Could Apo-E genotyping and alcohol be the key to my high LDL Cholesterol? An online anecdote

Cholesterol and Apo E

I’ve been trying to learn more about the relationship between low carb eating and a subsequent rise in both total cholesterol and LDL cholesterol and one of the more informative pieces I’ve come across was this  case discussion by Dr. Thomas Dayspring.

It’s important to note that while he’s a lipidologist with plenty of experience under his belt, the case discussion wasn’t a peer reviewed article or published in a journal.  There was also only one study that was cited which I’ve since downloaded and plan on reading.

While I definitely don’t know enough to say whether or not what he wrote is true, it definitely does give me some clues as to where to further investigate.

At this point I’m just trying to gather more information, so all I can do is keep digging around.

During one of my online excavations I came across, a blog written by a guy named Steve Kirsch.

From his self description he’s a lawyer, musician, crossfitter, and follower of the low carb primal/paleo template.  His profile picture shows that he’s a pretty fit guy.

He wrote two posts detailing his own experience with a new onset of high LDL cholesterol while eating low carb paleo and cutting out alcohol.

He’s a funny, engaging, and entertaining writer.  You can read the full posts here:  Part 1 and Part 2.

The Paleodrummer’s Cholesterol Experience

What I’ll be doing is similar to what I did for the Dr. Dayspring piece, summarizing and simplifying what Steve wrote for myself and sharing it with you:

Steve begins the blog by writing:

Ten days ago, I lost my mind just a little bit.

This was his reaction after seeing his NMR cholesterol panel showing that his LDL cholesterol went up 40% in just six months.  This included LDL-P, LDL-C, and small dense LDL-P.

After the initial panic he remembered that one big change he made in the prior 6 months was the removal of alcohol from his diet.

He also recalled a prior genetic test he did where he learned that his Apolipoprotein E genotype was Apo-E 2/3.  He goes more into the science of Apo E and the Mendelian heredity of it much better than I can, so go to his posts if you want to read more.

Steve then points to this study where they discover folks with an Apo-E 2 allele have significantly lower LDL cholesterol when they drink alcohol.

Using this information he added one alcoholic beverage back into his diet per day and did a followup exam four months later.  This time he found that he had completely reversed the 40% increase in all of his LDL numbers.

Every single one.  Without any increase in any of his inflammatory markers.

Does this apply to me?

In summary, Steve was eating low carb paleo, had great numbers, then he cut out alcohol and noticed six months later that his LDL numbers went crazy.  He then added one alcoholic beverage back into his diet per day and 4 months later his LDL numbers went back to normal [CORRECTION – Steve kindly chimed in in the comments section and added that his LDL didn’t quite go down to normal, but DID go back down to where it was before, which was still high].  The key for him was in his Apo-E genotype.

This is different from my situation because I don’t normally drink alcohol.  In fact I very rarely drink it and haven’t done so for the past 5 years or so.

When I turned 30 something changed in my body and I realized that I just couldn’t process alcohol like I did in my youth.  I jcan’t recover from nights out with the boys as fast as I used to.  In my 20s, if I went out Friday night, I’d pretty much be back to 100% Saturday afternoon.

Now if I go out Friday night with the boys, I’m pretty much destroyed the entire weekend.  Just a useless stinky mess that the poor BJJ Cavewife has to deal with.

So yeah… I now only imbibe on special occasions like weddings or when we visit places like Antarctica.

Not sure where I was going with this… except to say that alcohol isn’t really a part of my life at this moment and hasn’t been for a while, so I don’t think there’s a relationship in my situation between alcohol and my high cholesterol.

However, Steve’s experience does spark my curiosity into investigating Apo-E genotypes and how the various combinations of alleles affect serum cholesterol and the processing of saturated fat among other things (like risk for diabetes and dementia).

I’m also now curious as to what my Apo-E genotype is and am considering adding it to my next lab panel.

Wondering what Dr. Dayspring thinks about all this?

