Podcasts about lp pla2

I am excited to share our fourth class in our informative Lipid Masterclass series today, with the esteemed Dr. Thomas Dayspring. Dr. Dayspring is certified in internal medicine and clinical lipidology and is a distinguished fellow of the American College of Physicians and the National Lipid Association. He brings a wealth of expertise to our discussion today. In this class, we dive into lipid and lipoprotein dynamics during the menopausal transition, exploring the impact of estrogen on gut health and its effects on laboratory findings. We look at the differences between hyper absorbers and hyper synthesizers, sharing clinical insights on routine lipid panels that can let you know if you are one of those individuals. We talk about Boston Heart Testing, highlighting the impact of specific biomarkers on brain health lipids and lipoproteins, and we get into the staggering differences between the half-lives of peripheral cholesterol and brain cholesterol. We discuss lipid permeability across the blood-brain barrier, highlighting those at risk for brain health concerns as they age, and we reveal strategies for managing lipid abnormalities. We also focus on LP(a), an ApoB lipoprotein with potent atherogenic and thrombotic properties, and its implications regarding calcific aortic stenosis.  I am sure you will find this enlightening conversation with Dr. Dayspring invaluable. There is one more class yet to come in this masterclass series. Be sure to listen in! IN THIS EPISODE YOU WILL LEARN: How cholesterol absorption in the gut increases in perimenopausal women How hyper cholesterol absorbers tend to have elevated HDL cholesterol The impact of phytosterols on cholesterol absorption When should hyperabsorbers consider treatment? What research has shown regarding the differing effects of estrogen on brain health for older versus younger menopausal women What happens if a statin crosses the blood-brain barrier? How cholesterol synthesis relates to cognitive impairment  The importance of understanding LP-PLA2 test results How Lp(a) levels in women tend to fluctuate, particularly during menopause Should women with heart disease consider hormone replacement therapy?   Bio: Thomas Dayspring MD is a Fellow of the American College of Physicians and the National Lipid Association certified in internal medicine and clinical lipidology. After practicing in New Jersey for 37 years, in 2012, he moved to Virginia to serve as an educational director for a nonprofit cardiovascular foundation until mid-2019 as a Chief Academic Advisor for two major CV laboratories. Since then, he has served as a virtual cardiovascular / lipidology educator. Career-wise, he has given over 4000 domestic (in all 50 states) and several international lectures, including over 600 CME programs on atherothrombosis, lipids/lipoproteins (and their treatment), vascular biology, biomarker testing, and women's cardiovascular issues. He has authored several manuscripts and lipid textbook chapters and performed several podcasts. For several years, he was an Associate Editor of the Journal of Clinical Lipidology. He received the 2011 National Lipid Association's Presidents Award for services to clinical lipidology and the 2023 Foundation of NLA Clinician/Educator Award. He has over 34K followers on his educational Twitter (X) feed (@Drlipid). He has Gold Heart Member status as a professional member of the American Heart Association, and he serves as a Social Media Ambassador for the European Atherosclerosis Society and the National Lipid Association. Connect with Cynthia Thurlow Follow on Twitter Instagram LinkedIn Check out Cynthia's website Submit your questions to support@cynthiathurlow.com Connect with Dr. Thomas Dayspring On Twitter (@DrLipid) On LinkedIn

In this video, I'm going to share what you can do to help remove plaque from your arteries naturally. Plaque is made of cholesterol, calcium, and protein. These 3 ingredients form a band-aid if you have inflammation or other issues on the inside of your artery. There are 2 types of plaque: soft plaque (unstable, dangerous) and hard plaque (calcified, stable, less dangerous). Soft plaque is 4 times as common as calcified plaque! A CAC test gives you a score of how much plaque you have in your arteries. This test primarily detects calcified plaque, so the score usually won't reflect soft plaque. The CAC paradox is a phenomenon that occurs after you clean up your diet and get healthy, but your CAC score rises. This doesn't mean your plaque is getting worse. It means that some of your soft plaque has stabilized and become hard plaque. Soft plaque is associated with glycation and more oxidation of the LDL. There are 2 types of LDL: small-dense pathogenic LDL and large-buoyant non-pathogenic LDL. Myeloperoxidase and Lp-PLA2 both signify soft plaque on a blood test. An ultrasound can also detect soft plaque. Higher HDL can help clean up pathogenic bad LDL. You also want to keep your triglycerides low. High triglycerides can signify that your diet is too high in carbs. You may want to request to test your lipoprotein insulin resistance. This factor is associated with cardiovascular atherosclerosis more than any other. Here's how to determine whether you have small dense LDL or large buoyant LDL. Divide the LDL by ApoB—the part of the lipoprotein that indicates the number of particles. You want your result to be greater than 1.2. This indicates large buoyant LDL. The following nutrients may help remove arterial plaque buildup naturally: 1. Pycnogenol–150 mg 2. Gotu Kola–450 mg 3. Vitamin K2–Life Extension Mega K2 4. Nattokinase 5. Niacin Vitamin K2 is the most potent inhibitor of vascular calcification. Tocotrienols, berberine, aged garlic, magnesium, potassium, and vitamin D also help to clean out plaque naturally. Life Extension (Mega K2): https://www.lifeextension.com/vitamin... DATA: https://www.ncbi.nlm.nih.gov/pmc/arti... https://www.ncbi.nlm.nih.gov/pmc/arti...

