Dec 30

A Simple Guide to Cholesterol on Low Carb – Part I

If you’re on a Low Carb High Fat diet (LCHF), there are a few things you should know about cholesterol and how it is related to this lifestyle. In this guide I plan to cover the topic in very simple terms. It is by no means complete and is intentionally simplified to make it easier to read and understand for the layperson.

Our Energy on a High Fat Diet

Before talking about cholesterol, we have to talk about the energy you get from fat when on LCHF. Of course the main reason for food is to supply your body with energy. But how does that energy get to everywhere it needs to go in your body?

Like every other living thing, your body is made up of cells. Your heart is made of cells. Your brain is made of cells. So are your fingers, knees and toes. Almost all these cells need energy. And the vast majority of these cells ultimately get their energy from the blood circulating around your body.


The most commonly talked about source of energy is carbohydrates (carbs). Your body turns carbs into glucose to put in the bloodstream. From there the glucose can circulate throughout the body, allowing hungry cells to grab some for themselves, and this is done with the help of insulin.


The other major energy source for your cells is fat, and by that I mean fatty acids. And like glucose, your cells also get their fatty acids from the bloodstream. Only there’s an important catch: glucose can swim in the bloodstream easily, but fatty acids cannot.

Fatty acids and the bloodstream are like oil and water, they don’t mix well. To fix this, your body cleverly does two things:

  1. It packages three fatty acids into a combo pack molecule called a “triglyceride”.
  2. And it makes a kind of boat for these triglycerides to travel in called a “lipoprotein”.

In fact, the kind of lipoprotein that delivers all these fatty acids is known as a low density lipoprotein — but you probably know it already by it’s abbreviation, LDL.

Trigs vs Glucose

Common Confusion with LDL

Odds are you have most likely heard of LDL being used to describe cholesterol on a blood test. “Your LDL is high…” for example. So what gives?

Here’s the thing about cholesterol, like its triglyceride cousin, it also doesn’t swim well in the bloodstream. In the medical world, these molecules are commonly referred to as lipids. And lipids are actually repelled by water, so they are commonly called hydrophobic (hydro = water, phobic = repel). So when someone tells you they love to go to the beach but hate the water, mention they must be hydrophobic like cholesterol!

Yet what if the body has reason to have cholesterol available in the bloodstream as well? (We’ll get into that more in Part II) And while we’re on the subject, there are a few other things the body wants available to cells that are also hydrophobic, such as fat soluble vitamins (like Vitamin E).

So should it make a separate lipoprotein container for each of these molecules? No! It effectively packages all of them into the same boat: the low density lipoprotein.


That’s the genius of the human body. It has a kind of FedEx for all the hydrophobic elements needed by the cells. And most of whatever isn’t used gets recycled by the liver for many other possibilities, such as hormone or bile salt production.

Common Confusion with Triglycerides

The odds are likewise that you’ve heard “triglycerides go down on a low carb diet”. Indeed, blood tests for those going LCHF are almost universally lower in triglycerides. But a measurement of anything in the bloodstream is counting what is traveling around in that moment and not yet in use.

For example, Type 2 Diabetes has a common symptom of having very high glucose in the blood. This is because these diabetics are insulin resistant and have trouble getting the glucose out of the blood and into their cells. They may eat the same quantity of food as someone who isn’t diabetic, but glucose in the blood will spike higher and last longer by comparison.

If you have reduced your carbs and now get your energy mainly from fat, without question your cells are absorbing more of it from the bloodstream now. So even if you’ve increased the total amount of triglycerides going into the blood due to the diet, it is still brought down by the amount getting taken back out and used by the cells.

Common Confusion With Ketones

Another common assumption with LCHF is that you “get the majority of your energy from ketones” since you are in a state of ketosis. It’s certainly true your body makes many more ketone bodies from breaking down fatty acids, which will likewise feed your cells. This is especially important for proper brain function as ketones have special access that lipoproteins do not.

Yet while ketones are both produced and used much more on LCHF, they are still a secondary source of energy. The primary source of energy is still fatty acids brought to cells in LDL particles.


