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Aug 08

Cholesterol Code – Part V : More Fat, Less Cholesterol… to The Second Power

For the short version with pictures, see below. For the long version, read on after…

image

The Plan

A couple months ago I started talking to my sister about taking my data to the next level. But to do so, I’d need someone else’s help — to which she immediately volunteered. (Side note: my sister is uberawesome!)

In fact, my sister was perfect for what I wanted to test specifically. While her cholesterol numbers went up after going low carb last year, they didn’t rise nearly as much as mine. In fact, both her LDL-C and LDL-P were generally half of mine. Thus, we would have different starting points on our cholesterol when we ate, which is the goal.

Light Diet Day

Light Diet Day

I then started planning all our meals to be similar to my prior March week-long solo test. There would be the same day-by-day blood tests during one week. Only this time we’d add one test for the Friday before the week, and the trailing Monday that followed it, seven blood draws in all, each was an the advanced cholesterol test, NMR (Nuclear Magnetic Resonance).

Once started, we had to eat the same food at exactly the same time, no exceptions. Both of us had to take pictures of everything we ate, along with weighing them when possible. Half of the time she was in her state, then flew to me in my state where I’d then on prep, weigh, and cook our duel meals personally.

Generally, I tried to keep our food mostly home-prepared and stay away from processed or fast food. But both before the meal plan and following we ate out a little more. Also, my sister likes Zipfizzes, so we agreed to have one a day through the planned days as well.

Heavy Diet Day

Heavy Diet Day

Overall, the plan worked beautifully! My sister stayed religious to the diet and timing and we didn’t have any sudden surprises that thew us off the rails. I have a few fun stories that I’ll save for in person talks later.

The Comparative Data

Beyond the Total Cholesterol hook above, it’s worth looking closely at the other markers as well.

Our LDL-C was an impressive 88.9% correlative with each other! Did I put only one exclamation mark there? I meant three — 88.9% correlative!!!

image

And here’s a relative comparison to really see the match up:

image

This was especially relevant to me given my general theory encompasses energy trafficking as being the primary driver of these LDL cholesterol payloads. If I’m losing you here a little, don’t worry, I’ll cover this in a future post.

Like my own data before this, HDL doesn’t often move too much, but typically tracks with three day dietary fat in a positive correlation. More fat, more HDL. Between the two of us, we correlated a solid 71%.

ID_HDL-C

This next piece of data is extremely relevant to me (which I’ll get into in the theory post). It also tends to have a high standard deviation relative to the other markers from my past tests. However — in this case it was remarkably close in comparison to each other’s at a 77%. Incredible!

ID_TRIGS

So here is where things get interesting. On both LDL-P and Small LDL-P, Darla and I track very closely with the exception of the very last data point (7/18). In fact, the metric is so off course as to be suspicious to me. Up to that test, we had been eating everything identically as with the others, so what happened?

I’m loathe to suggest a lab error, especially since the non-P metrics appear to line up correctly. But unfortunately, there’s no easy way to find out as I have no direct contact with the lab (as it should be). For now, I’ll list both the complete results and what the correlation is without it and you can judge for yourself.

ID_LDL-P

ID_smLDL-P

It’s hard to quantify in words how happy I am that we captured this data and confirmed the previous patterns I’ve observed to this point. Our next steps will a new N, Nicole Recine, a Ketogenic Practitioner who has graciously accepted being our #3. We’re currently in the planning phase and hope to set up the next capture in the coming weeks.

I couldn’t end this article without given a very sizable thanks to my sister, Darla, and her contribution to this science.

39 comments

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  1. Bill Robinson

    Might 7/18 be hormonal?
    Great work (three exclamation marks here)

    1. Dave

      Thanks, Bill

      I’m skeptical if 7/18 was hormonal because of the drop off not matching the other baseline numbers. Why correlate with all the other data points regarding cargo, then diverge on the total boats against the formula?

      Of course, I naturally thought to myself, “man, if only we had done TWO weeks of the experiment.” This is a truly masochistic thought, btw, as it is actually very difficult to do even one week of those experiments.

