Update: Recent NMR Results, Cardiovascular Disease Risk, and What I Eat
I think the jury is still out on the significance of high levels of LDL-C and LDL-P in people following a low-carbohydrate, high-fat diet. My intent is never to offend anyone, and I’m certainly not an expert in this area by any means. But I did want to be 100% honest with people about my own experience and why I wasn’t comfortable with those dramatic increases in lipid values. Since writing that post, many ketogenic dieters have contacted me to report similar results and ask how concerned they should be and what they can do to get their numbers moving in the opposite direction. I’m happy to try to help in any way I can, and although I provide information about what has worked for me, I realize that people respond differently to various dietary changes. Also, there are other causes of hyperlipidemia, including major weight loss (1), as well as non-diet-related reasons, such as hypothyroidism.
My follow-up NMR last June revealed improvement two months after making changes to my diet, but I didn’t know if my numbers would continue to decline, stabilize, or increase over time. I’ve been eating a high-fiber, low-carb. lower-saturated-fat diet for about a year, and I recently decided to have another NMR (Nuclear Magnetic Resonance) spectroscopy LipoProfile done to see how things were progressing.
I’m really pleased with these results. My total LDL-P has dropped by 250 mmol/L and is now borderline-high, as is my LDL-C, which has further declined from 177 mg/dL last June. My small LDL-P has always been low, but it’s now less than 90 mmol/L.
Elevated LDL-C, LDL-P, Insulin, and Cardiovascular Disease Risk
How important are LDL-C and LDL-P in terms of cardiovascular disease (CVD) risk? It depends who you talk to. I respect the opinions and expertise of the professionals below and believe they all provide valid arguments.
I asked Dr. Thomas Dayspring to review my most recent NMR report. He feels that although my LDL-P has improved, it still places me at greater than average risk for a cardiac event. He said that given my age and the fact that I’m in the latter stages of perimenopause, I should definitely monitor this and other values and make appropriate lifestyle adjustments as needed. Also, there’s no arguing that I carry a lot of cholesterol in my HDL particles as well as LDL particles, and this cholesterol is transferred back and forth between all the particles within the bloodstream. He questioned whether the excess cholesterol is due to hyperabsorption, hypersynthesis, increased lipoprotein production and lipidation, or decreased clearance. Without further testing, there’s no way to know for certain.
Dr. Dayspring is a very progressive lipidologist, and I highly recommend his LecturePad presentations (sign up for free, and you’ll be able to access all content). In Part 1 of Have Cholesterol Measures Outlived Their Usefulness, he explains the reason oatmeal and other whole grain cereals aren’t a good choice to increase fiber intake for most people, why triglyceride levels should optimally be less than 100 mg/dL, and the dangers of relying on LDL-cholesterol measurements to evaluate degree of cardiovascular risk. In Part 2, he discusses the importance of controlling insulin resistance (IR); the interplay between hyperinsulinemia, hyperleptinemia, and appetite; and the benefits of carbohydrate restriction for those with metabolic syndrome: “Dr. Atkins was right.”
Although in my other blog post I referred to an article where he recommended statin therapy for anyone with an LDL-C level greater than 190 mg/dL, more recently, he said:
“That was written some time ago. I’d now amend that everyone with moderate to high lifetime risk for CVD events as determined by lipid/lipoproteins, family history, examination (BP, xanthomata) and smoking history – not simply LDL-C by itself.”
Dr. Dayspring also provides interesting information in the Cellular Regulation of Sterols lecture series, including the fact that vegans (who consume no animal products and therefore no cholesterol) absorb the same amount of cholesterol from the gut as do meat eaters and lacto-ovo vegetarians (about 55%, on average), but in their case, it’s entirely biliary in nature as a result of the gallbladder releasing hepatic cholesterol into the intestine. Even in non-vegans, most of the cholesterol in the gut comes from the bile rather than the food we eat, which is why limiting egg consumption doesn’t make sense as a strategy for lowering cholesterol levels. Even people who absorb more cholesterol than average (“hyper-responders”) experience only mild elevations in serum cholesterol concentrations when dietary cholesterol is increased (2).
Ivor Cummins is a chemical engineer known on social media sites as The Fat Emperor and is a prolific blogger on his website of the same name. He’s spent a great deal of time studying and writing about the role insulin and a high-carbohydrate diet play in CVD risk. While he agrees with Dr. Dayspring that LDL-P count is important, he feels that the combination of small, dense LDL particles and high insulin levels are the root cause of coronary artery disease (CAD) (3). He also believes maintaining adequate vitamin D3 levels is crucial to cardiovascular health, and I’ve recently seen him advise people with genetic defects (such as ApoE4) and very elevated LDL-P to replace a portion of saturated fat with monounsaturated fat and long-chain omega-3 fats. In addition to blog posts, he has several great videotaped lectures on his website, including “The Cholesterol Cunundrum.”
Dr. Peter Attia is a very-low-carbohydrate, ketogenic diet proponent who believes that elevated LDL-P values warrant dietary modification, including reduction in saturated fatty acid (SFA) intake. In a recent blog post, he describes a patient whose LDL-P dropped from 3500 to 1300 as a result of cutting saturated fat intake down to 25 grams per day while remaining on a ketogenic diet. He goes on to say:
“While I believe the population-based guidelines for SFA are not supported by a standard of science I consider acceptable, it does not imply I believe SFA is uniformly safe at all levels for all individuals.”
A few years back he wrote a 9-part series of blog posts entitled The Straight Dope on Cholesterol, which received a lot of attention and great feedback. Unfortunately, I’ve only read the first 2 parts at this point, but I’m hoping to read the entire series soon.
Dr. Spencer Nadolskey is a family physician who promotes a whole foods diet and healthy lifestyle. He’s recently done some experimenting with different diets (low-carb and vegan) and reported the changes in his biomarkers with each. He has a very balanced and moderate approach to health and wellness, recognizing the importance of taking people’s preferences and individual responses into account when making dietary recommendations.
As I said in my original blog post, most people who follow a low-carbohydrate, high-fat diet don’t experience significant elevations in lipids as I did, although it’s estimated that at least 25% do. In fact, Dr. Attia states in the blog post I linked to above that even when he was consuming 40% of his calories as saturated fat while following a very-high-calorie ketogenic diet, his biomarkers actually improved.
