appreciate that Dr. Dayspring made his information free.

          I do still think that he is a bit too cavalier about recommending statins… so that will be an ultimate last resort if it ever comes down to it.

  5. Chris says:

    Hey, in case it’s useful, I just did an N=1 experiment. I’ve been in ketosis for several years now, but my total and LDL cholesterol went through the roof. For the last four weeks I’ve swapped out added sat fats for olive oil (while still eating normal amounts of red meat and dairy in meals), and both numbers came down to the top of “borderline.” No increase in carbs at all. I feel like I could probably make some adjustments to bring the numbers down further, but I’m encouraged they came down as far as they did even now. This post on Peter Attia’s blog was very encouraging:

  6. Norm says:

    Assuming you have quite a bit of body fat, I would say your fat intake is quite high and saturated fat intake is very high with 100g carbs. If your carbs are high glycemic then that’s worse. Dietary fat does promote insulin resistence and impair glucose tolerence ESPECIALLY in the presense of carbs and when there is quite a bit of body fat present

    Perhaps you are one of those who dont process fat very well and migh do well on moderate good quality carbs (vegetables, legumes) and MUFAs.

  7. Norm says:

    Sorry BJJ the above comment was in response to your blood tests.

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