Remembering Kevin Moore

6-Month Lipid Panel Update On My Nutritional Ketosis N=1 Experiment

Ever since I began my n=1 experiment of the concept of “nutritional ketosis” in May 2012 that has resulted in a 50+ pound weight loss so far while consuming lots of healthy high-fat foods to raise my level of blood ketones, people have been asking me about what’s been happening with my lipid panel. But as we heard from Dr. Jonny Bowden in Episode 632 of “The Livin’ La Vida Low-Carb Show” podcast this week discussing his brand new book on this subject entitled The Great Cholesterol Myth: Why Lowering Your Cholesterol Won’t Prevent Heart Disease and the Statin-Free Plan That Will, is this something we really need to be concerned about? Whether the answer to that question is yes or no, what do the numbers really mean anyway? And are they different for people who eat a high-fat, moderate protein, low-carb diet to produce an appropriate level of beta-hydroxybuterate (blood ketones) that Dr. Stephen Phinney and Dr. Jeff Volek discuss as optimal for health and performance in their bestselling 2012 book The Art and Science of Low Carbohydrate Performance?

I’m currently on a personal quest to find the answers to these questions and more by speaking directly with as many of my expert friends in the medical, nutrition and research fields over the next six months researching and writing my book all about this topic tentatively titled A Patient’s Guide to Understanding Your Cholesterol Test Results (releasing Fall 2013). People are so confused about what to believe about their cholesterol test results that this book is way overdue. Arming people with solid information will help them make a more informed decision about what to do about the current state of their health rather than blindly following some dubious drug therapy promoted by their doctor to treat risk factor numbers. It’s high time we start treating actual DISEASE rather than risk factors anyway.

But every single week, I receive at least a dozen e-mails from people all over the world who are concerned about their cholesterol test results. Even for those people who have gotten away from the traditional lipid testing that only shows LDL-C, HDL and total cholesterol to the more advanced particle size testing from places like the Raleigh, NC-based LipoScience who created the NMR Lipoprofile test, there is pause for concern because their doctor tells them they need to be taking a statin drug lest they fall victim to a heart attack or worse. I’ve never understood the scaremongering that goes on regarding “high cholesterol” and the knee jerk reaction that taking a pharmaceutical drug such as a statin will somehow protect people from ever having a heart attack. A timely example of this is the late television newscaster Tim Russert who had “perfect” cholesterol numbers while ostensibly on a statin drug and yet tragically died of a heart attack in June 2008. Watch Justin Smith’s $TATIN NATION documentary for more information about just how insidious this push for a risky drug therapy to treat a non-existent disease has become.

I’ve been a big fan of having my cholesterol tested using the NMR Lipoprofile test for many years because they are the only truly accurate cholesterol particle testing company in the world. According to lipidologist Dr. Thomas Dayspring who addressed cholesterol testing in Episode 29 of the “Ask The Low-Carb Experts” podcast recently, this cholesterol test from LipoScience is the only one that he’s aware of that will directly measure your LDL-P (the total number of LDL particles in the blood) and Small LDL-P (the dangerous Pattern B LDL cholesterol that penetrates the arterial wall and leads to atheroschlerosis). Knowing where your numbers stand is a critical starting point for anyone wanting to optimize their health. Your doctor can actually run this test if you ask for it (although some will think it’s unnecessary or a “fad”) or you can use one of those online health testing outfits like Private MD Labs that work with your local LabCorp offices to pull the blood without a doctor being involved like I did last week to get my latest lipid panel update.

In mid-November before leaving on my trip to Australia for a three week, 5-city “Low Carb Down Under” speaking tour, I’ll be sharing a 6-month update about my nutritional ketosis n=1 experiment (read all of my updates for Day 1-30, Day 31-60, Day 61-90, Day 91-120 and Day 121-150). I’ve got some really interesting information to share with you regarding an experience that has happened to me during this 30-day cycle that could help those of you who might be wondering why your blood ketones aren’t where you want them to be. I’m amazed by how much I’m STILL learning about all this and look forward to passing along what I’ve discovered with you in the months to come. My target date for publishing my Day 151-180 results is November 11, 2012 or sooner. Stay tuned!

There’s still a lot of controversy about whether the LDL-P number (and the parallel marker of Apo B) is as or more important than the LDL particle size. Dr. Dayspring is adamant that it’s all about the LDL-P number and that the size isn’t relevant when it comes to heart health. He explained his reasoning for this position in Episode 585 of “The Livin’ La Vida Low-Carb Show” podcast. And in his popular “The Straight Dope On Cholesterol” blog post series, Dr. Peter Attia notes that the number of LDL particles and not just their size determine the atherogenic risk. But a Gilbert, AZ-based family physician who specializes in heart attack prevention named Dr. Rocky Patel (listen to him in Episode 62 of the “Low-Carb Conversations” podcast) noted in his September 2012 blog post entitled Does LDL-P Matter? that his personal LDL-P score of “over 3000” was initially “horrifying” until he had a Carotid Intima Media Thickness (CIMT) test showing his vascular health was equivalent to that of a 16-year old! Additionally, his low-carb diet has helped him lose weight, feel energized and brought his inflammation (CRP) levels to “not detectable.” Cool! Dr. Patel concluded his blog post by stating a truth that should be the basis of all healthcare decisions: “We must always remember to treat the patient/disease and not the number.”