Me too!  So I took to twitter and asked him (technology really is amazing these days), and this is what he said:



There you go. Dr. Dayspring doesn’t think there’s anything to this… but I’m not convinced at this point and will continue to look into it!

27 Responses to Could Apo-E genotyping and alcohol be the key to my high LDL Cholesterol? An online anecdote

  1. Chris says:

    Have you seen Jimmy Moore’s latest blog post on his own personal numbers? His cholesterol has started to come down. He credits his dental work cleaning up infections. Given that he’s gained some weight, I wonder if it’s due to not being in such fierce ketosis as he had been. Or it could be both. As the ketosis rash, ulcers, and various mouth diseases all seem to be set off by a combination of infectious agents and dietary factors, it wouldn’t surprise me if high cholesterol could be similar. Maybe it comes down to gut biome somehow 😀

    • BJJ Caveman says:

      I have seen Jimmy’s latest numbers… and have been saving it for a future post.

      All I’ll say right now is that it’s important to know that he wasn’t in keto for a while AND had gained back a fair amount of weight at the time those numbers were drawn…

      I’ll write more on this later.

  2. raphi says:


    I’ll add my N=1.

    My LDL-P was very high (ApoB 2.27g/L & ApoA1 1.61g/L ) when my TC was ~10mmol/L as of 16/09/2013 after being LCHF for close to 2yrs. I don’t know where it’s at now but I’d like to know since my TC is back down to ~7.42mmol/L as of 20/08/2014.

    I nearly never drink alcohol since about 3yrs.

    PS: all my other lab values were pretty spectacular compared to the (albeit, terrible) norms/averages which made the high LDL-P all the more intriguing. I had carotid, abdominal and aorta scans and everything is flowing marvellously without traces of calcium where it shouldn’t be. So, LDL-P is an open can of worms…interesting.

    • BJJ Caveman says:

      I would always encourage checking your numbers at least once a year to see where you stand. You don’t need to do it as often as I do.. but once a year seems like a reasonable interval.

      Great that your carotid and aortic scans were all normal. That is fantastic news and would lend more credence to the idea that an elevated LDL-P alone isn’t that dangerous.

      Obtaining those scans may need to be the next step for me.

  3. Zach says:

    Hey BJJ, you have a great blog (I’m especially a fan of your n=1 disclosures). Hopefully you don’t mind me linking to a few cholesterol-related sources here. Given your clear interest and willingness to scour the various articles/publications/etc. available about this topic, I thought I might be able to provide you with a couple that maybe you haven’t seen yet and may be of help for you.

    First off, I’m not sure if you’ve run across the work of Dr. Steven Gundry? He’s certainly well credentialed and has a very interesting take on TC and other lipid markers (his BodyIO podcast was informative: Cliff notes: 1) Steven Gundry tests everyone for APOE4 and believes that a positive test contraindicates the inclusion of animal products as a primary source of nutrition in one’s diet (use olive oil, coconut oil, etc. as alternative fats). 2) Gundry sees “cheese eaters” (specifically A1 casein as the culprit) as often having high LDL-P and the elimination of cheese can reverse the issue. 3) Gundry believe ApoB is an outdated marker, and that elevated (even very elevated) TC/LDL is a non-issue in cases of low (systemic) inflammation.

    Also, from just a general “how does cholesterol work physiologically”, I found this video from WellnesFX to be exceedingly helpful (there are a few reference’s to WellnesFX’s own panels, but the vast majority of the video is a great lipid primer): . One of the interesting points from the video (paraphrased) “High ApoB with low LDL = higher risk of CVD/atherosclerosis than the combination of high ApoB and High LDL” (however low ApoB and high LDL would actually be your best scenario as this would indicate fewer particles but that the particles you do have are of the “fluffy” variety).

    Lastly, this (3 part) series from Chris Kresser/Chris Masterjohn is lengthy, but can potentially help those that are questioning the current lipid hypotheses and the transcripts are available to make searching of the information covered much more convenient than most other audio sources:

    Thanks for your great blog, and, again, I hope you don’t mind the outside source links (my intention is not to violate any of your policies!).