      1. jan

        It would be interesting to know at what point in the cycle your sister was, because I’m speculating that it could indeed be hormonal (unless you also ovulate???;o).

        Isn’t that why most such studies are traditionally conducted with men, because then the whole “ovulation thing” doesn’t skew the data?

        So in your next trial with two women, I think it would be important to track their cycles to see if that has any effect. It may be possible to time the experiment so that neither will ovulate nor menstruate during the week of testing, or you may simply want to see what happens if either occurs during that trial. But to ignore those hormonal events is skipping a potentially significant confounder.

        1. Dave

          My sister is postmenopausal, but your theory is indeed interesting. I too would be interested in how much the present hormonal balance would play a part.

  2. Wenchypoo

    I just got through listening to your podcast with Jimmy Moore, and wrote to say I had my own inverse episode with fat and cholesterol. Only doing NMRs yearly (with the physical),, I noticed that over the last 3 years (starting with 2016 and going backward), my LDL-C, LDL-P, VLDL, and trigs all went down when I started using a combination of fats (MCT, butter, coconut oil, lard, and avocado oil) made into fat bombs for cooking and blended into my salad oil. HDL rose from 70 to 99.

    When I quit using this mix of fats, my NMR went to hell in a handbasket–my doctor (who THINKS I’m taking Crestor) wanted me to double the dosage. Instead of taking a statin, I just went back to my mix of fats. She wants to see me again in September for a cholesterol check, so it should be good (in her eyes).

    My recommendation: eat ALL the fat–blend your sources to make fat bombs for cooking, and/or using the blend in your homemade salad dressing. Blend your chain lengths, and blend your UFAs and SFAs, keeping to the heat-stable ones for the cooking, and going nuts in the salad dressing (such as red palm oil).

    Speaking of red palm oil, I recently read that it is supposed to lower LDL–I’m going to try an N=1 on this when my ordered bottle comes in Saturday. This oil will be used as a capsule, as my “cooking” fat bombs have already been made, and the salad dressing dressing already made (a full quart). If my September results show improvement, then I will add the red palm oil to the salad dressing fat lineup.

    I WILL NOT STOP EATING FAT JUST BECAUSE MY DOCTOR FREAKS OUT ABOUT AN OUT-DATED AND WRONG INDICATOR!!!

    1. Dave

      Hi Wenchypoo–

      I’m incline to think the higher content of fat you were mixing in with your diet pre-test probably had the same impact as my intentional outliers => lowering your score.

      But I wouldn’t be surprised if it wasn’t the specific fats themselves, just the higher total amount. My data suggests the body is downregulating VLDL (liver LDL) in response to more incoming Chylomicrons (gut LDL which expires after fasting time before test).

  3. Tim H

    My experience has been of my cholesterol increasing as the percentage of fat in my diet increased but over 3 years, not a few days. My recent total cholesterol is 323, LDL 238 and HDL 89 following a diet of around 85% fat calories, 2 or 3% carbs. The high cholesterol has not worried me unduly given research such as Ravnskov U, Diamond DM, Hama R, et al. Lack of an association or an
    inverse association between low-density-lipoprotein cholesterol and mortality in the elderly: a systematic review. BMJ Open 2016;6:e010401. doi:10.1136/bmjopen-2015-010401.

    What has made me curious, however, is my GGT (gamma glutamyl transferase) numbers. Eating 70% fat (coconut oil, butter, palm oil) it was 13 U/I in 2013. Eating 85% fat (lard, coconut oil, butter) it has become 44 U/I in 2016. Can anyone shed light on this?

    Rising GGT is normally associated with liver damage from alcohol (I manage a glass or two of wine in an entire month) or carbohydrate but I’m eating 2% carbs! Inflammation? Nope, my hsCRP is 0.872 mg/L! Both 2013 and 2016 GGT numbers are within reference range but at opposite ends. Why? Any ideas are welcome.