I'm excited to welcome back Dr Paul Anderson as we discuss the ins and outs of cholesterol and lipid labs. Understand what these numbers really mean for your health and how they can guide your wellness journey.   Dr. Anderson is an esteemed educator and clinician in integrative and naturopathic medicine, focusing on complex infectious, chronic, and oncologic illnesses. With over three decades of clinical experience.  He founded Advanced Medical Therapies in Seattle, Washington, for cancer and chronic diseases and still collaborated with various clinics and hospitals.  held positions at multiple medical schools, including Professor of Pharmacology and Clinical Medicine at Bastyr University. He has authored several books and articles and is actively involved in continuing medical education through online platforms and conferences.    In Part 1 we are discussing the following topics and more: Understanding the Basic Cholesterol Panel  Good vs. Bad Cholesterol The importance of LDL-P  Why do we need to fast for cholesterol labs? Why aren't detailed cholesterol labs ran on every patient?  Why is OxLDL important?   What is Lp-PLA2 and Lp(a)?   As always, thanks for watching and listening!   *****Connect with Dr. Anderson: https://dranow.com/ and on Instagram: @draonline   *****Click here to subscribe to my channel:   https://www.youtube.com/channel/UCM2Jjqb7MqtZ7VDIuRjguLA/?sub_confirmation=1     *****Connect with me on Instagram: https://www.instagram.com/doctorjones_doctorjones/  

This episode is my response to Layne's video about seed oils. Due to the pervasive mainstream support for seed oils, I believe it's extremely important to shed some light on the hidden truth behind these oils. There is a lot of conflicting evidence on seed oils out there. Looking at the totality of the evidence can be very misleading, so we must look at the details. By thoroughly breaking down each trial from Layne's video, we can see massive flaws in the methods and designs of each study. Trans fat consumption by the control group and multifactorial interventions in the experimental group were the primary confounding variables. In this video, Paul references several studies suggesting different ways in which seed oils are harmful to humans. He always appreciate differing views and these discussions because it's how we all learn. He has hope that a respectful debate will happen in the future so that we can dive deeper into this important subject. He strongly believe that seed oils are evolutionarily inconsistent, these are not the fats that humans have evolved on. In fact, we have evolved by consuming ample amounts of animal fats, rich in saturated fats. Saturated fats have been shown to lower markers of heart disease and they are an amazing source of essential vitamins like A, D3, K2, E. It's always meat / organs / fruit / honey / raw dairy. This is an ANIMAL-BASED diet, and I believe this is the most optimal diet for humans on the planet. Check out my ANIMAL-BASED CALCULATOR here: https://www.paulsaladinomd.co/ab-guide Listen on YouTube: https://www.youtube.com/watch?v=8QhWNBXamCM&t=1s Sign-up for Animal Based 30: https://heartandsoil.co/animalbased30/ 00:00 Intro 02:57 Randomized controlled trials in humans 03:47 Flaws found in the studies 04:42 Reviewing each trial 16:10 What's the takeaway 19:45 Studies against seed oils 26:30 Toxic compounds in seed oils 27:32 Responding to Layne's claims 36:10 Closing thoughts References: Meta-analysis of RCT by C. Ramsden - https://www.ncbi.nlm.nih.gov/pmc/arti... Meta-analysis of RCT by S. Hamley - https://www.ncbi.nlm.nih.gov/pmc/arti... PUFA increases lipid peroxidation - https://www.ncbi.nlm.nih.gov/pmc/arti... Linoleic acid metabolites in metabolic syndromes - https://www.ncbi.nlm.nih.gov/pmc/arti... Lower saturated fat increases oxidized LDL - https://pubmed.ncbi.nlm.nih.gov/14739... More linoleic acid increases oxidized LDL - https://pubmed.ncbi.nlm.nih.gov/9488997/ OXLAMs in atherosclerosis - https://www.ncbi.nlm.nih.gov/pmc/arti... Oxidized LDL and metabolic syndrome - https://pubmed.ncbi.nlm.nih.gov/19802... De novo lipogenis through oxidized LDL and linoleic acid - https://pubmed.ncbi.nlm.nih.gov/27020... Lower linoleic acid reduces oxidized metabolites - https://www.ncbi.nlm.nih.gov/pmc/arti... Soybean oil increase Lp-PLA2 and oxidized LDL - https://pubmed.ncbi.nlm.nih.gov/28503... Saturated fat lowers Lp(a) - https://pubmed.ncbi.nlm.nih.gov/9327759/ Benzene in seed oils - https://pubmed.ncbi.nlm.nih.gov/11064... Heavy metals in seed oils - https://www.mdpi.com/2076-3417/13/5/3020 Phthalates in seed oils - https://pubmed.ncbi.nlm.nih.gov/37726...

