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Found 6 results

  1. Todd Allen

    What's Wrong with Eggs Now?!

    [Admin Note: Over on the LDL particle size thread, Todd asked the question of why eggs are bad. Seems like a question that deserves its own thread, given the recent supposed exoneration of dietary cholesterol. So here it is.] The important difference between consumption of dietary cholesterol, which has a negligible influence on heart disease risk, and cholesterol produced endogenously in the body (which can be a marker of risk, depending on a complete profile).... So why exactly is it that eggs are so damn bad? http://www.whfoods.com/genpage.php?tname=foodspice&dbid=92
  2. Now this is pretty weird. on October 15, 2016, I had a glucose + lipid panel done , when I was still a alcto-ovo vegetarian. By chance, I akready had a 12-days cronometer record, so, even if the timespan is not much, I remember it's pretty representative of my diet at the time. Since I recently had another lipid panel done, and since in the meanwhile I turned vegan, a comparison is in order. I compared 12 days lacto-ovo prior to the test to 3 months vegan, prior to the test. The results are a little surprising: Lacto-ovo Glucose: 86 Total cholesterol: 153 HDL : 59 Triglycerides: <70 LDL : 80-90 Vegan Glucose: 83 Total cholesterol: 170 HDL : 65 Triglycerides: 69 LDL : 94 My intake of cholesterol when lacto-ovo was 264 mg per day, whereas as a vegan it was 7 mg per day (the occasional tablespoon of butter on the cookies sometimes I indulge in). So, it appears very weird that, with almost no dietary cholesterol at all, my blood cholesterol increased almost by 20 mg/dl, whereas other values are about the same. Also, as a lacto-ovo I ate a daily average of 39 g saturated fats per day, whereas as a vegan I ate, prior to tests, 21 grams, about a half. As a lacto-ovo I ate 133 grams net carbs, whereas as a vegan 176. But fasting glucose was lower as a vegan than as a lacto-ovo. Another strangeness. As a lacto ovo I ate 250 less kcalories and 32 grams of fiber rather than the vegan 63 daily grams. I mentioned the cholesterol issue to another friend who eats mainly palnt-based. He had his blood tests doen every year and observed that, as soon as he stopped eating cheese, his cholesterol went up. He also told me about another friend who, as soon as started a stint of total fasts, some of which of significant length (10 days) his cholesterol went up. I also asked about my first test who was taken at teh local pharmacy. The pharmacist told me that the test is pretty accurate and that, according to him, cholesterol in the summer season may increase. The paradox remains as why a vegan diet with almost no dietary cholesterol and 63 g daily fibers should result in more blood cholesterol than a lacto-ovo diet with 264 mg cholesterols and 32 g fibers
  3. All, We had a pretty long thread not too long ago about Total Cholesterol and Heart Attack Risk but as far as I can tell we haven't talked much about the relative value of a standard lipid panel vs. some of the newer tests for various LDL particle sizes, densities etc. I bring it up for two reasons: One is personal. A family member in their early 50s is an APOE4 carrier (single allele) and not surprisingly, has borderline high cholesterol (210 mg/dL total, 120 LDL, 55 HDL). They are otherwise thin, active, healthy with good fasting blood glucose. So it seems they are one of those borderline cases for statins, and I'm wondering whether getting their LDL particle sizes tested might provide some additional useful diagnostic information for making that decision. I would lean against starting statins in their case (due to possible side effects see below), but I'm wondering if the discovery that they have many (or very few) small dense LDL particles might tip the scales one way or the other. The second reason I bring it up is because I just listened to a long (1:20:00) but very interesting interview by Dr. Rhonda Patrick with Dr. Ronald Krauss, who appears to be a pioneer in research into cholesterol and CVD, the effects of diet on CVD risk, statin side effects, particle size testing etc. I found it really educational to learn more about the mechanics of atherosclerosis, e.g. the details of how inflammation is involved and why we might have evolved to work that way. How small LDL particles have the part of their surface structure occluded just where the liver's LDL-receptor tries