More Cholesterol is Trafficked on a Low Carb High Fat Diet

Now that you understand your body has need to move around more triglycerides to fuel your cells while getting the majority of your energy from fat, you may have already connected the dots.

  1. Your cells need energy
  2. On a high fat diet, their primary source of energy is triglycerides
  3. To get the triglycerides to your cells, your body sends them in low density lipoproteins
  4. All low density lipoproteins are made containing both triglycerides and cholesterol (but mostly triglycerides)

What are the Risks?

If you read the above and are struck with fear, I don’t blame you. It has been well drilled into our heads that more cholesterol in the blood = higher risk of cardiovascular disease and stroke.

But if you’re early in your research on this topic, let me help you skip ahead with one very crucial point (which I alluded to above). Making something available is not the same as using it.

Here’s a simple analogy – life rafts in the water and being used are typically a sign of trouble. Yet all ships sail with them on board. This is a good idea in case of an emergency, of course. But if you were only counting life rafts whether in use or not, then you’d assume a lot of ships entering view was by itself a sign of trouble.

Cholesterol is like the life rafts on the LDL ships. Even if it travels with your triglycerides, it is a much smaller passenger (in quantity) and mostly recycled back at the liver. You don’t actually care how much cholesterol is in your blood — you care how much cholesterol leaves the bloodstream and causes a build up of plaque in your arteries (atherosclerosis). And this is at the core of the inflammation debate with cholesterol. Is it a life raft for damage to the blood vessels? Or is the sheer presence of it risk alone? (You can probably guess where I fall on this one.)

In Part II we cover part of the journey of cholesterol in more detail through a very visual comic form. (Part III is coming soon…)


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  1. Samantha Baker

    Great post Dave, love it! Makes it all so simple to understand. Bravo!

    1. Dave

      Thanks, Sam — that’s what I’m going for. 🙂

  2. bill


    1. Dave

      Speaking of fun, I have a friend I collaborate with on some games we’ve made (I’m a software developer). He’s suggesting making this into a game for added fun / education. If we get some time (unlikely) in the next few months, we might Game Jam one out.

  3. Joe

    Thank you for the time you put into this excellent and simple summary. Looking forward to the series so I can share it with my less geeky friends in the hope that their eyes can be opened. Will likely also share with my doc who I have brought on board with LC but not HF. Gave him Big Fat Surprise for Christmas and hope it will have the same effect as Why We Get Fat!

    1. Dave

      Yeah — thus far it has already broken session hits relative to my other posts, and it’s barely 24 hours old as I write this!

  4. Dave Winebrenner

    I can see the particle count people circling the wagons now Dave:)

    I am with you on this!

    Awesome first part.

    1. Dave

      Yeah, but I welcome the debate. 🙂

  5. Diana

    Terrific explanation. looking forward to part 2

    1. Dave

      Thanks, Diana — should be coming soon.

  6. Wim Tilburgs

    Great explanation. Will share it. Looking forward to part 2

    1. Dave

      Thanks, Wim.

  7. Charles Grashow


    You said – “In Part II, I’ll discuss my own research and data, and why it has alleviated my concerns about having high cholesterol while on a low carb diet in greater depth.”

    SO – if high cholesterol on a LC diet is not really a concern why do all of these experiments with regard to cholesterol?

    1. Dave

      The research is key to illuminating differences in how the current perception of cholesterol management is in the literature vs how it is illustrated in my data.

      I’m extremely interested in the lipid system as a whole, not just with regard to cholesterol, but with the overall management of everything within — especially energy.

  8. Angela

    Great explanation! And way to leave me hanging. 🙂 Looking forward to part 2

    1. Dave

      Thanks, Angela!

  9. Doug

    Perhaps part II will answer my question, but you say: All low density lipoproteins are made containing both triglycerides and cholesterol (but mostly triglycerides). (Emphasis mine.)

    What are your sources for that? The trig/chol ratio in an LDL particle seems to be something that is highly variable, and IMO, clearly not true for folks with high LDL-C and low trigs – your point about the traffic vs content notwithstanding, at a given point in time, those people’s LDL are carrying mostly cholesterol. Also, mostly trigs in your LDL makes for small dense LDL, which is generally accepted to be a bad thing.