    1. Dave

      Hi Tim H,

      I realize this is going to sound odd coming from me, but I don’t react to reference ranges quite as easily as my doctors do. There’s a term I use frequently now, “Bold Face Text Medicine” — in that a doctor comes to the room with your labs in hand putting all his/her attention on the text in bold face that came outside the reference range. They then prescribe medicine to change that number almost as though it were a mundane game of Match the Medicine to the Symptom. (I’ve really lost a lot of respect for medicine in the last couple years)

      I’m not as familiar with the GGT to give much helpful feedback, but I’d encourage you to find out where the reference ranges ultimately originate from. Is it a series of studies? (Usually true) A group of specialists giving opinion? How new is this measurement?

      And it should go without saying that being fat-adapted changes the equation on a lot of “normal” data. So bear in mind the likely context that may or may not be baked into the data.

  4. Ela

    Hi Dave!

    Thank you so much for doing all this work and laying it out like this. I listened to your conversation with Jimmy Moore, and I’m struck by how much sense your picture makes (and how it vitiates many mainstream medical assumptions).

    I wanted to share some information that I think underscores the truth of your inverse correlation. I have a background history of extreme anorexia, probably developed to control my bipolar disorder, so I’m much happier now on a ketogenic diet (on the theory, which is borne out for me, that bipolar is a seizure disorder that responds to starvation, or keto).
    It turns out (perhaps you knew this) that people with a history of starvation often have high cholesterol. The last time I had my cholesterol checked before starting in a keto direction, my numbers were scary high. Over 400 total, and HDL and trig higher than I’d have liked but not terrible. At the time, I wasn’t eating much period, and certainly not much fat.

    Next time I had it taken, I was figuring out my ketogenic plan, was eating a lot of fat (especially coconut oil), more food in general, and my total cholesterol had dropped by 150 points; trig and HDL were fine.

    Obviously this is a very incomplete encapsulation compared to the work you’re doing, but it seems to correlate well with what you’re saying about the inverse relationship.

    Thanks again!
    Ela

    1. Dave

      Hi Ela-

      Yes, I was aware anorexia increases cholesterol — there are a few studies on the subject and of course the body is trying to mobilize what adipose tissue (body fat) it has for necessary energy supply.

      Thank you for your contribution and cheers for overcoming the disease!

  5. Nick

    Awesome stuff! But surely this can’t be “new science”. can it? You mention going to Vail, so did you talk to any doctors/researchers that had seen this type of data?

    Also, I noticed someone pointed you to Ken Sikaris’ excellent video (actually he’s done two that talk about hyper-responders) and since you went to Vail you no doubt saw Dr. Sarah Hallberg’s presentation on this (for those who haven’t seen it https://www.youtube.com/watch?v=w8jUmCe3zDs&list=PLrVWtWmYRR2BYjk-oQTlAtGCjnly3J7LB&index=5).

    Are there any other videos on this you’d recommend?

    Cheers,
    Nick.

    1. Dave

      Hi Nick-

      Yes, there are a number of videos that are mostly about cholesterol and will have a mention or two that covers hyperresponders. For example, Peter Attia’s excellent “Straight Dope on Cholesterol” lecture — https://www.youtube.com/watch?v=dAWdHYSrh7M, you can fastforward to around 36:00 and he discusses this briefly.

      Here’s the thing — I’m pretty sure this is new science, which is too bad, actually. There are at least a dozen key moments in the last couple decades where I believe medical studies should have undertaken what I’m doing now, only on a large scale. But in the course of trying to research this, the engineer in me said something like, “okay, forget this, I’ll jump in the trenches and expose the data I find for the next generation of hyperresponders so there’s at least there’s somewhere to start.”

      The irony is that I’m finding out a lot more than I thought I would in a pretty short time. I’ll be posting my general lipid network theory pretty soon, but it couldn’t have been possible without all this testing. There really is a lot to be said for just getting your hands dirty (or in this case, your blood drawn). 🙂

      1. Nick

        Thanks, but yes, Ken Sikaris’ videos were a more recent version of the same thing as Peter Attia’s: we’re outliers and there’s no data to suggest what we should do.