This week on ReInvent Healthcare, I have a very special guest, Dr. Ellie Campbell, and together we go over the connection between oral care and the risk of cardiovascular disease. We also go over the tests that can be done as well as signs to watch out for when it comes to assessing clients who are showing symptoms or are at risk. .Dr. Ellie Campbell is a functional medicine doctor who specializes in cardiovascular disease prevention and hypertension. She is also the author of The Blood Pressure Blueprint which is a holistic guide to tackle hypertension. IN THIS EPISODE:Oral Health and Cardiovascular DiseaseOral care can significantly impact cardiovascular disease through a complex interplay of factors. Poor oral hygiene and gum disease can lead to chronic inflammation in the mouth, which may release inflammatory molecules into the bloodstream. Harmful bacteria from the mouth can also enter the bloodstream, potentially contributing to the formation of arterial plaque and triggering immune responsesThe body's immune response to oral infections can lead to increased production of white blood cells and inflammatory markers, promoting atherosclerosis and clot formation. Also, oral health can influence existing cardiovascular conditions, such as increasing the risk of bacterial endocarditis in individuals with heart valve issues. That is why maintaining good oral hygiene and addressing oral health concerns can play a crucial role in reducing the risk of cardiovascular disease.Importance of BiomarkersBiomarkers play a vital role in understanding the relationship between oral care and cardiovascular disease. These biomarkers provide measurable indicators of the body's response to oral health and can help identify potential risks and underlying mechanisms.Some biomarkers to take note of are Lp-PLA2 as well as Myeloperoxidase. These biomarkers can provide clues to the presence of dental infections and inflammation.Collaboration between Medical and Dental PractitionersIn order to address the oral-systemic connection, there is a need for a collaboration between medical doctors and dentists. By working together, we can identify and treat dental conditions that may contribute to cardiovascular risk and improve the overall health of our clients. Dr. Ellie Campbell LinksGrab a copy of Dr. Ellie Campbell's book here.Visit Dr. Ellie Campbell's website here.Learn about the Campbell Family Medicine group here. Follow Dr. Ellie Campbell on Facebook here. Check out the Campbell Family Medicine Facebook page here.ReInvent Healthcare Links Get our FREE Guide to Taking a Detailed Health History that gets you to root causes.Access Additional Resources for Practitioners ready to improve clinical outcomes through our Nutritional Endocrinology Practitioner...