Increased vs. Decreased Risk for Cardiovascular Disease
ApoE genotype Apolipoprotein (Apo) E is a regulator of plasma lipid levels. I have two copies of the ApoE3 gene (3,3), which carries a low risk for atherosclerosis and cognitive disorders including Alzheimer’s disease (4). Those with the ApoE4 genoptye, who often have elevated cholesterol levels and are at increased risk for developing CAD, dementia, and other diseases, may find the ApoE4 Forums Heart Disease Discussion helpful for information and support.
Family history Regardless of genetic markers, a strong family history of heart disease is another risk factor for a cardiac event. Allthough I don’t have the ApoE4 genotype or familial hypercholesterolemia (FH), several of my family members have had CAD. My mom, who has stable atherosclerosis, has been on a low-dose statin for over 10 years. She is thin, active, and has never had any markers of insulin resistance (her lipid profile is remarkably similar to my own), although she was a long-term smoker before quitting eight years ago.
BMI and waist-to-hip ratio (WHR) My BMI is 19 (under 23 is optimal), and my WHR is 0.7 (less than 0.8 is optimal for women in terms of cardiac risk).
LDL-P Larger particles are generally considered less atherogenic than small, dense particles. I have very low small LDL-P and borderline-high LDL-P. While some would argue that my large LDL-P poses no concern, it’s still higher than what’s considered optimal. Also, in a study published after my initial blog post, large numbers of small and large LDL particles were both associated with increased CVD risk when compared with medium LDL particles (5). In addition, the MESA study researchers, who investigated CAD risk in more than 5000 people, reported this finding regarding carotid intima thickness (CIMT or IMT), a measure of subclinical atherosclerosis in the walls of the artery:
“Without accounting for LDL subclass correlation, small LDL and smaller LDL size were associated with IMT but large LDL was not. However, after accounting for their inverse correlation, both LDL subclasses showed highly significant and independent associations with IMT, with a greater difference in IMT per large LDL particle compared with small LDL. Smaller LDL size was no longer significant after taking into account the particle concentrations of the two LDL subclasses and risk factors. Thus, small LDL was a strong confounder of the association of large LDL with subclinical atherosclerosis, which may explain the widely-held view that larger LDL size is less atherogenic (6).”
Triglycerides, HDL-C, and HDL-P Low fasting triglycerides, high HDL cholesterol, and a large number of HDL particles are considered cardioprotective. Fortunately, I meet the criteria for all three. However, per Dr.Dayspring, my HDL-C/HDL-P ratio of 67 suggests potential dysfunction:
“In a recent study, individuals with the highest HDL-C/HDL-P ratios (>53) had a significant 1.5-fold increase risk for atherosclerosis progression compared with individuals with the lowest HDL-C/HDL-P ratio (<41) (7).”
However, at this point we don’t really know whether my risk is increased, and I’m comfortable with these values but will continue to monitor them.
Interestingly, 4 years ago, when I was following a low-fat diet with at least 50% of calories from carbohydrate, my triglycerides were 55 mg/dL, and my HDL was already quite high at 79 mg/dL. I think it’s safe to say that I’m not inherently insulin resistant.
Insulin levels I’ve had fasting insulin tested three times within the past three years, and each time my level was between 1 and 2 mIU/mL, which is considered very low (“Normal” ranges from 1 to 10 mIU/mL). Researchers have known about the connection between elevated insulin levels and heart disease risk for decades (8), and Ivor Cummins has discussed this extensively on his blog and in his lectures.
Fasting blood glucose, postprandial blood glucose, and A1c Elevated blood glucose, even at prediabetes levels, causes damage to endothelial cells that greatly increases CVD risk (9). My fasting blood glucose levels are consistently in the 80s, and 1-2 hours after eating, I am always under 130 mg/dL. I have an A1c every 6 months, and it has been 5.1-5.2% for the past 3 years. Prior to going low carb, my A1c was 5.6%, and my postprandial blood glucose values were routinely higher than 160 mg/dL.
Age I’ll be 49 this year, and as stated above, I’m transitioning into menopause, when changes in hormones, lipids, and body fat distribution increase CVD risk (10).
Low-carbohydrate diets are clearly beneficial for reducing CVD risk in people with metabolic syndrome and type 2 diabetes (11). But what about people with type 1 diabetes or those like me, who don’t have IR but follow a carbohydrate-restricted lifestyle for blood glucose issues, weight control, or simply because they feel better when they eat this way?
My Diet
I track what I eat in My Fitness Pal most days and have been doing this for over a year. While the nutritional information for the food database isn’t completely accurate (as I’m sure anyone who uses it would agree), it does give a good general idea of caloric and macronutrient intake.
Carbohydrates: I eat 30-45 grams of net carbohydrate per day consistently. Carb sources include nonstarchy vegetables, berries, Greek yogurt, cottage cheese, nuts, and dark chocolate.
Fiber: My fiber intake is very high, roughly equal to my net carb intake. A typical day includes half a large avocado, 1 cup of blackberries or raspberries, 2-3 oz unsweetened chocolate or cocoa (more than half the carbs come from fiber), 2 Tbsp flaxseed and/or chia seeds, 3-4 oz nuts, and 4-6 cups of nonstarchy vegetables. Fiber helps lower cholesterol levels yet doesn’t appear to compromise absorption of fat-soluble vitamins and other nutrients (12).
Total Fat: According to My Fitness Pal data, my fat intake ranges from 80-100 grams, which is around 50-60% of my caloric intake (I’m usually between 80-90 grams). Monounsaturated fat accounts for the largest percentage, and primary sources are avocado, olives, nuts, and meat. Eating fatty fish like sardines or salmon 3-4 times a week ensures that I get plenty of long-chain omega-3 polyunsaturated fats, including docosahexaenoic acid (DHA), which is anti-inflammatory and believed to be cardioprotective (13).
Saturated Fat: I don’t deliberately set a limit, but I generally end up consuming 20-30 grams of saturated fat daily. Although I’m usually on the lower end of that range, this still allows for modest amounts of cheese, half-and-half, coconut oil, butter, and fatty meat.
Protein: I’ve discovered that I feel best and most energetic with a relatively high protein intake of around 100 grams per day, which is just over 1.75 grams per kilogram body weight.
