Lipid Changes on a Very-Low-Carb Ketogenic Diet: My Own Experience
Moscarpone…
Cholesterol Results From June 2013 through November 2013
My cholesterol levels have always been higher than average. LDL has ranged from 120s-150s as far back as I can remember, long before I began following a moderately carbohydrate-restricted diet back in 2011. In June of last year, I reported my NMR (Nuclear Magnetic Resonance) LipoProfile results after almost a year of consuming a very-low-carb ketogenic diet (VLCKD) containing less than 50 grams net carb per day. I was very happy with these values and frankly a little surprised that I achieved them while eating delicious, satiating foods.
In November of last year, I had a standard lipid profile done as part of lab work for my annual physical:
Total Cholesterol: 300
LDL-C: 160
HDL-C: 128
TG: 56
My numbers had increased, but I wasn’t terribly concerned about the LDL-C, since on a few occasions it had been nearly that high in the past. Seeing a total cholesterol of 300 was a bit troubling, but I knew it was partially due to having extremely high HDL (Apparently high levels of some types of HDL can also be problematic, although I didn’t realize this at the time). Looking back, although I wasn’t tracking my intake online regularly back then, I’m pretty sure I was eating the same or perhaps a little more fat than when I had the NMR done five months earlier.
Nutritional Ketosis Experiment
At the beginning of January, I decided to experiment with lowering my carb intake further in order to achieve nutritional ketosis. I didn’t want or need to lose weight, but after speaking with a few people who’d reported improved mental focus and energy on minimal carbs and ketone levels between 1.5-3.0, I was intrigued. For the record, I felt great prior to this experiment: no symptoms of adrenal fatigue, excellent blood sugar control, lots of energy, good sleep, etc. But was there a possibility I could feel even better in deep ketosis? I’m a curious type, so I decided to try it for a few months. I had a ketone meter but didn’t test very often because the strips are ridiculously expensive. But when I did check prior to this experiment (first thing in the morning, the only time I’ve ever tested), my ketones ranged between 0.4-1.0 mm.
I began tracking my intake on My Fitness Pal, as many of my clients were doing. I lowered my net carbs to roughly 20 grams per day, although total carbs were often still around 50 grams because I ate a lot of avocados, unsweetened cocoa powder, and high-fiber vegetables like cauliflower. However, my consumption of berries dropped from 1-1.5 cups per day to 5 or 6 every morning at breakfast. I tried to keep protein around 70-80 grams daily (I’m 5’8″ and 125 lbs, so this isn’t all that low), and I ate more fat in order to maintain rather than lose weight. I never drank bulletproof coffee or added lots of butter or coconut oil to my food. But I did eat a fair amount of cheese, cream cheese, ricotta, and moscarpone, and I began using heavy cream instead of half-and-half in my coffee and tea. I still ate vegetables at every meal, although smaller amounts.
I tested blood ketones a couple of times a week in the morning, and results ranged from 1.2-1.8. After 3 months of eating this way, in all honesty, I didn’t feel any different. I still felt great, slept great, etc., but I can’t say I had more energy or experienced any cognitive benefits. My weight stayed the same, and my blood sugar control remained good. However, my lipids had definitely changed, and not for the better.
Cholesterol Results from April 2014
I had an NMR drawn at the end of April, and this time I’ll admit to being more than a little upset when I saw the results:
I was really surprised by how much my cholesterol had gone up since the prior test. My first thought was that perhaps my thyroid levels were off. (I have hypothyroidism that was diagnosed shortly before I went low carb, but my levels have been stable for the past few years on desiccated thyroid). However, I didn’t feel at all hypothyroid and wasn’t scheduled to have my thyroid labs re-checked until summer.
“Why Are You Concerned When You Have Such High HDL-C, Low Triglycerides, and Large, Fluffy LDL-C?”
While I’ve always been comfortable with higher than ideal cholesterol levels, having an LDL-C over 200 is a different story. The highest value I’d ever seen prior to last December was 158, I believe, about eight years or so ago when I was still following a low-fat, high-carbohydrate diet. But as far back as I can remember, my LDL-C was in the mid 120s to 150s regardless of what I ate, and my total cholesterol was never more than 260. My first NMR was the one last year, so I don’t know what my LDL-P values were prior to 2013, but I’m assuming they were above the optimal range, although likely not over 1600. You can see that my LDL and total cholesterol each went up about 100 points and my LDL-P increased by 700 points in a 10-month period. My triglycerides even went up somewhat, although 60 is still pretty low. Although it’s my understanding that LDL-C in an NMR is measured directly rather than by using the Friedewald equation (maybe a lipid expert can confirm this), when I plugged my numbers into an online calculator that estimates LDL-C, I got exactly the same number as in the NMR report, 221, for the Friedewald equation and 182 for the Iranian formula (The Iranian formula is believed to be more accurate when triglycerides are over 400 or less than 100).
You may be wondering what LDL-P is, since it’s not reported in a standard lipoprotein profile and most doctors don’t order it. Dr. Axel Sigurdsson does a great job explaining everything you ever wanted to know about it in his post about LDL-P, but I’ll try to give a quick summary. LDL-P is a measurement of the number of LDL (low-density lipoprotein) particles in your blood which carry cholesterol, triglycerides, and another type of fat called phospholipids. According to lipidologists (experts in the field of cholesterol and other lipids), LDL-P is the strongest predictor of risk for cardiovascular disease (CVD) and future cardiac events. Total cholesterol greater than 300 and LDL-C greater than 190 are also associated with significant CVD risk. High levels of LDL-C are prone to oxidation, and oxidized LDL has been linked to the development of arterial plaque and coronary artery disease (CAD). Sometimes people have normal LDL-C and high LDL-P or vice versa (the term for this is discordance), but most people with very high LDL-C have high LDL-P as well. These findings are from recent studies, not decades-old research reported by Ancel Keys.
I want to make it clear that this type of dramatic elevation in LDL-C and LDL-P doesn’t occur in most people who adopt a very-low-carb, high-fat diet. I’ve seen estimates that somewhere between one quarter and one third of low-carbers experience this. I’ve met and read about several who have. Most people who eat VLCKDs see their cholesterol rise only slightly, not at all, or even decrease, remaining within or near the normal range. I’ve met plenty of folks like this as well. I’ve also spoken with people who tell me their LDL cholesterol has always been over 200 and didn’t really change after switching to a VLCKD. This is in sharp contrast to what happened to me: going from relatively stable LDL-C between 120s-150s to 221 within a very short period of time.
Of course, many things can affect a person’s cholesterol levels, including stress, illness, and injury. Aside from familial hyperlipidemia (FH), there are other genetic disorders of lipid metabolism. Some people’s livers produce large amounts of cholesterol (hyper secretors), while others absorb a lot of cholesterol from food (hyper absorbers), and some have both of these issues. My past lipid profiles didn’t suggest FH, and I haven’t been tested to see whether I have increased hepatic cholesterol production or increased intestinal absorption. I assume I’m probably a hyper secretor, since my levels were higher than average even during my 10 years as a low-fat vegetarian who ate a lot of egg whites but very few yolks or other cholesterol-containing foods.
I do have a family history of heart disease on both sides. My maternal grandfather suffered four heart attacks (the last one fatal), and my maternal grandmother also had coronary artery disease (CAD). My dad’s brother has had two heart attacks, and his mother had CVD and died of a stroke. My mom has been on statin therapy since she was diagnosed with CAD ten years ago. (I’m not going to debate the risks vs. benefits of statin therapy in this post, but I’m not a big fan except in certain instances.) You may be wondering what kind of diet my relatives followed. Given that they all grew up and spent their entire lives in Switzerland (with the exception of my mom, who immigrated to the US at age 19), they obviously weren’t following the Standard American Diet, but they weren’t low-carbers either. My grandfather smoked and had diabetes, and my mom smoked for many years, but my other relatives didn’t, and all were moderately active. I’ve never had a calcium scan or a carotid-intima thickness test(CIMT) to check for atherosclerosis but am looking into having these done. Even if they show no disease at this point, my goal is obviously preventing CAD, heart attack, and stroke in the future.
My NMR results indicate I have the large, pattern A type of LDL with a low number of the more atherogenic small LDL particles (small LDL-P). This is definitely a good thing. However, although I’ve heard large, fluffy LDL characterized as “harmless” and even “protective,” I’m having trouble finding convincing evidence supporting this assertion, especially in the setting of cholesterol levels as markedly elevated as mine. In fact, the authors of the Multi-Ethnic Study of Atherosclerosis (MESA) study summed up their findings as follows:
“Contrary to current opinion, both small and large LDL were significantly associated with subclinical atherosclerosis independent of each other, traditional lipids, and established risk factors, with no association between LDL size and atherosclerosis after accounting for the concentrations of the two subclasses.”
Subclinical atherosclerosis is the period when changes are happening in the arteries but the hallmarks of atherosclerosis (i.e., plaque and fatty streaks) haven’t developed to the point where the disease can be diagnosed.
It’s been pointed out that no studies have been conducted on people following VLCKDs who have very high LDL-C and LDL-P levels, and that’s certainly fair to say. However, according to many MDs with expertise and/or personal experience in this area, we really don’t know whether CVD risk is lower in low-carbers with cholesterol elevations of this magnitude.
What Do The Experts Say About Very High LDL-C and LDL-P?
I studied lipid metabolism in college as part of the coursework required to become a registered dietitian, but I’ll be the first to admit that I have no expertise in that area. I think it’s important to listen to the experts in this field since they best understand all of its complexities, including the genetic variations that influence cholesterol levels and the development of CAD. Keep in mind that the physicians listed below are all advocates of carbohydrate restriction to some degree.
Dr. James Underberg is a lipidologist and hypertension specialist in New York City who told me that he has seen similar dramatic increases in total and LDL cholesterol in some of his patients following a carbohydrate-restricted diet. One of the interventions he recommends in these cases is replacing a portion of dietary saturated fat with monounsaturated and polyunsaturated fat sources.
Although technically not a lipid expert, Dr. Rakesh “Rocky” Patel is very familiar with current lipid research as a family doctor in Arizona with hyperlipidemia who treats many people with diabetes and metabolic syndrome. He recommends the CarbNite (cyclical low-carb) method for most of his patients and also follows this approach himself. Back in the fall of 2012, he wrote a fantastic blog post entitled Does LDL-P Matter? in which he described improvement in his carotid intima thickness despite a significant increase in LDL-C and LDL-P after switching to a carbohydrate-restricted diet. When I received my NMR results from April, I asked him if we’ve learned any more about very high lipids in the context of a VLCKD since he wrote that piece. He responded:
“Not really. It really is an understudied issue. Unfortunately, all the trials in the literature involve the Standard American Diet. Really, I think that before we engage in any discussion regarding cholesterol, one has to establish if atherosclerosis is present in any form. So using testing like CT calcium scoring, carotid intimal thickness testing (CIMT), and genomic scoring (Corus CAD, Cardiodx) becomes imperative and certainly provides context to the lipids.”
Dr. Axel Sigurdsson is a cardiologist who practices at a large university hospital as well as a private heart clinic in Iceland. In my opinion, his Doc’s Opinion blog provides some of the most balanced, easily understood information about lipids and cardiovascular disease online. I described my experience to him and asked for his thoughts. His response:
“I’ve seen this lipid response (a very high jump in LDL-C and LDL-P) a number of times in individuals who adopt a low carb/ketogenic diet with relatively high amounts of saturated fat. It seems that a certain percentage of people react in this way. In fact, the lipid response to this type of diet may be genetically determined. Of course, we know that high LDL-C and LDL-P are associated with increased risk of CHD (coronary heart disease). However, nobody really knows what it means in this metabolic situation (nutritional ketosis) and to what degree it is associated with increased risk. Some claim it’s not, but I think the evidence is lacking for such a conclusion. On the other hand, we also know that many people with high LDL-C and high LDL-P never have CHD. Of course, you may be one of those people. However, it is difficult to ignore altogether the possibility that high LDL-C and LDL-P may increase the risk of atherosclerotic problems.”
Lipidologist Dr. Thomas Dayspring wrote an excellent article about a woman who had an experience similar to mine on a low-carb, high-fat diet, although her case involved weight loss as well. The article is available from his Lecture Pad series, and I highly recommend reading it in its entirety. (You’ll have to register to view it, but registration is free). Although it may not always seem like it, he’s actually quite supportive of carbohydrate restriction, particularly for people with metabolic syndrome. I didn’t discuss my case with him, but here are two quotes from that article:
“We now recognize that the cholesterol usually gains arterial entry as a passenger inside of an apoB-containing lipoprotein (the vast majority of which are LDLs) and the primary factor driving LDL entry into the artery is particle number (LDL-P), not particle cholesterol content (LDL-C).”
“Could the low-carb crowd be outliers and in them we can ignore LDL-C and LDL-P? The advocates of those diets say there is no study showing harm of elevated LDL-P and LDL-C in patients who have eliminated or drastically reduced their insulin resistance and inflammatory markers by low carbing. That is true, but what they want to ignore is that there is no data anywhere that shows they are an exception. Their belief is that by reducing all other atherosclerotic risk factors and normalizing their arterial wall and endothelial biology, that apoB-containing lipoproteins like LDL cannot enter the arterial wall. Although LDL-C and LDL-P in plasma are high, none of the cholesterol content of the apoB particles gains entry into the arterial wall. Is that plausible??? Sure! But is that also erroneous or wishful thinking? Sure? Does one want to bet their CV health or life on a plausible theory? Some do and some do not. Seems to me the first step is to do what this woman did: adjust the nutritional regimen.”
He also states that when ketone bodies are present in excess, they can enter the cholesterol synthesis pathway, thereby increasing serum cholesterol levels.
While I agree with Dr. Dayspring on several issues, I disagree with his position (stated in another great article, Understanding the Entire Lipid Profile) that cholesterol-lowering medication is indicated for everyone with LDL-C greater than 190. I think nutritional intervention should be tried first, as it seems to be effective for at least a portion of people willing to do it.
Some of you may have seen spikes in cholesterol similar to mine after being on a low-carbohydrate, high-fat diet for a short period of time or possibly after a few years. You may not be that concerned, and I can understand that given the many positive effects LCHF can have on health, including certain cardiac risk factors. I also think there are still a lot of unanswered questions regarding the risk of elevated cholesterol in the setting of low insulin levels and optimal blood glucose control. But based on the evidence we do have, along with my strong family history of heart disease, I just wasn’t comfortable with my numbers. And although I haven’t seen this happen in any of my clients yet, I’d definitely recommend some sort of dietary intervention for them if it occurs in the future.
Dietary Changes and NMR Results from June 2014
Over the past two months I made a few small but significant changes to my diet in an effort to lower my cholesterol levels:
1. I cut back on saturated fat, particularly dairy fat and coconut oil, which contain the types of saturated fatty acids with the greatest potential to raise cholesterol.
2. I increased protein back to my previous intake of about 100 grams per day.
3. I doubled my net carb intake from 20 grams to 35-45 grams per day.
4. I began having chia seeds almost every day.
5. I ate sardines 4-5 times a week.
I still eat plenty of saturated fat, including some dairy fat. I drink coffee and tea with half-and-half (only 1 gram of carb in 2 Tbsp), always order Insalate Caprese made with fresh mozzarella at Italian restaurants, and continue to eat eggs cooked in a little butter for breakfast every other day. I still have burrata, ricotta, and moscarpone occasionally and continue eating red meat about 3 times a week. My total fat intake now ranges from roughly 80-100 grams per day, which is about 50-65% of my total caloric intake. That’s still a LCHF diet! And in my case, it’s also a mildly ketogenic one, since when I’ve checked my ketones in the morning (again, I only do this sporadically), they’ve been 0.4-0.8. Personally, I don’t see the need to be in ketosis for my own health; to control my blood glucose, I eat a low-carb diet which just happens to be ketogenic. My weight hasn’t changed (which was my goal), energy levels are good, sleep is excellent, etc.