With that in mind, let’s talk about my various health numbers. As you know, I’ve been actively losing weight and body fat (we’ll know for sure I’m losing body fat when I get the comparison results of my DEXA scan coming hopefully before I leave for Australia) on my nutritional ketosis plan and that has not stopped nor do I expect it to in the coming months. But before I even started on this plan in May 2012, I had a Berkeley HeartLab panel of tests run in February 2012 to see how my low-carb diet was working for me. Despite weighing over 300 pounds at the time, some key health markers were pretty remarkable:

  • C-Reactive Protein (CRP) – 0.7 (less than 1.0 is “low risk”)
  • HDL-C – 78 (over 50 is considered stellar)
  • Triglycerides – 89 (under 100 is excellent)
  • I’ve said it many times before, but reducing your carbohydrate intake, moderating your protein consumption and consuming higher levels of healthy fats that include saturated fat are the best ways to not just lose weight but making critical positive changes for the better in your lipid panel happen. Laura Dolson discusses Three Reasons Not To Worry About LDL Cholesterol On A Low-Carb Diet and notes that HDL over 50 and triglycerides under 100 will almost always mean your LDL size is the Pattern A (large, buoyant kind) that you want. Dr. Jeff Volek has found in his research patients a greatly improved triglyceride/HDL ratio eating a low-carb diet and that this is a much better marker for heart health than LDL or total cholesterol. As far as I know, the advanced particle size lipid testing has not been used by Dr. Volek, Dr. Eric Westman at Duke or others looking at low-carb diets in their research. I hope that they do add this extra bit of data for the benefit of those who may see some crazy numbers like Dr. Patel and I (and I’m sure many other low-carbers) are seeing.

    So what about my latest test results from my fasting blood draw on October 25, 2012? Some of the numbers shouldn’t be a surprise knowing that I’m eating a very strict high-fat, moderated protein, low-carbohydrate diet with a fat/protein/carbohydrate ratio of 85/12/3:

  • HDL-C is 65 (down slightly from Berkley but still over 50)
  • Triglycerides are 46 (virtually cut in half since Berkeley)
  • Small LDL-P is 221 (just 6% of my total LDL-P number)
  • VLDL was “too low” to measure exact number (A GOOD THING!)
  • LP-IR Score was 11 (means I’m no longer insulin resistant)

    As amazing as all of these numbers were, the ones people will likely be most interested in are the “high” ones. Let’s take a look:

  • Total cholesterol is 359 (not a relevant number at all)
  • LDL-C is 285 (again, this tells you nothing really)
  • LDL-P is 3451 (ideally it’s supposed to be below 1000)
  • Apo B is 238 (parallel to LDL-P and should be under 80)
  • What I want to know is how I can simultaneously have outstanding insulin sensitivity, an A1c score of 4.5, average blood sugars around 81, a heart scan score of zero, undetectable inflammation, 94% of my LDL particles are the large, fluffy kind (Pattern A), a microscopic triglyceride/HDL ratio of 0.7 and active weight/fat loss AND a greater susceptibility for atherosclerosis because of an extremely high LDL-P and Apo B. The answer is out there and I’m bound and determined to uncover it for my book next year.

    But this is more than about some book I’m writing…this is my life. I wholeheartedly believe my healthy high-fat, moderate protein, low-carb diet is vastly improving my health in ways that no other eating plan could even possibly touch. And yet the jury is still out on whether or not there should be concern about the direction my numbers have been going. I did an Excel spreadsheet showing how although my total cholesterol, LDL-C and HDL have all remained relatively constant for the past 4+ years, LDL-P has gone precipitously higher and higher (will it ever stop going up and what’s making that number continue to rise?):

    Interestingly, before I started on the Atkins diet in January 2004, my highest total cholesterol was only about 230. Of course, my doctor put me on both Lipitor and Crestor to lower that number and it did get down to 130 at some point (don’t know what the breakdown was of HDL and LDL nor do I know what my triglycerides or LDL-P were at the time either). But people have claimed I have familial hypercholesterolemia because my total cholesterol is now over 300. But I disagree. Something has happened since I began eating high-fat, low-carb and I can’t help but wonder if there is a purpose for that extra cholesterol in the body since we know there are benefits to higher levels of cholesterol in the body. The jury is certainly still out on this.

    If there’s one thing you know about me, it’s this: I won’t stop seeking the truth about this and sharing with you what I find. Dr. Dayspring has already invited me to visit him at the Richmond, VA-based Foundation For Health Improvement And Technology to see why despite all my incredible lipid numbers the LDL-P and Apo B seem to be out of whack. It will be interesting to see if these numbers are found to be less important for people on low-carb diets than those eating other kinds of diets. Now that’s some research that could help a whole lot of people. In preparation for my book, I’ll also be interviewing various health professionals from cardiologists to practitioners and everyone in between to get to the heart of what matters most. I’m anxious to get going on this project and can’t wait to see where my journey takes me on this.

    Got any comments about my latest lipid numbers? I’d love to hear your thoughts in the comments section below. Feel free to share any knowledge and experience you may have on this subject.

