»

Jun 15

Cholesterol Code – Part I : More Fat, Less LDL-C

I’ve thought a lot about how best to get this information out and knowing it will have many possible audiences. So I decided to just put it in a multipart series. This first installment will have some extremely surprising data with regard to dietary fat and its effect on LDL, HDL, and Triglycerides on a low carb / ketogenic diet.

Before we get started I wanted to emphasize two things:

  1. A big THANKS to all the doctors and engineers I swore to secrecy on the deeper data I was sharing. I really appreciate you keeping a lid on this until I had verified and re-verified. (With extra special thanks to the collaboration of Dr. Sarah Hallberg, Dr. Jeffry Gerber, and Ivor Cummins.)
  2. My cholesterol numbers are certainly high, and this might be distracting. I’m well aware of this and it is part of what started this data journey in the first place. But they’ll be more to this story by the time I get to my latest data.

The Brief Backstory

In March of last year, I got a marker for prediabetes from my blood panel, an A1C of 6.1. I was intent on avoiding future Type 2 Diabetes, so I researched and then began a low carbohydrate diet the month after. I lost 35 pounds, it raised my energy levels and seemed to improve my health in almost every way.

However, seven months later in November, I got back my first bloodwork and saw my total cholesterol had gone from 186 to a whopping 357, with LDL-C cholesterol climbing from 137 to 271. Given how incredibly great I felt the entire time, I was in complete disbelief. I heard some low carb dieters had exploding cholesterol, but assumed I wouldn’t, given I didn’t have higher than usual to begin with. From there, I began learning everything I could about Cholesterol Homeostasis.

The Idea

And this is where it got interesting for me. As a senior software engineer, the more I learned about the lipid system, the more I saw a familiar pattern –> a distributed network of objects. I read with particular interest on the assignment and apportionment of apolipoproteins and their potential role as a proxy for an information feedback loop to the liver.

Anyway, I’ll lay the general theory in more detail in a later post. Just know that if true, there should be two key presumptions:

  1. The cholesterol transporting lipid system would prove to be agile — much more so than is typically believed
  2. Discreet patterns should emerge between the diet and serum cholesterol now that disruptive inflammation is lower

So I went about testing these two points with my own blood starting in late November taking regular NMRs (Nuclear Magnetic Resonance – an advanced cholesterol test that directly measures lipoprotein particles and their sizes/classifications). Likewise, I kept meticulous track of my diet and nutrition values, both logging and taking pictures of just about everything I ate and drank. With blood taken every one to two weeks, I would make key changes between tests to see the outcome. Of course I was told over and over again that this was too frequent and that I needed to give the body more time to see results.

Initial Data

Sure enough, in eight tests over just three months I saw rapid changes, enforcing presumption (1). And yes, very discreet patterns did emerge, bringing evidence to presumption (2). In fact, both these behaviors were more pronounced than I could have imagined.

The tightest correlation appeared with total fat in my diet and LDL-C cholesterol. Now hearing this, you might not be surprised given that conventional wisdom seems to agree with the assumption higher fat (especially saturated fat) tracks with higher cholesterol in the blood. But that’s the first big twist — this isn’t a positive correlation, it’s a negative one. And get this –  the strongest time tracking appears to be not months or even weeks, but a three day rolling average.

fat3_vs_ldl_first8

Let’s use an example to illustrate. Imagine I took a blood test on a Friday morning, which we’ll call Day 0. Tuesday is Day -3, Wednesday is Day -2, and Thursday is Day -1 just before that Friday. If you took the dietary fat average I had between those three days, you get the score in the yellow line above. Put another way – all the days before that Tuesday (Day -3) appear to have very little to no relevance to my LDL cholesterol – I can practically ignore them!

To better show the correlation, I’ll flip the vertical axis of this same graph for the three day average of fat. (I’ll be doing this a lot moving forward)

fat3_vs_ldl_first8_reverse

At this point, I took my data to the Low Carb Vail conference and met with a number of great doctors there. I also had a particularly good conversation with Ivor Cummins who is likewise very versed in the subject as well as being a fellow engineer.