    One pertinent tidbit you glossed over is that on a high carb diet, once glycogen stores are high, the liver will convert calories not immediately needed into trigs, which of course, is why folks on high carb diets have high trigs.

    1. Dave

      Hi Doug-

      – Chylomicrons and VLDLs are the originating LDL particles (ApoB48 and 100, respectively). Chylomicrons start with 84% trigs, 8% cholesterol. VLDLs start with 50% trigs, 22% cholesterol.

      As each of these move through the bloodstream they release more and more triglycerides to cells and through CEPT, which is how they become more cholesterol rich (relatively) toward the end.

      This generally came from many biochem sources when I first began to study this subject, like here. While I think there could be arguments on the exact degree of percentages with variability, I don’t know of anything that argues the proportionality of triglycerides to cholesterol.

      – Again, a blood test is a snapshot of objects in transit and in their current state. LDL particles change their content over several stages and even their apolipoproteins to some extent.

      Here’s an analogy to illustrate:

      Let’s say you and are pizza delivery drivers. We both start off with 50 pizzas in our cars, and every three hours we return to the kitchen to refill our car back to that number. Throughout our shift you deliver a total of 100 pizzas while I only deliver 10.

      If someone were to randomly pick a time at some point during the shift to peek into our cars and count how many pizzas we had, I would likely have more than you did, of course. This makes perfect sense from a demand-driven perspective. It also illustrates why you can’t assume from a snapshot that one of us started out with more, nor does it accurately show how much is getting delivered.

  10. Deborah Burdette

    Thank you….I’ve always refused the medication for cholesterol and triglycerides……

  11. Chad Nordstrom

    Great job!! Enjoying your efforts and posts. Thanks for sharing all this.

    1. Dave

      Thanks, Chad!

  12. Karen

    What about HDLs I am interested in how HFLC increases HDL Levels, my skin and joints has never been better since being on this diet

    1. Dave

      No worries, I’ll be getting around to HDL soon for sure.

  13. Rob

    Great post Dave! I like the different way of looking at it. It all makes complete sense. I’ve had 10 NMR’s myself since starting LCHF in 2011, and my numbers have been high. I would be curious what Dr. Thomas Dayspring had to say, since he says”particle number, end of discussion”. I’m with you though Dave!

    1. Dave

      I’m occasionally pinging Dr. Dayspring, but haven’t gotten word back just yet.

  14. Chris Jones

    Hi Dave, this is all very new to me as I’ve started a LCHF diet last week but just got back the results for my cholesterol tests and they are high. That prompted the question “how am I supposed to reduce fat intake if I’m on a LCHF diet?”. Based on the misinformation surrounding the whole “fat makes you fat” nonsense, I don’t fully trust what the doctor is telling me regarding reducing fat to improve cholesterol numbers.

    So after reading this post a couple times, I came to the following summary. Please tell me if I’m misunderstanding:

    – The body packages three fatty acids into triglycerides

    – LDL carries both these triglycerides AND cholesterol through the blood stream

    – This allows the triglycerides to be absorbed and used as energy (“burning fat”)

    – Also allows the cholesterol to move through the bloodstream rather than to build up as plaque

    Now if I’m right on these points, then I also have the following questions:

    – Why is a high LDL count bad? It sounds like more LDLs would be better as that means more cholesterol can be carried through the bloodstream rather than building up.

    – Where does the cholesterol go if its not building up as plaque?

    – How does a LCHF diet affect this process, besides just having more fatty acids and therefore more triglycerides, and therefore more LDL(?)

    And to follow up on the last point, the impression I’m getting is that for a diabetic (or close to it) with high cholesterol would be better to just “ignore” the high cholesterol and LDL counts because the fat being burned from the LCHF diet is “worth it” overall, and that eventually it all balances out naturally over time because the body as a whole becomes healthier.

    I’m not the sharpest bulb in the box as you may have noticed, but I’m trying my best to at least understand at a very fundamental level what is going on when you combine LCHF with a high cholesterol number.

    1. Dave

      Excellent questions, Chris!

      >> – Why is a high LDL count bad? It sounds like more LDLs would be better as that means more cholesterol can be carried through the bloodstream rather than building up.