    • Scott

      It’ll be interesting to see what happens when your weight loss bottoms out. Some of this may be due to you being in an unnatural state of continual weight loss. Just a thought. I’ll be interested to see what you figure out.

      • LLVLCBlog

        That’s probably part of it. Although the continued progression of the LDL-P over the years seems to say otherwise.

    • Cp

      Could Dr Dayspring be wrong about apo b? I will have to re-read to see what your trigs to HDL percentage is.

      • LLVLCBlog

        Perhaps. That’s a key question I hope to answer in my book.

      • T Dayspring

        Not wrong about apoB – it is by far the most important CV risk factor. The rise in this case is almost certainly a paradoxical response to the amount of saturated fat in the diet: this is not an unknown phenomenon and is likely related to some genetic issue yet toi be determined. This response does not happen to most low carbers but it can be seen in some inducing ketosis

        • LLVLCBlog

          And I’d love to come see you in Richmond to see what’s going on.

        • Bill

          Dr. D., I’m curious why you are so sure that a “risk factor” (a correlation, really) found in one population, e.g. eating the SAD, necessarily applies to another population, e.g. eating low carb or other non-SAD diet. You’d have to be quite sure the mechanism of harm works the same way in both populations. But how could you know that without studying outcomes in *both* of them? I don’t believe it has been done in low carb/paleo eaters.

          It’s an anecdote, of course, but this doc tried hard to find evidence of cardiovascular harm from his high LDL-P on low carb and couldn’t:


          • LLVLCBlog

            I provided a link to Dr. Patel’s column in my blog post, Bill. I’ve already scheduled an appointment to go see Dr. Dayspring in Richmond, VA in December to discuss this further with him.

    • LLVLCBlog

      Interesting. I wonder why cheese and eggs would impact. Increased dietary cholesterol has no negative impact on serum cholesterol levels: http://www.awlr.org/1/post/2012/02/the-lack-of-effect-of-dietary-cholesterol-on-serum-cholesterol.html

      • kang

        I heard a lot of low carb gurus saying dietary cholesteral does not have a meaningful impact on serum cholesterol, but it does for me, and it does for 25%-30% populations as I read some research paper. I’ll dig out the paper.

        • LLVLCBlog

          Dr. Steve Phinney did a study that found weight loss alone mobilizes cholesterol temporarily, not the consumption of dietary cholesterol: http://www.ncbi.nlm.nih.gov/pubmed/2035468

        • ThatWriterChick

          25% of the population has at least one APOE 4 gene – the gene that has been linked to having a tougher time metabolizing fats, especially saturated fats, and Alzheimer’s. If you’ve never had your APOE genetic profile tested, this may be observational evidence that you are a 3/4 or 4/4.

          • LLVLCBlog

            I’m a 3/3.

    • LLVLCBlog

      What’s your CRP number? That’s a great measurement of inflammation to test your doctor’s theory.

      • Pat Semeraro

        It’s 1.8. They measured free fatty acid which was 1.30′ very high. Don’t have any idea if that is diet related or not.

        • LLVLCBlog

          Interesting. Depends on your diet.

    • LLVLCBlog

      I’m APOE 3/3.

      • Stuart Hechinger

        at Dr Davis TYP we have seen a few hyper-absorbers with 3/3 that cannot tolerate some kinds of saturated fat as trigs go up. A cardioChek meter will test for that or see get the hyper-absorber cholesterol test. I tend to agree with dr Dayspring idea but you may just have to eat just a bit less of some sat fat to get where you need to but you will never know until you experiment with the cardiochek just as you are doing with the ketone tester. We suspect that a very small percentage <5% have this problem more so with the genome type allee /4 as they can adapt to starvation better and then absorb fat quickly to recover.

        I just learned here that my small ldl <7.5% of my total particles but my doctor ordered a liposcan test to see the exact distribution and I am awaiting for my results.

        Johnathan Carey is a similar case as yours and it is likely liver enzymes malfunctiong so he supplement with those herbs that help the liver

    • LLVLCBlog

      Yes, I understand that could be part of it Ray. But why has there been a precipitous ruse in LDL-P since 2008? I haven’t been constantly losing over that time.

    • LLVLCBlog

      Yes, the Private MD Labs (I have no affiliation with them either) had the NMR for $125 plus the 15% discount in their newsletter. An awesome service.

    • LLVLCBlog

      Thanks buddy! I’m gonna get to the bottom of this.

    • bubba29

      what about your testosterone #s?

      • LLVLCBlog

        Testosterone is totally separate from lipids. Will likely test T at one year. But I have no symptoms of low-T.

        • kate, again

          “Testosterone is totally separate from lipids. Will likely test T at one year. But I have no symptoms of low-T. ”

          uhhhh—no, I am not sure you know that.
          low T can cause high cholesterol, according to some and body fat distribution is largely determined by hormones.

          You seem to have a very slight blind spot regarding this lipid dilemma, which is certainly understandable because you are very invested in “lo carb, high fat” in several ways.
          This is just my honest opinion, since you are very open and put yourself out there and asked. ( I have a lot of respect for this, and your work )

          • LLVLCBlog

            Not saying there is no relationship. I’m just saying I only measured lipids. This testing is all out of pocket expense. If I had unlimited resources, then I’d run everything under the sun. I’m not “invested” in anything other than helping people find what will make them optimally healthy.

