«

»

Jan 19

A Simple Guide to Cholesterol on Low Carb – Part II

In A Simple Guide to Cholesterol on Low Carb Part I, I gave a very broad overview of LDL particles and their important cargo along with common misconceptions about this subject within a low carb, high fat diet.

Without question, the guide was the most visited post on my blog. And many of my followers have remarked on how helpful the graphics were in getting across the information. So I decided to get ambitious with Parts II and III and tell it more as a visual story. In short – more graphics, less blog text. Enjoy!

cover

Page_01

Page_02

Page_03

Page_04

Page_05

Page_06

simple_guide_7b

Page_08

Page_09

Page_10

Page_11

Page_12

simple_guide_13a

44 comments

Skip to comment form

  1. Luke

    Simple and to the point. Look forward to the part 3.

    1. Dave

      Thanks — it will likely be soon after my presentation at Low Carb Breckenridge.

  2. Hyper-Responder Neville

    Using cartoons to explain lipid metabolism is so cool! really great work.
    In case anyone’s interested (apart from the above series ^), this is probably one of the best explanations of this topic [https://www.youtube.com/watch?v=998r-MyEEPc] that i have come across.

    1. Dave

      Yeah, that happens to be one of the earlier videos I saw when I started to learn about the lipid system. Really informative.

  3. Wim Tilburgs

    Great article shared it in the Dutch Low Carb community.

    1. Dave

      Great! Thanks, Wim, I hope it proves very useful.

  4. Nicole recine

    Thanks so much for this Dave. Am I right in understanding that the LDLs become small and dense when they are lacking in cholesterol and have a lot more trigs to drop off?

    1. Dave

      Hi Nicole,

      Actually, I believe it’s the other way around, generally. Trigs are distributed mainly at first and VLDL goes to IDL, then to LDL with this last stage being the smallest and most dense (due to being higher protein vs lipid content) and *cholesterol rich*. The assumption with the establishment is that the longer those last stage LDL particles continue in the system, the more likely they are to get oxidized and end up in our arteries, or get retained in our arteries and then get oxidized, thus starting atherogenesis.

      As we’ve discussed before, I have a very different leaning given my own data and research thus far. But more of that will be covered in my upcoming presentation at Low Carb Breckenridge.

  5. michael pollard

    Can’t see any way to subscribe.

    1. Dave

      As I’m a bit new to WordPress blogging, I myself wasn’t aware subscribing would be possible — but even if it were, I may have to wait until I move this site to the new host (probably in Feb or March).

  6. Dr Z

    Excellent site and excellent illustration!!

    Any info on Wellbutrin use and elevated cholesterol? Long and complicated history, but would love any leads if you have come across any associations in your research. Thanks again and keep it up! This information needs to get out!

    Megan

    1. Dave

      Hi Dr Z-

      No, I’m not familiar with Wellbutrin or it’s impact on cholesterol.

      If one went on a low carb, high fat diet while also starting the medication at the same time, then it might be difficult to determine what impact each had along with what they do in combination. Is this what happened?

      1. Dr Z

        Hi Dave,

        Thanks for the response.

        Here is a brief hx:
        At the time the 36 y/o female (now 40 y/o) pt started on 300mg/d bupropion (Rx’d by different dr) and within one month lost 5 pounds, going from 122-117 at 5’4″. She maintained that weight for 1.5 years as she was recovering from a foot injury that prevented her from being very active — even walking was not an option for about 6 months. Once the foot was healthy she resumed her previous exercise routine: weights, moderate cardio and in general significantly more mobility simply due to no longer being limited. The only dietary change she made was reducing alcohol intake. She said that she was drinking 2-3 beers/night, so she cut back to only twice per week and only 2 drinks at a time. After the reduction in alcohol and increase in activity level, she lost 10 pounds in 6 weeks. She stopped having her period and started to suffer insomnia, more depression and fatigue.

        Dietary wise: honestly, it’s not terrible or specifically high fat, low carb, etc, but she definitely could stand reduce sugar intake. She admits to eating chocolate, daily, and often gets a pastry with her coffee in the AM. Otherwise, she adheres to a whole foods diet. Not heavy on meat, however. Nor is she big on the carb front (excluding the pastries and chocolate habit).

        I ran some labs and sex hormones are in the tank — all postmenopausal. DHEA-s normal, testosterone – normal Thyroid markers are all low: TSH, T3, T4, free T3, free T4, all below RR. Anti-bodies are negative. Cortisol production is low, however, conversion to cortisone is high.
        The cholesterol is the interesting bit:
        Total: 308
        HDL-C 151
        Direct LDL-C 182
        Tri 75
        Non- HDL-C 157

        She does carry the E3/E4 genotype
        C/T MTHFR genotype
        She also tested high on her Beta-sitosterol and campesterol absorption markers

        I have 2 years worth of labs tracking her trends and the cholesterol numbers have slowing increased, the 308 was the most recent. Two years ago she was at 256 total.