    • BJJ Caveman says:

      I love that you’re linking to other sources and completely welcome it. The only reason I can see people being hesitant about linking is for fear of spam… you should see all the spam comments I get with links for viagra, porn, jewelry, handbags, etc…

      but if the links are relevant than the more the better!

      I know of the Gundry interview you mentioned and summarized it here:

      I remember his final recommendation to Rocky, which Rocky has repeated a few times in subsequent podcasts was to try removing Dairy from the diet… which will also be one of the options I’ll be considering.

      Thanks for the WellnessFX video. I’ve saved it and have added it to my “to watch” list. So much to learn… so little time.
      I’m not sure I understand the High ApoB with low LDL thing… my understanding is that ApoB = amount of LDL particles. So if you have a high ApoB that means you have a lot of particles… but that’s as far as my understanding goes. I guess before commenting even further, I should just watch the video.

      I’ll take some time to scan through the Chris Kresser stuff too!

      Thanks a lot for the links!

      • Zach says:

        Great summaries of the BodyIO podcasts (I hadn’t seen the one you did for Dr. Gundry yet).

        Regarding the the LDL and ApoB issues, you are correct that ApoB is used to calculate the number of LDL particles. So, again, ideally one’s ApoB would be on the lower side. That said, why would you want your LDL (LDL-C) to be high if your ApoB is high? This is because LDL (LDL-C) is a calculation of of the (cholesterol) mass within the actual LDL particles. Higher mass should equate with bigger “fluffier” LDL particles. So if your particle count is high (high ApoB), you’ve got to hope that you have a lot of the big, fluffy LDL particles (high LDL-C), and fewer of the small, beady, atherogenic LDL particles (which would tend to equate to lower LDL-C).

        Here’s a citation for the differences between the differences between the types of LDL particles:

        I am by no means an expert on this material, but also have an academic interest in getting to the bottom of it.

        • BJJ Caveman says:

          Got it! Thanks for the PDF.

          It seems like most of it is in reference to the VAP test… or trying to calculate your risk with just LDL-C and Apo-B… whereas if you just get an NMR, you can measure directly what the LDL-P and Small LDL-P is.

          I think that’s why I decided to use the NMR for my tests… to cut out the middle man and get a look at my damn LDL-Ps directly.

          I’m not an expert at this stuff either and am doing my best to fumble through it all too! Let’s do our best to learn together. Keep sending me more stuff!

      • raphi says:

        Their is 1 Apolipoprotein B100 wrapping around every chylomicron, VLDL, LDL & IDL particle. When we are counting the “# of LDL particles” we are counting all of these. Take a look at this graph for a better understanding of size relations You can see that LDL is the smallest (volume-wise) of the ‘larger lipoproteins’ & is thus used as the cut-off particle when measuring “apolipoprotein #”.

        As explained by Dr.Dayspring, arteriosclerosis is a “gradient driven process” which some would take to indicate that the smaller the volume of the aforementioned class of particles, the steeper the gradient & thus the sooner/more likely you are to croak!

        Dr.Dayspring is correct in calling it a gradient driven process but he is incorrect (IMO) in his assessment of the importance of contributing variables (endothelial composition, coronary infiltration, glycoprotein matrix composition, cell membrane fluidity, inflammatory processes gone awry, micronutrient depleting repair/growth & the biomechanics involved in our CV system experiencing appropriate loading etc…for the last point, see: Katy Bowman “Move Your DNA”).

        @BJJ Cavemen,

        Gundry’s guess is as good as any (meaning, not that great unfortunately). Yes I think it’s a good idea to keep testing if you know what to do with it. Otherwise, the uninformed might go running back to tofu & whole-wheat bread. However, there are many other markers worth the same if not more attention (it’s a long list).

        On another topic – I can tell you that my stock in LDL-P is quite conservative as the sea of positive biological markers changing for the better even when it doesn’t speaks louder. I say this based on clinical data showing LDL-P outliers (like myself). It’s harder to accept we need to revisit our model in a way. Yet, it also clues us in as to what’s missing around this gradient driven process.