    • Lions and tigers don’t get atherosclerosis. They don’t eat refined carbs. If high glucose causes amputation, imagine how much damage high glucose causes every cell in the body. I have very limited formal scientific education, but my feeling is it is the glucose that does the damage. Lets nourish ourselves with nutrient dense foods.

    • Tory Dutton


      Thank you for being so open about what you do. You are helping me get back on track since I have followed a very similar path as you. I lost 55 pounds on a low carb diet and quit taking statins, but slowly gained back about 20 and could not figure out why. Now, I’m back on track (lost 10) by making a better effort to be keto-adapted. I think I was making the same mistakes as you and I’m now experiencing the same things you talk about, like being able to effortlessly go without eating for 24 hours and still able to exercise in that state. I love, love, love being able to go about my day without worrying about what and when I’m going to eat. That is actually quite liberating.

      Also, I see a lot of group-think going on right now regarding starches to fuel activity a la Robb Wolf and Chris Kresser and obviously that does not work for everyone. I applaud you for being diligent to solve your problems and communicate it in real time because it is pretty clear to me that my body responds similarly to yours. Right now, I’m not as lean as I want to be, but feel confident that my health has never been better.

      Thanks again,

      Tory Dutton

      • LLVLCBlog

        Keep working at it Tory.

        • Lynn

          me too..I am losing again.

    • As you might remember from AHS12, I have very similar lipid numbers to you: high TC, LDL, and apoB, and awesome numbers/ratios in every other way. It’s confusing how by some measures I’m at extremely low risk, while by others I’m at high risk and should be begging for a statin. It doesn’t make sense. Please solve the puzzle soon!

      • LLVLCBlog

        Annika, I’m working on it.

    • Emily Baker

      P.S. Have you ever connected with Hyperlipid? Taubes is a fan of his. He has a way of explaining some of this seemingly contradictory data (e.g. Physiological insulin resistance).

      • LLVLCBlog

        Oh, I know Peter very well.

    • LLVLCBlog

      Thanks for the tip.

    • LLVLCBlog

      I’ll stand in line for that test too.

    • LLVLCBlog

      I have no doubt research will provide answers.

    • LLVLCBlog

      Interesting. I get plenty of omega-3. Never thought I’d need to supplement omega-6.

      • I note Thomas Dayspring’s comment on saturated fat in his comment
        imo it is not Sat Fat but the threshold omega 6 each individual needs with a given Sat Fat intake

        Sat Fat does down regulate the LDL receptors as TonyK states but only when there is a deficiency of omega 6

        Jimmy I bet what has changed since you earliest tests , Is a higher saturated fat intake and a lower omega 6 intake

        The correct amount of omega 6 will vary with the individual and with the amount of Saturated Fats eaten ( you could eat more mono unsaturated fats )
        upper threshold appears to be about about 6% of calories .

        Here is another paper.


        William S. Harris is a colleague of Thomas Dayspring .. I would be interested in his views on this omega 6 issue.

        Here is an interesting paper going well over the 6% threshold . ( maybe causing other problems )
        Differential Metabolic Effects of Saturated Versus Polyunsaturated Fats in Ketogenic Diets


        • LLVLCBlog

          You’re correct.

          • Kate again

            Hi Jimmy,
            On the one hand you say you are not worried and then other posts you sound like you “get it” about the LDL-P #. I’d be all over Dr Dayspring’s advice. Certainly, you must take one variable at a time and I think you have done an excellent job with that. Now let’s see if you can not “fall in love with the plan” and go where the evidence takes you.
            I am a great fan of your podcasts, you ask excellent, relatable questions. I did shake me head the other day when you were interviewing the Dr Avery Carpenter and tried to lead her into saying the downregulation of thyroid is a lot of bunk by saying “all the weird things they say” (the safe starch proponents, Jaminet, Kresser, etc) I heard Chris walk you through the studies…
            My own LDL went from below normal to high when I went high fat, low carb but the compounded t3/t4 seems to have resolved what was probably a clearance issue when I went 25 gms/ day for almost a year…..
            If you are satisfied with that particle count then don’t change anything, but you might be one of those people that needs statins even though they are generally not helpful.
            Don’t make it so dogmatic that you cannot make sound decisions based on the evidence. ( many of us have this pitfall )

            • LLVLCBlog

              THANKS Kate! When I say I’m not worried about this, it means I’m not going to stress out and let THAT impact me. I’m currently seeking answers on this and have an interview set up to meet with Dr. Dayspring in Richmond in December to see what may be going on.

              As much as I appreciate the work of Chris Kresser, the studies he cited were all low-CALORIE and not just low-carb as I explained in this video featuring a rebuttal of the claims about low-carb diets and thyroid:


              I’m not saying I have the answers to what is happening here which is why I’m blogging about it and actively seeking out a solution. I don’t think raising my intake of “safe starches” is going to solve anything except pack on the pounds and ruin my excellent blood sugar and inflammation markers.