        My thoughts are the bupropion which inhibits norepinephrine and dopamine re-uptake, in time, overly taxed the adrenals, which lead to the menstrual and thyroid dysfunction. I suspect she was hyperthyroid for a bit. And the the end result is increase in cholesterol as it is the precursor to sex hormones. I can’t find any literature on this, however. She presents almost anorexic, but is not. Her lowest weight was 106 and was extremely lean, if I were to guess, single digits. She has gained about 10 pounds, yet still no cycle and is still suffering from the symptoms that drove her into my care: fatigue, insomnia, depression and unintentional weight loss. The logical or trial run approach would be to take her off of the bupropion, but she says she has tried that (slowly tapering) but ends up feeling worse.

        Anyway … thanks for reading and for any thoughts or other minds that I could reach out to. It is disconcerting that so many medications are prescribed without truly knowing how they can impact the human system. Prior to the buproprion this pts cycles, sleep, energy, etc. were normal. Her only issue was depression and she says the bupropion has helped quite a bit.

        Thanks again for your incredible site and work in this field!

        Dr. Z

        1. Dave

          Hi Dr Z-

          First, as always, I caveat that I’m not a medical professional and this doesn’t constitute medical advice.

          – The first thing that popped out at me was her symptoms of insomnia, depression, and fatigue. Since going LCHF, I’ve found my biggest struggle was getting in the habit of consuming enough electrolytes and in particular sodium. I start my day with 3.5g of pink salt mixed in water and have one to two more of these drinks throughout the day along with salting many of my foods generously. If I don’t, I find I I have all the above mentioned symptoms, along with occasional cramps as well. It’s very unintuitive (more salt makes me less tired???) — but now that it is built into my routine, it is second nature. Given she’s actively eating better, she likely needs more sodium anyway as this is so common in processed foods.
          – Lower thyroid numbers certainly can have an effect on lipid numbers, though I concede that one is more outside my wheelhouse.
          – I too am a 3/4 and believe it to predispose me to higher lipid numbers. MTHFR genotype I’m still early on with research (and technically, everyone else is too – ha!)

          I’ve regularly joked that if I were female, I’d have have stopped researching any further and this site wouldn’t exist. The reason is because I’ve come across so much research that shows higher cholesterol has the lowest all cause mortality with women in particular.

          Here are some recent studies with very large population numbers:
          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%”
          https://www.ncbi.nlm.nih.gov/pubmed/21951982

          1. Dr Z

            Hi Dave,

            Thanks for the article link. Great information! And thank you for your thoughts on my question. Even though you may not have any formal medical training you are 100 times more informed than many medical providers that I know! I figured I would ask for any input that you may have simply due to your extensive research on the subject. So thanks again for your wisdom and time in responding to me.

            Megan

            Oh, and she does have an MTHFR variant that causes her to not methylate as efficiently … but what that means in the cholesterol world. Who knows! 🙂

          2. Dave

            Thank you, Megan! 🙂

  7. Joe

    Hello Dave….

    We chatted quickly on Twitter the other night, we had similar numbers and weight loss on LCHF. Here are my numbers again, before LCHF and one year later on LCHF. You said that you are taking no steps to lower your cholesterol at this point but told me to comment here for further explanation…Very interested!

    Thanks….Joe

    Jan 2016 Jan 2017

    Weight 206 173

    Cholesterol 223 373

    HDL Cholesterol 65 92

    Triglycerides 101 79

    LDL / Cholesterol 138 265

    Chol / HDLC Ratio 3.4 4.1

    Non HDL Cholesterol 158 281

    1. Dave

      Hi Joe — I’m going to build this into a blog post by itself. But this week I’m burning the candle at both ends, the reason why I’ll also be putting into a post soon.

      Please check back again next week…

      1. Joe

        Thanks Dave…

        Very interested in what you have to say, I will keep an eye out.

  8. Gale

    Hey Dave,

    Just wanted to say what a great job you did presenting at the Low Carb Conference.

    Keep up the great work.

    Gale Bernhardt

    1. Dave

      Thank you so much, Gale! I appreciate the encouragement.

  9. Eric

    Dave

    Love your work also loving LCHF. Got Lab work back after being LCHF for several months. Stopped 10mg Lipitor after taking for 15 -20 years six months ago.