I explained the next obvious step was to do a “reproduction test” and see if I could replay the experiment to get anywhere close to the same results. Except this time, it was going to be even more controlled with a tighter timeline. (And frankly, very unenjoyable!)

Reproduction Test

The plan was to have my blood drawn every single day, five days in a row (Monday-Friday). On the preceding days (Sunday-Thursday), I’d have a specific day of meals that matched the two of the extremes in my testing for LDL-P. The highest LDL-P score (3073) was Dec 19th, when I had just 68g of fat the previous day, which we’ll call the “Low Meal Plan.” The lowest LDL-P score (1967) being on Feb 19th when I had 222g the previous day we’ll call the “High Meal Plan.” All day Friday, Saturday, and Sunday I didn’t have a prescribed meal plan and just ate generally “high” fat. We’ll call this period the “General Meal Plan.”

The pattern would be:

  • Sunday – Low Meal Plan
  • Monday – Low Meal Plan
  • Tuesday – High Meal Plan
  • Wednesday – High Meal Plan
  • Thursday – Low Meal Plan
  • Friday, Saturday, Sunday – General Meal Plan (Uncontrolled)

For the first five days I ate the meals in as close to the same times and in the same order as the days they were modeled after. I also timed the blood test to have the same fasting time since the meal of previous day as well.

I was flying to a developer conference that weekend and hadn’t planned to take another test, but finally decided to add one more after I got there on the following Monday. So the Friday, Saturday, and Sunday meals when I went back to higher caloric intake with higher fat would likewise show as well, though they weren’t as controlled as the previous week.

So what happened? See for yourself:

fat3_vs_ldl_first14

 

And again – let’s flip that left axis so you can see the reverse correlation better…

fat3_vs_ldl_first14_reverse

This was especially meaningful, not just because it replicated the same three-day average, but because now we could actually see the changes in successive time to the cholesterol payload. (As an aside, the LDL-P had a more interesting story with this run of days. But again, I’ll detail that in the next post.)

The Intentional Outlier

Any engineer reading this is probably thinking the same thing I was by this point. “If this is an algorithm, then it stands to reason I can crank it up to a new level to generate a new extreme.” Which is exactly what I did.

I scheduled a test for April 8th, and for the three days before, I ramped up my diet to an average of 4,274 calories and 349g of fat per day. Just a little heads up… this is extremely hard to do on a low carb diet.

Let’s display all 15 data points together now with this last one on the end…

fat3_vs_ldl_first15

And again with the reverse axis…

fat3_vs_ldl_first15_reverse

Sure enough, the April 8th result was the lowest LDL cholesterol score of all the tests. Moreover, it likewise tracked to the correlative envelope of the previous 14 data points, giving the entire series a jaw dropping -.905 Pearson score.

Other Data Points

I could write another five posts on the other data points, but I’ll let the graphs speak for themselves with just a brief statement for each.


Three Day Average Total Fat (inverse axis) vs Total Cholesterol

fat3_vs_total_first15

Generally, I don’t care that much for the TC metric, but I thought I’d include it for those who do. It is worth noting that data point 9 started on 3/7 with a 348 TC, just two days later I peak out at 422, then six days later I’m down to 364. Again, this is one more example of where we are told frequently that these numbers take a lot more time to change when clearly my data suggests otherwise.


 Three Day Average Total Fat vs HDL-C

fat3_vs_hdl_first15

While the correlation at 0.742 isn’t as prominent as as the -0.905 of LDL above, there’s no question it is still a very strong relationship. The primary divergence is in the first data point going back to 11/24/15, but otherwise it tracks remarkably close – even during the day-after-day reproduction experiment.


 Three Day Average Total Fat (inverse axis) vs Triglycerides

fat3_vs_trigs_first15

Lastly, we see the trigs are pretty close in correlation as well. Ironically, a 0.6 correlation on at least one metric was what I was originally hoping for when I started this experiment. Yet here’s trigs showing such a strong inverse correlation and it’s the runt of the pack at -0.61. Go figure.