              I’ve taken both Lipitor and Crestor at varying doses and that’s no fun at all. If that pain is what I have to live with just to lower my LDL-P, then I’d rather take my chances. I’m open to other options if LDL-P is indeed a problem. I’m just not convinced right now.

              THANKS for your comments!

              • Kit

                What is Dr Kruse’s take on this. He has a commentary on every situation. He has not commented, but are you in touch.?

                • LLVLCBlog

                  No clue. Haven’t heard from him.

    • Thomas Dayspring

      Dr Lipid analysis: Using all the knowledge we possess today, all of the numbers that you are thrilled about have no meaning in the face of a 99th percentile LDL-P. You also should not say an LDL-C of 285 has no meaning. The cholesterol concentrations that often have no meaning are low levels (where an LDL-P is needed to evaluate risk). No one with an LDL-C of 285 with the exception of a Type III dyslipoproteinemia patient have a low apoB or LDL-P. If you have an LDL-C that high, particle testing is not needed. You need to significantly reduce the saturated fat in your diet and see what happens: repeat the NMR in 3 weeks and you will know if your nightmare LDL-P is sat fat related. I’ll bet your LDL-P drops. If it does not, you need serious lipid-modulating medication. We have seen this paradoxical horrific rise in LDL-P in some people who are on ketotic diets.

      • LLVLCBlog

        Thanks for your input Dr. Dayspring. My comment about no meaning was that it didn’t tell the whole story. So if I’m not supposed to consume saturated fat, then what sources of fat should I eat?

        • melancholyaeon

          Tuscan or Northern California extra virgin olive oil, Jimmy. Olive oil from cooler climates in general have more monosaturated fat and much less saturated or polysaturated fat. Tuscan olive oil is sometimes said to have the least omega-6 of all olive oils. Avocado oil is similar to olive oil in its profile. Mark Sisson likes macademia nut oil too. You may also want to add more fish servings to replace some red meat, if you decide to make this one of your n=1 experiments.

          • LLVLCBlog

            Hmmmm, another set of data points. Interesting.

      • Dr. Dayspring, is it possible that Jimmy’s hunch is correct? Namely that high LDL particle counts are not relevant for very low carb dieters on a ketosis dietary plan such as his?

        Look, he’s losing weight. Logically the adipose fat stores that he is consuming need to be transported within the body. Could it be that Jimmy needs the high LDL particle number to carry the adipose fat to the rest of the body as a food source? In other words, Jimmy’s body needs to produce the high number of LDL particles. So, “abnormally” high LDL-P is a healthy response by the body under his dietary conditions? It would make logical sense if this were in fact the case.

        Further, even if LDL-P counts that are sky high are indeed harmful, it seems reasonable that it is worth the risk. Why? Well, his fat loss will terminate when he achieves his goal weight. Let’s say that is 12 months of effort. His arteries and other organs will be “attacked” by the LDL-P high counts for one year. Once he is weight stable he can back off the ketosis potentially, and if his metabolism will allow for it, he can eat in a way that will normalize LDL-P counts. This is very unlike the long term sky high LDL-P counts that are present over decades in people who develop cardiac problems.

        • LLVLCBlog

          Great thoughts Derek! Listen to my “Encore Week” 2013 interview with Dr. Dayspring in Episode 635 on 12-31-12 of “The Livin’ La Vida Low-Carb Show” podcast where discuss this exact subject. 🙂

    • LLVLCBlog

      Different lifestyle? Low-carb and what else?

      • Grant

        Goat herding. The more goats you have the higher the reduction in apoB.

        • LLVLCBlog

          Translation please.

      • melancholyaeon

        I think Dr. Dayspring is suggesting you test after a few weeks without butter or coconut oil, using instead olive, avocado, or macademia, and eating a lot more fish. 🙂

        • LLVLCBlog

          Oh, I know what he’s saying, but for the benefit if everyone I wanted him to share how it can be done. Thanks for your list. I consume several of those foods on your list.

    • richelle jones

      hey jimmy. can i suggest “Minding your Mitochondria” by Dr Terry Wahls. Perhaps your problem is not being ketogenic (cause i think that is a great place to be) but you might be missing out of some key nutrients that your body needs to function at optimum homeostasis. You may need to increase your intake of greens, brightly coloured foods, organ meat. If your mitochondria are not functioning well then everything else gets out of whack.

      • LLVLCBlog

        Thanks Richelle! I have read that book and interviewed Dr. Wahls.

    • http://people.brandeis.edu/~kchayes/HayesOnFats.pdf note it is omega 6 that matters

      http://www.foodinsight.org/Content/5519/IFIC%20Omega%206-3%20Ratio%20Webcast%20Website%20Version.pdf again !

      Adipose tissue is 55% mono , Sat 27% poly 18% … That is what the body preferentially stores .. Makes sense that is what the body will do best on imo.

      Using that breakdown on a keto diet might be a good starting place

      Omega 6 is an essential fatty acid … the pdfs make the point that what matters is being above thresholds not so much worrying about ratios . Omega 6 and omega 6.

      you have had some guests that stressed how important omega 6 is

      eg http://www.thelivinlowcarbshow.com/shownotes/1240/dr-duane-graveline-statins-permanently-damage-mitochondria-episode-308/ .