I just received my new NMR results from labs drawn earlier this week:
As I said at the beginning, I’m a strong proponent of a low-carbohydrate lifestyle. I don’t think that’s ever going to change. But I feel it’s important to look beyond the benefits and address the changes in lipids some people experience that could potentially have adverse effects. This was an n=1 experiment, of course. Remember, most people won’t experience extremely high cholesterol levels on a VLCKD. But for me and others who do, I don’t believe in shrugging it off and dismissing the results of studies because their subjects weren’t following a carb-restricted diet. As a dietitian, I just can’t say, “Go ahead and eat as much butter, cream, and bacon as you want. It doesn’t matter how high your LDL-C and LDL-P are as long as you’re eating low carb and your other markers are low,” even if that’s what many want to hear. Because we just don’t know at this point. Maybe one day there will be evidence demonstrating that VLCKDs are cardioprotective even in the setting of significant hyperlipidemia. I truly hope that’s the case. But in the meantime, I’m going to eat a low-carb diet that keeps my lipids in a range I feel more comfortable with.
***UPDATE: Recent NMR results, cardiovascular disease risk and what I eat
References
1. Otvos JD, et al. Clinical Implications of Discordance Between LDL Cholesterol and LDL Particle Number. J Clin Lipidol. 2011 Mar-Apr;5(2):105-13
2. El Harchaoui K, et al. Value of low-density lipoprotein particle number and size as predictors of coronary artery disease in apparently healthy men and women: the EPIC-Norfolk Prospective Population Study. J Am Coll Cardiol. 2007 Feb 6;49(5):547-53
3. Cromwell WC, et al. LDL Particle Number and Risk of Future Cardiovascular Disease in the Framingham Offspring Study – Implications for LDL Management J Clin Lipidol. 2007 Dec;1(6):583-92
4. Mora S, et al. LDL particle subclasses, LDL particle size, and carotid atherosclerosis in the Multi-Ethnic Study of Atherosclerosis (MESA). Atherosclerosis 2007 May;192(1):
211-7
5. Waterworth DM, et al. Genetic variants influencing circulating lipid levels and risk of coronary artery disease. Arterioscler Thromb Vasc Biol. 2010 Nov;30(11):2264-76
6. Moriel P, et al. Lipid peroxidation and antioxidants in hyperlipidemia and hypertension. Biol Res. 2000;33(2):105-12
7. Ohlsson L. Dairy products and plasma cholesterol levels. Food Nutr Res. 2010 Aug 19;54
8. Mensink RP, et al. Dietary saturated and trans fatty acids and lipoprotein metabolism. Ann Med. 1994 Dec;26(6):461-4
Very cool! Pretty much the same thing I see with my patients (and myself)
Thanks so much, Spencer!
Its so interesting that you had this experience. Low carb made my numbers drop significantly….and I usually have high cholesterol. This is something to investigate further for sure!
Thanks, Ana! Lipid response to carb restriction is so individual. Some people do see their numbers go down. I’m glad to hear that’s what happened in your case!
Thank you for sharing your results. It is nice to hear other people’s approaches. I have been low carb (approx 30g net) for 3 years. My last numbers were Total Chol=277, HDL=85, LDL=171, Trig=105. I do not have comparison numbers because I never had a test before. I was concerned about all the numbers except the HDL. Compared to my previous diet (high carb low fat vegetarian) I suddenly started to eat a lot of red meat, eggs and high fat dairy along with non-starchy vegetables. (There’s not much good fish in my region.) The blood test results made me doubt what I was doing. My solution came spontaneously, as my appetite and overall interest in food decreased over the years. I eat very little now, although my macronutrient ratios have probably remained the same. I will be curious to see my next results.
Thanks so much for commenting and sharing your story, Anna. I wish you had a baseline prior to starting low carb just to see if your numbers improved, got worse, or stayed the same. I hope your next set of labs shows improvement all around.
Anna, I had a similar experience but I did have a baseline lab test so was shocked at my results. After almost 1 year in keto I feel fantastic, lost weight, great energy, sleep well but my total cholesterol went from 208 to 273 however my triglycerides dropped 85 to 66 which is good, my hdl went up 71-85 which is good but my ldl direct? also shot up 120 to 175 but my vldl dropped 17 to 13. My doctor is concerned but in researching more factors in CV disease it seems that the most important factor is total chol/hdl and mine is 3.2. Am i just looking for the answers I want? Any comments on this?
Hi Jill,
As you’ve no doubt seen, elevations in LDL cholesterol are fairly common in people who follow a low carb or ketogenic diet. Whether or not that is a concern in the context of other metabolic improvements remains a hotly disputed issue among nutrition and medical professionals. Your LDL response is less dramatic than many others I’ve heard from, or even my own personal experience.
1. Why was your first LDL-P labeled High when it was in the Moderate range?
2. Have you looked into the APOE-4 gene? It can affect the LDL receptor and is found in about 25% of people, which is about the percentage who don’t see lipid improvements on LC diets.
1. I think it’s just flagged as High for being above the normal range. Note that in my second set of labs, the LDL-C was flagged as High even though it was actually in the Very High Range.
2. No, I haven’t looked into the gene variants that much. Someone else suggested I might be APOE-3/4 or 4/4, but I need to look into this further. So interesting!
Nice post and well summarized. I do think that in the end, genetic variation is gonna be probably what we are looking at, so i do agree with Dr. Siguurdson. I will be very interested in seeing some studies regarding subclinical athero. for yourself once they come back
Thank you so much for the feedback, and for answering my questions the day I emailed you in a somewhat frantic state 🙂
1) When do you expect to get another NMR test?
2) Do you have any target that you would like your LDL-P to be?
1. I’m not sure right now. It will probably depend on how my labs look when I get my next basic lipid profile in a few months. I do want to have the other studies done (calcium score and CIMT), and they’re probably fairly expensive and not covered by insurance.
2. I’d be happy in the moderate range. Of course, <1000 would be fantastic, but it's not a realistic goal for me unless I start taking a statin or other antihyperlipidemic med.
You might research supplements like berberine, amla, bergamot, pantethine
for example
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3942300/
http://blog.case.edu/yxr10/2005/1/19/nm1135.pdf
http://herbal-powers.com/catalog/images/Bergamot%20Research%20Summary.pdf
http://www.lef.org/magazine/mag2008/nov2008_Preventing-Cardiovascular-Disease-Naturally_01.htm
Sorry, Charles — I’m unable to reply to replies, but I hope you see this. I appreciate the supplement information and the references. Thank you.
I think the data are actually in: watch Ivor Cummins’s lecture on cholesterol: https://www.youtube.com/watch?v=fuj6nxCDBZ0
Note the graph on *when* LDL-P seems to matter: when fasting insulin is high. When it’s not, you’ll note that it makes very little difference.
I think this is telling and important. Whilst we don’t have the data yet, my postulation is that for some people who metabolise fat well, the body works well with more LDL-P. I believe so long as there aren’t additional issues with regard to endogenous oxidation and glycation, and inflammation caused by excess insulin, the HDL will properly scavenge the particles back to the liver and you’ll be fine. Of course, I may be wrong, but remember my saying this in ten years time when the data’s (hopefully!) finally come in 🙂
Thanks so much for your comments and for sharing the video, NM. I don’t have time to watch it today but will definitely try to view it sometime soon.
That’s an interesting theory you shared, and I certainly can’t discount it. I would like to see what the lipidologists think about it. My concern is the strong family history, but it’s hard to say what their insulin and inflammation levels were like, as no one was tested for these things until very recently. I will remember your words, regardless of how it all unfolds in the future! 🙂
Exceedingly warm there NM, infectious agents perhaps playing their interactive part also – but I’m too impatient to wait 10 years for answer! ….so currently triangulating existing study data (such as it is with all the design flaws) to firm up on hypothesis – output will be in next seminar, and depending on the the direction the problem solving process dictates, may very well be titled “Insulin – the Rosetta Stone” 🙂
Thanks very much for responding here, Ivor! I very much enjoy and appreciate your work and look forward to seeing what you have in store for us next 🙂
Rather thank you Franzizka – for opening up such a timely and fascinating discussion, enabled by the excellent tracking of your response data versus inputs; on hols currently, but with 5 kids in tow I’m not reaching research goals(!) – will get there though…..!
Wow, I didn’t know you had 5 kids. No idea how you manage to get so much research done and put together such amazing presentations, but we are all very appreciative of your efforts.
Thanks for posting this, as I have noticed some of my lipid numbers moving in the wrong direction as well. While my triglycerides and HDL are fabulous, my LDL and overall numbers are not and I have been making some changes to my diet as well. My doc recommends statins, but I’m not comfortable with that at this point. Since I have been eating a lot of coconut oil, I think I will follow your lead and drop that for a while to see if it will help make a difference. I sure hope so, and hope, as you do, that our dietary choices will some day prove to be beneficial despite the numbers. But along with you, I’ll do what I can to keep those numbers low. 🙂
Sounds like we had very similar responses, Andy! Thanks for sharing your own experience. I wish you the best of luck on your next lab test, along with good health in general!
Franziska,
You know that I comment mostly about my n=1+family and friends experiences and personal opinions, and from such narrow perspective I can tell that that it could be more hormonal influences on the total cholesterol, than the thyroid gland. For example, in my case I always had TC around 200 even on LCHF diet, but it jumped 50 points after I turned 52. My doctor didn’t start to worry anyway because all my ratios were fine, HDL high and TG low, but I managed to persuade him to write a prescription for me for HRT. I hope it would prevent the age-related migration of my fat from appropriate places into my middle-section.
My husband claims that the key for a lower TC for him is taking fiber to prevent the cholesterol re-absorption at the rear end of GI tract at the end of a digestive cycle.
Thanks so much for sharing, Galina! Always a pleasure to hear from you!
Hello,
I eat low this way and been testing for almost 2.5 years… I have noticed my particles LDL-P going up each test , but my small LDL-P hangs at like 95-115 my HDL P was 37 my HDL 65 LDL 115
Now Before I ate this way I was sick and had crohns and ulcer colitis , it is all gone and EVERYONE IS LOST— I eat tons of low starch veggies , but eat my eggs, fat–avocado , almonds walnuts, meats etc .Same I feel great, sleep great, stomach is great, sinus is perfect , when I was sick,, I could no longer eat gluten, potato, beer ,starches…NOT that I really do now…But all my problems left and I can eat them again??? At the same time I have been testing my guts bacteria, yeast and bacteria and have seen huge changes in the types I now have….. Some deal with the stomach lining( making it thicker) others —well my make up isnt like most now–but I am not sick.. I would love to contact you and compare –eating and several things.. ( you should do the american gut project) 99.00 and see what you have microbe wise…will surprise you.. as well a lab like “”GREAT PLANS LAB””” there OAT test and COMP stool.. would love to hear from you.. Im starting to think the LDL particles are part of bacteria (HUNTERS) upping your immune system cholesterol can also be antimicrobial
Thanks so much for sharing your story, Eddie! I’m very glad your health has improved so much on LCHF and that you can now eat foods which previously caused such GI distress. I’ll have to look into the testing you recommend. Sounds interesting!
I will also say…..my insulin resistance was super LOW the NMR use to give you the real low numbers I was a 4 now they dont give you reading below 25 My inflammation crp is .07 and my inflammation in GI markers is down one count was 1300 below normal is under 600 today Im a 97 For my cardiac calcium score is a 1 Im 41 years old. Feel great… Me Im willing to roll the dice. As my particles LDL-P have gone up Ive felt better,. may sound strange. When my gut was a mess my heart would flutter. no more. I think these docs have no clue—–just as they have NO clue in gut problems and diseases…. to me heart disease is a leaking of bad bacteria and yeasts into the blood stream due to a bad gut…and the cholesterol is attacking and clogging up the site of inflammation. if you read certain bacteria are antimicrobial –and eating LC your changing your microbiome. It wouldnt surprise me in the future, that the fat turns on the microbiome as a hunter mode …if you have no issue the particles are flooding around in mass ready(actually protecting you)….time will tell.
I just got results back after trying to eat Keto and my HDL numbers jumped up wonderfully, triglycerides are crazy low…but my LDL’s are still higher than they should be. I was put on a statin three months ago, so they did go down some from last time, but I had hoped to see a bigger drop. Doc wants me to stay on the statin but I’m tempted to continue the LCHF diet without it and retest. I’ve seen the same theories out there on particle size and not much science behind it yet. I really enjoyed your story and hope to follow it more!
Thanks very much for your nice feedback and for sharing your story, Carly! It’s amazing to see how individualized lipid response to keto and carb restriction can be. Good luck with everything!
Hi Franziska
Love what you are doing. As someone who has met you, I can say you look ten years younger than your age, at the very least, so you are doing something very right. I follow the same diet as you, whole fresh foods, low carb. In my seventh year as a type two diabetic and all HbA1c numbers non diabetic, except from diagnosis. Only diabetes meds two Metformin pills per day and touch wood, no complications.
Keep up your great work.
Kind regards Eddie
Always great to hear from you, Eddie! Thank you so much for the compliment. As well, I truly appreciate your support. Yes, low carb is the way to go for people with diabetes. Your BG numbers and A1c say it all.
Kind regards, and all the best to you and Jan.
10/5/12
LDL-P 1430 nmol/L
Small LDL-P 132 nmol/L
LDL-C (Calculated) 199 mg/dL
TC – 274 mg/dL
HDL-C 69mg/dL
Triglycerides 31 mg/dL
Trig/HDH ratio – .45
Gave up – among other things – coconut oil and coconut milk
Still eat some saturated fat – grass fed ground beef, raw goat milk, nuts, seeds, fruits, veggies, etc.
Added supplements I listed above + a few more and started on 10mgs/day Atorvastatin
MNR test results – 2/28/14
LDL-P 401
LDL-C 47
HDL-C 44
Trigs 34
Small LDL-P 209
LDL size 21.5
HDL size 10.3
Wow, amazing changes in your LDL-C and LDL-P! Thanks for sharing.
http://atvb.ahajournals.org/content/34/7/1341.full
Is Carotid Intima-Media Thickness as Predictive as Other Noninvasive Techniques for the Detection of Coronary Artery Disease?
Interesting! Just read the abstract so far and will read the rest soon. Thank you.
Great post, with lots of valuable information. I’m going to take some of your suggestions on board.
Thanks so much, Lisa!
NM, thanks for linking that vid. It was a really excellent presentation, and that specific data on insulin vs. LDL particle was new to me, so thanks for that.
Franziska, if you don’t have time to watch the whole vid, at minute 56 he presents data from the Quebec CV Study that showed risk of ischemic disease with high LDL particle (ApoB) vs. insulin levels. Previous slide looks at same study data, risk of high TGs vs. insulin levels. His point being that context is important, and particle and TG may not be all that important to risk in the context of low insulin.
Thanks, JB! Will watch that portion now.
It’s pretty well established that ketogenic diets lead to low thyroid and that because thyroid hormone is needed to upregulate ldl-receptors the result is that LDL cholesterol spends too much time circulating in the blood, leaving it vulnerable to oxidative damage which in turn can lead to atherosclerosis and elevated LDL.
There is no reason to assume that a high intake of saturated fat had anything to do with your results on a ketogenic diet.
Two variables have changed at once, the first is that you removed carbohydrates from your diet and the second is that you increased your intake of SAFA, either or both of which could theoretically have resulted in the changes in your lipid profile.
I think that the first variable is a more likely candidate.
explain my disappearance of crohns diease and ulcer colitis No one has a clue why its gone….I can tell you in testing my yeast levels went down. and insulin resistance low now , but particles went up..
I have been tracking for 2.5 years and I see a difference in but microbiome now
Now I have no disease and all doc are lost –thyroid is normal
So very interesting, Ed. Very glad to hear this.