        • BJJ Caveman says:

          “I can tell you that my stock in LDL-P is quite conservative as the sea of positive biological markers changing for the better even when it doesn’t speaks louder. I say this based on clinical data showing LDL-P outliers (like myself). It’s harder to accept we need to revisit our model in a way. Yet, it also clues us in as to what’s missing around this gradient driven process.”

          Are you saying that you don’t put much stock in LDL-P numbers in the setting of everything else being normal/good? ie low inflammation, low fasting insulin, etc..

          • raphi says:

            What I mean to say is that context matters. Insulin & inflammation is a massive component of that context

            We have to consider the population in which the ‘gradient driven process’ was shown to occur in. Am I representative of that? We have to simplify risk profiles, but not too much – what other values are we trading on to lower LDL-P? Is what we’re doing evolutionarily concordant and if it isn’t, what specific data are you using to justify that?
            Furthermore, what genetic ‘assumptions’ are we making? People argue ApoE4’s should avoid cholesterol/sat. fat even > than non-E4s…this only makes sense in the fading light of an outdated lipid hypothesis of CVD. It really is not a viable theory any more. Statins are TERRIBLE drugs in terms of results & side-effects and this speaks directly to the value of that poorly supported theory. Disease requires less of the superfluous and more of the essentials: balanced omega3/6, protein/fat (the essential macronutrients) in the form of offal from meat/fish, plants as medicine as much as for food & CHO to maintain gut health etc..

            Although I respect Dr.Dayspring’s knowledge & extensive clinical experience, IMO he’s still taking a narrow view of health through mostly lipid numbers and isn’t doing a good enough job of addressing the glaring flaws in the statinization approach and consideration of other markers.
            Look at Ivor Cummins (@fatemeperor) the engineer. His approach to this issue is modern, it’s systems thinking. This is what is needed. This is what works. Classical medicine by subject specialization alone is outdated and (AFAIK) is pretty much still how the Daysprings of the world still operate.

            In the end it comes down to good science. Are you actively trying to disprove your theory or bolster it? The latter is by far the most common approach and it’s completely antithetical to sound scientific methodology.

            At I often clearly state my bias at the top of posts. I choose studies that seemingly contradict my bias because it allows me to both challenge my own beliefs & the science at hand. I think it is hard but also the most rewarding approach if you stick with it. I should say – my situation is easier/luckier than for most. I’m currently relatively unburdened by financial/legal variables & those things make good science much harder for health professionals – I don’t wish to downplay that.

          • BJJ Caveman says:

            I do agree that Dr. Dayspring is a bit cavalier about recommending Statin use, although I’m not quite ready to dismiss his other ideas, at least within the narrow focus of the that case… but I’ll be the first to admit that I’m quite ignorant and in the dark about this… so all I can do is keep my mind open to ideas.

            I found Cummin’s stuff through another site, and have added it to my to-read/to-watch list… so once I get around to it, I’ll probably be dedicating a post to it.

            You sound like you have a wonderful mind for this stuff, and a quick perusal of your site shows that you definitely know your stuff. Your latest post seems like it should be published in a journal!

          • raphi says:

            PS: this extract from “General Chemistry Principles, Patterns & Applications” (Ed. 1) may help clarify how I think about the competing arguments surrounding LDL-P:

            “Whereas a law states on WHAT happens, a THEORY attempts to explain WHY nature behaves as it does. Laws are unlikely to change greatly over time unless a major experimental error is discovered. In contrast, a theory, by definition, is incomplete and imperfect, evolving with time to explain new facts as they are discovered. The theory developed to explain the extinction of the dinosaurs, for example, is that Earth occasionally encounters small to medium-sized asteroids, and these encounters may have unfortunate implications for the continued existence of most species. This theory is by no means proven, but it is consistent with the bulk of evidence amassed to date”.

            The last sentence ==> cholesterol lowering by itself is healthful “is not consistent with the bulk of evidence amassed to date.” You can cut it how you want, that remains the case. So the question becomes, “what else should we look at not?” Not “how do we show this is the case?”.