Am I in ketosis? I rarely check urine ketones anymore, but when I do they’re usually trace or negative. Ketosis has never been my goal (aside from the 3-month experiment I discussed in the prior blog post); keeping blood glucose levels and other biomarkers under control, looking and feeling my best, and eating a healthy, well-balanced diet are what’s important to me. However, I realize that for some people, ketosis can be beneficial and desirable.
Further Testing
What about having Coronary Artery Calcium (CAC) scoring, a CIMT, or other tests to rule out subclinical atherosclerosis? According to Dr. Dayspring, CAC testing isn’t advisable for women younger than 60, who usually get a zero score even if trouble is brewing. He believes that a CIMT can be useful if done correctly.
Here are his recommendations for further testing in my case, some of which I’ve already had done. I plan to do the rest within the next year or so.
Sterol synthesis and absorption markers
Omega 3 index
Inflammation markers: MPO, Lp-PLA2, hs-CRP
Once per lifetime tests: ApoE, MTHFR genotypes and Lp(a) level (I’m negative for ApoE and MTHFR genotypes but haven’t had Lp(a) done yet)
Homocysteine (I received a score of 8 on a scale of 4-15 umol/L when last done 2 years ago)
Vitamin D (50 ng/ml as of February 2015, which is considered within the optimal range)
On Not Taking Sides
I’m a very moderate person. I don’t like confrontation and dislike the “us vs. them” mentality. It probably won’t come as any surprise that I’m a registered independent and vote Democratic as often as I do Republican (and increasingly frequently for another party altogether). In addition to the experts listed above, I like and respect the diversity of opinions on this subject that have been voiced by many other knowledgeable people, whether or not they’re advocates of carbohydrate restriction.
It’s generally agreed within the low-carb community that people have different levels of carbohydrate tolerance. So why is it considered heresy to propose that the same might be true with respect to optimal saturated fat intake?
As I said earlier, I think we still don’t know enough about what kind of risk elevated LDL-P and very high LDL-C carry in the setting of a very-low-carb diet where other markers improve. Because of this, I choose to eat in a way that allows me to enjoy all the benefits of carbohydrate restriction yet keeps my LDL particle number at a level I feel comfortable with. Some may think I’ve gone too far in making changes to my diet in order to improve my numbers; on the other hand, I’m sure there will be others who feel I haven’t gone far enough, since my levels still aren’t considered “optimal.” I understand both points, but I have to go with my gut on this one. Ultimately, it’s up to you to decide what feels right for you given what we currently know and don’t know.
References
1. Phinney SD, et al. The transient hypercholesterolemia of major weight loss. Am J Clin Nutr. 1991 Jun;53(6):1404-10.
2. Fernandez ML. Effects of eggs on plasma lipoproteins in healthy populations. Food Funct 2010 Nov;1(2):156-60
3. Phillips MC. Apolipoprotein E isoforms and lipoprotein metabolism. IUBMB Life. 2014 Sep;66(9):616-23
4. Lamarche B, et al. Fasting insulin and apolipoprotein B levels and low-density lipoprotein particle size as risk factors for ischemic heart disease. JAMA. 1998 Jun 24;279(24):1955-61.
5. Grammer TB, et al. Low-density lipoprotein particle diameter and mortality: the Ludwigshafen Risk and Cardiovascular Health Study. Eur Heart J. 2015 Jan 1;36(1):31-8.
6. 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.
7. Qi Y, et al. Cholesterol-overloaded HDL particles are independently associated with progression of carotid atherosclerosis in a cardiovascular disease-free population: a community-based cohort study. J Am Coll Cardiol. 2015 Feb 3;65(4):355-63.
8. Després JP, et al. Hyperinsulinemia as an independent risk factor for ischemic heart disease. N Engl J Med. 1996 Apr 11;334(15);952-7.
9.Maschirow L, et al. Inflammation, coagulation, endothelial dysfunction and oxidative stress in prediabetes – Biomarkers as a possible tool for early disease detection for rural screening.2015 Mar 6. pii: S0009-9120(15)00071-5.
10. El Khoudary SR, et al. Progression Rates of Carotid Intima-media Thickness and Adventitial Diameter during the Menopausal Transition. Menopause (New York, NY). 2013;20(1):8-14.
11. Volek JS, Feinman RD.Carbohydrate restriction improves features of the Metabolic Syndrome. Metabolic Syndrome may be defined by the response to carbohydrate restriction. Nutr Metab(Lond) 2005 ;2:31.
12. Ramprasath VR, et al. Consumption of a dietary portfolio of cholesterol lowering foods improves blood lipids without affecting concentrations of fat soluble compounds. Nutrition Journal. 2014;13:101.
13. Richard D, et al. Infusion of docosahexaenoic acid protects against myocardial infarction.ProstaglandinsLeukot Essent Fatty Acids.2014 Apr;90(4):139-43.
Nice post and congrats for sharing your numbers. They are for the most part insignificant in terms of heart and artery health. The key is inflammation of the endothelium, the most common cause is hyperglycemia. So the most important number for heart health is Hb A1c reflecting your average blood sugar. The particle size and number is just an attempt to extend the whole cholesterol theory, which is surely being discredited. The only way cholesterol ever gets deposited in the artery wall is when it is consumed by a white cell, activated by injury to the endothelial cell layer. Ignore the lipid numbers an keep your sugar and insulin low with your current diet.
Thanks very much for your comments and insight, Dr. Lundell. Appreciated!
I would disagree that A1C is the most important marker of heart health as we know that in non diabetics it can miss dysglycemia in over 90% of patients when compared to OGTT.
Endothelial cell finction is very important as this can predispose atherosclerosis by decades.
Cardiac dysfunction can be viewed in this term, very early on. It is one of the reasons cardiopulmonary exercise testing and peak VO2 determination should always be a factor in any treatment protocol (nutritional/lifestye and/or medication). This actually reflects the disease state, instead of the current paradigm of risk assessment. Shouldn’t we look for disease first, THEN figure out the risks associated. Instead we do things ass-backwards
On a side note, i believe the production/absorption issue is much larger issue then we think and by and large being ignored, both in medicine and in the low carb blogosphere. It will be interesting to see those when you get them.
Thanks for sharing!