Hi Marcus,
Thanks very much for your comments. Yes, I understand the thyroid down regulating LDL receptors which occurs in some cases (this isn’t universal, from what I understand), but didn’t want to get into that in this already very long post, particularly when I had no thyroid labs for confirmation. I think the increase in saturated fat and deeper level of ketosis likely both played a role, given that I’m still VLC and in mild ketosis, yet my labs have improved quite a bit in a short period of time. I truly wish there was a way to test thyroid levels at home in an easy, inexpensive manner, but sadly there isn’t. I do have thyroid labs tested twice a year, and they’ve been stable, as I stated in the article. Would staying out of ketosis entirely (i.e. >50 grams net carb daily) further improve my values? I can try that experiment after my next round of labs, provided my postprandial blood sugar remains within an acceptable range. Thanks again.
Thanks for your reply franziska. I think low thyroid becomes more common the longer you stay on a keto diet. That would explain why short term studies show that people eating keto diets have good cholesterol or even improve their cholesterol, but in the long term high ldl is very common. That is also consistent with your experience, your cholesterol gradually deteriorated over years of carb restriction. So given that background i think its premature to attribute your soaring ldl cholesterol to safa intake especially when the literature does not support an association between safa intake and poor hdl to ldl ratios.
Thanks, Marcus. You may very well be right. I’m still encouraged that my lipids improved quite a bit by increasing my carbs to only about 20 grams. Interested to see what they’re like next time I get them tested.
Correction in my response to Marcus: It should say “increased carbs by 20 grams” rather than “to 20 grams.”
Thanks for this post. Some folks on LCHF diets try to cycle carbs / insulin in order to maintain the thyroid function. They would once a week or prior to an intense exercise session eat carbs for either thyroid or athletic performance reasons. I don’t get the sense that many if any on this post cycle carbs, but I wonder if the carb cycling is effective or not, whether that would show up on thyroid tests and ldl-c tests. Likely there are subgroups of all of the above, but as a new low carber with increased ldl-c, thanks for your post as it gives me something to think about. Figure my increase may be mostly fat loss, but checking on thyroid is probably something I need to do in the event as my fat loss slows, my ldls don’t improve. Thanks Franziska for this post as many of us are struggling with this issue.
Thanks so much for your comments and sharing your own experience, Lance. In Dr. Patel’s article on LDL-P I linked to in my blog post, he confirmed that he follows a cyclical VLC diet, yet his LDL-C and LDL-P numbers are quite high. I don’t believe he has any thyroid dysfunction, however. I think it’s important to have thyroid labs done periodically regardless of diet, though, as changes can happen within months. Again, I appreciate your comments and hope that your lipids improve.
Not everybody believes that eating a LC diet is detrimental to the thyroid function, but a weight loss resulted from any weight-loss regimen may cause a hypo-thyroid symptoms in many people.
http://caloriesproper.com/?attachment_id=4235
“Hypothyroid-like symptoms occur relatively frequently during times of rapid fat loss, and this may be at least partially dependent on diet quality. Another component is the fact of being in an energy deficit, but this is difficult to evade on a weight loss diet.
Jane Plain has a post about how high fat oxidation and heat production induced by low carbohydrate diets is partially responsible for the relatively normal metabolic rate despite low thyroid hormones, similar to the Bisschop and Ebbeling studies discussed below. And another one, discussing the importance of energy balance. Sam Knox wrote about carbohydrate restriction and functional hypothyroidism, or lack thereof despite altered thyroid hormones. Also, Dr. Eades’ first-hand clinical experience; and Anthony Colpo’s take vs. Paul Jaminet’s response. And more on thyroid biology by Jack Kruse. Edit: Amber posted about thyroid levels & diet on Paleohacks.”
I have been following a LCarbohydrate diet myself since 2007, and I was diagnosed with under-active thyroid at 1996, so my TSN and thyroid hormones levels get checked on a regular basis by my general practitioner. I do not have an increased need in the hormones supplementation. Due to multiple allergies, my main form of entertainment is doing different exercise routines, so I am very psychically active, but my adaptation to the exercising in a fasted and ketogenic states took time.
A great reasoned discussion with particle numbers. BRAVO. I think different genomes respond to different diets. Folks with insulin resistance clearly benefit from LCHF diet. I hope the ADA comes around to this conclusion soon. To know if your diet works for you it is critical to get CAC & CIMT at baseline and follow CIMT every two or three years. Here is my report. https://docs.google.com/document/d/1a0Rp9WV1dSrbs_n5cXNv6TgdFZxdUBYUk95D5cYb61I/edit#heading=h.938fr74lv4ue Caution: False negative CAC in folks under 60 yo common. CIMT quality questionable. I have used different labs with different results but I posted KUMC as the most consistent and reliable for CIMT. Fran, I input your data of TC 280, HDLc 92, age 47, normal BP, no smoking, no DM into ACA/AHA risk calculator: http://clincalc.com/Cardiology/ASCVD/PooledCohort.aspx and found your 10 year risk to be 1.6% but your lifetime risk is 50%. If you have sub-clinical plaque on CAC or CIMT I would suggest trying Atorvastatin 10 mg a day and get LDLp < 1,000. My lipids & weight & statin intake did not change on LCHF but I stopped gaining weight. I actually decreased exercise over this 3.5 year period. Of course I am a big advocate of statins. I understand some folks just don't want to take them,
Thanks very much for the nice feedback, Brian! Thanks so much for all of the information and suggestions. Wow, a lifetime risk of 50%. I will look into having the tests you recommend. As I said, I have mixed feelings about statins and am hopeful that I can bring my lipids down to reasonable levels by dietary means. Thank you so much again for your comments! Very much appreciated.
First a personal disclosure. I am an engineer. In the past I followed official recommendations blindly. I am sure that following and promoting them I got to hurt some of my most near, dear kin. I don’t delegate preventive care to anyone anymore.
May I say that a lifetime risk of 50% is not so alluring to me… I would much prefer a number nearer to 100% because I would much prefer dying of a heart attack or massive stroke (cholesterol seems not to be a clear risk factor for this) than cancer for example. Anyway, I have no idea what my lifetime risk is since neither my total cholesterol of 369mg/dl nor my HDL-C of 105mg/dl are welcome by the ACA/AHA risk calculator. Go figure. Either way, since United Kingdom is quite nearer to me than USA (I’m Spaniard) I will take as good the 10 year risk from QRISK-2: 2.1%. I will be interested on epidemiological data showing the risk of a so high cholesterol level whenever I see the data myself for those with HDL-C higher than say 90mg/dl. I would much prefer that epidemiological data not being from USA though since it has been a long time since healthy food have been easily available over there. At least around here we still can buy not only full-fat yogurt but Greek one with cream added too. Anyone should read Nina Teicholz’s book. Until pertinent data is available I am not going to do anything on epidemiological data not representing those that eat like me.
Coming back to the cause of death issue. It has been quite a time since I asked about data linking apoB (I couldn’t measure LDL-P around here) and overall mortality in another blog. All I could find at that time was a study on NHANES III data (so on USA population) where all causes of death were evaluated. Hazards ratios per standard deviation increment with 95% confidence intervals almost not including the unity were HDL-C 0.87 (0.72,1.04), LDL-C 0.9 (0.81,1.01) —it is not a typo—, TC/HDL-C 1.04 (0.98,1.08). This last one was also the narrowest. ApoB hazard ratio was 1.17 (0.83,1.64) a quite wide confidence interval pointing toward a not too high sensitivity as a measure for longevity. I am still not moved.
I recommend you to look at the strategy of Dr. Davis (not updated outline by Dr. Dach), although I personally wouldn’t focus on the LDL-P at all and would add vitamin K2 to the vitamin D. There are some very interesting data from the Track Your Plaque experiment tank commented by DrBG too. We will have grand-grandchildren before their conclusions are refuted/confirmed by a proper intervention trial.
Personally I am mainly focused like you on the most important thing: postprandial blood sugar. That means not only controlling it by carbohydrate restriction but by trying several strategies designed to improve insulin sensitivity. I have had success (measured by postprandial improvement to the same triggers) but now I don’t know which of them (if any) is to blame.
I will change my mind about cholesterol whenever either I can get my sub-fractions measured or new data appear.
Thanks very much for your comments and sharing your story, Andres. I appreciate all of the information and your insights.
Andres,
I myself am an engineer too 🙂 I got sick crohns diease and ulcer colitis,,, I did nothing a GI doc told me (thank god) i looked into more in like what you are saying SUGAR!!!! and the role of yeast/fungus and bacteria..
What NO one talks about here in the USA is every dam thing has SOY, gluten or Dairy , or massive amounts of sugar added to it….
I wouldnt put much faith in data coming out of the USA –I think your right
When you look at who leads the world in Auto immune diseases you will notice–its US… —–As well many if not most who are SICK have HIGH antibodies to AMCA or ASCA youll notice there yeast—- many will call BS on this…. yeast eat sugar…..yeast also have proteins that look like soy ,gluten and dairy…
I looked at stripping my gut down of bacteria and YEAST/FUGUS to get healthy — and the way to do it was NO SUGAR….. even cutting massive fruits out.. The American diet is SUGAR– sugar, and tons of food that digests as sugar….added sugar drinks
Remove the sugar you remove most of the problems… as I moved up my fats and dropped the sugar I have lost all diseases( the real answer —-is I changed the GUT make up of bacteria and yeast/fungus…
I may drop dead at some point(my heart) — but now my blood pressure is 97/63 and pulse 65 as of today… my insulin resistance in NMR testing was a 5 until they stopped recording under25. My gut is great and no health issues —and I ve lost every doc ive seen———-my only issue now is HIGH LDL particles (total)…. so I’d say FAT is good….well it helped me some how
Now I am getting to much (fat per the standardized testing—well I guess I will find out —all my digestion markers are great now produce SCFA’s and my Lysozyme dropped from 1300 to 97 —- Lysozyme is an enzyme secreted at the site of GI inflammation (normal is below 600) as well my Lactoferrin –another GI marker for gi inflammation is 0.5 now down from 15 (normal is less then 7.3) So I guess I shifted my health problems from my gut body and GI tract to my heart..
time will tell— Im still playing (will see if my LDL particle total goes down with different bacteria added in…
I –still say its all what species of bacteria you have in your gut along with yeast—and all these Cholestrol numbers mean different things in different people ( with different genes and Gut make up( bacteria and yeast) theres nothing Accurate ( start testing there gut ) and blood for YEASTs
US Americans are totally un healthy — leaning toward HIGH yeast and bad bacteria—due to the over use of antibiotics( trashing our immune system, killing off good bacteria —and the lack of natural probiotic foods -which Europeans and South Americans still eat)
Yogurt is not yogaurt–when its ZAPPED and everything is killed and some crap is squirted in(bacteria you read on the label)….as well pasteurized. and made low fat.. ………..why everyone is sick( I woke up and now i am not)
Brian Edwards,
You seem to like to investigate like my self, when I read all your testing –I am no doc but have cured my self of crohns and ulcer colitis. What jumps out at me –you talk A1C, testosterone and other things as well statins your playing with and using to lower your number…..your not fixing the cause..
Being a doc , Im sure you dont believe in yeast/fungus as a problem. As well different bacteria in your gut — changing the out come of your problems… I have been doing the same thing your doing tracking things in many tests , its been 2.5 years now and I have a super gut, but my LDL- Particles are going up.. I have LOW insulin resistance markers , and so far everything seems good. I can also tell you I have changed my whole microbiome in my gut by testing, lowering yeast/fungus and up ing different bacteria strains.. One NOW very high akkermansia (research this one) a tip for your insulin and type 2 🙂 I will beat you money and lay the deck of cards –you will not have much of this gut barrier bacteria and your yeast will be high… you seem to like to investigate like my self… eat high does of inulin (onions , asparagus, leeks and garlic ) while lowering yeast by suppliments or antifungal drugs—- Watch your blood sugar and A1C i bet it changes… get a base line on your bacteria and yeast BEFORE YOU DO THIS… (GREAT PLANS LAB)(heres the lab http://www.greatplainslaboratory.com/home/eng/full_oat.asp) do there OAT test heres a sample http://www.healthlinkpartners.com/testkits/images/test-pdf/Organic%20Acid%20Test.pdf and there comp stool test sample http://www.healthlinkpartners.com/testkits/images/test-pdf/Comprehensive%20Stool%20Analysis.pdf………………….bet you money your YEAST are high in both fix this…. your akkermansia bacteria will rise….. you can get your basic RNA16 test for 99.00 thru american gut project http://humanfoodproject.com/americangut/
heres a basic article on akkermansia
http://www.nature.com/news/gut-microbe-may-fight-obesity-and-diabetes-1.12975
Ive been tracking this for 2.5 in me….cured my crohns( the cause yeast) bacteria secondary Yeast/fungus is believed to be the causes in many with diabetes— yet no one looks here. My family on my mothers side ALL have crohns or type 2….both simular
As well your a doc run a IBD PANEL on your self and IBD EXPANDED PANEL– labcorp test# 126045 I bet you come back with antibodies to AMCA or ASCA in expanded panel or IF your ASCA it will show in the IBD panel if your not….Bet AMCA will show in your EXPANDED PANEL along with ALCA — which is sugars…
be a good test for you…… 🙂 you seem to like to investigate
Im not so sure , the LDL-P is accurate — But I bet if you dig youll find YEAST/FUNGUS as your type 2 problem –and low akkermansia
Love to hear you do this and a follow up, I bet the house on it
Fungi actually thrive on ketones, ketogenic diets exacerbate fungi and also adversely effect gut microbial diversity.
Ive heard that one…………….too many times “”” fungi eating ketones.””” The problem its not as simple as that.. Depends on your PH , other bacteria..(which most are missing many strains from all the antibiotic use—why they have yeast overload to start with) too much fat and LC will kill many bacteria. If your missing many SURE it will eat ketones…..thats a lame answer –there missing many bacteria that would suppress them– due to the over use of antibiotics….add in to much you lose your good bacteria and add in antibodies to yeast/fungus— from all the penicillin.. foods with similar antibodies -gluten, soy and casein all look like yeast/fungus adding in the up tick of allergies and gluten issues…. diabetes… something no one talks about…. Im sure when you dig like I said above youll find YEAST as the cause with low good bacteria… investigate your type 2…. L@@K up akkermansia bacteria.. up this bacteria(eats real inulin) , and lower you yeast… Im sure your A1C will change and statins are also ant ifungal
So eddy, if i understand you correctly your solution to the problem of too little good bacteria and too much fungi is to starve the good bacteria even more and feed the fungi by staying on a ketogenic diet?
Fran, Thanks for sharing your results and thoughts. Unfortunately, we are left with expert opinion in 2014 regarding rising LDL-P on VLCKD diets and cardiovascular risk.
Dr. Dayspring agrees that we do not have all the answers yet, although he still feels strongly that those on VLCKD diets with rising LPL-P should reduce saturated fat and take a statin or Ezetimibe to lower LDL-P based on all the evidence, done independent of diet!
We won’t know anything about cardiovascular outcomes and diet until we do proper experiments that control for diet, unfortunately this will be a most daunting task. Like Ivor Cummins (The Emperor is fat & naked) says in his awesome cholesterol presentation unless you do proper experiments, in this case looking at diet, all you get is statistical noise.
Medications to lower cholesterol for primary prevention (as in your case) only reduce absolute risk by 1-2% regardless of LDL-C and Non-HDL. ApoB and LDL-P may have better specificity, we shall see if they become the new mainstream markers. The AHA and ACC still sya to look at non-HDL-C
What about Russell Ross and the response to injury hypothesis, inflammation insulin etc…? As I discussed in my talk on the cruise, maybe you should consider a Cleveland Heart Lab Profile inflammatory profile http://www.clevelandheartlab.com/ and see?
Also I do not think that the CIMT intima thickness (the wall or lining) correlates well with risk. We see patients with old blood vessels and no plaque. We see patients with young blood vessels and lots of plaque.