          • BJJ Caveman says:

            “The last sentence ==> cholesterol lowering by itself is healthful “is not consistent with the bulk of evidence amassed to date.”

            While I agree with this statement.. I don’t think we can extrapolate this quite yet to state that “LDL-P and/or Small LDL-P lowering is not consistent with the bulk of evidence amassed to date…” because there currently is no ‘bulk of evidence amassed to date’ when it comes to sky rocketing LDL-Ps in the setting of a low carb diet.

  4. NRC says:

    I don’t know if it will be helpful (probably not) but Dr. Rhonda Patrick had some interesting comments regarding Apo E when she was a recent guest on the Joe Rogan podcast.

    • BJJ Caveman says:

      Thanks for pointing that out. I remember hearing that a while back.. I believe the gist was that certain Apo-E genotypes/phenotypes are more sensitive to saturated fat ingestion. Which is another reason I’m getting more curious about my own Apo-E status.

  5. Dale Seng says:

    Great information, but a question…what about the carbs in the alcoholic beverages?

    It would seem to me that alcohol can, and usually does, come with significant carbs. PD has a barleywine image on his blog (probably the most carby style of beer) and mentions that he likes red wine (more carby than white). It would seem to me that he’d need to switch to diet coke and rum or something to eliminate the confounding effect of the sugars in fermented beverages.

    I don’t need much of an excuse to have a beer, so I’m happy to see this might be linked. See, I’m the same as you Mr. Caveman, VLC results in high LDL, so “permission” to have a beer would be great! I already have a beer on my carb night every week.

    I don’t know about my Apo-E. After a peek at wikipedia, I didn’t see any SNP’s mentioned, so I guess that’s not something I can see in my 23andme.

    • BJJ Caveman says:

      I’m not sure about the carbs in alcoholic beverages…

      I myself am partial to Cabernet Savignon’s… and you can see that in one glass there’s less than 5 gm of carbs.

      I think there may be other sweeter types of wine, but I’m not a connoisseur, so can’t comment any futher… except to say that I’ve heard that the ‘dry wines’ are better because they have lower carbs. I wouldn’t know a ‘dry wine’ if it slapped me in the face so that doesn’t help me too much… but you may know more.

      I’ve also read somewhere that straight liquor, like pure alcohol, whiskey, or rum is better because of the low carbs. So maybe jack and diet coke or Vodka soda can be options?

      Fruity drinks with mixers (like sex on the beach, long island iced tea, adios MFer) are a no-no for sure though.

      Beer can also have around 13 gm of carbs per bottle… so that may screw things up.

      • Dale Seng says:

        I found out from 23andme (in the Alzheimer’s technical report) that I’m E3/E3 (like 57% of the people of European descent, see It appears as if I have the “neutral” allele, and this effect apparently only “works” for E2. So much for the excuse to drink beer. I’ll do it anyway!

    • Zach says:

      Dale, I credit Dr. Rhonda Patrick with deciphering this information, but given your 23andme test, you can do the following:

      1) Browse your “Raw Data” (or just download the file and search it
      2) The SNPs you care about for APOE are going to be
      a) rs429358
      b) rs7412

      The lookup table is (sorry for the formatting):

      rs429358 rs7412 APOE
      CC TT APOE1/E1
      CT TT APOE1/E2
      CT CT APOE1/E3
      CC CT APOE1/E4
      TT TT APOE2/E2
      TT CT APOE2/E3
      CT CT APOE2/E4
      TT CC APOE3/E3
      CT CC APOE3/E4
      CC CC APOE4/E4

      It should be noted however that 23andme’s method for calculating these APOE specific gene polymorphisms aren’t perfect, so the results will not be guaranteed, but that’s how you can use the 23andme results to determine your APOE status should you chose to do so!