Hi Rocky,
I hope you get this notification, as I was unable to reply to your reply (the limitations of a Weebly website).
Thanks very much for your comments. Appreciate you weighing in with your expertise on these complex issues.
Bravo Franziska, and thank you for sharing these results.
My doctor told me yesterday that ANY fat or oil will raise my cholesterol, and to keep olive oil to 3 teaspoons a day if I wanted my LDL to go down. Mind you, she is a bit old. We’ll see, I’ve been eating olive oil in place of butter and plenty of veges to see if it goes down. Last time, about 3 months ago, this had made zero difference. I just had another test done, so we’ll see.
Does it matter? I can only afford a basic 4-count panel and HbA1c, plus BP, BMI and so on.
My opinion, which is all I really have to go on after taking into consideration everyone else’s, is that coronary artery disease is not caused by lipoproteins, with the possible exception of some oxidised particles. It is caused by chemical insults from smoke and similar environmental exposures, and perhaps from the elevated glucose too, and its growth is stimulated by the inflammatory repair process becoming deregulated by excess insulin.
LDL and VLDL particles can be captured by this process. They are not assailants, they are more akin to hostages. Like hostages, their being taken captive can make the situation worse, but if it didn’t already exist they would be incapable of initiating it.
Micronutrient deficiencies play a large role in the disordering of the repair system. Vitamin E is an obvious example because of its role in regulating protein kinase C, hence the protective influence of nuts in the diet, but there are many more. Diets that protect against heart disease are micronutrient rich, but this doesn’t mean that I think a restricted diet like an all-meat diet will cause heart disease – I think this unlikely. It is more about the micronutrition being appropriate for the macronutrition, whatever that may be.
Thanks so much for your comments and for sharing your own ideas on this subject, George. I find them both intriguing and plausible. You’re one of the “knowledgeable people” I was referring to above, and I appreciate everything you bring to such discussions.
Hi Franziska,
I think your results are excellent compared to the general population. Are they excellent in absolute terms? Hard to tell, but they definitely aren’t worrisome 🙂 !
To add to the anecdotes, my TC & LDL-c scores lowered significantly when going ketogenic & increasing SFAs (amongst other changes like increased sleep & sun exposure).
Not only should you tinker for your own sake but for the sake of adding to the pool of information for others out there. So thanks! You’re obviously about the science and objective data sharing, please don’t apologize for that.
“So why is it considered heresy to propose that the same might be true with respect to optimal saturated fat intake?” ==> it’s not heretical at all to my mind. I will say though that there’s a good argument to be made about looking at other variables first before looking at SFAs. I understand that this is also influenced by current discussion trends.
Like you, I learned a lot from Dr.Dayspring. However, I can’t ignore the fact that he’s wielding a (albeit sophisticated) hammer and see’s a lot of nails around him…that’s why I encourage people to purposely stray from mainstream theories (as Ivor so brilliantly does) because it makes for more fruitful progress.
Please keep it up!
Cheers,
Raphi
Thank you so much for your kind words and insightful comments, as well as sharing your own experience. You’re another of the “knowledgeable” ones whom I respect and learn from.
I just noticed Dwight Lundell M.D.’s comment and want to second it. He makes a fair point about “particle size and number is just an attempt to extend the whole cholesterol theory, which is surely being discredited”…look at it this way; even if LDL-p in & of itself exerts a substantial negative effect, we already know enough to say that dietary SFAs, cholesterol or CHOs can’t possibly explain much of it. It brings us back at square 1 to explain (hypothetically) why LDL-p has this (supposed) effect – we’d still want to look at endothelial status, mitochondrial processing, membrane composition, gaseous exchange effects (like NO) etc.,
Thanks for the additional interesting comments — much food for thought there! 🙂
Thanks Franziska for this great summary. Your approach is balanced and informative as always.
However, I don’t agree with Dr. Lundell. Although I believe that inflammation is important, the role of lipids shouldn’t be ignored. Oversimplifying these issues won’t help us.
Appreciate your writings.
Thank you very much, Axel! I believe you were the first one I contacted one year ago to help me interpret my results. I appreciate your continued support and enjoy your writings.
Excellent post! I am a nurse and follow the research very closely. I agree, you have to be objective and not take sides on these issues.
Thanks very much, Vicky!
Thank you for your kind words Franziska, it means a lot coming from you.
George’s ‘hostage’ metaphor is the single best one I’ve come across to characterize the role of lipoproteins in CVD/CAD.
To Dr.Axel F Sigurdsson’s point ==>
1) OK, but I can’t recall a 24hr period in the last century where the role of lipids have been ignored.
2) Even if we did try to ignore them, it’d be in vain since there’s basically close to nothing they don’t exert an effect on.
3) Even if the sole focus is to understand lipidomics, we’re necessarily obliged to look beyond the lipid-lipoprotein complex to learn about their ‘surrounding variables’ pulling the strings or ‘taking them hostage’ as George argues.
We’re at the point where there’s no evidence of cholesterol or lipoproteins causing INHERENT harm to us. In the same way that a good person can turn bad given the right environment, who’s to say this this isn’t what happens to lipoproteins? Regardless of whether or not this is the case, we’d still want to explore the biological milieu they find themselves in.
It’s truly hard to have the courage of ones convictions – especially when it relates to major health decisions.
Appreciate you raising these points, Raphi. Very intriguing!
Hi Franziska as always an interesting and thought provoking post.
As a type two diabetic I agree with Dwight Lundell M.D. Over the years I have seen many diabetics obsessing over lipid numbers, while running dangerously high blood glucose numbers. I equate this to worrying about the deck chair arrangements on the Titanic.
“For every percentage point drop in A1C blood test results (from 8.0 percent to 7.0 percent, for example), the risk of diabetic eye, nerve, and kidney disease is reduced by 40 percent. Lowering blood sugar reduces these microvascular complications in both type 1 and type 2 diabetes. Intensive blood sugar control in people with type 1 diabetes (average A1C of 7.4%) reduces the risk of any CVD event by 42 percent and the risk of heart attack, stroke, or death from CVD by 57 percent.”
Source: DCCT/EDIC, reported in December 22, 2005, issue of the New England Journal of Medicine.