The CIMT often includes a limited carotid doppler looking for plaque and plaque quality within the lumen. Do you have plaque or not and what is the quality of the plaque? Looking for plaque or not should become the new endpoint!
Hi Jeff,
Thanks so very much for your feedback and all of your comments. To be honest, I’m more confused about what these elevated values signify and what to do next than when I wrote this post 24 hours ago! So many doctors whose opinions I respect, including you, have differing opinions on these issues. I’m planning to spend several hours this weekend reviewing the papers, websites, and videos that have been suggested and go from there. Thanks again, Jeff!
Fran
To the contrary, yes you do understand!
Jeff
Can’t reply to your reply because Weebly set up the comments section this way, but thanks 🙂
Hi Jeff (I was your alternate cameraman on the low carb cruise).
Your comments about the Cleveland Heart Lab Profile inflammatory profile and potential CIMT shortcomings were not lost on me. My LDL-P makes Franziska’s look like the gold standard. Meanwhile, I found out that there is a local outfit that does calcium heart scans for $99.00. I had one yesterday and I’m anxiously awaiting the results. Got any general comments you could share on that test?
Tom, A Long thread here and you have already made some great comments. Regarding the calcium heart scan, I do hope that you went to a reputable facility. As in any imaging test, performing and interpreting requires a bit of art and skill.
The test will provide some historical information about calcium build up in your coronary arteries. I hope that you have a favorable Agatston score <100. Along with testing including lipids, insulin resistance and inflammatory markers you will get the big picture.
Here is an ACC/AHA expert consensus document on EBCT: http://circ.ahajournals.org/content/102/1/126.full. I find the discussion about reproducibility interesting.
BTW, your video came out nice (thanks for the help), however we were having audio problems.
Thank you, sir. Yes, hopefully it was a reputable facility doing the CT cardiac score. It was recommended by my doctor so I’m fairly comfortable with that choice. They said they don’t farm out the interpreting and the work is done by a local physician.
I have all zeroes. Total plaque burden – Agatston score = 0. I’m going to have the Cleveland Heart Lab tests done just because I’m an information junkie but it’s looking like the super high LDL-P is not something I’m going to lose sleep over so long as all other markers remain positive.
Congratulations on the great calcium scan results! Let us know what happens with the Cleveland Heart Labs testing.
Tom,
what were you total LDL particles ??? and small ldl P
I have 95 for small LDL-P and 1499 for total LDL particles
I had a scan and was a (1) having all the other things done monday for fun….Carotid Artery Disease Screening and Atrial Fibrillation (irregular heartbeat) Screening —had EKG’s in the past at 40 all perfect
will be doing in sept
antimyeloperoxidase MPO antibodies
Lipopretain -associated Phospholipase A2
What tests will the Cleveland Heart Labs testing will you be doing ???
Eddie – Here you go. The difference between 2013 & 2014 was I started taking fish oil twice a day.
I had information from disparate sources and finally started tracking it in the format below. It make it easier to follow for me and my doctor seems to like it too.
https://drive.google.com/file/d/0B7zDYCiIfElZeEh0eU5xMnlFWDA/edit?usp=sharing
Tom,
I find your scores interesting ,,, there some what like mine … If you look closely your total particles LDL moved a little…. the big jum was SMALL LDL P –and your inflammation CRP…. I ended up with crohns and colitis and a stomach a mess….gluten problems , starch problems etc… eating good fats–replenishing good bacteria and working on LOWERING yeast/fungus (mainly) I have noticed my insulin drop as well….. NMR use to publish below 25…. I was a 5 now Im always below 25. To me I think — just like with all other medical problems arthritus, diabetes etc —– there looking at symptoms not cause…. For me I think the cardiac thing is a leaking gut— allowing bacteria and or fungus to get in the blood stream,… the cholesterol clogging etc at the point of problem–bacteria and or fungus. My heart raced more , my inflammation was higher etc when my gut was a mess…….. when you research areas of fungus/yeasts/candida……. youll see almost anyone with an auto immune disease has low bacteria akkermansia muciniphila and high antibodies to yeast—-you wont hear that or see that from a cardo doc…. from my own study and research on my self… I have 3x more akkermansia muciniphila bacteria —–and now NO GLUTEN intolerance… at the same time My numbers for yeast dropped… both yeast and akkermansia muciniphila live in the same area…. and in my opinion fight for control…raise the bacteria lower the yeast— less or no auto immune disease….. close the gut less cardiac diease…. my opinion from family history of many with diabetes type 2, crohns arthritis and heart disease— many of this stuff started to happen to me—and its all revered so far…. other than a piece of paper saying my total LDL particles are 1499 …my secret…. LOWERING yeast—– which i bet a million will lower your insulin resistance…. up the good bacteria…lost from eating bad and the @SS jack American protocol of over use of antibiotics …. many yeast proteins resemble soy, gluten and cassien as they are very close…..A1 gene milk…. and meat also raises your cardiac risk,…. there are many factors not looked at….
http://www.drsinatra.com/what-is-the-best-heart-healthy-diet-plan
Thanks, Charles. Unfortunately, that is exactly the diet I followed for many years until I discovered my postprandial blood glucose reached 160s-190s after meals. Lowering my carbs significantly allowed me to keep BG under 140 at all times. My fasting blood glucose has always been and remains quite low, in the high 70s to low 80s.
Having said that if i am right then eating more safa would still probably exacerbate the problem. If your ldl receptors are working properly then they will clear dietary cholesterol readily and your cells will adapt by producing less endogenous cholesterol.
Perhaps if your ldl receptors are down regulated you are not only less able to clear dietary cholesterol, but your cells also fail to curb endogenous cholesterol production, because they still need cholesterol and thy’re not getting it. In that context it probably would be beneficial to reduce safa intake and dietary cholesterol.
Its a pity you didnt test your thyroid or cortisol levels.
Thanks for clarifying. Your reasoning makes sense. I do think both upping the carbs and protein while lowering saturated fat a bit helped both for thyroid function and perhaps via reducing ketone concentration, since they can be used in cholesterol synthesis. Yes, I certainly wish I’d tested thyroid and adrenal function back in April.
Thanks again for your insight.
“Sometimes when talking to someone about their cholesterol, I ask them to ask me what my cholesterol is. Then I answer: “I have no idea, because I never have it checked.” That’s not because I take an ostrich-like stance on matters that relate to my health – it’s because the great likelihood is that knowing my cholesterol numbers would not lead to me having a different view on my health or have any bearing on how I live my life. End of.”
Dr. John Briffa here http://www.drbriffa.com/2012/11/30/ask-me-what-my-cholesterol-level-is/
“There is no correlation between cholesterol numbers and heart disease, none whatsoever”
Dr. Malcolm Kendrick here http://www.youtube.com/watch?v=i8SSCNaaDcE
Elevated blood glucose levels are a different matter altogether and cause a multitude of serious health care problems and complications. The great cholesterol/statin con, the greatest con since saturated fat is a health hazard, and base your meals on starchy carbohydrates.
Praise the lard, I have seen the light ! Whole fresh foods and exercise, your passport to a healthy medication free life. “Start living your days instead of counting your years” Gerry Goffin
Kind regards Eddie
Thanks for your comments, Eddie. While I respect those doctors and their opinions, I have equal respect for the opinions of the doctors cited in my article and the ones who have posted here, who disagree that very high cholesterol levels do not increase risk of heart disease. So there is no harm and may be great benefit in modifying my diet the way I have. Thanks, as always, for your support.
Kind regards,
Franziska
Dr. Dwight Lundell has said that cholesterol is no indicator of CHD. I’ve also read that 200-250 may be an optimal range for total cholesterol. (Assuming HDL 60+ and Trgs 75 or lower) Seems odd that someone can have a TC of 220 and they are put on a statin. Will it reach a point that cholesterol is not even used for diagnosis?
Wow. There are a lot of parallels to my own experience here. I have been LCKD for 2 years. My doctor belongs to the particle size school of thought regarding LDL but I am not convinced:
LDL-C 231
LDL-P 2210 (I wish that was a typo)
LP Insulin Resist Score <25
CRP 0.14
CIMT all clear
I just may try cutting down on the saturated fat for a few months to see what happens. I had 2 NMRs four months apart and saw my Small LDL particle number go from 822 (bad) to 176 (good) with the only change being daily fish oil supplements. I also saw improvements in the various HDL markers (trying not to write a novel here).
Have you considered going to a health fair for the CIMT? I've done that twice and it's hard to beat the price. It's like a medical traveling circus and they are much more streamlined than a hospital (or so I am told). My insurance will not pay for it but the basic test, which includes the CIMT, runs $125. I use Life Line Screening.
Hi Tom,
Thanks so much for sharing your story and your lipid values. Congratulations on the small LDL-P going down so quickly and effectively and HDL improving as well! It certainly wouldn’t hurt to cut back on saturated fat. If you’re not trying to lose weight, just replace a portion of SFA with MUFA and to a lesser extent PUFA, preferably omega-3’s, and maybe add a few carbs back in the form of berries, nuts, etc. I can’t guarantee it will help, but it’s worth a shot 🙂
Thanks so much for the health fair suggestion. I didn’t realize they offered CIMTs and will definitely check into it. Much appreciated! And best of luck with everything.
Good luck with 23andMe! (Responding to your post below because I can’t reply to your reply and there are already so many responses to Marc’s initial one)
Yeah, that’s one long thread! I’ve followed link after link until my eyes are ready to bleed. I really hope the Irish guy with the stats showing that high LDL-P with low fasting insulin is harmless is correct! My fasting insulin was 4 (range 3-14).
I’ll post any relevant results from the DNA test. I really do want to learn what I can about my sky high LDL-P. I’ve cut back on saturated fat for now, just to see if it has an effect. Does anyone have any idea at all how long it might take a dietary change to show up on an NMR (if it has any effect)?
I hope Ivor is correct as well! My fasting insulin has been below the usual range ever time I’ve measured, right around 1.
Thanks for updating when you find out your results. As far as how long it will take lab work (primarily your LDL-P) to reflect the impact of any changes you’ve made, I think two to three months should be sufficient. Mine improved quite a bit in less than two months, but I’d imagine it would vary from person to person based on individual response to dietary change (some report stable values regardless of SFA intake), the degree to which nutritional composition is modified, and the starting point for your lipid values. Best of luck!
@Franziska
This is a test you might find very useful
http://www.bostonheartdiagnostics.com/science_portfolio_cholesterol_balance_test.php
“All individuals differ when it comes to the balance between cholesterol production and absorption. Some people synthesize cholesterol more than they absorb, while others absorb more than they synthesize.
Knowing how an individual produces and absorbs cholesterol can help determine the most effective LDL-C lowering therapy. Understanding in advance which therapy will have the greatest efficacy allows for a more successful and cost-effective CVD treatment strategy.
Lathosterol, the direct precursor of cholesterol, can be measured in plasma or serum. Eighty percent of synthesized cholesterol goes through lathosterol, while only 20% goes through desmosterol. Therefore lathosterol is the only valid marker of cholesterol production. People who overproduce cholesterol have elevated levels of lathosterol normalized to total blood cholesterol levels. Markedly elevated levels of lathosterol identify patients with increased risk of premature coronary heart disease.”
Here’s an interesting study
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2724787/
“Present study results demonstrate that individuals with CVD or ≥50% carotid stenosis have an altered cholesterol homeostasis profile, characterized by higher cholesterol absorption (plasma campesterol, sitosterol, and cholestanol concentrations) and lower cholesterol synthesis (desmosterol and lathosterol concentrations) relative to matched control subjects with comparable plasma cholesterol concentrations. Furthermore, the cholesterol homeostasis markers were highly significant predictors of CVD risk relative to established risk factors in this study population.
In conclusion, present results indicate that alterations in cholesterol homeostasis, namely high cholesterol absorption and low cholesterol synthesis, are associated with increased CVD risk in a subset of men and women with similar plasma LDL-cholesterol concentrations. Additionally, the cholesterol homeostasis markers appear to be better predictors of disease than traditional lipid risk factors in this study population.”
Your thoughts
Thanks very much, Charles. I am actually very interested in this test. I wish I could order it myself, but it looks like it requires a physician’s order. I’ll discuss it with my doctor at my physical next month.
@Franziska
You might also check this out
http://www.lifelinescreening.com/What-We-Do/What-We-Screen-For
Thanks!
I had planned on doing this test next month—-same place be interesting to compare results
marcus volke ,
What Im saying….if you dig and I mean dig deep, Im sure most have antibodies to yeast..the problem is all the tests are investigative as there is no real good test, as with all GI tests as you see they cant give you answer.(why millions are so sick—they dont treat to raise bacteria or even lower yeasts. My self I used may tests, some standard some non standard…some questionable I dont buy the fat thing…as I have watched in my tests my yeasts markers go down..not up…. But my diet is 70 percent low starch veggies , then fat and protein from nuts meats etc.( I GET MY FATS thou and cholesterol. I my self produce SCFA’s I have also lost all my disease and lost all docs.( super low GI inflammation and CRP For me I started HIGH fat lots of coconut oil fats etc then moved on…as stated above. What Ive found , I have far less firmicutes in stool testing yet my blood pressure is 97/65 and pulse 71 last checked… calcium cardiac score was a 1 i will check again this year…soon other heart tests for laughs(im not focued here—im more looking at the gut and blood)… Me i have been focused on bacteria/ yeast and heart third. But in my testing I have documented my life now in 2.5 years( adding the cholesterol as almost a laugh).. I hear all this ketones fat and candida… Im not seeing that…but what I have done different is focused on my self, why did I get gluten problems, why soy, why grains….and starch problems….all pretty much gone. The answer and hidden key FOR me appears to be bacteria akkermansia muciniphila.. As I worked on lowering yeast..which no dam doc will believe… my bacteria akkermansia muciniphila shot up high… this bacteria deals with lining (google it) the yeast also dig deep in the lining. today I can eat gluten, drink my self silly with beer…..I dont choose to do this , maybe on a rare day now. I ve done alot of different stool testing , and antibody testing —and in the back end particle testing. For me strange as it may sound as I have become better with crohns and colitis my small LDL-P dropped —today it is a 95 my LDL-P total has gone up…currently 1399 total particles… I now dont snore and chock in my sleep, sinus is great, no summer allergies, food problems are gone(except soy) no more migraines with weather change….no joint pain. As we can see NO one has a clue on gut , and really no one has a clue on cholesterol.. People argue all these different things for the gut…I did the opposite and didnt take the immune suppressant drugs. Im great now???? I wouldnt get to focused yet on total particle… maybe Im killing my self…..but my gut doesnt show it…and I feel the best I have all my life. For me I find it odd the HADZA tribes guts are full of bad pathogens…and there healthier then we are….and have less disease.
ALL fat diet, yeah Im sure your killing off many good microbes, but for me….im not seeing the candida going up on fat… my PH in my stool checked yesterday was 6.6 to 6.8 when I was sick and had more yeast i was a 5 ph… this goes against science but —we also dont know how to cure, heart disease, cancer and gut problems.
Its all a numbers game….its not as simple a saving your self by a particle number….im sure theres many other factors yeast to bacteria balance….missing bacteria— some bacteria lower cholesterol some make vitamins.. for me I am lower in cyano bacteria and action bacteria compared to others………… test your stool marcus
do the cheap american gut project 99.00 test…..do a GDX or GREAT PLAINS LAB compstool test….. as well great plains OAT test…. Im sure it will make your eyes blink —when you compare your yeast/ bacteria to your cholesterol….