Final Thoughts

While I’m glad both (1) and (2) of my theory above proved to open the door to these emerging patterns, I certainly didn’t think it would be such a perfect inversion of almost everything I’ve read to date with regard to Cholesterol.

My data over 15 data points suggest:

  • The more fat I eat, the lower my Total Cholesterol (87% inverted correlation)
  • The more fat I eat, the lower my LDL-C (90% inverted correlation)
  • The more fat I eat, the lower my Triglycerides (61% inverted correlation)
  • The more fat I eat, the higher my HDL-C (74% correlation)

Coming up in Part II – Particles, Particles, Particles. Results and analysis for my LDL-P, small LDL-P, and Pattern A/B.

 

45 comments

Skip to comment form

  1. Camilo

    I am just stating to read the article.

    1) thanks for sharing all the details

    2) please add a date somewhere at the top, end the article or where it mention ” The Brief Backstory In March of last year”, please change to March 201?

    Thanks again

    1. Dave

      Good point — I just noticed it doesn’t share the year. I may make that change to the skin itself, not necessarily the content…

  2. Zoziau

    I got the opposite : on ketogenic diet both my total and LDL cholesterol went much higher. Only the triglycerids went down.

    1. Dave

      It’s worth emphasizing that my original baseline numbers changed after I started ketogenic (see above where I mention TC of 186 pre-diet at the beginning). Thus, like you, my total and LDL went up, trigs went down. The main data above is the mechanism of the diet after having started.

  3. Rentius

    I have been doing LCHF diet for almost a year and a half now.
    My Cholesterol (mmo/L) is very high;
    TC 9.4
    HDLC 1.9
    LDLC 7.5
    TG 0.97

    Because of the above I decided to do the particle size test (Lipoprotein Electrophoresis) for LDL.

    To my horror the results was bad: Result = I/B
    Which means my LDL size is close to the smallest of the usual range.

    During the time I was eating allot of cheese (Mature cheddar), eggs and Macadamia nuts.

    The results have been done in April 2015 so more than a year ago.

    1. Dave

      I would recommend finding a low carb / ketogenic doctor to go over your bloodwork with you. While your Pattern B is something worth looking closer at, your Trig / HDL-C is actually very good.

  4. Wenchypoo

    When my doctor told me that cholesterol “bounced”, she wasn’t kidding! Thanks to your work here, I can see it for myself.

    1. Dave

      Thanks! Yes, I have quite a bit of bouncing with my data as well.

  5. mauricio

    hi Dave,

    Thanks for such a good post. I am impressed by the level of detail on your data. I too have a similar pattern that yours. My LDL (187) is not so high but my LDL-P ranges close to 2000 and sometimes more. HDL (70) is high and trigs are low (47).

    I have ready from Ivor’s posts that there is no real correlation to mortality of ldl-p yet, and that also saturated fat seems to do the trick to lower the ldl-p.

    Have had CAC scores 2 years in a row, bot to 0, so on the plaque arena I am happy.

    If you don’t mind could you share with me which resources did you use to perform the testing?

    Were the tests normally done by doctors appts. I’d assume you did them on your own since insurance companies don’t like paying for repeated tests and definitely insurance companies don’t like paying for the nmr nuclear test. I’d really appreciate if you can share that. May be there is a cheaper option that I don’t know about.

    Because like you I am also an engineer and have drawn some correlations through the years (don’t we all love data 🙂

    Thanks and excellent work
    Mauricio

    1. Dave

      Do be mindful not to get the CAC too often (I plan to do every 2 years at first, then 5 year intervals). It is exposure to radiation, even if at a low level. While the risk is generally unknown, it’s enough of one for me to be careful.

      Yes, I get my tests privately through requestatest.com at about $99 per NMR. I will sometimes order more to be coupled with it like a CRP, ApoB, and sometimes a full blood panel.

      Frankly, I’m very frustrated with going through my doctor even for tests the insurance company paid for because it’s so difficult to just get a copy of it for my own research. I believe all medical data collected on me should be owned by me and thus portable for my own use. (I could rant for hours on the bureaucratic state of our medical system)

      1. Diego Espinosa

        Hi Dave,
        I’m working on a diabetes prevention start-up that involves a public blockchain record component. I’d like to get your feedback on possible design features — your user stories. Please email me if you’re interested.