The MONICA study showed the people with the lowest cholesterol numbers had more heart disease than people with the highest numbers. There appears to be no correlation of cholesterol levels and heart disease. Whereas the correlation between HbA1c numbers and heart disease is irrefutable.
https://www.youtube.com/watch?v=i8SSCNaaDcE
It is commonly reported low carbing diabetics see triglyceride numbers plummet and improved HDL. As for LDL the rules and what is considered safe seem to change all the time. What do readers make of this.
New Cholesterol Guidelines Abandon LDL Targets
“Gone are the recommended LDL- and non-HDL–cholesterol targets, specifically those that ask physicians to treat patients with cardiovascular disease to less than 100 mg/dL or the optional goal of less than 70 mg/dL. According to the expert panel, there is simply no evidence from randomized, controlled clinical trials to support treatment to a specific target. As a result, the new guidelines make no recommendations for specific LDL-cholesterol or non-HDL targets for the primary and secondary prevention of atherosclerotic cardiovascular disease.”
http://www.medscape.com/viewarticle/814152
Kind regards Eddie
Thanks for your comments, Eddie. Appreciate you sharing your point of view.
I forgot to address the last quote about abandoning LDL targets. It’s because the new guidelines call for statin treatment for all people age 40 and over who have diabetes, regardless of LDL levels:
http://www.medpagetoday.com/Cardiology/Type1Diabetes/49300
Thanks for clarifying that point Franziska.
Whatever you decide in the future keep well away from statins. The latest horror story.
“New research published in Diabetologia (the journal of the European Association for the Study of Diabetes) shows that use of statins is associated with a 46% increase in the risk of developing diabetes, even after adjustment for confounding factors. The study is by Professor Markku Laakso, Institute of Clinical Medicine, University of Eastern Finland and Kuopio University Hospital, Finland, and colleagues.”
http://medicalxpress.com/news/2015-04-statins-diabetes.html
Kind regards Eddie
“I think the jury is still out on the significance of high levels of LDL-C and LDL-P in people following a low-carbohydrate, high-fat diet.”
Any science to back this up?
Hi Charles,
The point I tried to make in this post (and especially in my first post) that there are no long-term studies on elevated lipids in people following LCHF diets, so of course, there is no evidence either way.
Some doctors, researchers, and others who have done a lot of their own independent research (including some who have commented above) are proposing that maintaining low levels of insulin, blood glucose, and inflammation via low carb may prevent CVD even if LDL-P and LDL-C levels are high. This may very well be, but as I said, we don’t know for sure at this point.
This is true. There is simply no epidemiology of cardiovascular risk in populations with very low triglycerides. If you look at this study, the lowest TG measurement is over 88.5 mg/dL, or 1 mmol/L.
http://www.ncbi.nlm.nih.gov/pubmed/17635890
Another question is, or should be, what metabolic risk markers apply best to ALL diseases and causes of death, of which CHD is an important subset?
In the case of cancer, for example, LDL and TG are not significant, but HDL and insulin are. In the case of stroke, low LDL is associated with haemorrhagic stroke (as we might expect from blood-thinning effect of both PUFAs and liver disease), whereas high HDL is inversely associated with ischemic stroke.
http://www.ncbi.nlm.nih.gov/pubmed/15557504
http://www.ncbi.nlm.nih.gov/pubmed/23704101
The older people get, the less importance LDL has to their cardiovascular risk, but HDL retains its importance to the very end, and high LDL is associated with low death rate from infections
http://www.ncbi.nlm.nih.gov/pubmed/12860577
What no-one wants is high LDL, high TG, and low HDL.
Thanks so much for your comments and all the links, George. I wasn’t aware of several of these associations. Very much appreciated. I feel even better about my numbers now.
I wish you the best on your next round of labs.
George, thanks for sharing the study linking elevated triglyceride levels to heart disease and death risk levels. For those who may not have clicked through to review the study directly, I want to highlight two points:
1. The triglyceride levels being compared in the study were non-fasting. They are not comparable to the numbers most people get on standard fasting lipid panels.
2. Contrary to the contention that “the lowest TG measurement is over 88.5 mg/dL, or 1 mmol/L”, the lowest of the six categories being compared was “less than 1 mmol/L (<88.g mg/dL)", and it's clear from Figure 4 that many study participants fell into that category.
In summary, I don't think this study exemplifies a lack of "epidemiology of cardiovascular risk in populations with very low triglycerides".
Thanks for spotting that Marc. I’ll revisit that paper. So that’s the lowest cut-off (not measure, d’oh!) and they’re non-fasting.
This raises for me questions about what constitutes fasting/ non-fasting. My last lipids draw, the phlebotomist said a 17hr overnight fast was too long (was I meant to get up and eat in the night?), then when I said I had 10mls of cream in a coffee 4 hrs earlier, she said “that means I’ll have to mark it non-fasting”. Really? 5g fat 4 hours ago to break a 17hr fast? What-ever!
But yeah, low non-fasting TGs on normal diet = excellent insulin sensitivity, put in the “insulin => CHD” file.
Interesting post. I see a lot of lipid panels with the athletes I work with and the elevated total cholesterol is common and not unhealthy because the more critical markers like triglycerides, HbA1c, ratios, VLDL etc. are better than ideal. I also make sure their Vitamin D status is where it should be and they are actively supplementing with Magnesium. Stephen Phinney, Jeff Volek and Bev Teter are some of the researchers whom I communicate with on a regular basis. Bev can tell you that a female who is practicing carbohydrate restriction and has high total cholesterol is probably healthier…you can see her here: http://www.cbn.com/cbnnews/healthscience/2013/february/forget-cholesterol-inflammations-the-real-enemy/
Thanks for your comments and the link, Peter.
Hi, Franziska – I run a very low-key blog on the Science of Nutrition, Obesity and Diabetes and I want to commend you for being brave enough to post your test results online. I would also like to give you some food for thought. 🙂
After reading this thread and reviewing your test numbers, I believe you may be struggling with the wrong issue – and are in fact insulin and thyroid hormone resistant.
If I’m correct you have Metabolic Syndrome XX (you can read more about it at http://sugarfreegoodies.info/blog/metabolic-syndrome-xx ), which is quite different than Metabolic Syndrome and usually goes undiagnosed. That’s because in MSXX (formerly known as the Insulin Resistant variant of PCOS – polycystic ovary syndrome) your Trig’s are low, and your A1c and fasting insulin are ‘normal’. Even often great.