to attach to them, making the small particles harder to clear from the bloodstream, making them stick around in the bloodstream for longer to get oxidized / glycated and to infiltrate the arterial walls. Lots of good stuff I didn't know before. But a couple caveats. I'm not an expert on the details of how atherosclerosis works, or anything about particle sizes, so while I found it interesting, I can't vouch for the validity of Dr. Krauss's perspective or the information he shared. And I will note that Dr. Krauss co-authored with Dr. Patty Siri-Tarino and several others a pretty poor and misleading meta-analysis which appeared to call into question the link between saturated fat and heart disease. Their meta-analysis has been roundly criticized briefly by Michael in this thread and more thoroughly by PlantPositive here. He also mentioned he's been sponsored by the dairy industry, and has a patent and receives royalties on a new cutting edge LDL particle measurement test called Cardio IQ® Lipoprotein Fractionation, Ion Mobility which is now available from Quest. So all that is to meant to suggest that one should take what Dr. Krauss says in this interview with a pretty grain of salt. I'd be curious to hear what anyone with more knowledge in the area has to say about particle size testing, as well as the information Dr. Krauss shares both about the etiology of atherosclerosis and the significance of "small dense" LDL particle count vs the standard LDL measure on a lipid panel, particularly for people with borderline risk of CVD. To his credit, Dr. Krauss acknowledges that particle testing isn't for everyone. People at either extreme (i.e. very low or very high LDL cholesterol) probably don't need it - for obvious and opposite reasons. It's only in the borderline cases, like my family member, where it might be helpful. He also said the standard heart attack risk calculators, which don't take into account anything about particle size, do a pretty good job, and particle size and counts doesn't add very much to their accuracy / predictive power. But he sticks by idea that mechanistically, it's the small dense LDL particles that matter most for CVD risk. He also talks about how statins do work, but don't work as well as you might think because they upregulate the liver's LDL-receptor, which is pretty ineffective at clearly the most atherogenic particles - the small dense ones. He talks about statin side effects (muscle pain / weakness, but especially increased risk of diabetes, particularly in women). He is very much in favor of diet and lifestyle interventions to manage CVD risk, but as a researcher and clinician, he says there is trouble both proving the benefits of diet/lifestyle on CVD risk in clinical trials, and convincing his patients to adopt diet and lifestyle modifications, due both to compliance issues, and also in terms of getting the funding to do the research to make a convincing case. He says it's much easier to both get funding for, and to conduct, research on statins and other pharmacological interventions, because there is money to be made, and compliance is much less of an issue. Whether or not Dr. Krauss is blowing smoke about the value of particle size testing, it seemed to my (admittedly relatively naive) ears that Rhonda had a good set of questions and Dr. Krauss had clear and well thought out set of answers. For anyone interested in the topic, check out the show notes below and give it a watch/listen and let us know what you think. --Dean Begin Show Notes ============== Dr. Ronald Krauss on LDL Cholesterol, Particle Size, Heart Disease & Atherogenic Dyslipidemia In this podcast, I interview my friend and colleague Dr. Ronald Krauss. Ronald Krauss, M.D. is the director of atherosclerosis research at Children’s Hospital Oakland Research Institute, Adjunct Professor at UCSF and UC Berkeley. Dr. Krauss is really one of the pioneering scientists that changed the way we all think about cholesterol and saturated fat. The work of Dr. Krauss has demonstrated that smaller, denser LDL particles, which he pioneered a test for, known as the "Ion Mobility" test, has special significance when it comes to determining risk of heart disease. Regrettably, this test is not yet universally employed in a clinical setting in the manner in which total LDL cholesterol is, however. This test is called Cardio IQ® Lipoprotein Fractionation, Ion Mobility and is offered by quest diagnostics. Dr. Krauss is responsible