        By the way, my approach is called ‘network design’, wherein all network behaviors are taken into account at a holistic level. These include the organ/fat cells/microbiome network; the appetite/mind/social network; etc. Design solutions are only valid if they work at the network level, not at the individual node. I say this because I am quite interested in hearing the ‘network thesis’ that you allude to, especially the idea of the information feedback loop to the liver.

      2. Anita Gandolfo

        If you are in the US, you are legally the ‘owner’ of all lab test data. Your physician cannot deny you access. The most they can do is ‘charge’ for copying the info to you, but no doctor has ever done that to me. They all comply with my requests.

  6. Stacy

    Thank you for posting. This is really interesting, I look forward to seeing more.

    When thinking about lipid profiles and risk for CVD, the reference I often see is the Harvard study showing that the most important number we should be tracking is the Triglycerides/HDL ratio (getting it to about 2.0 or lower). The study indicated that this ratio is 16 times more predictive for a cardiac event.

    If that is the case, should we pay any attention to the total cholesterol number? Seems that it would become irrelevant in light of the Trig/HDL numbers but I don’t know.

    1. Dave

      I’ve read through literally hundreds of studies in the last several months and am fairly aware of every side’s *favorite* ones. Some have more credibility than most, but I don’t feel there’s one that is truly definitive.

      In a later post, I’ll be doing a deep dive on the risk analysis I’ve come to and why I haven’t taken any steps to lower my cholesterol holistically or medically. But as a spoiler alert, I’m no where close to a certainty on whether this course of action is a net lower risk or not.

  7. Timothy K Foxon

    Hi Dave.

    Interesting data, as you say, counter intuitive.
    I am a hyperresponder also and have been trying to determine risk since I got my first blood test post starting LCHF.

    I have “discovered” the following.

    LDL levels change because the LDL setpoint changes for the following reasons.

    1. Saturated (and maybe polyunsaturated) fat intake increases LDL since chylomicron remnants compete with returning LDL for uptake by the hepatic LDL receptor, so the catabolic rate of LDL declines while production is unaffected.
    2. Dietary cholesterol increases LDL since this cholesterol accumulates in the liver and pressures/down regulates the LDL receptors. Same mechanism applies, catabolic rate of LDL decreases.
    3. Insufficient intake of linoleic acid (18:2 n6) acts like a gate. Lower than 3% energy saturated fat, particularly lauric acid greatly increases LDL whereas above 7% of energy this activity is dampened (I don’t know why this occurs).
    4. Insufficient bile production in liver down regulates the LDL receptor.
    5. LDL can be considered as composed of two seperate pools that exhibit metabolic channelling controlled by triglycerides, for simplicity call them pool A and pool B. Pool A is composed primarily of LDLI and LDLII and is not as atherogenic. Pool B is composed of LDLIII/IV and is smaller, denser and considerably more atherogenic. These pools evolve under the control of triglycerides and insulin resistance. As trigs rise CETP and hepatic lipase activity rises and LDL/HDL is first cholesterol reduced and then lipid reduced by VLDL, resulting in small dense LDL and low HDL (since the ApoA1 protein gets shed due to the small size). Thus you can have high LDL that is benign or dangerous depending on your level of trigs. There is a threshold in males about 1.3-1.5 mmol where the changes start to become destructive, below this you are ok, above you start to accumulate small/dense LDL. Atherogenic dyslipidemia is characterized by higher trigs, low HDL but relativeley normal LDL (more particles but less density per particle). So most people in cardiac wards have low/normal cholesterol.

    LDL becomes dangerous because it becomes oxidised, small dense has less antioxidant defence so succumbs faster.

    Would love to see you debunk any of this or augment it.

    Thanks.

    1. Dave

      Interesting data, as you say, counter intuitive.
      I am a hyperresponder also and have been trying to determine risk since I got my first blood test post starting LCHF.