But women and men (yes, they can have it too; it has a genetic component though men are often the carriers) with MSXX do have recognizable and diagnostic symptoms.
First, they have *ineffective* (lazy) insulin. This usually results in 1-hour PP’s being higher than their 2-hr PP’s – a dead giveaway. Second, to make things worse, they usually have runaway Gluconeogenesis and convert a great deal of consumed protein into glucose. So someone with MSXX can eat an extremely low carb diet without understanding that they are in fact producing a great deal of glucose via consumed protein. That’s a double whammy, since they’re making sugars they’re unaware of in a body whose insulin can’t even handle what they’re eating with a fork! And if you really are eating 100 grams of protein a day, that’s about twice as much as you need, with far less fat (at 100 g per day) than you need. I’ve gone from 245 pounds eight years ago to 132 today, and I eat about 60 g protein (I do heavy weight training and have a lot of muscle to build/maintain), 150 g fat and about 100-125 g carbs daily. And I’m nearly 70. Definitely past menopause. 😉
One clue for my thoughts on your possible issues was your comment: “Prior to going low carb, my A1c was 5.6%, and my postprandial blood glucose values were routinely higher than 160 mg/dL”
A healthy working metabolism should be able to consume modest amounts (75-100 g) of carbs like potato, sweet potato, rice, pasta, corn, etc. every day with no problem whatsoever and no PP spikes or high insulin or A1c levels. If not, it just means that VLC abstinence has hidden your insulin problems – not resolved them.
And those particular carbs are all very important (especially for women, and double that for women who are Peri-menopausal) to keep thyroid hormones at peak levels, as Atkins discovered when all his pre-Diet Revolution book patients became hypothyroid. After consulting with a lot of Endo’s, he made sure to include ‘steps’ to ramp up carbs after the initial two-week induction stage – which you still appear to be on. If eating modest (not VL) carb sends your PP’s higher than 105, and your A1c to 5.6 – you have an insulin disregulation. Likely MSXX. Combined with what I will guess to be an extremely high Reverse T3, which is the Metabolic Black Hole of thyroid hormones. A few thyroid hormone tests: Free T3, Free T4 and Reverse T3 along with your Ferritin level will show this clearly if true. And all easily fixable if so.
My 2 cents/YMMV
Thank you so much for commenting here and for sharing your own story as well. Congratulations on losing over 100 pounds and learning to manage your symptoms!. I’d not heard of this variant of metabolic syndrome before, and it’s very interesting.
After reading the article on your blog, I don’t think it’s what I have, or at least not the same presentation as you described, however, as I’ve always been thin with no belly fat (aside from a few years in my teens), and my morning blood glucose levels are in the 80s, so not much gluconeogenesis is happening overnight. On the other hand, I was diagnosed with hypothyroidism shortly before starting low carb, and I’ve been on Armour thyroid supplementation for over four years with good results.
I really appreciate you posting this. I definitely plan to do more research about this little-known syndrome. Thank you so much, and best of luck to you.
Please provide references for further research on MSXX. Thanks.
Though way out of my league with the knowledgeable comments above, I want to thank you for taking on another tough topic & presenting thoroughly researched & fair-handed info. I’m going to take a Rip Van Winkle nap & awaken when the jury has reached a conclusion.
Thanks so much for the nice feedback, Gerri. Appreciate your continued support.
Thanks for the update of your results as well as the analysis and commentary – very helpful.
Thanks so much for taking the time to read and comment, Marc.
Can you explain the math behind the HDL-C/HDL-P ratio? I’m having a hard time with that… 96/36 = 2.66? Sorry, I’m missing something..
Thanks for the awesome update with the latest NMR. Looks like SFA contect definitely has an impact on P…
You have to convert from mg/dL to mmol/L. I apologize for not doing that. HDL-C = 96 mg/dL = 2.5 mmol/L . HDL-P = 36.8 umol/L. The ratio is 67.
Thanks again for the feedback. Yes, reducing SFA appears to have a significant impact on my total particle number, but of course not everyone responds this way. And small, dense LDL-P generally doesn’t improve with lower SFA intake (as it does with carb restriction), so I think that’s likely related to something else.
Ahhh, nice thank you for the explanation on how to get that ratio..
I mentioned in another thread that my NMR is essentially identical to yours.. I saw the same swing in my ldl-C and ldl-P, even as every other risk factor improved. I’m VLCMPHF (2ish years now) – swing in and out of Keto but don’t obsess about stayin there..
I get a feeling that this pattern may be even more common than your 25% guestimate, time will tell I guess.
The $64,000 question remains, “in the context of a VLCMPHF diet, is high ldl-C and high ldl-P a possible driver of atherosclerosis?”
We’re not sure. And chances are, it won’t be a cut and dry “yes” or “no”..
It’ll be like every other question we try to answer regarding our amazingly complex metabolic machinery… Hell, we’re still not exactly sure of the exact etiology and pathogenesis of CAD.
Current accepted theories (and it’s easy to forget that that’s what these are) seem to be falling apart before our eyes.. They are built upon an incorrect understanding of arterial morphology if believe the arguments made by William E. Stehbens or Vladimir Subbotin:
http://www.tbiomed.com/content/4/1/41
Can we correctly theorize about cause of disease and mechanisms of disease development when we have an incorrect understanding of coronary artery design?
Maybe, but only because we got lucky – not because we figured it out.
We threw enough at the wall and something stuck..
Thank you so much for this thread. You’ve done a wonder job of putting all of this information in context. I enjoy your blog, very much.
KellyT
Thank you so much for all of your insightful comments. Agree strongly with all of your points. It’s so hard to keep saying, “We’re not sure” and “I don’t know.” People often want definitive answers and tend to place trust in those who argue their positions most vociferously without acknowledging that they may be wrong.
I’m extremely grateful for all of the intelligent readers who have commented on this post and shared their viewpoints in a civilized, respectful fashion.
Thank you also for your very kind words about my blog. Much appreciated!
I’m not a scientist or anything–just a practicing LCHFer with a question. My own LDL numbers have been rising from NMR to NMR, and I wonder if I (or you, or both) could have some sort of saturated fat intolerance? IS there such a thing as a saturated fat intolerance?