Buck and Alan Viglione, MD discuss the Cardio IQ® report in detail and battle it out to see has the best numbers in this 2 part episode. Part 2 will drop as Episode 22. 0:01:31 - What exactly is a Cardio IQ? 0:03:15 - the cost of Cardio IQ 0:05:18 -Lipid panel, Total Cholesterol, HDL, Triglycerides, LDL Cholesterol 0:08:29 - HDL the so-called good cholesterol 0:13:55 - Lipoproteins 0:15:42 - LDL Particle Number 0:22:46 - Apolipoproteins 0:25:40 - Apolyte protein tag 0:27:48 - Apolipoprotein B or apoB 0:28:31 - Lipoprotein(a) or Lp(a) 0:31:41 - Statins: Crestor and Livalo 0:32:41 - How do Statins work? 0:33:11 - Repatha 0:36:58 - Inflammation and Atherogenesis 0:39:39 - High-sensitivity C-reactive protein (hsCRP) 0:40:43 - Lp-PLA2 activity  0:41:43 - Oxidative LDL 0:42:04 - Myeloperoxidase enzyme 0:45:07 - F2-isoprostanes as a marker of risk

This week, Paul interviews board certified cardiologist, Michael Twyman. Michael comments on Paul's blood lipids and they both chat about apoB, cardiovascular risks, oxidized LDL, and, of course, seed oils. They both share what they believe the true indicators of cardiovascular risk really are, aside from LDL.  A note from Paul: Throughout my training and practice as a physician I have come to one very disappointing conclusion:  Western medicine isn't helping people lead better lives. Now that I've realized this, I've become obsessed with understanding what makes us healthy or ill. I want to live the best life I can and I want to be able to share this knowledge with others so that they can do the same. This podcast is the result of my relentless search to understand the roots of chronic disease. If you want to know how to live the most radical life possible I hope you'll join me on this journey. Time Stamps: 00:01:25 Podcast begins 00:04:15 Interpreting Paul's labs 00:10:05 ApoB particles & atherosclerosis/endothelial dysfunction 00:27:09 The insulin resistance pandemic 00:30:49 Do we all need Statins? 00:36:59 Integrative cardiology 00:40:24 The importance of nitric oxide 00:45:39 The problems with glyphosate 00:47:20 Thoughts on seed oils 00:56:39 Lp-PLA2 test 00:58:39 Lipoprotein (a) & endothelial dysfunction 01:11:59 Mitochondrial health 01:16:21 How to take care of our hearts Connect with Dr. Twyman: @drtwyman on Instagram drtwyman.com Sponsors: Heart & Soil: www.heartandsoil.co Carnivore MD Merch: www.kaleisbullshit.shop Make a donation to the Animal Based Nutritional Research Foundation: abnrf.org  White Oak Pastures: www.whiteoakpastures.com, use code CarnivoreMD for 10% off your first order or Carnivore5 for 5% off subsequent orders Marek Health: marekhealth.com/fundamentalhealth, use code PAUL for 10% off your first lab order Colima Salt: drpaulsalt.com, for a free bag of Colima Sea Salt Our Sponsor LetsGetChecked: 20% off your order at www.TRYLGC.com/paulsaladino for 25% off   

This week, please join authors Paul Ridker and Eric Van Belle, editorialist Robert Harrington, and Guest Editor Allan Jaffe as they discuss the original research articles "Effects of Randomized Treatment With Icosapent Ethyl and a Mineral Oil Comparator on Interleukin-1β, Interleukin-6, C-Reactive Protein, Oxidized Low-Density Lipoprotein Cholesterol, Homocysteine, Lipoprotein(a), and Lipoprotein Associated Phospholipase A2: A REDUCE-IT Biomarker Substudy" and “Cerebral Microbleeds During Transcatheter Aortic Valve Replacement: A Prospective Magnetic Resonance Imaging Cohort” and the editorial "Trials and Tribulations of Randomized Clinical Trials." Dr. Carolyn Lam:             Welcome to Circulation on the Run, your weekly podcast summary and backstage pass to the Journal and its editors. We're your co-hosts. I'm Dr. Carolyn Lam, Associate Editor from the National Heart Center, and Duke National University of Singapore. Dr. Greg Hundley:           And I'm Dr. Greg Hundley, Associate Editor, Director of the Pauley Heart Center at VCU Health in Richmond, Virginia. Dr. Carolyn Lam:             It's double feature time Greg. We've got two totally unique and interesting papers that we'll be discussing. The first, a biomarker substudy from the REDUCE-IT trial, that is looking at the effects of randomized treatment with icosapent ethyl, versus a mineral oil comparator, on inflammatory biomarkers. Now, don't use roll your eyes at me, because I'm telling you, this has results that you may not expect, and very, very important clinical implications, and implications for clinical trials. The second paper, very much up your alley, Greg, is a prospective MRI study of cerebral microbleeds during TAVR. But okay, enough now to whet your appetite, let's now just first grab coffees, and discuss the other papers and the issue, shall we? Dr. Greg Hundley:           You bet, Carolyn. And how about if I go first? Dr. Carolyn Lam:             Please. Dr. Greg Hundley:           So, Carolyn, my first paper comes from a group of investigators led by Dr. Araz Rawshani from the Institute of Medicine, and it included 715,143 patients with diabetes, registered in the Swedish National Diabetes Register, and compared them with over two million match controls, randomly selected from the general population, to determine the role of diabetes in the development of valvular heart disease, and particularly, the relation with risk factor