        The fact that it hasn’t been studied is both astounding and – of course – to be expected. ; – )

        What I’m really hoping for from Sarah’s clinical trials is perhaps some genetic association, though I don’t know if she’ll be testing for that, which combined with NMR data might then give some suggestion as to which path to follow. Using the minimum daily dose of carbs that restores a relatively normal lipid profile is what I’m choosing for now.

        Anyway, looking forward to your next update!

  6. Bosse

    Is it possible to get day-by-day data on dietary fat for the three day averages.

    Fyi it’s not really correct to use averages for this kind of data. Especially without presenting deviation.

    Also what’s going on at 7/15?

    1. Dave

      – Sure, you can friend me on MyFitnessPal (DaveKeto) which has about 9 months of my diet. I’ll soon be open sourcing my spreadsheet for macros too, which will make it easier to analyze.

      – “not really correct…”? Please explain.

      – Not sure what you’re asking with 7/15. Can you elaborate?

      1. Bosse

        The inverse correlation disappears on 7/15.

        1. Dave

          A correlation is determined by comparing two series of numbers. When you say the ‘inverse correlation disappears on 7/15″ — it seems to suggest the 7/15 data point is an outlier to the extent of nullifying the correlation. But if that is what you mean, this isn’t the case as the inverse correlations above include 7/15 in their mutual series and still show the inversion (where applicable, like LDL).

          1. Bosse

            I mean correlation to average fat.

          2. Dave

            I still don’t know what you’re referring to. Inverse correlation is present when including 7/15 average fat.

      2. Bosse

        Averages are used for data with normal distribution.

        1. Dave

          Sure, but that’s just one of many uses for the (arithmetic mean) average with data modeling.

  7. Eric

    Look at doctor pandas work on time restricted feeding. The Salk institute has a free app to track time a d photo food intake. Eric

  8. Dr. I

    I am a 47 yr. old Family Physician, following initially a low carb, high protein, and low fat diet, now following a low carb, mod protein, high fat diet. I have lost 25 pounds to bring my body fat to 8 – 9 % and am as fit as ever. I have seen my Chol, HDL, HDL-P, LDL, LDL-P and LDL Size to increase significantly while my TG, TG/HDL ratio, small LDL-P to decrease significantly. I have read all of Peter Attia’s info and Ivor’s posts and video’s. Currently my HDL, TG, TG/HDL ratio, HDL-P, small LDL-P, LDL Size, and LP IR are as good as they have ever had measured but my LDL is exceedingly high at 292 and the Chol 385! HDL 80, TG 60.

    I have read Taubs, Teicholz, Cholesterol Clarity, and Dr. Fung, and Dr. Gerber’s info. At this point my LDL makes my doctor, who is one of my partners, lose sleep but I am unconvinced the meaning of this outweighs my incredible HDL, TG, and TG/HDL ratio. Given the very high number needed to treat for statins to prevent one nonfatal MI for primary prevention and their side effects, I’m so far not treating the LDL.

    In high responders such as us, is there any good data on the association of isolated elevated LDL-p with development of CAD? The mixture of indicators is confusing. Surely an HDL of 80 and a TG/HDL ratio of 0.75 can’t be incredibly good on the one hand while also having a really bad LDL-P. Which is more predictive? Does anyone even know?

    Thanks for your very interesting observations and contributions to the discussion.

    1. Dave

      Hi Dr. I

      Your numbers are almost identical to mine. My TC averages around 380 and my LDL to 270.

      My short answer is no — I haven’t found data to my satisfaction that demonstrates LDLp is an independent driver of atherosclerosis while controlling for endothelial damage/disfunction, oxidative stress (ROS), and/or inflammation.

      A lipidologist would likely counter my requirement from above by saying it is too difficult to control for those factors given how hard they are to measure effectively. (Whereas blood tests for cholesterol are EASY to measure) But this doesn’t excuse the fact that we know all three of the above have been very powerful drivers of atherosclerosis.