      “the importance of Vitamin E from tocotrienol, and the importance of vitamin D and Omega 6 supplementation.”

      • LLVLCBlog

        True Raymund. I’ve also interviewed a guy who said fish oil is horrible and that we all need to be eating a lot more omega-6 in our diet:


        • I thought Omega 6 was bad and you were supposed to get an even balance of 3 to 6’s… I thought omega 6 was inflammatory?

          • LLVLCBlog

            It is in excess. But it is still an essential fatty acid meaning the body can’t make it. So you need some for the proper balance of EFAs.

            • If you have a high poly unsat fat intake as you do – with your intake of omega 3 and 6 you can reduce anit-oxidant vitamins. I’d suggest popping your food into Cron-o-meter and see how the fat amounts come out. Lots of poly unsat fat means anti-oxidants can get used up keeping them stable in cell membranes. Vit E 500iu per day and vit C 1000iu per day and lots of polyphenols (colourful plant compounds) I use Dr Sears Zone polyphenols if people have high PUFA and low vege + fruit intake.

              I did a post which lists the amounts of omega 6 and 3 PUFA’s in oils, fats etc – I agree that switching to more coconut oil and mono oil sources might be better. Some long chain sat fats do increase LDL, as does fish oil.http://paleozonenutrition.com/2011/05/10/omega-6-and-3-in-nuts-oils-meat-and-fish-tools-to-get-it-right/

              • LLVLCBlog

                Thanks Julianne!

    • ThatWriterChick

      The high cholesterol statin scaremongering can be explained in three little words: Follow The Money. It’s no coincidence that Lipitor is the world’s best selling pharmaceutical drug.

      • LLVLCBlog

        YEP YEP!

    • bubba29

      have you had any imaging done to actual measure any plaque accumulation in your arteries? that would interesting to see if the continual rise in LDL P has lead to accumulation of plaque. betcha dr. davis would recommend a cat scan and/or ultrasound to get a full picture. the story on risk factors seems to be ever evolving. in the end, what one should be concerned with is actual plaque accumulation.

      • LLVLCBlog

        Yes, I had a heart scan done as recommended by Dr. Davis and my score was ZERO.

        • bubba29

          when was that done and was it a heart CT scan? as i said, heart CT scan tells you what is actually going on in the artery. the blood test risk factors seem to be ever evolving and i am not sure if we have a conclusive blood biomarker yet.

          • LLVLCBlog

            It was done in 2009 and Dr. Davis noted that if your score is ZERO that you don’t have to do another one for 7 years. Perhaps at the end of this 12-month n=1 experiment, I’ll have another one just to see. But I’m confident my heart calcium score is still ZERO. Here’s the test I had done where my wife Christine had it done in 2011: http://www.youtube.com/watch?v=XeAhhWn2h_Q

            • bubba29

              yes, if you want for your own satisfaction, probably a good idea to retest. it just seems crazy to me how total cholesterol was the gold standard, then LDL, then hdl/trig ratio, then LDL particle size, now LDL particle number. they seem to continually change what the gold standard is because new evidence shows that the previous gold standard is a poor predictor. i am appreciative of this science but even the scientists should admit these correlations are disproven. imo, there isn’t a decent blood test to hang our hat on….yet.

              • LLVLCBlog

                Which is why I’m not personally worried.

    • The High Fat Hep C Diet

      Thanks for this Jimmy. We have to be able to understand what this “healthy hyperlipidemia” picture really means if we’re goingg to convince the sceptics.

      • LLVLCBlog

        I agree which is why I want to seek answers about this.

    • JohnG

      Jimmy, great experiment! Were you eating primarily range-fed meat? Also, were you taking fish oil? If you were, I’d say that likely dismissed most of the discrepancies between you and the eskimo. I’d love to know what the eskimo LDL-P/apoB numbers were before they began eating more modern foods.

      • LLVLCBlog

        Fish oil everyday. All I eat is pastured and grass-fed foods.

    • LLVLCBlog

      I’m investigating what that diet would look like in food. I’m going to see Dr. Dayspring in December.

    • LLVLCBlog

      I had low T around 400 earlier this year. But T cream for a couple of months got the levels up over 900. I look forward to checking again at some point. I feel fantastic!

      • Cara

        Jimmy, I have never been overweight, not on a ketogenic diet, but low carb in the sense that I don’t eat fruit or starches, am very lean, and I have been told that I have the familiar Hypocholesterolimia too. My HDL-C is 85, Trigs 50, HDL-P total are 41.6, Small LDL-P are 173, LDP-P 1,981 and LDL-C are 204. I have been researching this issue lately since my doctor has called several times demanding that I go on a statin. I have some thoughts that maybe some of the medical community can comment on. First, I believe that cholesterol elevates due to an underlying problem which I think is hormones. Cholesterol makes hormones and if hormones are not properly being made, then maybe the body sends out more signals to have more cholesterol to make the hormones. (Similar to the thryoid process with why TSH would be elevated) However, there is also an enzyme that helps the body clear out LDL’s and it’s possible that you are deficient in that enzyme maybe the same way that people are deficient in digestive enzymes so if you had more of that enzyme, then the body would be able to clear LDL better and all your numbers would be ideal. Then my last theory is that it is a pituitary issue since that’s further up the chain and if the signaling is not in place, then a cascade of issues would result affecting hormones and LDL. I just starting taking a Burdock root tincture since that is supposed to help the body the LDL’s maybe in the way that bitters help with digestion. I also found a product which I have ordered but have not started called Imu-Stat from this website http://saponins.com/ and will give that a shot. I’m getting blood work done in 2 weeks so I’ll see if any of this will make a difference.