control. Dr. Carolyn Lam:             Huh? Interesting, diabetes and valve disease. All right. What did they find, Greg? Dr. Greg Hundley:           Right, Carolyn. So they found, that individuals with type one and two diabetes, have greater risk for stenotic lesions. Whereas, risk for valvular regurgitation was lower in type two diabetes. Patients with well controlled cardiovascular risk factors, continued to display higher risk for valvular stenosis, without a clear stepwise decrease in risk between various degrees of risk factor control. So Carolyn, diabetes and a link with valvular heart disease. Dr. Carolyn Lam:             Wow. Really interesting, Greg. Thanks. Well, the next paper is a preclinical study with really interesting clinical implications. Now, we know the human heart has limited capacity to regenerate new cardiomyocytes, and that this capacity declines with age. Now, because loss of cardiomyocytes may contribute to heart failure, it is important to explore how stimulating endogenous cardiac regeneration, to favorably shift the balance between loss of cardiomyocytes and birth of new cardiomyocytes, occurs in the aged heart. Now, these authors, Doctors Rosenzweig, from Massachusetts General Hospital, and Dr. Lee from Harvard University and colleagues, previously showed that cardiomyogenesis can be activated by, guess what? Exercise in the young adult mouse heart. However, whether exercise also induces cardiomyogenesis in aged hearts, however, is not yet known. So in today's paper, the authors aim to investigate the effect of exercise on generation of new cardiomyocytes in the aged heart. And here, we're talking about 20 month old mice, who were subjected to an eight week voluntary running protocol, and age matched sedentary animals who served as controls. Dr. Greg Hundley:           Wow, Carolyn. Really interesting evaluation of exercise on cardiomyogenesis. So what did they find? Dr. Carolyn Lam:             Endogenous cardiomyogenesis can be stimulated by exercise in aged hearts. Comparative global transcriptional analysis further revealed, that exercise and age specific changes occurred in gene programs. The regulator of calcineurin RCAN1.4 was specifically found to be induced with exercise in aged hearts, and was accompanied by reduced calcineurin activity. So what's a take-home message? Exercise induced cardiomyogenesis may counter the increased cardiomyocyte loss and reduced cardio myogenic capacity in elderly patients. Dr. Greg Hundley:           Great, Carolyn. Well from the mail bag, there's an exchange of letters to the editor from Professor Zhou and Veith regarding a prior letter to the editor from Professor Jin and associates, pertaining to the previously published article “SPARC, A Novel Regulator of Vascular Cell Function in Pulmonary Hypertension.” And also, there's a Perspective piece, from Professor Mentz entitled, “Catastrophic Disruptions in Clinical Trials.” Dr. Carolyn Lam:             There's also a Research Letter by Dr. Kumar on [entitled] “von Willebrand Factor Is Produced Exclusively by Endothelium, Not Neointima, in Occlusive Vascular Lesions in Both Pulmonary Hypertension and Atherosclerosis.” There's also this beautiful tour of Cardiology News from the literature, from Tracy Hampton, which ranges from a study linking COVID-19 to higher long term cardiovascular risks, which was published in Nature Med, to uncovering alternative metabolic pathways involving cell fate transitions, published in Nature, to designing an autonomous biohybrid fish, from human stem cell derived cardiac muscle cells, that was published in Science. Wow. Isn't that amazing, Greg? Well, let's get on now though, to our two feature papers. Shall we? Dr. Greg Hundley:           You bet. Welcome listeners, to these two feature discussions on this particular day. And our first feature today, we have with us Dr. Paul Ridker, from Brigham and Women's Hospital in Boston, Massachusetts. Dr. Bob Harrington, from Stanford University in California. And also, Dr. Allan Jaffe, from Rochester, Minnesota. Welcome to you all. And Paul, we're going to start for you. Can you describe for us, the background information that really went into the construct of your study, and what was the hypothesis that you wanted to address? Dr. Paul Ridker: Sure, Greg. So first of all, my thanks to the AHA and the Circulation for publishing this paper, we always want to support the AHA, and we're delighted to be here today for these podcasts. The field of omega-3 fatty acids has been a complicated one for a long time. Epidemiology suggested that, fish consumption would lower cardiovascular risk, and there was a number of trials done. And my friend and colleague here at the Brigham, Deepak Bhatt, was the lead of a very big trial, called REDUCE-IT. Some 8,000 plus patients who received EPA alone, and they got a terrific result. A 25% reduction in their primary endpoint. And this was a New England Journal paper, back in 2019 or so. But another friend of mine, Steve Nicholls, ran another large trial of a combination of eicosapentaenoic acid, or EPA, plus docosahexaenoic acid that's DHA called STRENGTH. And that one showed, really, no benefit. And so, there's been some controversy out there. In any event, when Deepak and his colleagues published