for having played a part in the actual guidelines used by the American Heart Association in his role as chairman of the Nutrition Committee. Additionally, Dr. Krauss has also served on both the Committee on Dietary Recommended Intakes for Macronutrients and the Committee on Biomarkers of Chronic Disease of the Institute of Medicine of the National Academy of Sciences. In this podcast, Ron and I discuss what HDL and LDL cholesterol are, what they do in the body and how they play a role in heart disease. We talk about what small, dense LDL particles are, how they form, what effect eating saturated fat versus refined carbohydrates have on LDL particle size and heart disease risk and more generally what the main risk factors for heart disease are. Ron also talks about the good, bad and the ugly of LDL-lowering drugs known as statins and much more. In this conversation, Ron and I discuss... Changes in the availability of funding for good nutritional research."It's a fact that NIH, which is the major funder of biomedical research in the world, has basically pulled the plug on clinical research support as a general area of emphasis. The infrastructure for doing good nutritional studies, in particular, has relied on a mechanism that is now being withdrawn." - Dr. Ronald M Krauss The important difference between consumption of dietary cholesterol, which has a negligible influence on heart disease risk, and cholesterol produced endogenously in the body (which can be a marker of risk, depending on a complete profile). The good, bad and the ugly of LDL-lowering drugs known as statins and much more. What differentiates fructose from fruit versus fructose as an added sugar, namely: speed of absorption, presence or absence of other beneficial compounds (fiber, micronutrients, polyphenols, etc.), and differences in dose. How LDL (low-density lipoprotein), and particularly the ApoB protein inside of LDL, is needed to transport cholesterol, triglycerides, and fatty acids throughout the bloodstream in order to deliver them to other tissues in the body that may need them. What small, dense LDL particles are, how they form, what effect eating saturated fat versus refined carbohydrates have on LDL particle size and heart disease risk and more generally what the main risk factors for heart disease are. The functional difference between large, buoyant LDL particles and small, dense LDL particles and introduces us to the traits of what he terms "atherogenic dyslipidemia." These traits consist of: High levels of small, dense LDL cholesterol. Low levels of HDL cholesterol. High levels of triglyceride-rich lipoproteins (very-low-density lipoproteins or "VLDL") and their remnants. How small, dense LDL particles increase the risk of atherosclerosis. There is only one ApoB protein per LDL particle, which is what enables ApoB to be a surrogate blood biomarker for LDL particle number. How access to the ApoB protein can become obscured due to conformation changes in the small, dense LDL particles. As the size of the particle decreases, this conformation change reduces the ability for the particle to bind to the LDL receptor and be recycled by the liver. How VLDL particles, the precursor to LDL, demonstrate an interaction with LPS (also known as endotoxin, a component of bacterial cell membranes), and how it's possible that some of the negative associations with this particle size may be a result of their simply being in the blood stream longer: this gives them a greater opportunity to undergo inflammatory transformations.This part is especially exciting to me because it may be an interesting link by which gut health (where much of the bacteria and immune cells in the body are located) and the importance of controlling inflammation to cardiovascular health. How saturated fat appears to increase the larger, more buoyant LDL particles, which do not have the same robust correlation to heart disease risk that the smaller, more dense particles do. Dr. Krauss also takes the stance that consumption of saturated fat does not have as strong of a link to heart disease risk as previously suggested by others, and may be less relevant except in the case of what he termed "hyper-responders." These "hyper-responders" have gene polymorphisms that cause them to respond differently to saturated fat. How increased carbohydrate consumption, especially simple sugars may have been an unintended consequence of the push for low-fat diets, and how this