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!
















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  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!


    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.”

          Key lines from Norwegian study:
          “Among women, cholesterol had an inverse association with all-cause mortality [hazard ratio (HR): 0.94; 95%”

          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.


            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!


    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


    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?



    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


        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?


        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!

          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


            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?



          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,


  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?


    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?

    1. Dave

      The short answer is: we don’t know.

      Obviously, I’m operating at a higher level of cholesterol that came with my keto diet given all the information I have to this point and my low markers of inflammation. But If I see any signs of atherosclerosis, I’ll change gears with the data (and report it here, of course). But in short, I’m cautiously optimistic.

  19. greylearning.com

    Foods like oatmeal, apples, prunes, and beans are high in soluble fiber, which keeps your body from absorbing cholesterol.

    1. Dave

      I plan to do some experiments with fiber soon. But in tracking the fiber intake I already have, I’m not seeing a significant change based on inputs.

      To be sure, 85% of cholesterol is endogenous (produced within the body), and this is counterbalanced with existing absorption anyway. So while it might have some impact, I’m guessing it won’t be as significant as say 15 or 20% or more.

  20. rebt.com

    Foods like oatmeal, apples, prunes, and beans are high in soluble fiber, which keeps your body from absorbing cholesterol.

  21. stan straub

    I have been on LCHF for about a year. I have lost weight, feel good. I had a cholesterol PARTICLE test done. My doctor who ordered it then called, and said “we need to do something about your cholesterol”. Before I started LCHF, my cholesterol levels were moderate, NOT high (according to the standard cholesterol test and my doctors opinion). Now they are high. But I’m not able to interpret the results, and I’m a little fearful. My doctor won’t help me interpret the results…..he just sees “high”. If I give you the results, can you help me with deciphering them? I sent them to Dr. Andreas Eenfeldt at Dietdoctor.com and he said “As far as I can see these numbers are relatively average for the population. Hard to give a more useful reply without knowing your other health situation and what the numbers looked like before LCHF, etc.”. Not too helpful.
    These are my results. I would sure like some peace of mind, one way or the other, if you would be so kind as to help me.

    LDL-P = 1836
    LDL-C = 208
    HDL = 47
    Tryglicerides = 65
    Cholesterol = 268
    HDL-P = 26.1
    Small LDL-P = 371
    LDL Size = 21.7
    LP-IR Score = 33

    Thank you so much.

    1. Tigris

      This is the rabbit hole many of us have fallen into, finding out that establishment nutrition/health practitioners have serious flaws in their understanding of cholesterol, but not sure what to do about it.

      If your concern is CVD, from my understanding of the research, the best test is to get a calcium score from a CAC. LDL is only very weakly predictive and possibly only so because its a marker for insulin resistance.

      For me, my wife is in the category of concerned and not (yet?) well-read. Getting the CAC test (assuming my result is good) will be sufficient for her to let me KCKO. As far as my doc, I’m not sure if I want to switch, educate, or ignore. I’m gathering some data using the Feldman protocol so that my next appointment will be more interesting.

    2. Michael Lawson

      Your numbers are very similar to mine. I too have been LCHF for about a year and half now and feel great because of it. My reason was not so much weight loss ,but to get relief from post concussion syndrome, which it helped greatly.

      I was concerned about the LDL-P being high after reading Dayspring/Attia thoughts on this, but Jimmy Moore says high LDL-P isn’t necessarily a problem as he has carried an absurdly high LDL-P (over 3000) with a CAC of 0 and CIMT scan showing no arterial blockage.

      This doc also shares the same sentiment on LDL-P:

      My numbers:

      1. Craig

        Thanks for sharing that your numbers and that link, it was a great read. Certainly relevant for my situation.

  22. Pieta

    I am a medical doctor from South Africa. Hyper-responder on LCHF. Cholesterol now at 9mmol/l (360)
    would like to partake in your study.


    1. Dave

      I may have a write up for a remote one up pretty soon. Stay tuned. 🙂

  23. Vaduvur Kumar

    Part 1 & 2 are really informative.

    1. Dave

      Thanks! I hope to have Part III up in the near future, but these take a lot of work, so no promises.

  24. carmelchamba.org

    Foods like oatmeal, apples, prunes, and beans are high in soluble fiber, which keeps your body from absorbing cholesterol.

    1. Dave

      I’ll have some future experiments that will actually test that variable (soluble fiber) directly.

  25. kk lim

    Hi Dave,
    My mum have been on LCHF for close to 10 months now and a comparison of her lipid panels shown below (before and after LCHF):

    (in mg/dL)
    Total Cholesterol : 313 to 444
    Triglyceride : 242 to 102
    HDL : 50 to 60
    LDL : 214 to 364
    TG/HDL : 4.84 to 1.7

    1. Is she what you would consider a “hyper-responder”?
    2. Obviously the worry here is the upshoot in her LDL. But I told her that all her other important markers have improved – increased HDL, reduced Triglyceride, improved TG/HDL ratio. Her BP is normal and she has reduced her BP medication by half (50% less frequent intake of BP pills).
    Are her worry confounded? Or am I too optimistic?
    3. She also conducted a lipid sub-fraction test and she has about 27% small LDL (percentage excludes VLDL). Her VLDL number is 51 mg/dL. I.e. she has overall Pattern B particle size. Is that something to worry about?