    HDL-C 71 was 46 on HCLF +10mg Lipitor
    LDL-C 170 was 95 on HCLF + 10mg Lipitor
    Triglycerides 65 was120 on HCLF + 10mg Lipitor
    HDL-P total 34.5unmol/L first time measured
    Small LDL-P 625umol/L first time measured
    Large LDL-P 1552umol/L first time measured
    Total -C 254 was 161 on HCLF + 10mg Lipitor

    Only number that I don’t like is the Small LDL-P which is just slightly out of range it’s 625 and reference high is 527. I know your not a MD but what’s your take?

    Thanks

    Eric

    1. Dave

      I’m probably a lot more skeptical than most on small LDL-P being causal of atherosclerosis specifically. I’ll have a blog post on this in the near future (I hope). This is not to say I’m sure it isn’t, only that my own data and research shows just how quickly these numbers change, showing the level of control the lipid system has in the first place.

      Two points to consider:

      1) Small LDL-P can be cleared far faster than is presumed (in as little as 3 days). I’ve shown this several times now, including my Extreme Drop experiment at the Ketogains Seminar (441 to <90 -- http://cholesterolcode.com/infographic-of-prediction-experiment/). The common assumption with atherosclerotic build up is that it is due a “traffic jam” of LDL-P (and in particular, smLDL-P) as the body can’t seem to clear it, yet my data is showing it can.

      2) More importantly, the causal assumption also presumes the body wouldn’t intentionally upregulate LDL to meet an emergency state. But we already know this to be false. LDL has been shown to be upregulated in an infection event. Likewise, it can be increased to repair injury. In other words, it shouldn’t be surprising to find those near the end of their life to have more LDL given its immunological and reparative benefits. Which is why I’m actually surprised after learning of these factors that LDL levels are not actually *higher* when found near death in the aggregate.

      But then, I also know the presence of doctors being frequently found in proximity to people who have died doesn’t mean they must be killers.

  10. Eric

    Do you have any concern over Large LDL-p?

    1. Dave

      Current thinking by lipidologists like Dr. Dayspring is that total LDL-P (large or small) is the factor that matters most. While I’m not as convinced, it’s definitely something I don’t rule out.

      1. Eric

        Dave

        Thanks again! I am still losing weight since diet change have gone from 187 to 165 in 9 months very steady slow decline. I wonder if while losing weight some how LDL-p numbers go up?

        Eric

        1. Dave

          Many in the LC community (like Volek and Phinney) will point out that subsets have shown higher LDL-P when losing weight. I’m actually more skeptical of it being a 1:1 with released TG now due to my data. It’s a bit technical to explain, but to simply state it — I think the body has more effective LDL-P clearance control than is currently believed in the medical community, and that the higher numbers could be transitory or even upregulated by preference of the body. (Again, it would take a bit of time to really break this out)

          1. Eric

            Just found your interview with Ketogains https://www.youtube.com/watch?v=QUjbvK2U1D8 My A1c was 5.7 when I started changing my diet. Did your A1c lower over time how long did it take?

            Thanks Again!
            Eric

          2. Dave

            My A1C being 6.1 was the reason I started the diet, actually. It was around 5.4 seven months after a started, but has since bounced up to around 5.5-5.6 in my most recent tests. This appears to be due to higher glucose sparing where my body keeps my glucose closer to 100 mg/dl (which is higher than usual for a keto diet), yet my fasting insulin is extremely low (typically 2-4 uiu/ml).

          3. Eric

            Dave

            I’m suprised your A1c is not lower. I read on Dr. Attia’s blog his hemaglobin size was small giving him a higher A1c reading than his acutal blood glouse average. He compared his A1c to the Average BG from the Dexcom CGM he was wearing. Implying the CGM average blood glucose reading is more accurate. I wonder if your hemaglobin size also is small?

            Thanks

            Eric

          4. Dave

            Actually, I want to do an entire blog post on that. Both my A1C and fasting glucose is now higher than when I started (5.6 and 100-ish, respectively), but I suspect strongly this is due to glucose sparing on the part of my body. The reason is due to my low relative fasting insulin (typically 1.5 to 3.5).

  11. Lita Santos

    OMG I’m so glad I found you. Just heard your Breckenidge talk. I’m Jill. I’m her. 7 months on keto and took the cholesterol test and almost fell off my chair. I couldn’t believe it had shot up so much. total cholesterol went up, LDL went up, HDL went up but not by much. My ratios were worse I couldn’t see a way to explain it favourably. I wrote to Dr Ken Sokardis, Gary Taubes, Jimmy Moore, Dom De’Agostino, Stephen Phinney, Malcolm Kendrick and a few others. Most wrote back some with good news others not so much. How can I email you please? I’ve encouraged my mother and sister onto this diet – I’ve even started a degree in Nutritional science and now I am feeling so deflated. Scared to eat fat. Scared not to and put on all the weight I lost. I don’t know what to do.