      — Welcome fellow hyperresponder!

      1. Saturated (and maybe polyunsaturated) fat intake increases LDL since chylomicron remnants compete with returning LDL for uptake by the hepatic LDL receptor, so the catabolic rate of LDL declines while production is unaffected.

      — I hadn’t come across this before. My understanding was chylomicrons and their remnants had a very short lifespan (30-90 minutes, depending on the source). This would make me less confident it was crowding out LDL uptake given the short window of possible conflict.

      2. Dietary cholesterol increases LDL since this cholesterol accumulates in the liver and pressures/down regulates the LDL receptors. Same mechanism applies, catabolic rate of LDL decreases.

      — This hasn’t been the suggestion of my data thus far — at least with regard to the transitory changes. As with the graphs above, when lowering my dietary cholesterol, my LDL-C increased (see data points 2 and 5 for example). And conversely, when increasing my dietary cholesterol, my LDL-C dropped (See 1 and 8 for example).

      — Now it’s possible the higher fat from the beginning of the diet set a high LDL *baseline*. But the presumed baseline appears to be very static in this data, allowing most of the movement to be the inversion shown above.

      3. Insufficient intake of linoleic acid (18:2 n6) acts like a gate. Lower than 3% energy saturated fat, particularly lauric acid greatly increases LDL whereas above 7% of energy this activity is dampened (I don’t know why this occurs).
      4. Insufficient bile production in liver down regulates the LDL receptor.

      — Interesting… I’d have to learn more as I’m not as familiar with the research on either of these points. Do you have links to the studies?

      5. LDL can be considered as composed of two seperate pools that exhibit metabolic channelling controlled by triglycerides, for simplicity call them pool A and pool B. Pool A is composed primarily of LDLI and LDLII and is not as atherogenic. Pool B is composed of LDLIII/IV and is smaller, denser and considerably more atherogenic. These pools evolve under the control of triglycerides and insulin resistance. As trigs rise CETP and hepatic lipase activity rises and LDL/HDL is first cholesterol reduced and then lipid reduced by VLDL, resulting in small dense LDL and low HDL (since the ApoA1 protein gets shed due to the small size). Thus you can have high LDL that is benign or dangerous depending on your level of trigs. There is a threshold in males about 1.3-1.5 mmol where the changes start to become destructive, below this you are ok, above you start to accumulate small/dense LDL. Atherogenic dyslipidemia is characterized by higher trigs, low HDL but relativeley normal LDL (more particles but less density per particle). So most people in cardiac wards have low/normal cholesterol.

      — That’s an interesting theory… but I can’t comment on this too much right now as it will be partially covered by the next part in the series (which will be released tomorrow).

  8. Timothy K Foxon

    Hi Dave.

    Thanks for your quick response.

    The reference for cholesterol and linoleic acid effects is “Saturated Fatty Acids and LDL Receptor Modulation in Humans and Monkeys” K.C. Hayes, P. Khosla, A. Pronczuk. For chylomicron remnant uptake by the LDL receptor it is “https://en.wikipedia.org/wiki/LDL_receptor”.

    I think you are correct that chylomicron remnants have a shorter lifespan, however if the effect is strongly pulsatile the pulse in LDL may last much longer (since the plasma residence times of LDL I/II is about 2 days and LDLIII/IV about 5 days so the pulse generated on your day-1 would last past the test point further confusing me). Reference for residence times is “http://atvb.ahajournals.org/content/17/12/3542.long” fig 4. This paper is also the reference for my point 5 (metabolic channeling)

    I think it is very strange that your pre/post LCHF experience with LDL is similar to mine but the within LCHF response is totally unexpected. I look forward to your subsequent posts.

    Regards.

    1. Dave

      The study you’re citing I did read a while ago, but it has a number of core assumptions that haven’t been directly observed. This is part of my problem with many of the lipid studies in general.