their original paper, they said it's interesting, because they got this big risk reduction, but it wasn't apparently due to the triglyceride lowering of the drug. And so, my interest, as many people know, has largely been in inflammation biology. And so we said, well maybe we should just do a test. Well, we said, we'll measure a number of biomarkers that we know were associated with atherosclerosis, some inflammatory, some with coagulation. And so, that was the core hypothesis, was simply to look at some other markers, and see what we might learn. And sometimes, you learn things that you didn't expect. And I think, that goes to the heart of what complicated clinical trials are all about. And I'd also say perhaps, what the roles of surrogate endpoints are, as compared to hard clinical endpoints, and things that make this whole field kind of interesting. Dr. Greg Hundley:           Right. Very nice, Paul. So you mentioned REDUCE-IT, so describe a little bit more for your study. What was the study population, and what was your study design? Dr. Paul Ridker: We were fortunate enough to work with REDUCE-IT investigators, to use their biobank. They had put together, again, it's 8,000 plus patients. I think, it was two thirds secondary prevention, one third primary prevention. And when they received the combination of EPA and DHA, as I said earlier, they had about a 25% reduction in the risk of their primary endpoint, which was cardiovascular death, nonfatal AMI, nonfatal stroke, coronary revascularization, and the like. What we did is, we basically said, "Okay, since the mechanism was uncertain, why don't we go ahead and measure a series of biomarkers?" Things that a lot of us are interested in, homocysteine, LPLa, oxidized LDL, my own interest in inflammation. We measured, IL-1β, we measured, IL-6, we measured CRP. We measured another molecule, Lp-PLA2, that people have been interested in. And the hypothesis, of course, was to see what the drug did, as compared to the comparator did. And the findings were interesting to us, in that, to simplify them, the actual icosapent ethyl arm didn't do much to most of those biomarkers, very little change. But the mineral oil comparator arm had some small to modest effects on all those biomarkers, all of which went up again. Now, some of these effects are pretty small, two to 3% for things homocystine, LPLa. Others were moderate, 10 to 20% increases in oxidized LDL, Lp-PLA2. And the inflammatory markers went up about 25%, sometimes, even a little more. So it's complicated. It's important to point out, that these changes on an absolute scale are relatively small. On a percent scale, they're different. The REDUCE-IT investigators themselves, to their credit, had earlier published that, they saw some increase in LDL cholesterol as well, about 10, 11% in those who had received the mineral oil comparator. So it's not exactly what we thought we were going to find, I guess, is the simplest way to express it. Dr. Greg Hundley:           Very nice. And so, describe for us just a little bit more, any differences in men and women, and what about age? Or for example, premenopausal, postmenopausal women. Dr. Paul Ridker: No, the effects were quite consistent across all various subgroups. It's a very large study. There were, again, 8,000 patients, lots of blood samples been drawn. And I should again, commend the REDUCE-IT investigators, for allowing us to do this work with them. And again, as I point out, sometimes you find things out that weren't what you expected. And the hard part, I was glad this got tossed over with Dr. Harrington, is sort to figure out well, what's it really mean? Because again, as a clinical trial list, I will say, my instincts are to trust the primary endpoint of the trial. That's what they did. They're going to go out and lower heart attacks and strokes. And then, here we are a couple years later, trying to figure out what the mechanism might be, and just came across some puzzling results. Dr. Greg Hundley:           Very nice. Well, next listeners, we're going to turn to the editor that actually processed this manuscript, Dr. Allan Jaffe. Allan, what drew you to this particular article? Dr. Allan Jaffe:   Well, I was asked to be a guest editor this week, by the Journal, because of some conflicts that were intrinsic to the editorial board. And since I have an interest in biomarkers, and had for a long time, it made perfect sense for me to become involved. I was particularly interested in this particular area, because I was aware that there were these two trials that had found different endpoints, and that there were some controversy as to what the mechanisms might be by which these effects could occur. And so I was pleased to get involved. And I think it's a compliment to the REDUCE-IT investigators, and to Dr. Ridker, that they were willing to put the data out there so that everybody could see it. And we could then begin to look. So it was of interest to me. I thought it was important to the field, to get really good reviewers who would be, make sure that the data that would eventually be published was clear, so that readers would understand it. And so that, at the end, we'd be able to at least, come to some conclusions that we could end up having an expert in clinical trials. And