        • LLVLCBlog

          I think you’re on the right track with your theories, Cara. THANK YOU for sharing them here. 🙂

        • Kate

          Cara that is very intriguing, but didn’t Peter Attia MD send up a big warning about Plant Sterols in his series “The Straight Dope on Cholesterol?”
          Maybe I misunderstood, I will go look for what he said. Maybe Dr Dayspring knows….

    • LLVLCBlog

      My ATLCX podcast with Dr. Peter Attia from last night addressed whether LDL-P matters on a ketogenic diet. Still unknown.

    • LLVLCBlog

      Thanks Kate! I have. 🙂

    • Plague without calcification is more dangerous and unstable than plague with.
      You can certainly have atherosclerosis without calcification..

      HDL is certainly something else again and daily their seem to be new mechanisms that HDL acts through.
      EG preventing LDL from oxidising

      to this new finding http://www.uphs.upenn.edu/news/News_Releases/2012/11/arteries/

      One thing a keto diet usually always does is raise HDL..

      • LLVLCBlog

        Almost like clockwork, a high-fat, low-carb diet will raise HDL and lower triglycerides.

    • Why do some studies indicate that saturated fats are unhealthy while others show they’re fine? It depends on the essential fatty acids consumed with the saturated fats, according to Brandeis University nutrition scientist K.C. Hayes. He says that it takes just a little bit of essential fatty acids to go with saturated fats, so you don’t have to chug a bottle of cod liver oil. In fact, that would be a bad idea. What’s a good idea?

      http://www.meandmydiabetes.com/2010/11/13/saturated-fats-need-omegas/ .

      • LLVLCBlog

        I take 2 Tbs of Carlson’s fish oil every single day.

        • “Just a little bit of essential fatty acids” . note the plural !
          He is referring to omega 6 more so than omega 3 .

    • LLVLCBlog

      Yes, I’ve cited that and it’s one possibility about what’s going on. I know I’m doing more good for myself with my current plan than harm.

    • LLVLCBlog

      Who says I’m not already doing that? 😀

    • LLVLCBlog

      It is a multi-faceted disease.

    • LLVLCBlog

      I enjoy all of those fat sources. And I am quite active daily.

    • http://www.ncbi.nlm.nih.gov/pubmed/21612461

      Some studies on Mediterranean and Spanish Keto diets.. They all seem to lower LDL-C ,, ,More use of Mono fats

      And Jimmy this finding was interesting implicating maybe Iron from RON KRAUSS

      “. In this case, the surprise was that the combination of the high beef diet and the high saturated fat diet caused very serious increases in all of the cholesterol related risk factors we had been measuring, including total particle numbers, small LDL, total LDL cholesterol, inflammation, whatever we looked at, we saw an adverse effect.

      Everything went wrong.

      This was in contrast with our earlier studies where the same amount of saturated fat and very similar carbohydrate intake but a diet not loaded up with red meat, had no adverse effect even if it had lots of saturated fat in it.
      So if you put on your Sherlock Holmes hat and get our your magnifying glass, what is it you found was the likely smoking gun here?

      I wish I could give you a definite answer to the question. But fortunately, the fact that we had these two very different results with two different kinds of protein led us to propose to the National Institutes of Health, one of the nation’s leading funders of health research, which hopefully will stay that way, a new study. We are glad that it’s being funded by the National Institutes of Health, as a neutral ground if you will, between the world of sponsors from the food industry. NIH is allowing us now to investigate in a detective-like matter what is going on, and also test directly in a head to head manner, three different diets. All the diets will have the same amounts of saturated fat. But one is high in red meat, one is a non-meat, vegetarian diet where the protein comes from vegetable sources, and one is an intermediate diet, with meat from chicken, primarily. We’re doing this study to determine whether the source of protein influences the response to saturated fat in the way we suspect it will from these earlier results, and we’ll do some blood work that will allow us to investigate possible underlying mechanisms.
      You think there are clues in the beef.
      Perhaps some other component of beef, not necessarily the protein, but something that comes along with it, such as iron would be one example, that may have an adverse effect in conjunction with saturated fat.


      • LLVLCBlog

        I know my friend Chris Kresser has implicated an iron/LDL connection. I’m definitely looking into that.

        • Lynn

          Mike and Mary Eades say to give blood, So you won’t rust…

          • LLVLCBlog

            I give every 58 days.

        • Lynn

          I love this lively question and answer thing you are doing. I am doing this. It is working. I have not retested my blood but am avidly watching you. If I am losing the TIRE around my middle…How can that be bad?? That is what you are doing. Today My mothers doc put her on Lipitor. She has HDL of 100….crazy!!! She bought the lipitor to appease the insurance company but refuses to take it.