      The data I posted thus far already runs diametrically opposite this and many other studies’ suppositions that increased SFA will increase serum cholesterol (whether through reduced LDLr expression or some other means). A large portion of my total dietary fat is saturated, and as I eat more, my LDL-C (and LDL-P) drops. (As an aside, between data points 6 and 7 I had dropped my SF to 25g a day and replaced with MUSF and PUSF to see if it changed any major outcomes, but it effectively hadn’t)

      The part that keeps being brushed over is whether there is an actual regulatory response in play with serum cholesterol as an end point (in part or entirely). A higher cholesterol result is always treated as though it is the tragic event that happens after all the other normal mechanisms have failed. The possibility the body is up-regulating LDL out of its own intention and that there is a net benefit is ruled out at the beginning. I’m not saying I feel confident this is the case, only that I think it needs to be falsified in the first place before dismissing the possibility.

      I’ll be posting a risk analysis piece soon that will explain why I have a kind of grading system for studies and how I weight them for my own purposes.

  9. Timothy K Foxon

    Hi dave.

    Sorry, one more point. The conflict time may well be extended since a high fat meal may take up to 8 hours or so to be digested and you will be producing chylomicrons throughout this time so your conflict window may extend to as long as 9-9.5 hours which is probably enough to raise LDL given your very short response times elucidated in your graphs.

    Regards.

    1. Dave

      Possibly — but longer gut CM synthesis is usually tied to multiple inputs of energy (high carbs and/or high protein in parallel with high fat). I’d be surprised if lchf took up these longer resident times pre-lymph given how singular the energy source.

  10. Joan Day

    most people do not have ferritin levels tested, but i ask for one. as it has been just a little high over the years, at 308 the end of nov/2015, now june I just had it done it has shot up to 491. I have been doing low carb high [good] fats for around 3 to 4 months, My ketons with urine test was 2..so that was great–but my cholesteral has gone from 5.6 last nov to now 8.22 –my dr is going to flip out for sure. trig moved from 2.54 in nov to 2.22 june so this has improved. My HDL was . 93 last nov and now is .93 –so the good one is not improving and still low, non LDL was 4.66, now up to 7.29, LDL was 3.51 now up to 6.28–and my cholesterol /HDL ratio is far worse, from 6–to 8.8–does anyone know much about he genetic mutation , and perhaps i have it and this is creating the problems. Others see improvements with there good cholesterol and lipids etc. –my bg has improved fasting was 6.1 now good at 4.5, and my A1C/ is gone down to 5.7, from 6.0 last end of nov. 29/15/ I have lost over 34 lbs, and feeling so much better–now this ferritin and cholesterol situation–I think I really need a specialist to help sort this out. but have no idea where i can find one to work with. My gp will be wanting me to take drugs, and i want to see what kind of diet I can use to fix this if it needs fixing.. i would be interested to know how many other people ever check there ferritin levels on high fat low carb diets, and with higher A1C–

    1. Dave

      Of what I know of ferritin, it is typically a good marker for Iron regulation. But I haven’t reseached much beyond that as mine has come back normal in my labs. I do remember seeing a study of ferritin levels being elevated during acute malnutrition in anorexic patients. I agree you should find a specialist and likewise check if is diet related.

    2. Simon

      You could have hereditary hemochromatosis, you can read about it on my blog
      Hereditary Hemochromatosis
      What is your age? I’m assuming based on your name you are female which means you have a built in iron reducer until you hit menopause. You want your ferritin levels to be in the range of 50 – 150 for optimal health. Ferritin is also an inflammation marker so it can go up with inflammation. I would definitely look into giving blood with those ferritin levels but I’d also get the gene test to rule out hereditary hemochromatosis.

  11. Jas

    Great post Dave. In regards s to Tim’s post, I have had total Cholesterol at 11.0 with HDL at 2.2 and tried at 0.7 yet after a subtraction analysis I had some small dense Ldl, – phenotype B. This was after a year of LCHF and training for endurance sports. Previously followed at high carb diet and previous lipid analysts for the past 10 years showed “normal lipid profiles. Total chol 4.2 HDL 1.7 trigs 0.5. Hard to know which way to go for the best of health

    1. Dave

      Wow! That’s a hardcore Trig/HDL ratio. Even though I’m a strong Pattern A and should be comforted by the lack of small LDL-P, I’m not so sure of how much that matters either in non-inflammatory circulations. Note how in Part II I my smLDL-P moved up and down with the entire score, but at a higher gain-loss ratio. This has led me to theorize that perhaps the two day delay effect in smLDL-P clearance could be a kind of earmarking for outbound particles right before they are cleared.