For me the holly grail has been bacteria akkermansia muciniphila GOOGLE it…for me I wonder if this does something to your particle count total…. I have 3x more then anyone else in a study im in…I also had a low insulin resistance score with NMR when they use to give you reading under 25…. now they dont tell you under 25 all my health markers seem great….This is just my thought and not anything proven… but depending on your diet , Im starting to think the total cholesterol LDL-P may be scanning and part of your immune system depending on your bacteria make up. Its normal role is to got to the site of injury etc… bonding and clogging…from what I read– it wouldnt suprise me if those that have clogs you notice a high amount of bacteria or yeast that have leaked in from there gut…
Be nice to test OLD people that live long—to see what microbes they carry… and DEAD sick people…
Well im glad to hear you’re feeling better eddie. Ketogenic diets can be therapeutic for crohn’s and any condition related to gut dysbiosis and small bowel overgrowth. Generally these diets remove food toxins and stomach irritants which can be problematic if you have a permeable gut (i.e grains). Fibre can also be antagonising to a sensitive gut. The other reason they work is that starve the pathogens, including the SIBO pathogens. The downside is that you also starve the good bacteria and possibly feed fungi.
If you have the money you should try fecal microbiota transplantation to restore the many hundreds of species of good bacteria to your gut. If you cant afford that, taking prescript assist might help. You would then need to reintroduce vegetable carbs like potatoes and slowly introduce resistant starch and fermentable fibres to feed your good bacteria.
THANKS, NEED MY FRIEND
All problems are gone… I spent two years building back my gut….I carry 4 genes for gluten, I can drink beer again, eat gluten,,, slowly been adding some starch veggies in… not potato yet. I have lost all docs
my fecal ph hangs about 6.6 to 6.8 no fungus issues now..(sounds strange—I did at a ph of 5– all testing each time showed less and less. My magic key GOOGLE IT akkermansia bacteria heres just one link http://www.nature.com/news/gut-microbe-may-fight-obesity-and-diabetes-1.12975 I have 3x more then most people now….( this bacteria eats inulin—I eat high amounts of onions and asparagus….. I eat fermented kraut ,kimchi and my probiotic is 7 strains lacto 5 bifo… Ive been slowly building my gut , over 2.5 years.. plan to write a book about my experience , how lost GI docs are and what has happen to me. I went from gluten intolerant to fine with gluten…..you see– my research and testing points to amoxicillin creating a monster.(in me) I say with many—..a killing off all my good bacteria and then my body creating antibodies to mold(and amoxicillin) and to yeasts…. then making my immune system weaker…food proteins like gluten look like yeast as well soy and milk….add this in …its a mess also wearing down the barrier…gave me sinus issues , seasonal allergies, etc GONE… caused a leaky gut and un digestable starches and hard digestible sugars in.. (ANSWER FIX THE BARRIER –lower the yeast but grow the akkermansia) first problem solved. the second getting the bacteria back that block yeast and bad bacteria… all pretty much done now… I need to get my action bacteria up( which I can get from some soil based probiotics) feed with RS… in the end Im going to add high doses of Lactobacillus reuteri as a fun test to see if over all total particles come down…
I have lost every doc…..stomach is like steel now.. no allergies, no nasal drip…no snoring ENT lost ,GP lost and GI…..as well RECTAL doc…..fix the gut fix your health—its all bacteria and yeast balance( YEAST is as import or more then bacteria) one day docs will wake up on yeast
Thats fantastic eddy, it sounds like you know what youre doing. Can you tell me how you increased your levels of akkermansia bacteria? Did u take a probiotic form and prebiotic to feed them? How Did you fix your gut barrier integrity? Just diet and probiotics?
Marcus,
sure– since I was sick….I figured my balance of bacteria and yeast was off.( reading hundreds of studies on yeast and bacteria)..No one talks of the fungus /yeast— which I believe has more to do with disease and gut barrier.—lowering akkermansia –certain foods are known to wipe way the barrier –gluten as one healthy or not..
I spent thousands of dollars in tests –and found everything I stated in other posts.. One factor I zoomed in when I laid all my papers on the table was yeast…. So I worked hard on lowering yeast and stripping done my bacteria( i wanted to lower kill most—antibiotics only target certain ones…..( figuring my balance was so off) taking herbs olive leaf , oil of oregano , grapefruit seed extract caplyric acid neem many things….NOT ALL AT THE SAME TIME!!!!! then I worked hard on PROBIOTIC FOODS real sauerkraut, kimchi… probiotics I used RENEW LIFE 50 billion and 80 billion 10 -14 strains of bifido and lacto While upping the good bacteria , I work HARD eating lots of inulin ( akkermansia bacteria food source is inulin—-gralic leeks , onions asparagus) for me I then switch to things that only attacked yeast…pau d’arco , caplyric acid LC diet —no starches sugars grains milk, etc while doing this I watched the akkermansia bacteria population grow more( switching from yeast to akkermansia >>>…. now in this process my gut make up is strange in testing — but to me you cant fully focus here as different strains live in different places in the gut.. ( as well the PH will be different in different places) we focus so hard on the exit area and stool… when I was sick the exit was 5 ph today Im 6.8 PH My population is more—my guess is it rises as it get down to the lower colon now
My make up is odd as my most abundant strains are
Genus Bacteroides 37.3%0.19%
Genus Parabacteroides 20.1 %
Genus Akkermansia 13.2%
In other testing I have other strains—these are my highest thou but thats on exit.
In testing –my lacto is low , but I dont think so–I think it stays up in the top end now. and doesnt ride down to the end..
….I eat alot of fermented stuff…and take high does if you look at a chart of the gut if things are working correctly youll see bacteria stay in different places. Youll also have different PH’s which the avg person cant test. ..
Look into yeast and Akkermansia youll see many with auto immune dieases have high antibodies to yeast AMCA or ASCA at the same time they have low Akkermansia bacteria… FOR ME A BIG KEY science is missing….you see all the mouse studies on Akkermansia but no human testing—I decided to do the testing — but you see there are other factors — for it to work right I think the yeast have to be lowered and the Genus Bacteroides /
Genus Parabacteroides work with the Akkermansia to re build…
some strange links in stuff I see happening to me http://aem.asm.org/content/early/2013/09/23/AEM.02545-13.full.pdf
http://cmr.asm.org/content/20/4/593.full
plus all the http://cmr.asm.org/content/20/4/593.full
if you want we can chat more in email.. if you send me a facebook message to eddie belschner I will send you my email address
Thanks for the info. So you didnt actually take an akkermansia probiotic at all?
Congratulations on a well thought out discussion Too simplistic for some to comment such a response is genetic as every single chemical reaction in the body is under genetic control, and thus everything is influenced by genes. I have that found most folks with your response have evidence of induced cholesterol synthesis which is evident if one measures desmosterol or lathosterol in serum. If so the therapeutic approach has to be reducing the synthesis by dietary alteration (reducing or changing type of fat or for those unwilling to do that or do not have a response at moderate to high lifetime risk for CAD, a cholesterol synthesis inhibitor (statin)
Thank you so much for your comments, Dr. Dayspring. Thanks very much as well for your LecturePad series, where I found the case study that prompted me to make modifications to my diet that got my numbers moving in the right direction. Such a fantastic resource.
Dr DAYSPRING,
is addressed to me??? maybe Id be a good test subject for you to look at?? I know you looked at jimmy moore. I believe your in VA , I am in MD. You can see the effects of cholesterol on me I am APO 3/3 Many Genes in the HLA DQ area for gluten… As I ate more fat and cholesterol I got better… and life long problems are gone… snoring , stomach, sinus . allergies… You could test the effects of cholesterol my high particles with desmosterol or lathosterol showing the good effects of the fat on my disease but bad on my cardio part ???? be interesting for you i would think
My cholesterol went really really high recently too – total 10 at its peak and 7.5 LDL (285)
So I got advanced testing. My small dense LDL were a little bit high, but it was mostly the large type. Worryingly though – my oxidised LDL was through the roof. Most people dont get that done with high cholesterol. My husbands on the other hand was high LDL with very low oxLDL.
I am post menopausal and have (well controlled, symptomless) hashimotos. Another post menopausal low carb client cam back with very similar results to mine – high oxidised LDL.
I’ve made big changes to my diet – leaner protein, dropped the saturated fats, and increased carbs to 100 – 150 grams a day from root veg and berries. I must say I’m feeling and sleeping better and have not put on any weight. Like you heart disease is rife in my family.
I’ve not yet got updated blood tests – but will soon
Thanks so much for sharing your story and experience, Julianne. Here in the US, oxidized LDL testing requires an order from a physician, unlike the NMR, which anyone can order on his or her own. Most doctors don’t order oxidized LDL for their patients, but of course I’d really like to know the status of my own. It’s good to know that the majority of your husband’s LDL wasn’t oxidized, but I’m sorry to hear about yours. I’m so glad to hear that making those dietary changes resulted in improved sleeping and stable weight. Good luck on your next round of lab tests!
Julianne, The oxLDL test is part of the CHL testing and also HDL lab does most of the panel. We are getting a lot of unexplained high oxLDL results and they just lowered the threshold on that test. I think the full panel is helpful.
I have spoken with Dr, Mark Penn from CHL and he places more emphasis on the hs-CRP, LP-PLA2 and the cardiac myleopeoxidase tests: https://www.youtube.com/watch?v=SmGxfz8WUn0
I am not connected with the lab but like the focus on the inflammatory component of CV disease. Understand that most of these tests, like any new tests, are still considered investigational.
Just a follow up, dropping out animal fats, butter and coconut oil, increasing starchy root veg carbs, taking a couple of supplements, – hesperidin, my LDL went down to 4. I also had my hsCRP done and it was 1 – so fine.
I’m continuing on the lower fat/ lower SFA diet with plenty of starchy carbs and some berries.
@Franziska
You might consider this test which can be ordered without a doctors prescription
http://www.plactest.com/patients/about.html
http://www.bhlinc.com/clinicians/clinical-references/reference-manual/chapter12
“Lp-PLA2 can be viewed as a biomarker that measures the pathologic link between the toxic effects of oxLDL, the resultant unstable vulnerable plaque formation, and future cardiovascular events.”
http://www.clinchem.org/content/52/9/1645.full
Thanks very much, Dr. Gerber and Charles.
@Jeffry Gerber, MD @Franziska Spritzler
“We are getting a lot of unexplained high oxLDL results.”
Perhaps this means that Dr. Dayspring is correct in that TOTAL LDL-P is what’s important – maybe it’s the number of particles that count and not just the size – the more particles there are the more chance one has that they will penetrate the endothelium and become oxidized – maybe people on a LCHF diet that have high LDL-P should be concerned
Your thoughts
Your thoughts
Charles, I’m not really qualified to opine on that but will say that it sounds like a reasonable postulation. I’d love to hear the doctors weigh in on this.
Wonderful article and blog
Thank you very much, Cindy!
Franziska, thanks for the excellent blog post and for supporting an incisive commentary discussion.
This topic of high LDL on ketogenic diets arises often on the ApoE4 Forum (http://apoe4.info/forums/index.php). From anecdotal evidence, I perceive a lot of overlap between these two groups:
1. People whose LDL rises dramatically on ketogenic diets.
2. People with one or two ApoE4 alleles.
With some variation among ethnic groups, one ApoE4 allele doubles Alzheimer’s risk, and two alleles increase the risk ten-fold and drive earlier onset. ApoE4 carriers also face increased cardiovascular risk.
The good news is that some traditional cultures with many ApoE4 carriers experience low levels of AD and CVD. The alleles survive in the gene pool because they confer certain advantages, and one of our missions on apoe4.info is to learn how to live in ways that maximize those advantages and minimize the concomitant risks.
Most of us on the ApoE4 Forum learned our status from 23andMe. Even though the FDA has restricted 23andMe’s ability to share health-related information with new customers, raw data can still be downloaded and fed to Promethease. It’s an amazing bargain at $99 for the genotyping plus $5 for the Promethease interpretation.
Mark, thank you so much for the nice feedback and all of the insightful and helpful information. I will definitely check out the ApoE4 Forum. I did have the 23andMe genotyping done, but I didn’t see anything regarding ApoE4, only that I do not have FH. Thank you very much again.
The two SNPs of interest are rs429358 and rs7412. If you log in and choose the “BROWSE RAW DATA” option from the “Franziska Spritzler” dropdown, you can find your values. The nexus of those two SNPs define your two ApoE alleles:
E2: rs429358 = T and rs7412 = T
E3: rs429358 = T and rs7412 = C
E4: rs429358 = C and rs7412 = C
For example, I’m CT at rs429358 and CC at rs7412, so one of my alleles is CC (E4), and the other is TC (E3). In common parlance, I’m an ApoE3/4 or, in context, just a 3/4. 24.0% of people with my ethnicity (European) have that combination, and 2.9% are 4/4.
Mark, thanks again for the information. I downloaded my info to Promethease, and it appears I do not have the ApoE4 gene, although I do have several SNPs indicating my risk for CAD is 1.5 times higher than average. According to the report, I am Apo E3/E3.
I just wanted to add, I am ApoE e3/3, so that is not a contributing factor for me. My cholesterol has been completely fine up until post menopause. I also have a client whose results are similar to mine – high HDL, low TG, high LDL and ox LDL. We got our tests through Imupro. Another aspect could be fish oil supplementation. Although my husband supplements he used OmegaRx which is batch tested for oxidation. I was using fermented codliver oil. My client – I have yet to check.
So far I see some commonalities – post menopause, low carbohydrate diet (50g/d approx), fish oil supplementation.
Mark, thank you again for that guidance with interpreting the Apo E information. Although in my 23andMe data is states I do not have the Apo E4 gene and on Promethease it states I am E3/E3 in the Alzheimer section, when I enter the SNPs as raw data, I get 2/4. So I’m a little confused at this point but am grateful that there’s so much information that will allow me to sort it all out. Thank you so much again!
Hi Julianne,
Thanks for the additional information about yourself and your client. I hope your next set of lipids shows much improvement for both of you!
Franziska, to be 2/4 you would have
rs429358 = CT
rs7412 = CT
To be 3/3 you would have
rs429358 = TT
rs7412 = CC
I don’t understand how you could get one result from 23andMe and Promethease and a different one by checking manually. Incidentally, 2.2% of people with European ethnicity are 2/4, and 57.4% are 3/3.
Thanks, Mark. It didn’t make sense to me either, and I was going to look further into it today but now realize that I incorrectly transposed the letters. I am indeed a 3/3.
Here I go down another rabbit hole. I just ordered the 23andMe test. Fingers are crossed!
I am ApoE3/3 and my LDL went up to 7.5 with low carb, high fat diet
I am also ApoE e3/3,
http://www.atherosclerosis-journal.com/article/S0021-9150%2814%2901164-2/abstract
Cardiovascular risk in patients achieving low-density lipoprotein cholesterol and particle targets
Results
Among 15,569 patients with LDL-P measurements, the risk of a CHD event increased by 4% for each 100 nmol/L increase in LDL-P level (HR 1.04; 95% CI 1.02–1.05, p < .0001). The comparative analysis included 2,094 matched patients with ≥12 months of follow-up, 1,242 with ≥24 months and 705 with ≥36 months. At all time periods, patients undergoing LDL-P measurement were more likely to receive intensive lipid-lowering therapy and had a lower risk of CHD/stroke than those in the LDL-C cohort (HR: 0.76; 95% CI: 0.61–0.96; at 12 months). Conclusions In this real-world sample of commercially insured patients, higher LDL-P levels were associated with increased CHD risk. Moreover, high-risk patients who achieved LDL-P <1000 nmol/L received more aggressive lipid-lowering therapy than patients achieving LDL-C <100 mg/dL, and these differences in lipids and therapeutic management were associated with a reduction in CHD/stroke events over 12, 24 and 36 months follow-up.
Thank you, Charles. I’m going to put the full text of the article on my rapidly growing reading list. But the abstract of this new study looks quite interesting.