I wouldn’t call it a saturated fat intolerance, as that would indicate you’re unable to eat any amount (i.e., lactose intolerance, celiac intolerance). I’d say it’s just a response to increased saturated fat intake that occurs in a sizable minority of the population who eat LCHF.
My LDL is usually high on any diet, 5-6, but with all other risk factors minimal (BP, ECG, BMI, HDL, TG, CRP, HbA1c, FPG) I’m fine with that usually.
However, just for an experiment, I lowered total fat and SFA (much less butter and dripping, more olive oil, nuts, fish oil supps, fibre and “safe” starch) for the past few months.
Now my LDL is 7, which is too high even for me to be comfortable with. Which is probably an example of what Franziska talks about, that some people don’t get an LDL shift from diet (or drugs, for that matter – there are plenty of statin non-responders).
Luckily the glycemic lipids – HDL and TG – are easier to improve.
My HbA1c has gone from a steady 5.1 to 5.6.
Now, this is a different lab. I had a steady stream of 5.1s from an American lab when I was in the Hep C drug trial, and now I’ve had 2 5.6s from this local lab. I wonder how accurate the count of a tenth of one percent actually is between labs.
Alternately, more unsaturated fat, less ruminant fat, and a little more carb is harshing my insulin a bit, and this is pushing the HbA1c and the LDL.
I have some hacks left to try – I eat a lot of eggs so I’m going to lower my egg cholesterol intake from 12 a week to 4 (the USDA just said it’s not an issue, so it probably is now), also coffee was giving me migraines so I’ve cut that too.
If it’s still the same after that, I’ll stop the experiment. I’ll have learned an important lesson, sometimes diet isn’t everything.
Thanks so much for reporting back on the results of your experiment, George. Sorry to hear that your LDL-C increased rather than declined, as you’d hoped. Agree that HDL-C and TG improve almost across the board with LCHF, while the LDL-C response is anyone’s guess.
You make a great point about the differences in HbA1c between labs. It would be great if it were possible to have 2 blood draws the same day in order to compare. Hard to know whether it’s the dietary changes or variation among labs due to technique or other factors.
Smiling at your comment about decreasing eggs because of the USDA’s latest position on dietary cholesterol 🙂 Looking forward to hearing about the results of that experiment.
Always appreciate your insight on these issues. Thanks again.
Hi Franziska,
I finally got results of this experiment. Last time LDL was 7.7 mmol/L and HDL was about 1.2 mmol/L.
So – I stopped eating eggs every day (2 a day), stopped drinking coffee every day (4 cups), and replaced the olive oil in my breakfast with ghee.
Today, my lipids are
Total cholesterol 8.0 (309.4) (down from >9) mmol/L
Triglycerides 0.9 mmol/L (79.7) (12 hour fast)
HDL 1.64 mmol/L (63.4)
LDL 6.0 mmol/L (232) or Iranian 5.3 mmol/L (206)
Chol/HDL ratio 4.9 (<4.5 is supposed to be good)
The internet says
Your Total Cholesterol of 309 is HIGH RISK
Your LDL of 230 is VERY HIGH RISK
Your HDL of 63 is OPTIMAL
Your Triglyceride level of 80 is NORMAL
Your Total Cholesterol/HDL ratio is: 4.90 - (preferably under 5.0, ideally under 3.5) GOOD
Your HDL/LDL ratio is: 0.274 - (preferably over 0.3, ideally over 0.4) AT RISK
Your triglycerides/HDL ratio is: 1.270 - (preferably under 4, ideally under 2) IDEAL
I'm happy with that.
Hello George,
Thank you very much for sharing your lab results following your latest dietary experiment. Congratulations on the improvement in lipids across the board! I’m wondering which of the changes had the most impact. Also, I assume you’re still eating eggs but no longer 14 per week?
– Franziska
I have been following a ketogenic diet for about four months. (“low carb”/New Atkins before) I wanted to lose about 20 pounds that had crept up over the 5 years of menopause, I am now post-menopausal, and I have mild hypertension. The diet has been wonderful. I feel great, huge amount of energy, sleeping well, etc. I exercise quite a bit; marathoner and Pilates and have been able to run half marathons without carb loading. I had lost 10 pounds and about October decided to do a modified egg fast to lose the last 10. I had my labs checked the second week of January and was a bit dismayed: Total chol: 322, total LDL 168, triglycerides 80 and HDL138. Three years ago, my HDL was 153 and TG only 43 with LDL 133. I’m going to get NMR to differentiate the LDL, but I’m wondering your opinion of the benefit of HDL so high. I mean, is it a case of diminishing returns?
Hi Martha,
Weight loss can found cholesterol and triglyceride results, so your results may possibly change in another few months or so — which way the LDL-C will go is hard to say. I’m really not sure what to make of your extremely high HDL. I’ve honestly never seen one that high and I know that in some cases it can be a problem. You’d need to speak with a lipidologist and have further testing to determine that.
You have my best wishes for good health.
Thank you so much for this update Franziska, it’s really helpful 🙂
Franziska,
I never knew high HDL can be bad. My last test my HDL was 124 and LDL was 147 – trigs/64 – CRP/1.48 – homo/8.6 I’m having the Boston test later this month. I just found your blog this morning and will be reading more. I think I’ll lower my saturated fat levels – maybe delay the test a month. Unfortunately I’m hypo and post meno/55 and have gained significant amount of weight despite being pretty good with a LC diet. I was skinny in my 30s with a BMI around 19 so this is very depressing. Also on numerous drugs for HBP which is familial. Don’t know what to do but I’m working with a new and what I feel is a good practitioner. I appreciate all your work and honesty and I agree that we are all different. Sometimes the LC world can as dogmatic as the vegans. I stopped frequenting a LC board for that reason. Thanks again Franziska.
Thanks so much for your kind words of support and for sharing your story, Eliza. I’m so sorry you’ve been struggling with weight gain even though you’ve been following a healthy LC diet. That’s extremely common in women during and after the menopausal transition. I hope your new healthcare practitioner can provide helpful guidance.
Thanks especially for your last couple of sentences regarding LC dogma. I’ve seen downright cult-like behavior recently, especially in the keto community.
I wish you the very best with everything!