  6. Ben G says:

    Good post again. I have been meaning to comment on your cholesteral post, since I have my own story. Early 2014 I started following Peter Attia and did get into ketosis briefly before I spent two week in Peru, which made ketosis unsustainable. A couple month after I got back start following BulletProof, including butter/mct in my coffee. Knowing was an unconventional approach, I had blood test at the beginning of this experiment. My numbers were similar to my previous test, infact they had been very consistent for the prior 5 years. My cholesterol had been gradually going up.
    LDL-d 190 HDL 63 cholesteral 271 ( this was up about 25pts)
    My CRP was elevated 7.07, which at the time I thought was due to a bactieral infect I got in the Amazon.
    Two months later
    LDL 244 HDL 47 cholesteral 330 CRP 0.5
    My AIC was unchanged at 5.5 but my Tsh rose from 2.35 to 3.6. It was 2.35 for the five years prior. Subsequently on a more rigorous test my LDL-P was >3500 ( it was outside the measurement range.)
    To try to get this resolved I I had a battery of test which all came back with no answer. I had a cartiod IMT which had a score of 0.611 which put me in the 20% (good). I also had a ct calcium scan which put my in the 30% (all of these percent are age based and I was 63 at the time.) Having drunk the koolaid I was commited to the low carb high fat approach. I spent the next 6 months trying to get my gut diagnosed and resolved. Believing that the cause of my elevated lipids was caused by underlying inflammation. Ultimately the gut test came back normal. So due to life circumstances I didn’t have any additional tests for 18 months. So May of this year I want back for tests. My lipid panels were unchanged, My tsh was unchanged my A1C was 4.9, my stress test was slightly inproved. My CIMT was unchanged although there were several plaques. My ct calcium score was in the 90% ( the bad 90). Needless This got my attention. Over the roughly 2 year period I experiment the coffee thing among others. I tried no butter only coconut or mct then cream and cocnut milk. I read Dr. Gundry’s book and listened to the podcast. the oly dairy I eat is goat cheese or goat yogurt (which seemed to have no effect.) Ultimately after looking at all the research I concluded that short to medium chain saturated fats raise cholesterol in what I will call res-ponders.
    I spent 6 weeks with only source of fat being of the mono or poly unsatured type with the execption of goad cheese and dark chocolate and one egg for breakfast. I ate only lean meat. During this time I also took a low dose statin and thyroid meds. My tsh fell back to 2.35 and my cholesterol fell to 106. Good new is I can lower my cholesteral, but this is below any reasonable target. I hate chicken breast and I also miss the fat in my coffee. The first week was worse for me than going into ketosis. I also use a paper filter for my coffee. For what it is worth I have no symptoms. In fact had I not had these lipid panels run I would never have changed, eating this way made me feel better than I had. I did not start this to loose weight, but to feel better. FIY didn’t drink much alcohol before and I don’t now (1-2 drinks per week)

    • BJJ Caveman says:

      Wow, it’s great that you obtained all the correlative imaging to go along with the lab test.

      It looks like it the drop in the A1C from 5.5 to 4.9 was a big change in the positive direction.

      I’m surprised that your CT calcium scan went from 30% to 90% in the span of 18 months… I mean.. holy cow. That really lends credence to the idea that a sky high LDL-P CAN in fact lead to worsened coronary risk!

      Although such a drastic change from 30% to 90% would lead me to suspect an error in the test… or the interpretation of the test. There may have been artifact in the imaging confounding the just a potential example.

      Did you happen to get a followup NMR and CRP during the second Calcium scan?

      With the changes that you made that lead to the improvement in TSH AND cholesterol, I wonder how much is attributable to the statin vs the change in diet vs the thyroid med.

      Are you going to get a followup Calcium scan? It would be interesting to see if your improved numbers corresponded to an improved scan.

      Thanks so much for sharing your information. I hope you will come back with any followups, since I know there are a lot of people out there, myself included, that really want to learn more about this.