I thought about Bob Harrington, right from the beginning, might be able to comment on. Dr. Greg Hundley:           Very nice. Well, Bob he's setting you up here nicely, both Paul and Allan, to really help us put these results in perspective with other studies that have been performed in this space. What are your thoughts? Dr. Robert Harrington:   So first off, Greg, thanks for having me. And Allan, thanks for inviting me to review and comment on the paper. As both Allan and Paul have indicated, that I've spent the last 30 plus years doing clinical trials of all sizes. Very small, where we try to understand mechanisms, and very large, where what we're trying to understand is clinical outcomes. And I've been intrigued in this field, because of the inconsistency of the data across the field. Where in some trials, Paul had indicated this STRENGTH, there seemed to be no effect of omega-3 fatty acids, and in REDUCE-IT, there was quite a pronounced effect of the test agent. And so, when one sees discordance in a field, one tries to understand, well, why might that be? And so in the editorial, I took the position that, well, what are we trying to do in clinical trials? And in outcomes trials, we're trying to figure out what matters to patients. Do they live longer? Do they feel better? Do they avoid bad stuff happening to them? Like having to undergo revascularization procedure. So you're trying to do things that are really clinically meaningful, but that doesn't say that you're also not trying to understand mechanism. And as Allan said, there have been some questions raised. And so, trying to understand mechanism in the edit in trials can be quite useful, not just to understand that trial results, but to really form hypothesis for a field going forward. And so, I took the approach of, we learn things from different trials, and sometimes we learn things in the same trial. Meaning that, there's mechanistic work embedded in the large trial. One of the most famous examples of this, in the GUSTO trial 30 years ago, we learned through the mechanistic substudy, that it was rapid reprofusion TIMI-3 establishment of TIMI-3 flow, that really explained the difference between TPA and streptokinase. So I was very intrigued by how we might use these data to explore the results. And I find the findings fascinating, as Paul said. It is complicated, but it raises a really fundamental issue in clinical trials. There's an assumption in a placebo control trial, that because randomization is allowing you to balance everything, except for the randomized treatment groups, and therefore, that comparison has causal information in it. There's an underlying assumption that's really important. And that is, that the placebo is inert. That it has no biological effect of its own. Well, that assumption was violated here. The placebo is not inert in this clinical trial. Now, the investigators, I think to their credit, have said, "Well, this is small, probably doesn't matter." And that might be right, but it also may be wrong. And you can't just say, well, it doesn't matter, these are small effects. As Paul said, some of the effects are small, some are medium, some are large. So what explains it? And I made a point in the editorial, you could model all of this. If you get 5% of this, and 10% of this, and 20% of this, you could make some assumptions and say, well, the magnitude of the benefit was so great that it couldn't have been overcome by this. But that's just modeling, and there's uncertainty. So for me, as a trialist, and somebody who really believes in using evidence to guide practice and to guide public policy, I think there's uncertainty here. It's likely that the treatment effect is not as large as was observed, but how large is it? And how large is important? And how large might we want to consider to put into our practice guidelines? I think all of those open questions, particularly in a field where there is inconsistency across trials, in terms of the observation of the outcome. So my conclusion is, we need more work. We need another trial, if we really want to understand this. And we need to use an inert placebo, to really understand what the contribution was. I'd like nothing better to see that it didn't matter. But I can't say that it doesn't matter because I don't know. Dr. Greg Hundley:           Well, listeners, boy, we've got kind of some interest here in that an unexpected result. So Paul, it's nice doing an interview like this listeners, because each speaker sets up the next one. Paul, Bob is saying, well, what should we do next to clarify the results here? So maybe we'll go through each of you, and start with Paul. Just describe for us, what do you think is the next study that we need to perform? Dr. Paul Ridker: Well, Greg, it's a really interesting issue. We saw it, as authors, to write as neutral a paper as we could possibly write, and sort of do our academic job and say, here are the data. And I think we did it that way because, we don't really know what the interpretation should be. On the one hand, you have a very big beneficial result, which is great for patients. And there's a prior clinical trial called JELIS, which was open label, the same drug, and also got a large benefit. And we were trying to figure out mechanism. That being