      This is anecdotal, but in my current hyperresponder findings and one-on-ones, there seem to be a slightly higher proportion of athletic ketoers having more smLDL-P / Pattern B then sedentary. Fortunately for this subgroup, I myself will be doing some distance training and half marathon running for the second half of this year and will keep posting my data as I go. So if there is a movement from pattered A over to pattern B from having lots of exercise, I’ll help to show it.

  12. Adam Nally, D.O.

    Superb . . . Thank you for posting this information.

    1. Dave

      Happy to advance the data… I think you’ll enjoy what I have upcoming as well…

  13. Dustin Gerken

    I comment each time I especially enjoy a post on a blog or I have something to contribute to the discussion. Usually it is caused by the passion communicated in the post I read. And after this article Queen Of Charms |. I was excited enough to post a thought I actually do have 2 questions for you if you do not mind. Is it just me or do a few of the responses appear like they are coming from brain dead visitors? And, if you are posting on other online sites, I would like to follow anything new you have to post. Would you make a list every one of your community sites like your Facebook page, twitter feed, or linkedin profile?

    1. Dave

      To your first question, I’m happy for any/all questions I get, even if some are at different levels of knowledge on the subject. I myself feel like I’ve learned so much in such a short time, but yet have only spanned the tip of the iceberg.

      The the second, my twitter is @DaveKeto where I do most of my shortened, but frequent posts. Beyond that I’ve posted to various forums under the username DaveKeto, so it’s pretty easy to search out my earlier learnings. (Though some also have that name)

      However, most of my n=1 research and detailed thoughts will be posted here on this blog.

  14. Han Sanson

    I have not checked in here for some time because I thought it was getting boring, but the last few posts are good quality so I guess I¡¯ll add you back to my daily bloglist. You deserve it my friend 🙂

    1. Dave

      Thanks, Han. Glad you’re enjoying it.

  15. Jason Bellotti

    Great info, very interesting, I’ve been Keto for about 6 months, just had a second lot of bloodwork done, shows an increase in tg, only .2 from 1.2 to 1.4, my hdl went up .4 from 1 to 1.4 so my ratio went from 2.7 to 2.2 which is good, my total LDL went from 3.5 to 6 in the same time frame, any thoughts on the small tg increase? I’m very active (grapple/bjj regularly) and while I’ve dropped over 20kg on Keto, I’m currently sitting at about 10-12% body fat. Side note, the preceding day to my most recent test I dropped just over a kilo of weight, (mobilized tg theory?)
    Thanks
    Jason

    1. Dave

      Hi Jason–

      Your Trig/HDL ratio has definitely improved, which is likely very good.

      To requote myself from a response to another commenter –> From my own testing, I find trigs to be the most volatile number, which makes sense being fat adapted. Given more rapid and sporadic fatty acid diffusion/consumption, the distribution consistency in a single blood draw seems likely to vary.

      With regard to Trig mobility on weight loss, I’ve heard many accounts but don’t have a lot of my own data to show either way given my weight has been relatively stable by the time I started rigorous recording.

  16. Raymond

    It would be interesting to see the same experiment on a person who have been eating a non LCHF diet.

    1. Dave

      Indeed! I have some theories on that I’d like to test against. But I need standard western dieters, not ketoers like myself stepping off low carb briefly.

  17. Dr. Steven Horvitz

    Dave

    Great blog so far.
    Only issue is you write like my engineering friend Ivor ; )

    Your results are an N=1 experiment. It raises interesting questions.

    I too, when going LCHF had a dramatic rise in all my lipid fractions, other than Trigs which remained normal.
    Of course the elevated ldl-c and ldl-p still get my attention, even though I am a physician. Don’t worry, I do not believe in statins.