      • BenG says:

        I should make a couple things clear since they may not have been in my post. The change in my ct scan from 30% to 90% was a population ranking. My actual score which is the area of plaque detected in a 2d scan (as I understand it) increased by 3x so it was a significant change. I would have questioned the data, but my cimt showed the addiontion of several plaques. I have had my CRP tested regularly and it will be 0.5 one test and 6 or seven the next, I have not been able to determine the cause. I will probably have the calcium score after I have had my numbers stabilize for several months. The ct scan has limitations, but without symptoms it is hard to get an angiogram. I started committed treating the problem not the symptom, but so far it has been elusive. According to “Theraputic Lipodolgy” my APOE type is the norm and does not dispose me to abnormal cholesteral problems. My diet is low carb paleoish, pastured pork, grass fed beef, pastured eggs, organic veggies. I ate sardines for lunch for 2 years, and my blood omega 3-6 ratio was slightly greater than on ( more 3 than 6.) I am assuming that the thyroid meds caused my TSH to fall, although in my last test, acouple of weeks ago it was back up. I do know that thyroid meds should be taken with out other food since many things reduce the absorption, I may have gotten a little careless, I am being more careful now. The plan is to get a basic lipid panel about every 8 weeks until the numbers are stable. In the mean time I am going on a bike trip across the south Island of New Zeland in a couple days

        • BJJ Caveman says:

          A 3x change in amount of calcium is pretty scary! Especially considering that it seemed like you were doing everything right.

          Your CRP related changes are strange however… and may indicate the presence of some other underlying inflammatory process that waxes and wanes.

          Enjoy your bike trip!

          Please keep us updated on your followups!

  7. raphi says:

    Thanks for the compliment – much appreciated. It was an essay I wrote for my Msc Molecular Biology that earned me a good grade so I thought, why not put it up?

    I am not saying LDL-P lowering isn’t a fine target.
    I am saying though, that achieving this as a function a cholesterol lowering (aka HMG-CoA inhibition) is nearly nonsensical considering the “bulk of evidence amassed to date”. Hence my insistence on asking better questions. To take an extreme analogy, cholesterol lowering therapies for the most part are akin to arguing that someone should lose weight by cutting limbs off..’no bueno’ as Dr.Lagakos says. Too much downside. Read up on HMG-CoA reductase and tell me if you want a spanner in those works hehe!

    Cummins is fantastic – to be followed closely. His systems approach is what better modern medicine is evolving towards.

    Dayspring is encyclopaedic in his knowledge. But how you apply that is ultimately what counts. His statinization approach doesn’t do his intellect justice (in my non-medically trained opinion).

    You should follow computer scientist Dr.Seneff of MIT ( as well. She’s taking the best researchers in the biomedical field to task and is doing so in a very convincing way so far…

    PS: My next posts will be about ketosis and high-intensity performance. your N=1 might be a nice contribution. My bias is that ketosis &/or a FFA oxidative metabolisms in humans – aka fat adapted ones – are fine for such activities…BUT, the modern context appears to make this easier with HC diets. The question I’m interested in is, WHY??

  8. Steve Kirsch says:

    Hey man, thanks for checking out (and enjoying) my APOE-related posts. I don’t know why Dr. Dayspring is dismissing the alcohol link to LDL-p numbers (both positive (APOE2s) and negative (APOE4s)). That Framingham study that I cite in my blog posts is pretty well-respected. And my own N=1 experiment was, for me, pretty dramatic.

    But I wanted to clear one thing up for you. My LDL-p as of my last test (late May) was not back down to “normal.” It just went back to where it was, which is still kinda high (1700), just not wacky (2500). Wacky is where it went with six months of no-alcohol.

    So, actually, since May I have been trying a new experiment. I still have a drink a day — usually whiskey, sometimes red wine — but I am trying to dial down the added fat in my life. I’m now eating what I’ll call “normal” paleo, but ditching all the “extra” fat, like butter/MCT-oil in my coffee, tons of coconut milk, etc. I still eat fatty cuts of well-raised animals, but I’m not going nutty on the added fat. Sometime in early Dec, I am going to get bloodwork done again, so we’ll see how that goes. A blog post will surely follow…. Thanks again for reading.

    • BJJ Caveman says:

      Thanks for chiming in! I added in the correction.

      I’d love to see your followup results!

      As I’ve mentioned already in this post, I really enjoy your writing!

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