      I also have an extreme dislike for “studies” that rely on diet recall from the participants. I track literally every single thing I eat (not only logging, but taking a picture of it with my iPhone) since Nov of last year and I’m still pretty sure I have a 15% error rate. And believe me, it pretty much feels like a part time job! Throughout that time, I find I often look up many things I thought to be of certain weights or nutrients before eating them only to be shocked at how wrong my presumption was. So as you can imagine, when I’m presented with a study where others are filling out a form to estimate what they ate over the last six months, I’m highly skeptical of their accuracy.

      There are a number of other things to this that I’ll be putting in blog post I plan to have up soon. But overall, I haven’t yet found anything that has convinced me of the LDLp concentration theory. This isn’t to say I’m drinking the low carb community Kool Aid and assuming everything is fine, I may very well find my CIMT and CAC scores in five years jump, in which case I’ll be sharing that here as well.

  9. Nancy

    So I went high fat and my LDL cholesterol shot through the roof, similar to your experience. I’ve read all your posts and listened to your interview with Jimmy Moore. It’s interesting data but I’m not sure how to apply this for my situation. My questions:

    1) How dangerous is very high LDL?
    2) Do we need to treat this with diet and statins?
    3) If not dangerous, can you point me to further reading?

    For now, I’ve cut back on fat, especially saturated fat, have added a statin and have started using olive oil as my oil of choice. Thanks in advance.

    Nancy

    1. Bill Robinson

      A woman taking a statin?

      Why?

    2. Dave

      Hi Nancy–

      1) Short answer is — we don’t know. I’ll have a post later on why I have a problem with almost *every* study regarding LDL-C and LDL-P.

      2) I don’t yet accept the premise that it needs to be treated as I’m not convinced it is a net negative. If I were to be convinced it were, I’d first try to fix through diet before medication. (And statins would be one of the very last things I’d do, given the research I’ve worked through so far.)

      3) In particular, I find a lot of the more recent research shows a fairly clear distinction for women with higher cholesterol = lower all cause mortality. With men there’s either more ambiguity or a “U” shape curve. Two of the largest recent studies are the Ibaraki Prefecture
      Health Study (91,219) Norwegian HUNT study (52,087).

      Key lines from the Japan study:
      “Overall, an inverse trend is found between all-cause mortality and total (or low density lipoprotein [LDL]) cholesterol levels: mortality is highest in the lowest cholesterol group without exception. If limited to elderly people, this trend is universal. As discussed in Section 2, elderly people with the highest cholesterol levels have the highest survival rates irrespective of where they live in the world.”
      http://www.karger.com/Article/Pdf/381654

      Key lines from Norwegian study:
      “Among women, cholesterol had an inverse association with all-cause mortality [hazard ratio (HR): 0.94; 95%”
      http://www.ncbi.nlm.nih.gov/pubmed/21951982

      Not that I’m a fan of taking one or two studies and making them the only thing that matters. But that said, the most relevant one to me is the hospital admittance study that’s definitely made the rounds in the low carb community. I like it because it’s far less selective, very large in sample size, and had researchers that were actually looking for the opposite result.
      http://dietheartpublishing.com/Cholesterol/10/09

  10. IanA

    Really appreciate the work you are doing and yes, I have readings like yours (when converted into Aussie units). So many unanswered questions in this area.

    1. Dave

      Hi Ian–

      Thanks! I have a very time consuming business, which has had me pretty occupied as of late. But I hope to have much more to post soon.

  11. Tim F

    Hi Dave.

    Thanks very much for your efforts, they are incredible and really appreciated.

    I am very much looking forward to your lipoprotein system theory.

    In particular I will be looking for the following question answered:

    If dietary fat is inversely related to LDL-C/LDL-P cholesterol on a relatively short term basis is there anything that would explain the very large rise in cholesterol on a long term basis for us LCHF hyperresponders, which is a sizeable group. IE if fat is supplying 65-75% of energy needs why does the body need such higher cholesterol and why in only some people.

    I am thinking since chylomicrons are relatively short lived maybe the extra cholesterol is needed for trafficking lipids around the body and the cholesterol is mainly along for the ride (ie more efficiency means more activity).

    Alternatively when insulin levels drop and fat can be manipulated more efficiently maybe the higher cholesterol numbers reflect cholesterol coming out of the body, not being ingested with diet or produced endogenously. This would seem to be supported by evidence that cholesterol numbers do stabilize over time.