Hi Franziska, I am having somewhat the same reaction to a LCHF diet that you did. I have been watching your two blog posts for awhile hoping for another update. Have you checked your particle number again since you wrote this post? I am very curious if the lower saturated fat has worked for you. So far I have checked mine twice with lower sat. fat and it has gone up instead of down but I think I may have had some carb confounders. I am preparing to try again, hopefully without any confounders.
Sincerely,
Diane
Hi Diane,
I have not had an NMR to recheck my particle numbers since I wrote this blog post. However, my LDL-C levels have always mirrored my LDL-P levels, and my most recent LDL-C from July was 145, which is well within the range I feel comfortable in. I’m fairly confident that my LDL-P levels have further declined, given that my LDL-C has decreased, my HDL-C has increased to 119, and my Triglycerides remain very low at 54.
I’m sorry to hear that your LDL particle number increased when you reduced saturated fat, but an increase in carbs could certainly affect this. My intake remains consistently less than 50 grams net carb per day and usually around 30 grams net carb per day, with roughly the same amount of carbs in fiber daily.
I wish you the best of luck going forward.
I’m 78 and just lost 32 lbs on keto in 4 months (214 to 182). I’m a retired legal federal appeals research specialist, and really appreciate your non biased approach to understanding increased LDL cholesterol levels on keto. I’m responding as there is little info about seniors on keto anywhere, and thus this may offer some insight.
Lipids after weight loss: HDL: 30, LDL: 161, TRIGS: 149, TC:221. Only changes were an increase in LDL and decrease in TRIGS.
I was not on any meds before keto, and am on none now. However, BP reduced from 139/89 to 120/82, and reduced waist size from 40 to 36. Pain associated from slipped L-4 is gone. I am essentially sedentary now, after a lifetime of moderate exercise (I’m a very cerebral type anyway.) I still smoke cigars, but don’t drink alcohol. I have played guitar for 65 years, and still play in local clubs with my sons and grand daughters (blue eyed soul music) as a social outlet.
I average 1300 calories daily, with 20 grams of carbs, 60 grams of protein and 80 grams of fat. I supplement with fish oil, magnesium, vitamin D3, Vitamin E, prebiotic fiber, probiotics and alpha lipolic acid.
I am going to substitute olive oil for coconut oil, and increase carbs after reading Mrs. Spritzler’s results after doing this, with the increased carbs coming from frozen berries daily. I live alone and only cook with a microwave and a toaster oven.
I do believe that cholesterol helps elderly people with infections, helps the brain, and also that combined with reduced sugar from low carb inhibits dementia, heart disease, diabetes and so much more. When I see so many elderly people that have such chronic diseases I’m convinced that diet is the major culprit.
Thanks for all of the valuable information you publish.
Warm regards,
Mike Strauss
Hi Mike,
Thank you so much for the nice feedback and for sharing your story. Congratulations on losing weight and improving several heart risk factors. In your case, I don’t think replacing coconut oil with olive oil is necessary, although consuming a variety of healthy oils is a good practice. I wish you the best of luck and great health!
Thanks for this post – I have incorporated chia seeds, walnuts, spirulina and turned over to leaner sources of meat to reduce my LDL-p and it worked!
Cooking with olive oil and using it on my salads.
I still eat some lean steaks a few times per week and am not regretting it.
Dairy never suited me well so I’m fine there 🙂
I think if you put more PUFA in your diet it might get even better.
Thanks so much for your comments and for sharing the strategies that helped you lower your LDL-P, Mike! Sounds like you have a very healthy low-carb lifestyle. I’m eating pretty much the same as outlined in this post, albeit with more walnuts and flaxseed over the past year or two.
After several years low-insulinogenic and time-restricted eating I started having high LDL cholesterol. I suspect the cause is Reverse T3. (rT3). rT3 is considered metabolic inert by nearly all medical professionals with few exceptions like Dr Westin Child. rT3 may not enter cells like T3, but can replace T3 on liver cell LDL receptors disabling those receptors causing LDL-C to soar. Per Dr Child rT3 rises during infection and starvation to fight infection and to conserve energy. Various diets are known to increase rT3 over time. It would be interesting to know the rT3 status of all low-carbers with high LDL-C.
Thanks for your comments, Robert. Your premise is interesting, although my own rT3 is actually very low and has been for several years. However, it’s possible that other people who follow a low-carb way of eating may have elevated rT3 levels.
That is interesting; we have to ask what the purpose of such an adaptation to reduced carbohydrate intake could be.
Are LDLs kept in circulation a bit longer to enable the TGs on them to be more completely used up when glucose is less available?
It is normal for healthy individuals to have higher LDL when they fast; in fact this is really a sign of health as LDL will go down in obese subjects. You don’t say what your reason was for eating this way, but if it was to lose weight or reverse metabolic disease, then I think it very likely that LDL would rise once you were successful.
See for example Dave Feldman’s blog cholesterolcode.com or the recent podcast with Dr Nadir Ali.
https://www.ketovangelist.com/episode-134-dr-nadir-ali-is-a-keto-cardiologist/
Dr Ali prescribes a keto diet for his cardiology cases and finds that LDL rises after a year or two – once health improves.
This is LDL rising for a good reason, one different from the reasons for higher LDL being associated with CVD.
Starts around min 25 in that podcast
Wow, this has been one wonderful post. Your honesty is beyond amazing, and speaks much for your character. Reading this, I thought back to my teenage years in the early 70’s, when I experimented for a short time with the then new Atkins diet, and borrowed his first cookbook from the library. I remember the chapter on him recommending low saturated fats for high cholesterol, because heart disease ran in my family. Maybe he wasn’t too far off base back then.
My specialty is low carb baking, but what I do now is substitute 1/2 cup unsweetened applesauce and oil, for the butter I used to use in my coffee cake. It actually tastes lighter and better. That 1/2 cup applesauce adds 12 grams (total) carbs to the recipe, which only adds a small amount per serving. For me, keeping my carbs down is primary, but if I can lower my saturated fat, and still keep the carbs down, all the better. I still eat sat fat, but not as much.
Thank you for this wonderful blog! I am in the same boat and following your journey! I love the info and also the references to various thinkers in the field. I will look for updates. Thank you for taking the time to provide this information. It’s so valuable!
Thanks so much for your kind words and feedback, Lisa! I wish you the very best going forward. – Franziska