Charles
I wonder what all these peoples small LDL-P scores were??? not just TOTAL LDL-P
Id also wonder what bacteria and yeast they had in there stools
and how many had constipation– and ate hardly no fiber
http://www.lecturepad.org/pdf/tomdayspring/human_lipid_transportation_system.pdf
Lipid and Lipoprotein Basics
Thomas Dayspring MD, FACP, FNLA, NCMP
It is crucial to have a clear understanding of how particle size contributes to atherogenesis (it does not). All LDL particles, large or small are atherogenic (will enter the arterial wall) if present in increased numbers (elevated LDL-P). If LDL-P is low (physiologic), there is little risk whether one has large or small LDL particles. Indeed, once LD-P is known, LDL size is no longer an independent risk factor for CHD.
If LDL-P is high, CHD risk is high no matter whether the high LDL-P is driven by toomany large LDLs, too many small LDLs or both. Keep in mind that the most lethal lipid/lipoprotein disorder is familial hypercholesterolemia. Such patients typically have very increased numbers of the larger (PatternA) particles. All of the older studies that suggested risk is related to small LDLs per se, were never adjusted for LDL-P.
Once that adjustment is made, the risk related to LDL size is no longer statistically significant.
Because the volume of a sphere or circular particle is a third power of the radius (V = 4/3π r3), there are considerable volume differences between particles that vary only slightly in diameter. Thus if a patient has an LDL-C of 100 mg/dL it will take 40 to 70% (depending on the exact diameter) more small LDL than large LDL to carry the 100 mg of cholesterol. Therefore, even though an LDL-C may be 100 mg/dL, the LDL-P will be
40-70% higher in patients with smaller rather than large LDL. Also if one has TG-rich and thus cholesterol-poor LDL particles, it will take increased numbers of particles to traffic a given level of cholesterol. And it is LDL-P that primarily determines risk. Since any apoB particle 80-100 mg/dl. Ideal is less than 80mg/dL or perhaps even 60mg/dL in very high risk patients. It is more accurate to measure LDL particle concentration (LD-P) using the NMR(nuclear magnetic resonance spectroscopy) technique (n<1000 nmol/L).
Key points
"If LDL-P is low (physiologic), there is little risk whether one has large or small LDL particles. Indeed, once LD-P is known, LDL size is no longer an independent risk factor for CHD."
"Since any apoB particle < 70 nm in diameter can penetrate the vascular endothelium, LDL size does not influence LDL particle entry into the subintimal space(the largest LDL is 23nm. Likewise the number of cholesterol molecules per particle has no influence on LDL particle entry. The only variables that affect vascular entry are LDL-P and endothelial integrity." http://www.dislipemias.com.ar/pdf/apoBandrisk.pdf
Apo B versus cholesterol in estimating cardiovascular risk and in guiding therapy: report of the thirty-person/ten country panel
In brief, this paradigm posits that the total number of atherogenic particles is a more important determinant of the risk of vascular disease than any of the conventional lipid measures. This is the case because the number of particles within any lipoprotein fraction determines the likelihood of any member of that class entering and lodging within an arterial wall. The conventional lipid indices equate the risk due to a specific lipoprotein fraction to the plasma lipid concentration of that fraction. Thus, triglycerides are the estimate of the risk due to VLDL, LDL cholesterol the estimate of the risk due to LDL, and non-HDL cholesterol the estimate of the combined risk of VLDL, IDL, LDL and Lp(a). But there is an error in this equation. The lipid composition of the principal atherogenic lipoproteins differs substantially amongst individuals. Therefore, lipid levels do not automatically equal lipoprotein particle levels.
Most studies divide LDL into only two subclasses: large and buoyant LDL particles that are relatively enriched in cholesterol (LB-LDL) and small and dense LDL that contain less cholesterol (SD-LDL). Whilst useful, this is an oversimplification and it is biologically and clinically more accurate to recognize at least three subclasses: very large LDL (LDL I), large LDL (LDL II) and small LDL (LDL III) (Fig. 1). Indeed, none of us have just one subclass, although one does tend to predominate at any time. A correspondence between the predominant LDL subclass and disease was noted first by Teng et al. Low-risk individuals were characterized by a lower than average number of LDL particles and the dominant LDL subclass was LDL II. Patients with familial hypercholesterolaemia (FH) were characterized by markedly increased numbers of LDL I and LDL II, whereas patients with hyperTg hyperapo B were characterized by markedly increased numbers of LDL II, particularly LDL III particles . Because the amount of LDL cholesterol per LDL particle varies substantially both between and within individuals, LDL cholesterol does not necessarily equal the most critical variable, the total number of LDL particles. This is the key point.
So – it would appear
Thanks, Charles. Great stuff on LecturePad.org. Highly recommended!
So one more question, If one has surgery and there cut open Like I was….do to a fistula,, 7 inches long and 5 inches deep and left open to heal..
Wouldnt ones cholestrol RISE.. as the role of cholesterol is to be sent to the area in need of repair and cell growth. Would ones LDL particle GO up??? or LDL score???
Hi Eddie, It’s my understanding that cholesterol often temporarily increases after surgery or injury as part of the healing process, yes.
Franzika Spritzler,
Would your guess be LDL-Particles or the actual LDL score.?? Love to see some of the docks chime in( as well on (phospholipids—from krill)You know My test results have been similar to yours as my LDL small P is low and total particles have been going up each 3 to 4 months of testing… for me thou im not so sure its going up from food… as I fought a fistula and hard a large surgery– where alot of tissue has had grow back… But I also noticed you ate avocado .(Monounsaturated fat ) HIGH
Im still testing , I have tested alot of things in the process of rebuilding my gut– yeast, bacteria, antibodies , etc cholesterol.. until I am fully healed pretty close I wont be able to say about the particles… If its the surgery I will know , but two things I did was add 1000mg of krill oil for my healing which has 525mg of phospholipids.. My cholesterol total number has peaked and doest really move now over 110-115 (LDL) same with HDL (58 to 65) but size change all the time as well LDL particles going up.. I also suspect the AVOCADO raising my LDL P totals.. as I ate limted diet for 1.5 years to heal my gut…. since the introduction of avocado and higher krill oil dose (more phospholipids) my particles have gone up.. im in the process of testing this now… as I have take krill for 2.5 years and added avacado in 9 months ago
Have you cut back on your avocado I am eating half of what I use to and half the nuts I use too…
Hi Eddie,
I don’t think MUFAs would raise LDL-P; if anything, they are believed to lower or have a neutral effect on cholesterol. I still eat the same amount of avocado, 1/2 to 1 per day. I’ve heard conflicting information on n-3’s in fatty fish, but increasing sardine intake seems to have improved all of my numbers. I actually increased my nut intake when I decreased saturated fats. So I’m getting more MUFAs and PUFAs than when I was doing the NK experiment.
I doubt most of the MDs are following this very long string of comments, but of course I’d welcome their thoughts on this as well.
I may be crazy but for me it seems the krill or fish has lowered my small ldl p…. I eat almonds and walnuts and seem to see more up tick witg the avacado….. fish seened to lower small ldl p not total ldl p….maybe crazy
Thank you so much for sharing your experience and what you do to improve your cholesterol levels Franziska. It is greatly appreciated and I will be sharing your post with everyone!
Thank you so much, Martina!
Just an interesting tidbit from a recent interview with Dr Steven Gundry:
http://body.io/body-io-fm-24-dr-steven-gundry/
19:00 to about 30:00 he talks about high cholesterol and A1 milk / milk products… found it interesting… am probably a genetically challenged individual … so i went out and found some A2 cows and milk… may just go with heavy whipping cream in my coffee (my personal physician just spit her coffee all over her screen) as that evidently doesn’t have much A1 casein in it.
He also mentions some cheeses as being not with A1 … I think its probably goat cheese. Mentions that butter should also be A2 not A1.
He also talked a little about genetically challenged folks and said that they just have to watch out for animal fats in general, and work on reducing A1 milk and products but that even then it was about reducing the small dense LDL. This is in conflict with other doctors who are all about the overall particle count. But I guess you can only control that which is controllable. No idea where that discussion takes place in the podcast, sorry just haven’t had the time to relisten.
Anyway, just thought I’d share…. if this was pointed out elsewhere in this thread I apologize. Cheers.
Thanks so much, Lance. Listening to it right now, as I was alerted by someone on Twitter as well 🙂 This hasn’t been brought up yet in this thread, so I very much appreciate you sharing this.
I d like to know why even test SMALL LDL-P it seems several of these docs like DAYSPRING are focused on the the TOTAL LDL PARTICLES
So why even record the small LDL-P ????????? I see many are fighting is it small LDL-P or is it total LDL particles
looking at Franziska numbers if DAYSPRING is right her total numbers are bad ??? IF the other DOCS are right on small LDL P then she is GOOD???
seems no one can tell you so all we have is basic answers be in the range of both …………………………………………………..
Thanks, Eddie. I think your last line says it all, and at least until we have evidence showing us otherwise, that’s what I’m trying to do.
Franziska
I would like to see what happens when you change your diet over the next couple months
you had HIGHER total LDL particles
and real LOW small LDL P
I was the same
lets see if your TOTAL LDL particles drop which you say they are
BUT watch your small LDL-P is it rising ????
another test try adding in lactobacillus reuteri ncimb 30242 (bacteria probiotic) they say eating Low Carb you loose alot of your lacto bacteria. many(lacto) will pull down your cholesterol.
Me Im playing and watching to see if this lowers my particles (LDL total particles ) or ( LDL cholesterol number)
Hi Eddie.
Responding to your second comment:
My small LDL-P went down as well as total LDL-P, so I think my dietary changes have me on the right track.
what did your total LDL P particles start at as well the small LDL p
what is it now
Eddie,
All of my small LDL-P results are included in the 3 sets of NMR results in my blog post.
Great article! Special thanks for always listing your sources!
Thank you so much, David!
I have very similar data total 283, HDL 76, LDL Iranian 166, TG 66, apo B/A1 0.68, LDL P 1577, LDL size 22.3, LDL pattern A, LDL large 69 %. My TG/HDL ratio has gone from 3.2 to 0.9 when switching to low carb. Unfortunately all current recommendations based on averages of a population that uses a SAD diet and these values most likely not relevant for very low carb people. It would be helpful if someone asked for us low carb people to volunteer our data and perhaps collect a 1000 data points to get our averages and compare those values to SAD members. For me personally, I will never go back to eating pizza or pasta etc. I have never felt so good in my whole life and I eat very few carbs while going from 26 % to 15% body fat. Thanks for your blog.
Hi Gary,
Thanks very much for sharing your lab values and low-carb experience. I agree that studies should be done on people following very-low-carb diets long term and assessing lab outcomes and rates of CVD as compared to people following an SAD. I’ll be low carb for life right along with you. And congratulations on that change in body composition!
Most long term population studies are difficult to do because of compliance. With us low carbers compliance is typically not a problem since once we see the positive effects of the diet on weight and blood chemistry not to mention the feeling of well being we won’t revert to a SAD diet. In my case compliance is even more assured since I had a myocardial infarction Feb 2012 with a SAD diet. They said I died twice during the operation to install the stent. My nickname on the third floor of intensive care was “miracle man”. Fortunately the stars were in alignment for me that sunny day. On low carb, my blood pressure went from 143/89 to 115/75 and my trigs from 290 to 66 as well as a doubling in HDL and I no longer suffer chest pains. So for me to go back to eating carbs would be life threatening.
Wow, what an amazing story! So happy to hear about all of the improvements you’ve seen as a result of following a low carb way of eating. I wish you a healthy and happy long life.
Got labs back in today and I feel like you. Except I don’t have the partical size numbers. I have been doing VLCKD for 6-8 weeks now.
I will post my labs BEFORE starting LCHF. Cholesterol – 163, Trig.- 78, LDL – 73, HDL – 74
Labs as of 7-23-14- Cholesterol- 291, Trig. – 86, LDL – 133, HDL- 141
Both labs were drawn not fasting. Of course, the doctor has called and wants me to come back in to discuss this. I am not going on cholesterol medicine. He admitted to eating a high junk food diet, so this won’t be in my favor. My regular doctor moved, so this is my first time seeing this doctor.
Hi Judy,
I know it must have been a shock to see your levels increase so much in such a short period of time. However, although you don’t have your particle sizes and numbers — and understand that I’m speaking as someone who’s recently learned quite a bit about lipoprotein profiles but still has a long way to go — I don’t think you have much to worry about at this point based on the fact that your LDL-C doesn’t suggest a high apo-B/LDL-P, and your HDL-C increased even more than your LDL-C did.
I’m assuming you’ve lost weight on the LCHF diet, which can further confound things — make sure to read Dr. Dayspring’s case study if you haven’t already, as I think that woman’s experience was much more like yours than my own.You can choose continue on the diet as you’re doing and have your labs checked again when you’re no longer in the weight loss process, or you can try making some of the changes the woman in the case study and I did if you’re not comfortable with the numbers and want to bring them closer to where they were before. Best of luck to you!
Thank you so much for taking the time to respond to my post. I only lost about 3 pounds and don’t really need to lose weight. That is what also surprised me about my numbers. I would have expected it if I had lost a lot of weight. Before I started (5’2) I weighed 115 # and now weigh #112, so no major weight loss.
I am hoping the doctor will agree to wait for at least 6 months but preferably 1 year to check my levels again and then I will feel like my body had time to adjust to this new way of eating. I had already cut out the grains and almost all sugar, but did increase my fat in take in the last 6-8 weeks. I eat so much less and stay full/satisfied for usually 6-7 hours-that’s wonderful.
I mainly took this approach to be healthier and hopefully prevent diabetes which runs in my family. Best of luck to you also. Even those I was prepared to see a slight rise in my cholesterol, I never expected such a dramatic increase and I admit that bothers me.
I will read the case study, thanks for pointing that out.
My pleasure! I’m glad you’re enjoying low-carbing but also recognize that lipids can change and should be monitored every 6-12 months. I’m hoping to get my LDL level back to where you’re currently at 😉
I walked in and the asked me why I was there? I explained that he wanted me to come back because of my lab results. Soon as he got my labs pulled up, he said we need to get you on cholesterol medicine. Whoa!!!!! Didn’t even talk with me about my diet or ask any questions, suggestions to try and lower it with diet. Mind you, he doesn’t know me, unlike my former doctor of 24 years who moved.
Didn’t make any reference that my ratios were great though despite my other lab values. Wants me to stop this “unhealthy diet” and come back in 8 weeks for repeat lab work. He asked me what type of diet I was on and I told him, “low carb-high fat”. He said, I kid you not, “I’ve never heard of it before”. I was told to go back to doing what I was doing before this diet.
I am in utter disbelief.
After he asked me what I ate. I was told to stop all coconut oil and no nuts after the age of 50 (I will be 46 next month) because of diverticulosis. This diet will lead to diabetes versus doing what I was doing before.
So sorry to hear that your doctor isn’t supportive or even aware of the benefits of LCHF. Any chance you can find another doctor in your area who’s more progressive and knowledgeable?
While your labs may normalize on their own after being on the diet longer — this happens to some people — there’s also a chance that cholesterol will continue going up rather than down. I’d stay low carb but make a few of the changes the case study woman and I did, i.e., cutting back on dairy fats including butter, increasing fatty fish intake, increasing protein and/or carbs a bit depending where you’re currently at, and making sure you’re getting plenty of fiber. Some reading this may disagree and say that your lipid profile is great the way it is, but as I said before, I understand your concern with such a dramatic increase in a short period of time, and at the very least they require monitoring regardless of the diet you choose to follow
Good luck, Judy!
Lotsa your issues are discussed here:
http://www.lecturepad.org/index.php/2014-04-09-18-46-55/lipidaholicsanaonymous/1140-lipidaholics-anonymous-case-291-can-losing-weight-worsen-lipids
Sorry if already posted, but it is a view from a respected doc who spends considerable time thinking about lipids and is addressing people in your current situation. Lots of info for a layperson here, some of which can be skipped.