increased traits associated with atherogenic dyslipidemia: namely, a shift from the larger, more buoyant LDL particles to the smaller, more dense LDL particles. Broadly, the differences between the various types of lipoprotein particles, including very-low-density lipoproteins (VLDL), and high-density lipoprotein (HDL) and what their roles are in the body. This really is one of the better science-based podcasts I've posted to date. It's often a bit nuanced, but hopefully with the help of some of the annotations in the video you will find it as enriching as I have. Dr. Krauss is a real pioneer in the field and drops huge amounts of knowledge, so go check it out now! ============== End Show Notes
  4. Dean Pomerleau

    Total Cholesterol and Heart Attacks

    [Another one for the "non-CR diet and health" forum. If such a forum ever gets created, I promise I'll use my moderator super-powers to move all these threads to the new forum!] Dr. Greger's latest video titled Everything in Moderation? Even Heart Disease? has this interesting graph from [1] of cardiovascular disease and heart attacks as a function of total serum cholesterol level (click to enlarge): It shows that 35 percent of heart attacks occur in people with total serum cholesterol between 150 and 200 mg/dL. I had no idea it was that high. And virtually no heart attacks occur in people with cholesterol below 150 mg/dL, which is why many people (including me) have said it makes you virtually "heart attack proof". But then I started thinking, wait a minute. Couldn't this simply be a reflection of population statistics, and not reflect a causal relationship between cholesterol level and heart attacks? To understand this possibility, consider a similar plot of height vs. # of heart attacks. Assuming heart attacks are totally independent of height, you'd still see a similar bell curve of the number of heart attacks plotted against height, for the simple reason that height is distributed along a bell curve. So 50% of heart attacks would occur in men below the median height of 5'10" in the US, and furthermore only a tiny fraction of heart attacks (~3%) would occur in men shorter than 5'2", which is two standard deviations below the median. Does that mean that having a very short stature makes you heart attack proof? Of course not, it just means that there aren't many men shorter than 5'2" to contribute to the heart attack statistics. As an admirer of both Dr. Greger's work, I am sometimes disappointed when he uses potentially misleading statistics like this one to advance his perspective on diet and health (i.e. the value of following a plant-based diet - which I very much agree with). So what is the more accurate picture of the relationship between cholesterol and heart attack risk? Here is a graph, from [2], which BTW has a very good overview of various blood markers, including cholesterol sub-components and their association with CHD: As you can see from the graph on the right, CHD mortality rate (as opposed to total # of heart attacks) appears to be pretty asymptotic below 200 mg/dL. It's only when you get up to a total cholesterol of about 225 mg/dL that you see CHD mortality rate rising significantly, above which it goes through the roof. This is what's called evidence-based medicine, and it is why the American Heart Association and European equivalent (the European Societies for Cardiology, Hypertension and Diabetes) recommend keeping total cholesterol below 190-200, rather than necessarily trying to push it below 150 using diet or statins. With the latter, you might end up like this guy : So despite what Dr. Greger suggests, keeping one's total cholesterol below 150 mg/dL, as opposed to somewhere in the range of 150-200 mg/dL, doesn't appear to provide a dramatic benefit in terms of heart attack risk. To be fair, Dr. Greger has another video on the optimal cholesterol level for heart health that does seem to get the science better. It ignores total cholesterol level, and instead looks at all the randomized control trials of cholesterol lowering drugs, which suggest that an LDL level below 70 mg/dL (about 1/2 the average LDL level in US adults, 130 mg/dL) does make one virtually "heart attack proof". But then again, the relevance of results from people who are taking statins, not to mention the relevance for us of statin-induced LDL reduction or other positive effects of statins, make it far from certain that these results apply to people keeping LDL cholesterol low through diet and lifestyle choices. --Dean --------------- [1] Atherosclerosis. 