      That’s a difficult to answer question. The pro Diet Heart Hypothesis people would suggest more total LDL particles circulating in the system = higher overall risk of atherosclerosis. I feel quite different given a number of large scale issues with the overall outcomes observed. (For example, those with higher cholesterol in the elderly population present lower all cause mortality.)

      >>– Where does the cholesterol go if its not building up as plaque?

      Most of the cholesterol in LDL particles ultimately end up at (or back to) the liver. I often describe them as “life rafts” on boats or “spare tires” on cars as their behavior is appears more as an emergency backstop instead of a constant usage like triglycerides. Remember, almost every cell membrane is made up of both cholesterol and phospholipids, both are inside LDL particles which can be consumed for spare parts by the cells. But most people assume the more you have circulating in LDL particles, the more you *necessarily* deposit them in your vessel walls as atherosclerosis. I definitely don’t share that opinion as the correlation isn’t very strong at all (given the hypothesis, it should be a very solid line with a near logarithmic curve).

      >>– How does a LCHF diet affect this process, besides just having more fatty acids and therefore more triglycerides, and therefore more LDL(?)

      You’re getting the most important part right there. To complete the thought, more LDL particles (LDL-P) means more *trafficking* of cholesterol (just has having more ships circling the bay means more liferafts technically circling with them).

  15. Nicole Recine

    I love this! This helped me understand why Peter Defty told me cardio may help lower my trigs. I just need to use them. On to part 2 🙂

  16. Drifter

    Thanks for taking on this topic…Several things, in case you haven’t seen it, here is Dr. Rocky Patel’s post where he describes how his particle count was “high” when he went LCHF, however his arterial plaque actually reduced during that same period. That to me is the holy grail so evidence like that from clinicians seems particularly important. He also has a good discussion of the inflammation markers he uses and some good discussion in the comments section. Unfortunately he doesn’t seem to be blogging or podcasting anymore, but here is the post:


    Also, I haven’t seen you cover oxidized cholesterol, but maybe I missed it. I would strongly recommend Chris Masterjohn’s writing on this topic if you haven’t seen it. I am also a hyper-responder so I have been following this topic for a number of years. While it seems fairly clear that many people can have what mainstream “medicine” would consider elevated cholesterol and still be perfectly healthy, there are also some other issues which can also creep in which are likely worth addressing. Specifically, Dr. Gundry has said that in his experience he often sees people with a high level of oxidized LDL which resolves if they switch to A2 casein instead of A1 casein and reduce cheese consumption. It seems that while LDL is far from the most important issue, it is still worth considering if related factors like problem foods are creating an unnecessary elevation.

    1. Dave

      Hi Drifter-

      Sorry for the late reply, this one somehow flew under my Comments Radar.

      – Yes! I’m very familiar with Rocky’s post and even tried to reach out to him a few times. It’s true he isn’t as active lately, but I can understand that. Social media can be unrelenting sometimes. 🙂

      – Yes, I’m familiar with and have read much of Chris Masterjohn’s work (and highly recommend it). But I haven’t done much specific oxLDL testing because I still feel the technology is in its infancy. Moreover, there’s almost no test I will take unless I can take it several times over — as you can see by my blog. There are several reasons for this, but the biggest is to help disqualify tests that appear erratic and error-prone given how they do/don’t match up with other markers appropriately. If you’ve been closely following this subject, I’m sure you understand why I’m less willing to spend the $$$$ on emerging tests, particularly when the initial studies on the tests involve researchers with stakes in the patents/IP.

      – I think I came across the A1 v A2 casein discussion before but it was early on in my research before I understood the lipid system as I do now. It is probably worth a revisit – thanks!

      – “It seems that while LDL is far from the most important issue, it is still worth considering if related factors like problem foods are creating an unnecessary elevation.” — I couldn’t agree more. BUT, my research is exposing why the use of a single LDL test as a marker is so problematic given how dynamic it is with regard to food just consumed in the previous 3-5 days. So much of where this leads me is to respecting the technology that gets me the data, but being much more skeptical of studies that use it outside this context (which is all of them, for now).