Hi Lance,
Thanks very much for sharing. That article by Dr. Dayspring is actually included in my article under “What Do the Experts Say About Very High LDL-C and LDL-P?”
Dr. Dayspring and I had never talked prior to my publishing this post, but we have several times since then. He’s going to be publishing my post on Lecturepad along with his own commentary. I hope you’ll read that, because I know it’ll be extremely informative. I made quite a few errors in nomenclature and interpretation, and I’m very happy to have constructive criticism in this area, as I’m very new to this field and still have a lot to learn.
Franziska, thank you for the information, and sharing your experience.
My LDL went higher after I started to use more saturated fats – butter , heavy cream,coconut oil, full fat cheese. I will reduce the amount of those , and hope to get better results. thanks again !
Thanks very much for your commons, Kapka! The LDL-C itself isn’t the biggest concern; it’s the LDL particle size (LDL-P). But if you’re not happy with the LDL-C number, reducing saturated fat a bit might help.Best of luck to you!
Thanks for the post where we come to know more details on lipid test with nice pictures and sharable information……
Thank you very much, Annie!
i ran across your website after getting my most recent lab results.
baseline (June 2013):
cholesterol (total) – 181
LDL-C – 87
HDL – 45
September 2013 (low carb, but not keto diet):
cholesterol (total) – 159
LDL – 103
HDL – 33
June 2014 (keto diet):
cholesterol (total) – 222
LDL – 51
HDL – 40
December 2014:
cholesterol (total): 255
LDL: 177
HDL – 49
while my HDL has been steadily increasing (except for the dip in 2013), the upward cholesterol and LDL trend have me a tad worried. i did have cleveland heart lab run NMR+lipid profile in 2013 so here’s that baseline:
LDL-P: 1790
HDL-P: 37.8
i’m not quite sure what to make of all this. i do love being low carb but i’m worried my doctor may start pushing statins if this trend continues. (so far, she has been quite supportive of me not taking statins).
Hi Mihir,
Although your results aren’t as dramatic as mine, you’ve had the same response. I don’t know what your current LDL-P is, and that’s tied to increased CVD risk much more than cholesterol. I’d have your NMR redone. If you’re concerned, try the same measures I used to bring my levels down somewhat: more fiber, less saturated fat, enough protein, fatty fish.
Best of luck to you!
Franziska
thanks Franziska. (by the way, the LDL in june 2014 was supposed to be 151, not 51).
i’d planned to talk to my doc and have her order the NMR again. i just need to see if my new insurnace will cover it. i’ll post back if i am able to get it done.
Just thought I’d post back. current LDL-P is 1638. you mentioned you started taking chia seeds daily. my doctor said something about them as well. but, i forgot to ask how much to take. how many did you take?
Hi Mihir,
I’m glad to hear that your LDL-P went down about 150 points. I mix 1-2 Tbsp of chia seeds with 1/2 cup of water and let it sit in the refrigerator overnight so the seeds become thickened and gelatinous. Taking them dry can cause problems with constipation, so make sure to let them soak for at least 4 hours.
Hi Franziska ,
Do you know what Apo B level would correlate as a surrogate for an ldl-p level you would be happy with for a female of your age. Ldl P levels not available in Australia . Given that they measure the same thing I hoped a conversion formula might be available but have not found one. Recommended levels of apoB also vary most are looked at in pts with known CHD. And tend to be quite low.So is there anideal level to be at /under in low risk pt?
( i am 48 yo female ,normal wt, insulin sensitive following low carb for 3 yrs, NO FHX OF CHD. I tried NK and found same , but less dramatic spike in TC/LDL C , all pattern A. As a medical practioner this still felt concerning and I also followed Dr Daysprings approach less sat fat , inc fibre with return to prev numbers.)
Hi Sam,
Thanks for your comments. It seems we have a lot of similarities in terms of age and lab response to a VLCKD. As far as the Apo B value I’d be comfortable with, I’d say anywhere <130, but again, it's not known whether a higher number increases risk for those on VLC diets who are normal weight and insulin sensitive with good BG control. I'm glad your numbers improved by employing the same dietary interventions that worked for me. I wish you the best of luck in maintaining good health and helping others do the same.
This was an awesome, awesome article. Thank you. I have cholesterol issues as well, and that is why I’m following a sensible low carb (weight maintenance will be moderate carb), way of eating with an eye on fats. So refreshing to read this. My days of pork rind nachos are now long gone.
Thanks so much for your comments, Sheryl! Each person needs to find what works best for him or her, and it sounds as though you’ve got it figured out. Best of luck to you!
hi there,
thanks for documenting this. I thought I was reading MY story there 😉
I’m wondering if you’ve continued to limit satfats, while upping mufa/pufa?? And if so, have you checked ApoB/LDL-P since you wrote this blog??
Thanks again for the education.
Kelly T
Hi Kelly,
Thanks for your comments. Glad you can relate.
Yes, I try to limit saturated fatty acids to less than 30 grams per day, and some days I’m well below this. MUFAs comprise the largest component of my fat intake, and I get a lot of omega-3 PUFAs in sardines and other fatty fish.
No, I haven’t had my LDL-P or Apo-B checked since writing this blog post. My doctor ordered a lipid profile to be drawn this month, and based on those results I’ll decide whether I need another NMR at this time.
Awesome. Please keep us updated 😉
as a side.. I feel like I’m talking to a unicorn.. You know low-carb dietitians don’t really exist, right????!!!! haha!
have a good one.
Funny you should say that — the first line of the book I just published reads:
“A low-carb dietitian? I didn’t think there was such a thing!” 🙂
Curious as to why you’re not getting NMR, or can LDL-P be obtained without? Thought is that with possibility of LDL-P being in discordance with LDL-C, one would be more concerned with the former. A drop in C means nothing.
I too have had LDL-P go up considerably with going deeper into ketosis. I was close to 2800 on last test. I decided to reduce mostly dairy fats, heavy cream and cheeses, and increase fish, olive oil, and avocados. After seeing your article it looks like I might cut back a little on coconut oil too. I am a type 2 diabetic who had quit metformin but have recently started taking it again after reading of its benefits in lowering LDL-P.
You’ll need the NMR if LDL-P is a target you think is worth watching and manipulating downward, right?
FYI.
My story and NMR is virtually identical to yours. In the context of VLCMPHF-Keto Diet… I’m starting to think this isn’t all that rare..
I resisted my Doc’s immediate reflex to throw a statin at the LDL-C number.. Consuming Dayspring’s information (and others) I know that LDL-C is just one piece of the puzzle that you’ve got to put in context before you can make an informed descision about whether or not the side-effects of statin therapy are worth accepting..
I paid for a Calc Heart Scan – score of zero
I paid for a CIMT – age appropriate thickness, no plaque detected
hsCRP very low, homocystein very low..
All good new and good to have as baselines moving forward as I watch this…
There are a few more tests that I’ll pay for on my own over the coming year as I can afford them.. but with ALL other markers moving in the right direction, thanks to this lifestyle, I’m not losing any sleep over this..
Context matters.
Hi Kelly,
Thanks for your most recent comments today. You’ve probably read my most recent blog post with my NMR results from earlier this month. I’m very happy with my current numbers and glad to hear that your CAC and CIMT came out well.
Best, Franziska
Doh! I totally missed that. Thanks for mentioning it. Going to read it now 😉 I’m hoping the tweaks you made in your diet made a difference in LDL-P…
Hi Franziska,
Great article and I hope your next lipid tests come out to your liking.
I went low carb (<50 g/day) about 5 weeks ago and had my yearly blood tests about 7-days ago on 3/14. I was anxious for the results since I was hoping to see my lipid profile significantly improved on the low carb, but to my surprise, I got a mixed bag of results which I am not sure what to make of it.
To clarify the larger picture a little bit, I am a 47 years old male 183-cm tall and weigh around 85 kg with a BMI of around 24 (border line overweight). I decided to go on a ketogenic diet to lose few pounds and improve my lipid profile which was hovering at borderline over the past few years, especially my HDL which has always been low. When I took the blood tests I had lost around 2 kg over two weeks and had been on a slight calorie deficit over that same period. I was feeling great and getting plenty of sleep.
Below are results of the tests from a week ago. They also indicate the results of the same tests done last year, since I always have them done at the same lab.
Cholesterol mg/dl 218 181 (20/03/2014) Desirable: 120-200
Borderline: 200-240
High risk: >240
Triglycerides mg/dL 406 H 236 (20/03/2014) ( 30 – 200 )
HDL-Cholesterol mg/dL 27.2 26.4 (20/03/2014) Desirable: >45
Borderline: 36-45
High risk:<35
LDL-Cholesterol mg/dl too low 107.4 (20/03/2014) Desirable: 60-130
Borderline: 130-160
High risk: >160
Chol/HDL Ratio 8.0 6.9 (20/03/2014) <4.97
Glycosylated Hb( HbA1C) 5.28 % 5.60 (11/02/2013) Normal:4-6
Controlled diabetes
mellitus:6-7
Uncontrolled diabetes
mellitus:>7
Alkaline Phosphatases 41 IU/L 52 (20/03/2014) ( 35 – 120 )
What concerns me is that my LDL, which were previously normal, were too low to measure and my triglyceride which were on the high side went through the roof. The total cholesterol went up a bit but so did my HDL but now the ratio of Total Cholesterol/HDL is very high at 8.
I have been researching this online for a week but haven’t found a convincing explanation. I am still on the keto diet and plan to get another blood test in 2 months or so or around the time I reach my target weight of 80 kg and when I am not in weight loss mode.
Meanwhile I will keep researching this, but would highly appreciate any input you may have or articles that may shed some light on this.
Hi George,
Thanks so much for the nice feedback and for sharing your story and lab reports.
I think there must be an error regarding the LDL cholesterol value. If your total cholesterol is 210 and the HDL is only 27, the LDL must be at least 100 and is likely higher. Total cholesterol = HDL + LDL + VLDL. Your VLDL wasn’t measured, but it’s generally not very high — the lower the better, for that marker.
Also, had you fasted for 8-12 hours before having your labs drawn? Triglycerides will definitely go up after eating a high-fat meal.
Congratulations on losing 2 kg and improving your A1c. Sometimes people experience increased lipids while they’re losing weight, although this is typically seen with significant weight loss:
http://ajcn.nutrition.org/content/53/6/1404.long.
At any rate, the high TG and low HDL are concerning, and I think you should have the test repeated in 2-3 months. As I said above, the
LDL cholesterol being classified as “too low to measure” doesn’t jibe with your total and HDL cholesterol.
Thanks again for sharing your story. I wish you the very best.
hi I’d like to know what test should I get for cholesterol and how will I know if the test is ok?
Hi Rio,
I would start with a standard lipid panel: Total cholesterol, LDL cholesterol, HDL cholesterol, and triglycerides. Any numbers outside of the normal range will be flagged, and your doctor can help you interpret whether further testing is warranted.
Really glad to have found this discussion as I was surely unpleasantly surprised at my labs yesterday after LC keto diet! I’ll throw my data points into the mix because I can tell you how was eating before three of my last test results. Let me preface by saying I am a 52-year old female low-carber (have been for 15 years), generally keeping my carbs around 50 to maintain a normal weight. APo-E 3/4, blood type A.
1. April 2013: Went on a 3 week anti-inflammatory diet where you give up caffeine, dairy, gluten, etc. and focus on vegetables, rice, beans and alkaline proteins. The middle week was vegan, so mainly beans. Aware of carbs, I limited rice. When I tested shortly thereafter, my LDL-P was 1752, up from 1580. However, my cardiac inflammation/oxidation scores were improved and have never been as good since (note to
self, there was something I was doing right!)
March 2014: Diet was LC and focused on getting protein (from animal sources) and 2 cups of cruciferous vegetables daily, main fats EVOO and a little butter. LDL-P dropped to 1372 (lowest so far). Inflammation scores worsened again, however. Hmm . . .
March 2015: By now, I’m up 10 lbs. Blaming travel splurges and approaching menopause (although I just learned I am severely calcium deficient which causes the body to hold on to fat, so that may have contributed to weight gain). Anyway, low carb for 3 months and ketogenic diet for 4-6 weeks where I enjoyed (probably too much) lots of grassfed butter. I also was juicing green vegetables (including cruciferous) most days. LDL-P jumped 50% to 2089! Inflammation/oxidation highest ever . . .
Based on the advice I’ve read here and analysis of my own results, I’m going to switch back to mostly MUFA fats, add back the 2 cups daily cruciferous vegetables and enjoy high fiber foods, including some beans and the occasional sweet potato. Basically, back to a more Mediterranean diet, but really bumping up the vegetables and focusing on lean protein. Will retest in 4 months and will try to remember to report results here.
Thanks to everyone for your contributions to this discussion!
Ellen, thanks for sharing your results. I hope you’ll drop by http://apoe4.info/forums/ sometime as we are a community of ApoE4 carriers like yourself who are interested in optimizing health to prevent / delay / reduce our tendencies toward Alzheimer’s and cardiovascular disease. Member strategies vary along the entire spectrum from low-fat veganism to very low carb / ketogenic. From your post above, I think you would fit in well there.
Thanks so much for your comments and for sharing your story, Ellen! I agree with your plans and second Marc’s suggestion to check out the ApoE4 forums — a wonderful, supportive community. Best of luck to you!
– Franziska
Dear Ms. Spritzler,
I have had the following tests done-I am low carb, moderate protein, medium to high fat and non-diabetic, no medications, calcium score 4.5 years ago was zero, 47 years old male.
APO(B) 132 mg.dl
Fasting Insulin 2.1 uu/ml
hs-CRP 2.4 mg/l
Fasting Glucose 85 mg/dl
All Lipid profile is mg/dl below
TC 248
HDL 120
TC/HDL ratio 2.1
LDL 123
VLDL 5
Trigs 67
Concerned obviously on APO(B) and hs-CRP, any thoughts please?
Thanks.
Hi James,
I can’t give medical advice, but in all honesty, your lipid profile looks very good to me.Your Apo B and CRP-HS are only a little bit elevated. I don’t like people placing too much faith in CRP-HS anyway, as that number can vary greatly from day to day depending on illness, injury, stress, sleep, etc. There are other markers of inflammation, such as homocysteine and Lp-PLA2, that you can have measured as well. In my most recent blog post, I share some of the other Dr. Dayspring recommends: https://www.lowcarbdietitian.com/blog/update-recent-nmr-results-cardiovascular-disease-risk-and-what-i-eat.
Best, Franziska
Great post. I am trying to find out where /how to get the absorption versus production markers (campesterol,sitosterol, lathosterl)ordered. I called my local hospital and they were clueless. I normally order my labs online at walk in lab . com but not finding where to order these. I’m also wondering how much the test costs as a cash payer. Glad to see there are others whose ldl-p and LDL-C went from bad to worse on lchf diet. I was so bummed. Feel and look better than have in 20 yrs but with LDL-C 300 and ldl-p of 2500 I Had to leave ketosis behind. Trying to just go paleo and begin taking plant sterols (Cholestoff )to see if that helps.
Thanks so much for the nice feedback on my post and for sharing your story, Eric. I believe you’ll need to see an MD who uses Health Diagnosic Laboratory (HDL, Inc) testing in order to get the absorption testing. They can’t be ordered by the patient. It’s my understanding that insurance might cover most of the charges, but don’t quote me on that. Low-carb Paleo or even moderate carb Paleo is still a healthy way of eating. In fact, for most people I’d argue that it’s significantly better than strict leto. I wish you the best of luck in improving your LDL-P and LDL-C.
– Franziska
Found your article, while doing research after a recent cholesterol test. Rewinding a bit, I was suffering from chest pains, and due to a recent loss in the family, anxiety (or curiosity) got the better of me, and I went for a blood test. Turns out that my LDLs are high (but no advanced blood work was done). It seems my HDLs are 58, LDLs 147, TG 60, total 217. I’m 31 years old BTW. My recent loss wasn’t much older then I am (42). And was way more fit, went from being unfit, to super hero fit with two years on keto, then to a vegan (still very fit) for a year before the incident.