    1. Dave

      1. Yes — that definitely fits a Hyper-responder.
      2. Yes, I’d consider her markers substantially improved, particularly triglycerides. BP, in particular, has a very strong association with CVD (where LDL does not).
      3. 27% small LDL is actually in line with most hyper-responders. I’m not sure why they are coming to Pattern B unless it’s quantitative, not qualitative. Is she thin or average, but not overweight? The VLDL being at 51 is further indicative she is properly using triglycerides for energy (as would be appropriate for low carb) and isn’t likely very insulin resistant.

      Honestly, I think this lab looks good from a lipid standpoint. I always want to see TG and HDL because they can tell the larger story as to whether LDL is high for a *bad* reason (IR, infection, injury), rather than a good one (energy transport due to being LC).

      Oh — and by the way — let me cut paste these comments I made regarding women and high cholesterol. I’m confident you’ll find it quite powerful:

      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.”

      Key lines from Norwegian study:
      “Among women, cholesterol had an inverse association with all-cause mortality [hazard ratio (HR): 0.94; 95%”

  26. Chuck W


    Enjoying your blog, videos, and cartoons!

    I had a couple questions regarding lipoproteins:

    Are VLDLs/LDLs _delivering_ cargo to fat tissue, _picking up_ cargo from fat tissue, or a little bit of both?

    During conditions of fasting and/or low carb dieting, what is the primary energy transport from fat tissue to other tissues of the body? LDLs? HDLs? Free fatty acids?

    -Chuck W

    1. Craig


      Glad you found us! Fat is continually cycling through the body.

      To adipose (fat tissue):
      1. VLDLs deliver TG from the liver to various parts of the body, including adipose.
      2. Chylomicrons deliver TG from the gut to various parts of the body, including adipose.

      From adipose:
      3. Adipose releases FFA (free fatty acid), which gets picked up by Albium and returned to the liver. Other tissues can tap into this stream of energy, but I’m not sure the exact uptake mechanism.

      I don’t haven numbers or ratios, but I my guess is VLDL are going to be doing the bulk of the work during fasting. Especially during periods of energy demands, like exercise.


      1. Chuck W


        Thanks for the reply, I had trouble finding this info from other sources.

        So from the perspective of the adipose cell, release of FFA is the only “way out” for fat energy?

        -Chuck W

  27. annie

    Hi Dave –
    I think that I’m a hyper-reponder as well and would be in a study if possible.
    I realize that you’re not a Dr but you do have lots of experience reading the #s and I would love your opinion.

    I’m 55, female and have been on a keto diet for 7 months. I’ve lost 35 lbs and am within 5 lbs of my maintenance weight. My bloodwork prior to keto was all great. Last week I had my first blood work since keto and some of the #’s are now through the roof.
    Cholesterol 302
    TG 60
    HDL 78
    VLDL calc 12
    NonHDL Chol 210
    LDL-P 2274
    LDL-C 218
    VLDL size 70
    HDL-P 27.9
    My Lipidologist (who is on keto but has normal bloodwork) thinks I’m possibly a hyper-absorber.

    I’m seriously concerned about CVD and would love to hear your thoughts

    1. Dave

      Hi Annie,

      Your numbers are actually very standard for a hyper-responder. VLDL count is low, TG are very low, yet your HDL is nice and high — everything IMO looks very solid.

      Moreover, as a 55 year old female, you’d have more reason than not to *want* higher cholesterol. I actually address this in a comment earlier in this thread –> http://cholesterolcode.com/a-simple-guide-to-cholesterol-on-low-carb-part-ii/#comment-11199

      I often joke that if I were female, I’d have long abandoned my research and probably continued doing software development given how much *stronger* the case is for high cholesterol with the opposite sex. 🙂

  28. Annie

    Thank you, I appreciate your response!

  29. Jim

    Just watched your presentation at Low Carb Breckenridge and thought it was great. I will be starting (again) a LCHF diet in January and will get some blood work for your “study”. I am going to lef.org to purchase the CBC panels for $35 each. I think that is the best price around for blood work. Do you know of another I should look into?
    Just started following you on Twitter as well. Thanks for your work

    1. Dave

      CBC = Complete Blood Count. It’s great for a number of markers related to such things as White Blood Count (WBC) to check when sick, etc — but it isn’t a lipid panel.

      I recommend seeing if you get a “Standard Lipid Panel” which is typically cheap ($20-40), or “Nuclear Magnetic Resonance” (aka “NMR”), which is typically not as cheap (typically $99). These will give you cholesterol markers. The former will be LDL-C, HDL-C, Triglycerides (and hopefully VLDL-C). The latter will give you all those and a complete breakdown of your LDL particles (total, small, etc).

  30. jim

    Thanks for the info…and here is what Life Extension does for the $35…they do an annual sale too where you can buy a years wort of tests: http://www.lifeextension.com/Vitamins-Supplements/itemLC381822/Chemistry-Panel-Complete-Blood-Count-CBC-Blood-Test

  31. jim

    Just noticed they call it this: Chemistry Panel & Complete Blood Count (CBC) .. Sorry for the confusion

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