  17. Ray Klepper

    Thank you so much for your continued pursuit of this topic. I am a physical therapist and have been relentless with my self education regarding nutrition over the past 2 years. I am scheduled to speak with a cardiothoracic surgeon who is very into nutrition and primary prevention as well. His interest is how to best lower LDL without a statin. I’m not sure how he will respond when I bring up the idea that LDLc is a terrible biomarker per Dr.Dayspring and per other articles, data and experience. What I would like is to use your examples to tell the story and also to pick your brain a bit more regarding specific nuances to make sure I have my bases covered. If you are able to could we communicate through email? I will leave my email below and hope to hear from you. Thanks again.

    1. Dave

      Hi Ray-

      Per your comment and my response on Twitter, I did reach out to you through the email you provided.

    2. Rob

      Hi Ray and Dave–I’m a speech therapist at a major hospital in DC and am developing nutritional advice for stroke patients along with help from clinical dietitians. Unfortunately they are very usda guidelines focused and tend to recommend way more grains and carbs than I do and they definitely steer patients away from saturated fats. Any luck developing good advice for lowering patients risk of cardiovascular disease? Feel free to email me or connect me to Ray. Thanks.

  18. Pat

    I see your previous comments re: Dr Attia so no need to respond!!

  19. Andrea Mikler


    just found your site today and can’t stop reading. I love your analytical engineering aproach to it. When are you going to write about HDL?
    I am very interested to know the mechanism of my HDL increasing on ketogenic diet to the point that is much higher than my LDL. I have been on low carb for about 4 years with the last year being mostly keto. My Total chol in 2013 was 200, HDL was 94, LDL 100 and Trigs 0.38. My last test in Sept. 2016 Total chol. 238, HDL 125, LDL 103, Trigs 0.5. What does it mean when HDL is higher than LDL and is that ever a concern? I do not see this ratio very often.

    Thank you for all your work

    1. Andrea Mikler

      Oh just noticed I converted cholesterol numbers from mm/l to mg/dl but did not convert triglycerides. They went from 34 to 44.

    2. Dave

      I ultimately care much more about my HDL than my LDL. And I want it to be high! Or at least above 60…

      I can’t say for sure that unusually high HDL such as yours is problematic, but I’m very doubtful. In your shoes I’d want to get an NMR to determine both my HDL-C *and* HDL-P. Not to set off your alarms, but its a theoretical possibility that you have normal or low HDL-P that are very engorged with cholesterol, which I’ve seen before in one other person’s lab.

      But again, I’m pretty sure you’re more than fine. 🙂

  20. Dave Braatz

    Might need another category: My cholesterol and triglycerides have always been high, but I remained skeptical of taking statins. From 2001 to 2017 (N=22), my TC averaged 260; TG avg 356; HDL avg 37; LDL avg 169; glucose 94 (all after 12-hr fast, and on HCLF diet).

    In 2010, my blood after a 4-day water-only fast showed TC=312; TG=271; HDL=34; LDL=224; and glucose=62. I assumed my TG dropped because my glucose fell, but I was surprised at the jump in my TC.

    I went keto in 2017, and my June bloodwork (non-fasting; LCHF) showed a huge spike in TC to 397; a spike in TG to 740; a drop in HDL to 29; LDL not calculated; and glucose at 92. The rise in TC fits the hyper-responder profile, but WHY would my triglycerides skyrocket (especially with a modest non-fasting glucose at 92), and why would my HDL drop?

    I did the June blood test as non-fasting because of the logic in the Life Extension article “Should you fast before a blood test?” in their May 2017 issue. Good reasoning, and I’d appreciate your opinion. http://www.lifeextension.com/Magazine/2017/5

    1. Dave

      Hi Dave–

      – Your bloodwork is very unusual. Obviously, it suggests hypertriglyceridemia. But I haven’t seen a series at your level that also had pre- and post-keto.

      There appears to be a lack of uptake for your TG at the cell level making me wonder if it is something genetic with LDL lipase or similar mechanism at that phase.

      It is certainly odd to see TG rise and HDL stay the same or fall after going LCHF.

      – I most definitely DO NOT advise eating near a test. I always strongly recommend having at least a 12 hours fast given the clearance of Chylomicrons isn’t strongly determined in the hours after a meal — but it IS fairly assured to be cleared in the 12 hour time span.