1996 Jul;124 Suppl:S1-9. Lipids, risk factors and ischaemic heart disease. Castelli WP(1). Author information: (1)Framingham Cardiovascular Institute, MA 01701-9167, USA. Over 200 risk factors for cardiovascular disease (CVD) have now been identified. Among these, the three most important are (1) abnormal lipids, including the fact that there are more than 15 types of cholesterol-containing lipoproteins and four different types of triglyceride-rich particles, some of which are very atherogenic, (2) high blood pressure, and (3) cigarette smoking. In addition, many other factors including diabetes, haemostatic factors such as fibrinogen, factor VII, plasminogen activator inhibitors, and new factors such as apolipoprotein E4 and homocysteine, are known to increase the risk of developing clinical CVD. A low risk for CVD requires that these various factors are present in the circulation in the correct proportions. Two simple tests for determining plasma lipid levels can be used to identify those individuals with an atherogenic lipid profile and who are, therefore, at increased risk for CVD. Firstly, the ratio of total cholesterol to high density cholesterol (HDL cholesterol) should be determined, followed by measurement of plasma triglyceride concentrations. This will allow differentiation of whether the low density lipoproteins (LDL), HDL cholesterol or triglyceride-rich particles such as the small dense beta-very low density lipoproteins (VLDL) are the major cause for concern. Once identified, those individuals with a high lipid risk profile should be treated before, rather than after, experiencing coronary heart disease (CHD). PMID: 8831910 ------------------- [2] The Journal of the International Federation of Clinical Chemistry and Laboratory Medicine Vol 13:2 (2003) THE ROLE OF LIPIDS IN THE DEVELOPMENT OF ATHEROSCLEROSIS AND CORONARY HEART DISEASE: GUIDELINES FOR DIAGNOSIS AND TREATMENT Victor Blaton Department of Clinical Chemistry, Hospital AZ Sint-Jan AV, Brugge, Belgium pdf: http://www.ifcc.org/ifccfiles/docs/140206200306.pdf
  5. All, Al Pater posted a study [1] that compared the effects on biomarkers of health for various types of vegetarian diets vs. omnivores in a group of Taiwanese men and women of all ages. The study divided subjects into four groups: vegan, lacto-vegetarians, ovo-lacto-vegetarians, and omnivores, as ascertained via a 26 element food frequency questionnaire, and explicit questions about how they self-classify their diet. They matched each of the 10,000 vegetarians in the study with five omnivores of the same age and sex. Here are the main findings comparing all the vegetarians as a group against the omnivores: With adjustment for age, sex, physical activities, alcohol consumption and education, vegetarians had significantly lower abnormalities [i.e. values in the unhealthy range as defined by health authorities - DP] in WC [Waist Circumference], BMI, SBP [systolic BP] DBP [Diastolic BP], FBG [Fasting Blood Glucose],TC [Total Cholesterol] and LDL as well as in TC:HDL ratios, with OR ranging from 0·37 to 0·90, but higher abnormality in HDL [i.e. low HDL] (OR ranged from 1·17 to 1·52), when compared with non-vegetarians cross-sectionally. <snip> Overall, we observed lower values for WC, BMI, SBP, DBP, FBG, TC, HDL and LDL, along with lower TC:HDL ratios, in vegetarians compared with non-vegetarians, which replicated the findings of previous Taiwanese studies(9,22,23). Except for [lower] HDL and [higher] TAG [triglycerides] values in lacto-ovo-vegetarians [only], the vegetarian diets showed significant beneficial effects on metabolic traits, which may be partly due to the lower BMI of vegetarians. <snip> With additional adjustment for BMI (Table 3), the beneficial effects for blood pressure and blood glucose were partly attenuated, whereas the effect on lipids remained consistent. <snip> Lacto-ovo-vegetarians appeared to eat more carbohydrates and fructose, which could be one of the main causes for TAG elevation in this group. <snip> Whether the lower HDL in vegetarians can be regarded as a risk factor may require further study, as vegetarians generally had better TC:HDL ratios. In addition, previous studies have found that low HDL due to reduced fat intake was not associated with poor cardiovascular health(25,26). Strangely, they apparently didn't ask the subject about smoking