I was half hoping the my LDLs would be lower, as I’ve been on the ketogenic diet religiously for two years, and my health has skyrocketed (more on that below). My carb intake is minimal at best (I only eat spinach, cauliflower, broccoli, lemon, avocado, and the rest of the food I eat is high fat animal products, no dairy, minimal butter, and lots of coconut oil). It’s a very boring way of eating, but I like it. Since my stress is almost non-existant and mental clarity has skyrocket, plus I never get sick anymore, no allergies, no trouble sleeping, or waking up (which is a big thing, I use to not want to get out of bed). Little to no anxiety (use to be very bad, and I refuse to take any pills a doctor tries to give me). And although I wasn’t planning on it, weightloss. Which I really regard as loosing excess fat that I don’t feel was necessary. I am 6ft, was 185lbs and in two years got down to 160lbs two jean sizes. And I think the only real reason I’m that slim now is I’ve not worked out seriously in the last two years due to work (though my work has me doing a lot of cardio oddly enough). Some of it muscle loss, but most of it was weight taken off my face, though I carried my weight really well, athletic looking even at 185lbs.
Rewinding a bit again, two years ago, I said enough is enough. I grew up in Canada, and the Canadian health care system pumped me full of antibiotics as long as I could remember, every sniffle I was given amoxicillin or something similar. I had stomach problems, always getting throat infections, I was told I was allergic to dust mites, dogs, everything under the sun.. I felt tired all the time and missed class a lot. Moving across the world also didn’t help. I was exposed to fungal spores and etc that I wasn’t use to, and my allergies flared up the whole year round. So one night at new years I met an ENT who seen how unwell I was, and recommended I see him. After I did, I was diagnosed with chronic tiredness (forget the medical term), stemming from mono. He gave me nasil spray for my allergies, and pills for the mono. Later I found out that my body was very adverse to gluten. And that helped with a lot of my issue, but one thing that really helped was that I started taking probiotics. At first it was sugary probiotic drinks, which turned into probiotic pills, then I started brewing my own Kefir, which I feel was godsent. Later, I went over to keto, and still maintained myself with either kefir or probiotic pills. I got a lot better, and keto was the surge I needed to feel even better. Fast forward a year, the loss happens. Fast forward another year, and I decide to get a blood test due to chest pains and numbness in my arm. My doctor says based on the tests I’m fine, but I have to cut my red meat. The weird thing is, I feel so good when I eat red meat, and other aniimal fats.. I feel less good with vegetable fats (avocado and coconut oil). I test my ketone levels every day, and I range from moderate to high.
Anyway, now I’m worried about the LDLs so I have to cut out animal fats, which I think sucks. I also have been reading the comments, and I’m worried that I’m killing off my good bacteria. So I’m wondering if there are any fats I’m not considering right now, which would help my good bacteria. Also what would be a good way to reboot all my bacteria, and how would I maintain it, while being on large keto, while still not eating bad LDL fats?
Any comments or suggestions would be great. And sorry for the long post, I’m just trying to give everyone as full of a picture as I can.
Thanks for sharing your story, Michael. I’m very sorry for your loss.
I cannot provide any medical advice, only nutritional advice.
I don’t think you have to cut out all animal fats, but cutting back on saturated fat might lower your LDL cholesterol, as it definitely did in my case (read my latest blog post; the one you’re commenting on is almost a year old). Then again, in some people, saturated fat intake doesn’t affect cholesterol much. Healthy fat is found in both plant and animal foods, including nuts,olives, and fatty fish, among many others.
Gut health isn’t my area of expertise, but I believe soluble fiber is important for the health of your gut bacteria, so eating plenty of vegetables, berries, nuts, and seeds would be my recommendation, as their fiber will be fermented to short-chain fatty acids that nourish the gut.
I wish you the best of health.
– Franziska
1 full year following a no sugar, no wheat, virtually no grains (occasional white rice, oat meal), no alcohol, little dairy, high fat (80%) low carb (30-50g daily) moderate protein (@80g daily) Low cardio 2.5 mile run once a week, 4 x 20 second sprints once a week, lifting heavy twice a week, standing desk 3-5 days a week, walk a lot.
52 yrs male around 13% BF 169lbs 5′ 9″ tall. No medications No supplementations.
I was 20 hours fasted for this blood work. I very occasionally intermittent fast.
Totals:
Cholesterol 303 mg/dl
LDL 228 mg/dl
HDL 61 mg/dl
Tris 70 mg/dl
Fasting Glucose 81mg/dl
Ratios:
Total Cholesterol / HDL -> 303/61 = 4.96 (Ideal < 5) Trig/HDL -> 70/61 = 1.14 (Ideal < 1.0) LDL / HDL -> 228/61 = 3.73 (Ideal < 5) Fasting Glucose 81mg/dl-> 4.5mmol/L (Ideal < 5) LDL Subfraction: LDL1 82 (<58) LDL2 42 (<31) LDL3 8 (< 7) LDL4 2 (< 1) LDL5 0 LDL6 0 LDL7 0 LDL Particle Size 26.9 (Greater or = 26.8 Presence of mainly LARGE LDL indicative of Type A profile) I didnt see a particle count test result so I assume that falls under some other test? I had to specifically request the LDL Subfraction test by my Doctor. Funny but expected, my Doctor called me after reading the results and by results I mean just the TC and LDL values and wanted me to immediately begin medication. Time to find a more educated doctor.
Hi Franziska,
So glad I found this blog. I’ve been reading reddit, bjj caveman’s, and some other Keto blogs as well in search for the same problem that you had. We don’t have NMR profile here in our country so the most that I can do is the traditional lipid testing:
After more than 3 months of Keto, these are the results:
May 2015 Dec 2015
TC 208 335
LDL-C (Direct) 138 242
HDL-C 68 92
TG 72 77
FBS 94 92
TG/HDL 1.06 0.84
Uric Acid 8.3 10.6
Obviously, my TC & LDL-C went up more than 100 points.
Another problem is the elevated uric acid. Although literatures say that the elevation in uric acid should be short lived after starting Keto, theoretically, it should have dropped down considering that I am already more than 14 weeks into the diet.
In the meantime, I will follow the dietary path that you have taken and I’ll check again after 3 to 4 months.
Your feedback will be much appreciated if you have anything to add.
I also wonder what are your current numbers? =)
Thank you and God bless!
-Alex
Hi Alex,
Thanks for your comments and for sharing your story. I can’t really speak to the elevation in uric acid other than to say you’ll need to continue monitoring it. 14 weeks is actually not a very long time, so you may indeed see improvement on your next round of labs.
You can read about my most recent labs in this post: https://www.lowcarbdietitian.com/blog/update-recent-nmr-results-cardiovascular-disease-risk-and-what-i-eat
I wish you the best of luck with everything.
Hi Franziska,
Thank you very much for your response.
Yes I will just do the dietary modifications and see how it goes.
Your articles by the way are all fantastic!
Keep spreading the good information – many people hungry for knowledge like me need it.
Take care and all the best!
Ta,
Alex
Thanks so much, Alex! Appreciate your kind words.
Hi Franziska. I put a long post on the fb group Optimizingnutrition which may clarify some parts of the problem. I’ll post it below, sorry its quite long….:)
This post discusses a possible reason why some people get very high LDL cholesterol on LCHF diets.
KINETICS OF LDL SUBFRACTIONS (1)
LDL presence in plasma is not homogeneous but can be divided into relatively heterogeneous subfractions (called here Pool A and Pool B, each further divided into subfractions) that have separate and distinct etiologies; the LDL content of plasma at any point in time can be considered the sum of these two pools and as such exhibits a complex behaviour due to their interaction.
Although the behaviour of each pool considered seperately is relatively simple the dynamic resulting from their interaction is complex and can include extrememly high LDL values within normal non atherogenic conditions and low LDL under atherogenic conditions.These subfractions exhibit metabolic channeling and separate structure, function and metabolism. This is important because they have different atherogenic potential. The principal division is into two separate LDL pools that embody their separate creation and evolutionary dynamics primarily under the influence of triglygerides. Triglycerides are the key component catalyzing lipoprotein metabolic disturbances involving LDL and HDL and channeling these lipids into atherogenic pathways. These disturbance and channelling mechanisms produce the defining characteristics of atherogenic dyslipidemia, high triglycerides, high small and dense LDL and low HDL.
Pool A consists of LDLI/II which contains relatively larger amounts of cholesterol ester and triglyceride and is essentially normal and non atherogenic. It has a pedigree and evolution bound intimately to lower levels of plasma triglyceride in the range of .5 – 2 mmol/l. Characteristics of this pool include:
1.Assembly within the smaller diameter ranges for VLDL.
2.Assembly of LDL, IDL and smaller VLDL pools.
3.Delipidation from VLDL->IDL->LDL occurs under mediation of lipoprotein lipase and hepatic lipase.
4.Triglyceride levels <1.3 mmol/l in males <2 mmol/l in females.
5.Pool A concentration varies with triglyceride levels and follows an arc of increasing size from .5-1.3 mmol/l in males to .5-2 mmol/l in females. Pool size peaks at 1.3-1.5 mmol/l in males (2 mmol/l in females) and decreases thereafter. Since triglyceride levels below 1.3-1.5 mmol/l are normal and LDL can vary considerbly among individuals this can give rise to a very sharp increase and very high level in LDL-C within normal triglyceride ranges for a minority of people that does not recur (until much higher triglyceride levels and then occurs due to Pool B) and can be exaggerated under LCHF. The reasons for this appear to be twofold. First the increase in the Pool A size is accompanied by a reduced catabolic rate of LDL which follows a similar but inverse dynamic. That is as pool size increases catabolic rate decreases. This appears to be supercharged under LCHF for a minority of people because of the higher saturated fat component of these diets (monounsaturated and polyunsaturated fats seem not to influence LDL unduly, although they may be implicated to a lesser degree (5)) and presumably other factors tied to individual variation. Higher levels of saturated fat result in higher levels of VLDL LDL and IDL since more lipid is available during assembly and more ApoB protein may be cued for assembly. However it is important to realize that these higher LDL-C levels occur under normal lipid conditions and are not indications of metabolic disturbance.
6.High clearance rates (ie typically Pool A LDL is cleared within 2 days).
Pool B consists primarily of LDLIII whose particles contain relatively smaller amounts of cholesterol and triglycerides and is inherently atherogenic. It has a pedigree and evolution bound intimately to higher levels of plasma triglycerides. Characteristics of this pool include:
1.Assembly within the larger diameter ranges for VLDL due to higher lipid availability during assembly and possibly more ApoB cued for assembly, features exaggerated under insulin resistant conditions.
2.Assembly of VLDL pools only.
3.Delipidation from larger VLDL-> smaller VLDL occurs under mediation of lipoprotein lipase and
CII/CIII.
4.Delipidation of LDLI/II to LDLIII occurs under hepatic lipase.
5.Triglycerides levels >1.3-1.5 mmol/l in males >2 mmol/l in females.
6.Pool B concentration varies with triglyceride levels and follows an arc of increasing size; the pool size does not decrease with increasing triglycerides as does Pool A but increases continually.
As pool size increases the proportion of small and dense LDL increases and that of larger LDL decreases and the pool becomes increasingly atherogenic. The phenomenon of a sharp peak in LDL-C values does not occur. The catabolic rate of LDL sharply rises with increasing triglycerides and LDL-C value
Nope, looks like it was too long. Sorry, if interested try Optimizingnutrition. Thanks.
Hi Tim,
It looks like your post, or at least the majority of it, did go through. Thanks very much for all of the information. I will need to read it again in order to understand it all 🙂
I appreciate you taking the time to post here, as well as in the Optimizing Nutrition forum.
Hello there, I had my cholesterol tested two weeks after starting my keto diet.
My LDL was 255, HDL 85, total cholesterol 355. Trigs were under 100. My doc thinks its familial hypercholesterolemia. Unfortunately I have no previous values to compare with.
After reading your blog post I’m wondering if the high LDL is related to my newly acquired low carb diet.
Do you think two weeks of low carb eating is long enough to impact my LDL like this?
Thank you!
Hello Nas,
It’s really hard to say whether your elevated values are due to your leto diet since you have no prior labs to compare with. If you’d like to see what I did to reduce my LDL-C and LDL-P levels, please read the follow up to this blog post: https://www.lowcarbdietitian.com/blog/update-recent-nmr-results-cardiovascular-disease-risk-and-what-i-eat.
Best of luck to you.
Thank you Franziska 🙂
It may relieve your mind to take a look at the latest post by Peter at Hyperlipid. http://high-fat-nutrition.blogspot.com/2016/07/arteriosclerosis-6-and-subbotin.html
and the paper he references http://www.ncbi.nlm.nih.gov/pubmed/27265770 by Subbotin VM
The latter shows that plaque starts in the outside of the intima media in areas where the media is extra thick and develops microvascularization from the outside stimulated by hypoxia caused by being so far from the oxygen diffusining in from the vessel. This vascularization causes the plaque to form. (perhaps some of this, if not found in this paper, was from Subbotin’s earlier paper(s))
Pete’s thesis is that the over thickness of the media is mainly caused by elevated insulin levels. So a low insulinogenic diet will not cause plaque or CVD.
Thanks so much for your comments and the link to Peter’s post, Robert. Very intriguing theory! I appreciate you taking the time to share.
And let’s not forget Dr. Joseph Kraft’s argument that “Hyperinsulinemia IS Diabetes IS Heart Disease…” He backed that up with the data from his life’s work in his book “Diabetes Epidemic and You.”
Congratulations! Great post! My total cholesterol is now 376, and I am a bit scared, but your post has clarified many points. I´d love to know you have reached the normal levels and how long did it take to achiev it?
Thank you very much.
Thanks for your kind words, Fabiano. I’m sorry to hear that your cholesterol has increased. I have a follow-up blog post written one year later that shows all values returned to my normal range: https://www.lowcarbdietitian.com/blog/category/cardiovascular%20disease
I continue eating lots of fiber (35-50 grams daily), around 100 grams of protein per day, and keeping saturated fat intake moderate. I haven’t had a new NMR for a while, but my most recent LDL-C was only 142.
Best of luck to you! – Franziska
thanks for the article, well written and lots of info, would love to chat sometime!
thanks, dR 212-243-1276
Thanks very much for the nice feedback!
Check out Dave Feldman’s work, and his definition of a “lean mass hyper-responder.” You’ll find excellent videos of his on YouTube. Your previous self (as described here, according to your labs) suggests you fall into that category.
Hi Greg,
I’m well aware of Dave Feldman’s work. Check out my most recent article on lipids, where I discuss LMHRs and my own results following his protocol: https://ketodietapp.com/Blog/post/2017/11/07/high-cholesterol-on-a-keto-diet-should-you-be-concerned.
I wrote a couple of years ago about my own high LDL. At one point it went up to 7.5mmol/L. With more carbs, and cutting saturated fat and switching to more monounsaturated fats it came down to 4.5 to 5.5. Still far higher than I would like. I heard about a person getting fantastic reduction using Psyllium fiber – I added 1 -2 teaspoons at each meal, with a glass of water. I’ve just had my lipid results back – LDL is now 3! My total is down from 8 to 5.2. HDL down slightly to 1.7, and TG 1.2 slightly up. Given high HDL might also be problematic as you pointed out, I’m not worried. My ration total:LDL is now 3.1 down from 3.8. So all in all a massive improvement.
Thanks for the updates, Julianne!
Hi! I know this is somewhat off topic but I was wondering if you knew where I could find a captcha plugin for my comment form?
I’m using the same blog platform as yours and I’m having difficulty finding
one? Thanks a lot!
I don’t have a captcha plugin. So unfortunately I can’t help you with this. Best of luck!