      Because of this, I’d want to retest your June 2017 bloodwork with a 12-14 hour fast to see if you get the same results. As always, be sure to eat to your “general” range in the three days before as well, given the Inversion Pattern.

      – If it’s okay with you, I may pass your numbers by a few of my doc friends to get their opinions. I’m curious how many have seen anything similar.

  21. David

    This is a subject close to my heart cheers.

  22. Scout Dawson

    Dr. Michael Eades linked to your website, so I thought I would check it out. This ‘beginner’s guide’ is amazing and really informative. The cholesterol thing is something I have always been quite confused about (and I did wonder why long-term keto’s had “high” blood pressure after many years).

    This has cleared up any worries I had. Time for a steak? 😉

    1. Dave

      Thanks, Scout!

      Although I am curious about your comment on long term keto bringing “high” blood pressure. I find it is the opposite.

      And yes, it’s always time for steak. 😀

  23. Roger


    Your work is awesome! I use your data to disrupt conventional medicine every chance I get. That said, what is your generic advice for FH patients?



    1. Dave

      Hi Roger–

      Actually, almost everyone who is a Keto/LCHF hyper-responder has LDL levels consistent with one who is FH, but only a few have been *genetically* FH.

      Have you confirmed your FH status as genetic? For example, if you have 23andMe, you can check against specific SNPs to determine: https://www.snpedia.com/index.php/Familial_hypercholesterolemia

      Generally, if your cholesterol was “normal” or low before starting the diet, then changed to very high levels soon after, then it is unlikely to be genetic FH as you’d have likely had high cholesterol your entire life.

  24. Leslie

    This article is very good in helping me understanding cholesterol. I started a LCHF way of eating about 5 weeks ago. I lost some weight but didn’t have much to lose. I went to my yearly appointment and they checked my labs. My TC was 290 and my LDL was 210. I am 37 years old, 5’4″ and weigh 117. I don’t know if that information matters. From my understanding, these numbers don’t mean anything and I would have to have my particles checked to see if there is a real issue. thanks in advance for any information.

    1. Dave

      Hi Leslie–

      I’d want to know a little more to give my opinion —

      What is your HDL, Triglycerides?

      Also, are you lean and/or athletic?

  25. Mansoor

    Hi Dave thanks for the invaluable insight you gave me about cholesterol. After 4 months of keto I had my blood work done I realized my cholesterol was high.My weight is 70 kg and I’m 178 cm high.I’m moderately active .

    Total: 238
    LDL : 160
    HDL : 66
    Triglyceride: 62

    I have heard if LDL cholesterol is over 130 it’s not healthy and the small dence particles are high. I don’t know how they came up with this number.In my country NMR test doesn’t exist.I really love this diet but there are alot of confusion. How can i get more information about my condition? Thanks you so much.

    1. Dave

      After now seeing hundreds of labs, I can say the pattern is generally true that if you have high HDL and low TGs, you typically don’t have many small dense LDLp.

      If you’re concerned about lowering your LDL, you will likely have success replacing more of the dietary fats with carbs.

  26. Pratik Jhaveri

    Been on a LCHF diet for the last 2.5months (was in keto for a bit). Lost ~20lbs during that time. Went in for my blood test last week and was surprised to find that my cholesterol went up. Good news is that A1C dropped.

    A1C – went from 6.3 to 5.7
    Total Chol – from 257 to 292
    LDL – from 181 to 212
    TG – from 194 to 215
    HDL – remained same at 37

    I read through your simple guide to cholesterol and was trying to understand the reasons for the possible increase. In addition, what other tests should I do to get a more accurate picture of the risks?

  27. Dave

    Hi Pratik

    That’s a pretty unusual profile for low carb. I’d like you to consider tracking your food closely moving forward. When I’ve seen HDL low and TG high *despite* going low carb, I’ve found there have been “leaks” in the diet. This has been predominantly the case with my family and friends when working with them directly. It’s possible you have other forms of carbs you’re not catching as easily (in my f/f case, it was usually condiments, sauces, drinks, and often one or two favorites they assumed were fine and turned out not to be).