    1. Dave

      Hi Lita – I’ll reach out to you. But to be sure, my communication is sporadic these days as I’ve got quite a bit on my plate. 🙂

    2. Brian Williams

      Hello Jill,

      I have exactly the same situation. The important things are the two ratios: TotCl/HDL and TG /HDL

      As long as they are ok, I don’t worry about cholesterol. You can improve HDL with fish oil EPA & DHA.

      I use this for my guidelines: “Cholesterol Conundrum – Know Your Metrics” on Youtube https://www.youtube.com/watch?v=YRFRRqe0vrE

      Good luck,

      Brian

  12. Pat

    Do you follow Dr. Peter Attia at all? He has had quite a change of position on Ldl(a)-P in the last few years mainly I think through lots of feedback from Dr Tom Dayspring. Large particle number=arterial damage. Any comments?

  13. Pat

    Hi Dave–Do you follow Dr. Peter Attia’s Eating Academy blog? Nice detail and for sure he has an increasingly negative standpoint re Lp(a)-P. I think from more in-depth conversations with Dr Tom Dayspring. It is indeed a hot area of research but Dr Attia seems to be settiing the tone of high-P=artertial damage (no matter the particle (i.e. any Cholesterol). Any thoughts?

    1. Dave

      Yes, in fact I consider Attia and Dayspring the most read (and watched) in my core education on this topic. I have come to a few different conclusions mechanistically than they’re teachings, mainly due to my own experiments and the patterns that have emerged — but that’s for a different post.

      The subject of risk is actually a pretty long one, but I intend to do a post on it in the near future.

  14. Ben

    Very cool illustration. One detail seems to need attention, though. Perhaps I’ve missed something somewhere, but from what I understand, small LDL particles and vLDL are not the same thing. I used to think they were, until I was called out on it, and did more some research on it.

    Further research showed me that there are actually five major groups of lipoproteins: (1) chylomicrons, (2) vLDL, (3) LDL, (4) IDL (intermediate density lipoprotein) and (5) HDL.

    LDL particles vary in size and density, as we know. Larger, less-dense particles are referred to as Pattern A LDL, whereas smaller, dense particles are referred to as Pattern B LDL (or “LDL-P small”).

    vLDL is a completely different lipoprotein than LDL, and tends to have a direct relationship with trigylcerides. Higher triglycerides = higher vLDL, and smaller triglycerides = lower vLDL. However, I’ve seen cases in which small LDL particles can be high, even when trigylcerides are low.

    I’d be interested to know your thoughts on this. Thanks!

  15. Dave

    Hi Ben-

    – Note I don’t actually address “small LDL” particles as a classification in this story, only that as triglycerides are being dropped off, the particle continues to get smaller. In fact, this first portion pretty much covers their journey as a VLDL until the last couple pages where the run into the HDL and it gets remodeled (read: turned into IDL).

    > vLDL is a completely different lipoprotein than LDL, and tends to have a direct relationship with trigylcerides. Higher triglycerides = higher vLDL, and smaller triglycerides = lower vLDL. However, I’ve seen cases in which small LDL particles can be high, even when triglycerides are low.

    VLDL is characterized by the added apos and being more triglyceride rich and larger. LDL (as a classification) is really just a possible end stage of VLDL-origination (if it isn’t absorbed by the liver first).

    And yes, there are definitely cases where trigs are low with high small LDL – Pattern B. I see a higher proportion of this with keto athletes.

  16. Ben

    Thanks for the clarification. It just seems easy to misunderstand from your sixth slide, which states that there are two types of LDL, and it seems to say that one form of LDL is vLDL. The 7th slide seems to state that the other form of LDL is the chylomixron. Glad to hear that this is not truly what you were trying to communicate.

    1. Dave

      I *am* trying to make that distinction between Chylomicrons and VLDLs. I consider those the two major classifications.

      I know in the literature the term “LDL” is often in reference to a *stage* of the VLDL. (VLDL > IDL > LDL) And this is why I just typically say “LDL particle” in casual conversation given the blood test for LDL-P encompasses all apoB containing lipoproteins. It’s frustrating for many who are trying to learn this process how unintuitive these terms are.

  17. Brian Williams

    Hello, this is a great series! Any idea when Part 3 will be out?

    Thanks!

    1. Dave

      Thanks — at the moment I’m spread pretty thin, but my hope is that I’ll have Part III out this summer.

  18. Rafael

    So basically I don’t have to worry about having a 321 mg/dl cholesterol and a 240mg/dl LDL right now?

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>

*