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  1. 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
  2. All, Anyone who has been following discussions around here will realize that I've been criticizing salmon as a healthy food, and Saul has been vehemently defending it, which has lead to some amusing exchanges, e.g. here, here and especially here, where Saul wrote: Well, the evidence just keeps piling up against Saul's sacred cow, er, fish. Background Summary: PCBs are bad sh*t. PCBs (or polychlorinated biphenyls) are man-made organic chemicals widely manufactured and used in a variety of industries, but mostly for cooling and insulating fluid for electrical devices, all over the world up until 1979 when they were banned. Unfortunately, PCBs are very persistent, remaining in the water and soil for many years, and bioaccumulating the in flesh (mostly fat) of animals. Fish, especially fatty fish, seems to be the food in the human diet where the most PCBs bioaccumulate, as illustrated by this graph (data from [2]) of PCB content in 12,000+ food samples from around Europe: Notice that fish oil is off the chart, but people typically only consume a gram or two of FO per day, and this graph represents micrograms per kilograms. Fish itself (all types) was about 5x higher than any other animal products. Fruit, vegetables and cereals had close to zero PCBs. Interestingly though, most exposure in North America comes from beef, dairy and other animal flesh rather than fish, since we eat so much more of them than fish: So how bad are PCBs? Pretty bad across the board, including causing cancer, endocrine disruption, reproductive and neurological effects. See here for more details about all the bad effects PCBs have on human health. With that background, this new study [1] posted by Al (thanks Al!) looked at dietary PCBs levels based on self-reported food-frequency questionnaires from ~36,000 elderly Swedish women, and then followed them for an average of 12 years to see how heart attack risk related to dietary PCB exposure. First, off a helpful chart of demographics of study participants by quartile of dietary PCB intake: As you can see from my highlights, the dietary PCB (and mercury) levels in these women was strongly correlated with fish and long-chain omega-3 intake. Women who ate the most fish had almost 3x the level of PCBs of those who ate the least. So what about heart attacks? Here is what the authors' found: Women in the highest quartile of dietary PCB exposure (median 286 ng/day) had a multivariable-adjusted RR of myocardial infarction of 1.21 (95% confidence interval [CI], 1.01–1.45) compared to the lowest quartile (median 101 ng/day) before, and 1.58 (95% CI, 1.10–2.25) after adjusting for EPA-DHA. Stratification by low and high EPADHA intake, resulted in RRs 2.20 (95% CI, 1.18–4.12) and 1.73 (95% CI, 0.81–3.69), respectively comparing highest PCB tertile with lowest. The intake of dietary EPA-DHA was inversely associated with risk of myocardial infarction after but not before adjusting for dietary PCB. In other words, having the highest intake of PCBs (mostly from fish) was associated with a 21% increase in the risk of heart attack relative to being in the lowest PCB intake group. But it was only a 21% increase because EPA/DHA was pulling the other way, helping to prevent heart attacks. If you statistically factor out the EPA/DHA benefits, PCBs alone would raise heart attack risk by 58% in the top vs. bottom quartile group. Analyzed the other way, EPA/DHA intake wasn't associated with fewer heart attacks, largely because of the PCBs that typically accompany them, it would appear. In fact, those in the highest quartile of DHA/EPA intake had a (non-significant) 11% increase in risk of heart attack. But when they statistically factored out the PCBs, DHA/EPA was (weakly and non-significantly) associated with a 26% reduction in heart attack risk. The relevant data is summarized in this table with my highlights, for anyone who wants to see the details: To summarize, it looks like if you can get DHA/EPA without the accompanying PCBs, it may be a slight win for heart attack risk. But when the DHA/EPA comes as a package deal with PCBs (would you like fries with that?), as it did for these fish-eating Swedish women, it's bad news. And its looks it might be even worse for us skinny folks, since they found: In a stratified analysis, we observed a higher RR [of high dietary PCBs] (2.39; 95% CI, 1.15–4.96) among lean women (waist circumference b80 cm) than among those with abdominal adiposity, however the interaction was not statistically significant (p value = 0.18) and the confidence interval was wide. ... Our results indicate a stronger association between PCB and risk of myocardial infarction among lean women meanwhile no association among women with abdominal adiposity. One likely explanation behind the observation is the higher concentrations of circulating PCBs in blood and lower dilution of PCBs in adipose tissue of lean than of obese woman [22]. Fortunately, it is possible to ensure one gets DHA/EPA without the PCBs, by choosing an algae source of DHA/EPA, like this one, rather than taking one's chances eating fish what one hopes is low in contaminants like PCBs, but which can often be mislabelled. --Dean ------------ [1] Int J Cardiol. 