    This was especially the case with my dad. When his TG went up and HDL went down following a better period, we went closely through his diet and found two key leaks — an asian dish he thought was “light cheating” and heavy whipping cream he didn’t know had 1g carb/5ml (different brand than he normally gets, but he wasn’t watching the label).

    For more expanded tests, check out Craig’s excellent article — http://cholesterolcode.com/lab-testing/

  28. Lisa Mayo

    Hi Dave
    Thanks for your work.
    Trying to understand the numbers and conversions and just looking for some clarity of direction. If you have the time please can you check my recent blood work.
    I am a 54 yo female , train 3-5 times weekly weights / cardio 62 kg and 154cm.
    total cholesterol 8.3
    trigs .0.9
    hdl 2.1
    ldl 5.8
    fasting glucose 4.2
    CRP 0.5
    Thinking low trigs , CRP and fasting glucose good and HBAiC in range probably a good predictor. however high LDD and total cholesterol still a red flag but with low trigs my be a indicatory of minimal risk of small dense LDL particles ? Think a cac scan and lipid subtraction analysis will give greater clarity?
    Appreciate your thoughts
    Thanks again
    Lisa M

    1. Dave

      Hi Lisa,

      You definitely appear to have the profile of a Lean Mass Hyper-responder. Take a look at this post and some of the many comments within… http://cholesterolcode.com/are-you-a-lean-mass-hyper-responder/

  29. Lisa mayo

    Thanks Dave yes thought I might fit into the hyper responders group . Thanks for your teply . Also great presentation at the Gold Coast gave more clarity to my numbers and my understanding

  30. Stefan

    Great ..is there a write up where you explain HDL (Good), LDL (Bad) Cholesterol and Triglycerides. New to this an my doc always wants to put me on pills to lower my cholesterol ..like to get more informed before I swallow a pill. ( sorry about my english I am from europe) . thx

    1. Craig

      Start with the Simple Guide.

  31. Lou Malinow

    Very well done. I am an internist, a lipidologist, and a hypertension specialist and I preach ketosis for many patients. I would make one constructive comment……a “typical” LDL particle is 4 parts cholesterol to 1 part triglyceride, so most of the baggage on the ships isn’t triglyceride (unless you’re dealing with an insulin resistant patient with high VLDL). VLDL (recipe: combine a bunch of triglyceride with a little cholesterol and wrap it with a lipoprotein called ApoB which you might refer to as the hull of the boat) has a triglyceride to cholesterol ratio of 5:1……..and that may be what you’re referring to.

    1. Dave

      Hi Lou!

      Firstly, constructive comments are *always* welcome, especially from those in the know. 🙂

      Since you’re a lipidologist, I can speak geek with you!

      LDL particles picked up from a fasted cholesterol test are mostly VLDL-originating. Which is to say, they start with many more TG than cholesterol but quickly drop them off in the initial stage while they have their apoCII for delivery. So in a sense, distributing energy is their biggest job from both a payload and activity perspective (just not a time-based one).

      Imagine someone who delivers meals all day Monday and Tuesday, and is then a volunteer fireman the rest of the week, but rarely does more than being on call. Their material impact is primarily on those first two days… unless of course, there’s a lot of fires going on!

      This is why you’re exactly right that having high TG matters quite a bit — it is common in a dysregulated state (typical of hyperinsulinemia/T2D) where the energy isn’t dropped off given the lack of takers now, thus leading to unremodeled VLDLs having much longer residence time.

      But likewise, it matters in the reverse! In a LCHF diet, if there’s a lot of LDL-C, yet low TG, this is very suggestive of proper energy distribution if it is concordant with LDL-P. More “boats” to carry more energy, and sure enough, the energy is depleted (remodeling the boats to LDLs that are TG poor). Thus, it seems pretty clear the upregulation of VLDLs is met with a likewise usage of the energy they bring, which makes perfect sense in a lower glucose, higher fat use environment.

      This energy distribution model is the core of my research and how I’ve been able to manipulate my own cholesterol numbers substantially (see presentations I’ve given linked throughout the site, such as the one I’ve given at Breckinridge: https://www.youtube.com/watch?v=jZu52duIqno).

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