habits, and therefore didn't control for it. Here are the two main tables of results comparing the various types of vegetarians to the omnivores (click to enlarge): They also tried doing a longitudinal analysis of the data, but the results weren't too informative, and for most of the subjects (63%) they only had one (baseline) measurement. Most of the baseline differences remained significant and mostly improved for those people who remained vegetarians at follow-up visits. Comparing the various types of vegetarians vs. omnivores, it appears that lacto- and lacto-ovo-vegetarians had a slight advantage over vegans across most of the health markers when compared with omnivores, both before and after adjusting for BMI (see Tables 2 and 3 above). Besides the obvious difference between consumption of eggs and dairy, the biggest difference in the vegan food intakes relative to the other two vegetarian groups were they consumed less beans, less "sweet breads" and less fried vegetables. Perhaps a poorer B12 status or lower bean intake could explain the less advantageous health markers of the vegans vs. the other two types of vegetarians (but all three vegetarian types were better than omnivores). So overall, vegetarians of all types appeared to do better compared with omnivores in all of the commonly acknowledged biomarkers markers of health, except for lower HDL and higher triglycerides among the lacto-ovo-vegetarians. This is pretty much consistent with previous studies, such as the Epic Oxford and Seventh Day Adventists. --Dean --------- [1] Br J Nutr. 2015 Oct;114(8):1313-20. doi: 10.1017/S0007114515002937. Epub 2015 Sep 10. Cross-sectional and longitudinal comparisons of metabolic profiles between vegetarian and non-vegetarian subjects: a matched cohort study. Chiu YF(1), Hsu CC(1), Chiu TH(2), Lee CY(1), Liu TT(3), Tsao CK(3), Chuang SC(1), Hsiung CA(1). Several previous cross-sectional studies have shown that vegetarians have a better metabolic profile than non-vegetarians, suggesting that a vegetarian dietary pattern may help prevent chronic degenerative diseases. However, longitudinal studies on the impact of vegetarian diets on metabolic traits are scarce. We studied how several sub-types of vegetarian diets affect metabolic traits, including waist circumference, BMI, systolic blood pressure (SBP), diastolic blood pressure, fasting blood glucose, total cholesterol (TC), HDL, LDL, TAG and TC:HDL ratio, through both cross-sectional and longitudinal study designs. The study used the MJ Health Screening database, with data collected from 1994 to 2008 in Taiwan, which included 4415 lacto-ovo-vegetarians, 1855 lacto-vegetarians and 1913 vegans; each vegetarian was matched with five non-vegetarians based on age, sex and study site. In the longitudinal follow-up, each additional year of vegan diet lowered the risk of obesity by 7 % (95 % CI 0·88, 0·99), whereas each additional year of lacto-vegetarian diet lowered the risk of elevated SBP by 8 % (95 % CI 0·85, 0·99) and elevated glucose by 7 % (95 % CI 0·87, 0·99), and each additional year of ovo-lacto-vegetarian diet increased abnormal HDL by 7 % (95 % CI 1·03, 1·12), compared with non-vegetarians. In the cross-sectional comparisons, all sub-types of vegetarians had lower likelihoods of abnormalities compared with non-vegetarians on all metabolic traits (P<0·001 for all comparisons), except for HDL and TAG. The better metabolic profile in vegetarians is partially attributable to lower BMI. With proper management of TAG and HDL, along with caution about the intake of refined carbohydrates and fructose, a plant-based diet may benefit all aspects of the metabolic profile. PMID: 26355190
  6. All, Here is a short video (1:30) and a longer one (13min) profiling a Ellsworth Wareham, 100-year vegan man who appears to be still going strong, both physically and mentally. He was a heart surgeon who didn't retire until 95. He is (not surprisingly) one of those long-lived, clean-living Seventh Day Adventists from Loma Linda California. He attributes his longevity to his low-fat vegan diet (which he adopted ~50 years ago) and his ability to avoid stress. His total cholesterol is 117, which he says makes him very unlikely to develop heart disease. He now sees it as his mission to educate people about preventative medicine. Here is his wikipedia page for more information. He is quite an inspiration and the kind of person I think CR practitioners should aspire too! --Dean