    Whatever, really looking forward to your theory.

    Congratulations again on a job well done.

    1. Dave

      – Thanks!

      – Yes, I believe for many of us the long term LDL-C and LDL-P increases on a low carb diet. I often refer to this as “The Baseline” given it is a kind of starting point, and is seemingly very static given my behavior pattern (though I’ve always suspected exercise would impact this and am currently testing this now). “The Inversion” is the ups and downs above the baseline that I’m manipulating with my diet. So why does the baseline go up for some and not others? I don’t fully know that answer yet, but as I say repeatedly, it doesn’t surprise me as a general principle given we are trafficking more fat.

      Okay, so with all of that said, here’s where I want to point out cholesterol is the red herring. It isn’t that the body is SPECIFICALLY upregulating cholesterol, it just has more of them in play because they come standard with LDL particles. Your body will not make an ApoB containing lipoprotein that doesn’t include both triglycerides and cholesterol (as well as some other components). This is actually the genius of the human body because it pretty much packages all hydrophobic elements it wants in the bloodstream for various reasons to use the same container.

      So paying attention to the cholesterol count is like counting the life rafts on boats. Seeing a lot of life rafts doesn’t mean there’s a problem, it just means there’s a lot of boats with a whole lot of life rafts. What IS a problem is seeing the life rafts being used — THAT is the real signal of a problem. Otherwise the boats are being used for their primary purpose: to move around people and cargo, and the life rafts are there in case of emergency. (Hope that analogy helps)

  12. Richard B Arnesen

    Hi Dave,

    So glad I stumbled across this site. So much information! Also thanks for the link to the APOE4 forum (I am 3/4). Still not sure what the answer is but it is great to be part of the discussion. I’ve been LCHF for several years and keto off and on but in January of this year decided to get into keto again. I also finally convinced my doctor to give me the NMR test in March. Not great news as you would expect for a 3/4 (which i found about in February of this year). LDL-P was 1916, LDL-C was 140, HDL was 48, Trig 81, TC 204, Small LDL was 919. These all freaked me out a bit but now i have a better understanding. I’ve cut down on sat fat, a bit, and dairy, and I also started regularly IFing (basically not eating except for coffee with MCT and sometimes grassfed butter until 2pm or so). I just got retested Thursday and will have the results next week. Anyway, i am glad to hear you are going to do some experimenting with fasting and blood work. I will be very interested to see those results. Also, i am wondering if you have thought about doing some experiments with different types of fat? Seems like most people are saying that APOE4 types should replace most sat fat with MUFA.

    Thanks!

  13. Dave

    Hi Richard-

    – Thanks! One of the very first reasons I wanted to start a site is for others like me who saw their cholesterol spike on LCHF and wanted to understood what it means.

    – I wish I could say more about your numbers, but I feel so much depends on existing diet. FWIW, I do believe that having higher carbs proportionally to fat would likely reduce my LDL — though I think it would likewise reduce my HDL. But I’m not convinced this is a good thing on net, and I mainly care about my All Cause Mortality. (I’ll have a post that breaks this out more in the near future.)

    Something I never feel I can drive home enough is that you are *literally* getting your energy primarily from fat when you are fat-adapted — and that fat is carried in the bloodstream by your LDL particles. Yes, some get converted to ketones, but the majority get *trafficked* as triglycerides in LDLs, so having a higher count doesn’t surprise me too much given the new metabolic pathway. The question that matters to me more is inflammation.

    – I actually did do one experiment where I specifically dropped SF to 25g while upping MUSF and PUSF way up to see what difference it made. (Lots and lots of avocados!) I think this is datapoint number 7 and it was for a total of 11 days. Overall it had little impact, and frankly, I just felt awful. I’m pretty sure my body craves saturated fat in particular as when I went off the experiment and came back, I felt a burst of both energy and joy!

  14. Richard B Arnesen

    Thanks Dave!