          • LLVLCBlog


    • How can you not see how it looks to post your extremely alarming lipid results, mention that you’re working with a doctor you trust who thinks said results indicate you are doing tremendous damage to yourself, and, IN THE SAME POST, talk about how you’re writing a book to help people interpret their own lipid results?

      Doesn’t listening to Dr. Dayspring (which is a GOOD thing) and considering what he is saying as arguably valid disqualify you from writing such a book? How can someone not sure how to interpret their own results help others?

      Now, it is possible you could go through this whole experience, learn a lot, and then, if you’ve clearly learned some good information that helped, end up writing a book about what you’ve learned. But that’s not what you’re doing. You’ve already signed to do the book and have a deadline, while you sit there confused by your own results. This is madness.

      • LLVLCBlog

        Talk to my publisher. In the meantime, I’m interviewing the best and brightest people who know their stuff in this arena (Dr. Dayspring included, who I am visiting in VA next month). The reality is nobody knows what the importance of LDL-P and/or Apo B are for people on a ketogenic diet. Maybe I can help solve this mystery for the many others out there who are in this same situation that I am. I appreciate your concerns and your feedback, Charles.

    • Jimmy – you said “My blood work from October 2005 showed my lipid profile as nearly ideal with HDL at 71, triglycerides at 57, VLDL at 11, LDL at 119, and total cholesterol at an acceptable 201. This was what my numbers looked like after livin’ la vida low-carb for about 22 months and I was proud to see them doing so well.”

      What have you changed since then and why don’t you go back to what you were doing then??

      • LLVLCBlog

        What was working then doesn’t work for me now 7 yeas later. Thus, I adjust.

        • Why did you change what was working then and why do you think it won’t work now??

          • LLVLCBlog

            Because what was working then stopped working or me. You adjust and make appropriate changes as I’ve done.

    • MarkES

      “Dr. Ron Rosedale recommends 50% monounsaturated, 25% polyunsaturated, 25% saturated”
      Hi Joshua, do you have web link or book page number reference to this recommendation. I cannot seem to find it. Thanks.

    • Lynn

      I have no problem with it… I can live on raw meat with no fruit and very little veggies.. I make my meat hot and rare.

    • LLVLCBlog
    • Kenneth MacKillop

      Hi Jimmy. My experience (with serum cholesterol markers) matches yours after changing to a low-carb diet. I have done an enormous amount of reading on the utility of markers such as LDL-P, and come up with conclusions similar to your own.
      To ANYONE who makes the claim that LDL-P is a definitive marker for CVD risk independently of whole-body insulin resistance, I challenge him/her to explain the results of this study:
      Tg/HDL-c ratio is a much more reliable marker for insulin resistance than is LDL-P or any other LDL-based marker whatsoever. And the association of IR and CVD is fairly well demonstrated. Also, while markers such as Tg/HDL-c are reliable for individuals, LDL-P is decidedly NOT so. All of the (weak) associations drawn with CVD are based upon mean statistics from huge study cohorts. The one conclusion that has been drawn from these studies with which I DO AGREE is that LDL particle size is a meaningless parameter with respect to CVD risk and etiology. The detailed research focused on LDL particle size independently and overwhelmingly suggests the same conclusion. It is my guess that something like the response-to-injury theory is roughly correct, and that the triggering injury process is in the endothelium, and that the presence of cholesterol in atheromas is due to the role of LDL and HDL particles in the innate-immune response to this injury. And that the injuries themselves are probably normally occurring, but that a compromised ability to properly respond to the regular injuries is the real cause of atherogenesis, leading to an adaptive (i.e. second-best) cellular response involving cholesterol-carrying particles. And that the compromised first response is due to chronically-induced metabolic damage in the cardiovascular tissues.
      Liver cholesterol metabolism is only one (very complex and mostly not understood) indicator of metabolic/diet problems that themselves MAY be a cause of CVD — i.e. the so-called “atherogenic profile”. But this profile includes low HDL-c and high Tg as the stronger indicators and high LDL-c (or LDL-P — it’s not that much stronger) as the weaker indicator. Ron Krauss et al (ref. Malmo, Sweden study) have developed some more sophisticated lipid markers (that require research-grade instrumentation to measure), but this very recent research supports the same basic idea. High HDL-c and low Tg easily override the significance of high LDL-P, especially on an individual basis — I am absolutely stupified as to how anyone who has studied all of the available data can conclude otherwise, unless he/she simply does not understand the mathematics of statistics (which is probably true of at least 99 in 100 US residents).
      As more people adopt a ketogenic diet, it becomes increasingly clear that hepatic cholesterol homeostasis like yours and mine is pretty common — it happens in a significant minority of individuals (I estimate 1 in 6). The “normal” serum concentrations are simply derived from large cohorts of people eating industrial diets. Barry Groves is a good example (TC=8.2mmol/L) — he has probably been “hypercholesterolemic” for four decades! And healthy as a horse. He has been eating low-carb since before this serum cholesterol madness really got rolling, and well before the clinical means to measure LDL-c, much less LDL-P, have been available:
      Thanks for sharing your numbers, Jimmy. Keep up the good work.

      • LLVLCBlog

        Great info, Kenneth.