2015 Mar 15;183:242-8. doi: 10.1016/j.ijcard.2015.01.055. Epub 2015 Jan 27. Dietary exposure to polychlorinated biphenyls and risk of myocardial infarction - a population-based prospective cohort study. Bergkvist C(1), Berglund M(2), Glynn A(3), Wolk A(1), Åkesson A(4). Sci-hub.io full text: http://www.sciencedirect.com.sci-hub.io/science/article/pii/S0167527315000820 BACKGROUND: Fish consumption may promote cardiovascular health. The role of major food contaminants, such as polychlorinated biphenyls (PCBs) common in fatty fish, is unclear. We assessed the association between dietary PCB exposure and risk of myocardial infarction taking into account the intake of long-chain omega-3 fish fatty acids. METHODS: In the prospective population-based Swedish Mammography Cohort, 33,446 middle-aged and elderly women, free from cardiovascular disease, cancer and diabetes at baseline (1997) were followed-up for 12 years. Validated estimates of dietary PCB exposure and intake of fish fatty acids (eicosapentaenoic acid and docosahexaenoic acid; EPA-DHA) were obtained via a food frequency questionnaire at baseline. RESULTS: During follow-up 1386 incident cases of myocardial infarction were ascertained through register-linkage. Women in the highest quartile of dietary PCB exposure (median 286 ng/day) had a multivariable-adjusted RR of myocardial infarction of 1.21 (95% confidence interval [CI], 1.01-1.45) compared to the lowest quartile (median 101 ng/day) before, and 1.58 (95% CI, 1.10-2.25) after adjusting for EPA-DHA. Stratification by low and high EPA-DHA intake, resulted in RRs 2.20 (95% CI, 1.18-4.12) and 1.73 (95% CI, 0.81-3.69), respectively comparing highest PCB tertile with lowest. The intake of dietary EPA-DHA was inversely associated with risk of myocardial infarction after but not before adjusting for dietary PCB. CONCLUSION: Exposure to PCBs was associated with increased risk of myocardial infarction, while some beneficial effect was associated with increasing EPA and DHA intake. To increase the net benefits of fish consumption, PCB contamination should be reduced to a minimum. Copyright © 2015 Elsevier Ireland Ltd. All rights reserved. PMID: 25679993 ------------ [2] EFSA Journal 2010; 8(7):1701. [35 pp.]. doi:10.2903/j.efsa.2010.1701. European Food Safety Authority; Results of the monitoring of non dioxin-like PCBs in food and feed. Free Full text: http://www.efsa.europa.eu/sites/default/files/scientific_output/files/main_documents/1701.pdf ABSTRACT Non dioxin-like polychlorinated biphenyls (NDL-PCBs) are persistent organic chemicals that accumulate in the environment and humans and are associated with a broad spectrum of health effects. Processing and distribution of PCBs has been prohibited in almost all industrial countries since the late 1980s but they still can be released into the environment from electrical appliances, building paint and sealants and waste sites that contain PCBs. In 2002 the European Commission prescribed a list of actions to be taken to reduce the presence of dioxins and PCBs in food and feed and Member States were recommended to monitor the situation. A total of 12,563 food and feed samples collected in the period 1995 - 2008 from 18 EU Member States, Iceland and Norway were retained for a detailed analysis of the occurrence of the six indicator NDL-PCBs (# 28, 52, 101, 138, 153, and 180). Overall, 18.8% of the results for single congeners were below the limit of quantification (LOQ) but their distribution varied highly between food and feed groups. PCB-153 and PCB-138 were the most commonly detected congeners. In food, the highest mean contamination level was observed in fish and fish derived products followed by eggs, milk and their products, and meat and meat products from terrestrial animals. The lowest contamination was observed in foods of plant origin. A similar pattern was observed in feed where high contamination was reported in feed containing fish derived products and comparatively very low levels in feed of plant or mineral origin. The sum of the six NDL-PCBs was on average close to five times higher than the sum of the 12 dioxin-like PCBs. This relationship varied across food groups and is presumably related to the origin of samples and the contamination source. Country-specific clustering has been observed in several food and feed groups.
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