    My question for you is:

    Have you had any of the following tested along with the numbers you shared above?

    Fasting insulin
    Uric Acid
    ferritin
    Adiponectin
    Leptin
    Tsh, free t-4 and free t-3
    testosterone
    Apolipoprotein Genotype??? Actually are you and E4 genotype carrier?

    Steve

    1. Dave

      Fasting insulin — Yes. Most recent = 3.3
      Uric Acid — I don’t believe so, but my PH is generally 6.5-7.0
      ferritin — No, but I did take an Iron and TIBC test that had all markers within range
      Adiponectin — No, but would like to know more about it.
      Leptin — No
      Tsh, free t-4 and free t-3 — Yes, slightly out of range on t3 on a recent test, but was within range before. Will test again soon to see if one-off.
      testosterone — I may have in a previous batch of tests, but not sure.
      Apolipoprotein Genotype??? Actually are you and E4 genotype carrier? — Yes, I’m a 3/4 allele

  18. LK Taylor

    I am as lost as a fat cell or is that a bug in the rug. I began a no sugar carb about 3 months ago and went to the doctor and cholesterol is up and thyroid is high. I am not a pill popper so figuring out how to get both measures lowered is the plan of the day. More fish possibly!

  19. Vincgoara

    Hello. And Bye.

    1. Dave

      Ditto.

  20. Andrea Mikler

    Hello Dave,

    you have so much knowledge! Could you, please comment on higer HDL than LDL numbers. My total cholesterol was 6.16 with HDL 3.24 and LDL 2.69. Trigs were o.5 mm/l. I am on LCHF for about 4 years now. Normally I would not be concerned as we hear that HDL is the “good” cholesterol. However, I read few opinions (do not remember where) that high HDL is associated with higher mortality from all causes. Any thoughts on this?

    1. Andrea Mikler

      Dave, I just noticed you commented on my numbers in part 1 just few days ago. Please, disregard my comment here and thank you so much for your opinion. Thanks for all your research and sharing it with the community :).

  21. ARUNACHALAM RAGUNATHAN

    Hello Dave, just went through your narrative of the experiment. I was shocked to see my recent blood tests after being on low carb diet. Total Cholesterol 371.1; Triglycerides 100.3; HDL 73.9; LDL 210; Apo A1 177.8; Apo B 198. Before dieting Total Cholesterol 152; TG 81; HDL 31. Reading your notes gave me some solace. I was having high blood sugar previously. Now settled with HbA1C 4.9. Will be continuing this diet. Have increased my fat intake from 120 to 180. Will check blood and post you the results. Your comments on my reports?, please.

    1. Dave

      Actually, your numbers are nearly identical to mine except your LDL is lower and HDL higher. Apos A1 and B are likewise nearly the same. And your A1C is excellent — mine hovers around 5.4 to 5.7.

      As far as where you came from, your HDL going up from 31 is a massive improvement, IMO. As you may have read here in many places, I consider HDL the most important marker I track. Trigs are much noisier and have the loosest correlation in my patterns, but this makes sense given their erratic usage throughout the system for energy. (In fact, I’d bet if you took blood from multiple places in the body at the same time, trigs would have the highest variance)

  22. David

    Just coming into this with 9 months LCHF behind me and the results of my first blood lipids test. Results very similar to the ones you had that set you off down this road. Total Col – 8.6 mmol/l, 6.3 LDL, 1.6 HDL and 0.6 Trigs. Had a massive argument with my doc over these results because I had stopped taking statins 6 months previously which he wanted to get me on. But onto my question, Considering your study findings that higher fat intake lowers cholesterol then why do you think your (and mine) lipid results jumped when you started LCHF which by definition means your fat intake was higher ?

Leave a Reply

Your email address will not be published. Required fields are marked *

You may use these HTML tags and attributes: <a href="" title=""> <abbr title=""> <acronym title=""> <b> <blockquote cite=""> <cite> <code> <del datetime=""> <em> <i> <q cite=""> <s> <strike> <strong>

*