    I will post my new numbers next week when get them. I too like my sat fat, and substantially all of it comes from pastured/grass fed sources. I just get a little freaked out being a 3/4 when i hear several sources (Steve Gundry and others) talk about eliminating most sat fat for 3/4 and 4/4s. I recently replaced bacon with sardines and salmon with my afternoon “breakfast”.

    Regarding my numbers the thing i am most concerned about is the small LDL. Of course your experiments call in to question the relative importance of all the lipid markers. I mean, if they are that variable and “agile” what good is it to get a once a year test etc. I cant help but wonder what Peter Attia and others in this space would say about your experiments.

    I guess after reading all that i have read (and I do not have a science or engineering background) my hope is that the answer is keep BG, Insulin, and inflammation markers low and don’t worry about the rest. It would be nice to have an answer on whether or not to be in ketosis. I get that it is likely my lipid numbers may improve if i went to say, 100-150 grams of good quality carbs, but is that necessarily a good thing given that the carbs could affect by BG, Insulin and inflammation..

  15. Richard B Arnesen

    New numbers from 10/27/16
    TC: 267
    LDL-P: 2069
    Small LDL-p: 1028
    HDL C: 56
    TRIG: 101
    hsCRP: 0.3
    Ha1C: 5%

    So my HDL went up from 48 to 56 which is great, and my hsCRP is low. All the other numbers stayed the same or went up marginally. I should also point out that my BG which i check frequently, is almost always between 75-90 and my ketones are usually 1.0 – 3.5. Generally i feel good, I workout often and have bodyfat of around 10%. I think my step would be a CAC scan. My doctor of course wants to put me on a statin. For most of my life (i’m 51), my Total C has been below 200 and LDL-C has been low but those early tests were not NMR so i don’t have anything to compare to.

    1. Dave

      Hi again, Richard —

      I’ve noticed some patterns with LDL-P and in particular, smLDL-P that are anecdotal, but still very much worth investigating.

      In general, I keep coming across athletic Keto-ers who have higher levels of smLDL-P. A prominent blogger I was first reading (and who you are likely already familiar with) is BJJCaveman. He too has high smLDL-P. I have likewise had a few conversations with Ketogainers who were very lean and muscular that had NMRs and saw higher smLDL-P.

      Given my general theory, this actually makes sense metabolically. Your body is very insistent on mobilizing Trigs via LDLs in anticipation of energy demands you keep putting on it. And you indeed USE those trigs, depleting their LDL carriers to potentially top off cells exhausted of their energy supply, making it more likely that your LDLs will be likewise smaller.

      So here’s the cool thing — since I personally will be doing much more resistance training soon, I’ll have some very strong baselines to compare the results to. If my smLDL-P climbs out of the <90 it is usually in, that would be a strong sign this is really in play.

  16. Richard B Arnesen

    Thanks again Dave! It is very frustrating not knowing what direction to go. I eat what i think is a very health keto diet. No sugars or grains of course, lots of leafy green veggies, all or substantially all animal fats and proteins are pasture raised etc. I have recently cut back on dairy (I am in Wisconsin so not easy to do) and added more olive oil but my numbers, with the exception of the HDL and Trigs look like i am on a SAD. I have a hard time believing that the answer is to go back to eating carbs when by BG is low and stable and my hsCRP is low at .3. I may try to get out of keto for 3 or 4 weeks by eating 100 grams or so carbs (sweet potatoes or similar) and cutting out the daily dose of bulletproof coffee and then test again.

    Yes I am familiar with BJJ. Haven’t been on his site for awhile so i will check it out. If you are ever looking for another n=1 let me know if meet up for it.

    Rich

  17. Leo Tat

    Hi Dave,

    Back a few years in 2014 when I started a low carb high fat diet, I tested my blood after 4 months.

    TG and HDL ratio is one of the best indicators of cardiovascular disease risk.

    Heres mine:

    TG/HDL = 70.88/69.66 = 1.05

    My wife started at the same time as me, took the test too and got

    TG/HDL = 70.74/69.66 = 1.15

    These are pretty much perfect figures.

    1. Dave

      Hi Leo – these indeed look impressive. Great job!

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