said, as Bob pointed out, I think what we stumbled into is some level of uncertainty. And the question is, how uncertain would it be, and does it matter in the big picture? Allan was interesting, because the Journal asked us to use the word comparator, rather than placebo. Now this was designed as a placebo controlled trial, but our paper uses the word comparator, because of the possibility, that as Bob Harrington points out, it may not be totally inert. So the writing of this was quite carefully done. I think, at the end of the day, my REDUCE-IT colleagues, who I have great respect for, and really worked terribly hard to do the main trial, understandably feel, that the trial would've showed, and I have a lot of sympathy for that, because it's the hard endpoints we should go with. On the other hand, I have sympathy with the idea that it never hurts to have more data. And if there could be a way to have a second trial, and I might change the population a little bit, maybe I'd do it in true primary prevention. This was one third primary prevention. My colleague, Joanne Manson had done her, she had a trial where they showed some potential benefit in the black populations. Maybe you might over sample some minority groups. But just the pragmatic issues here, make it tough to have a second trial. And so, uncertainty is just part of what we, as physicians, have to learn to live with. Dr. Greg Hundley:           Allan, turning to you. What do you think is a next study to perform in this space? Dr. Allan Jaffe:   Well, I think what Paul has said is correct. That it would be very hard to generate enthusiasm funding for a large trial. But it might not be nearly as difficult to begin to explore the effects of the mineral oil comparator, versus the active agent, versus perhaps, another potential placebo, and see over time what happens in primary prevention patients, as a way of beginning to put some context around what these results might mean. So for example, it could turn out that, the active agent actually kept the values from rising as they normally would've, and mineral oil had no effect at all. Alternatively, mineral oil may well have been a negative. It had a negative effect. And I think, those are the sorts of questions that could be explored reasonably in the short term, without doing another multimillion dollar randomized trial. Dr. Greg Hundley:           And Bob, your thoughts. Dr. Robert Harrington:   Well, and I mentioned this in the editorial, Greg. I didn't make my recommendation lightly. I know that these trials are expensive. I know these trials take a great deal of time, a great deal of energy. And I know that the REDUCE-IT investigators worked enormously hard over the years to get this done. So I don't say tritely, "Oh, just do another trial." But if you think about the magnitude of the public health issue here, there are millions of people to who this kind of therapy might apply globally. And so, shouldn't we be more certain than less certain, if we want to include it, for example, in ACC/AHA guidelines? I would say, the answer to that is yes. And so, I think of it as, okay, let's make some assumptions. Let's assume, that the effect that was observed in JELIS and REDUCE-IT, is the true effect. That's ground truth. Well, there are different study designs one might think about, from an analytic perspective, using Bayesian statistics, as opposed to frequency statistics. One might think about an intense interim analysis plan, to understand where the data are going, and be able to pull in the prior data for evaluation. I would advise getting a smart group of people together, who spend their lives thinking about trials in the atherosclerotic space, and the REDUCE-IT team is pretty darn good, and say, "How could we do this efficiently?" I do think, there's enough uncertainty that it would be ethical, from an equipoise perspective, to include high risk patients in a second evaluation, because we do have uncertainty. And if we really want to nail this down, I think we could look at high risk patients with hypertriglyceridemia, and try to use some interesting design issues, and some interesting analytical issues, to try to reduce the sample size, lot of attention in interim analyses, to try to answer the question. I'd like, as I said, nothing better to say, "Oh look, REDUCE-IT was the truth." This next trial is consistent. That'd be, to me, a terrific outcome of this. On the other hand, if you said to me, "Well, the effect's not 25%, it's more in the 15% range." Well, maybe then we think about how we apply it to our patients a little differently, maybe a little more cautiously. So I don't make the recommendation lightly, as I said, but I do think that there are some conversations that could be had, being respectful of the effort and the expense that goes into these kind of things. To try to answer the question efficiently. Dr. Greg Hundley:           Very nice. Well listeners, we want thank Dr. Paul Ridker, from Brigham and Women's Hospital, Dr. Bob Harrington from Stanford University, Dr. Allan Jaffe, from the Mayo Clinic, for bringing us the results of a substudy of the REDUCE-IT trial, that assessed a variety of serum biomarkers, pertaining to systemic inflammation, and highlighting uncertainty around the mechanism regarding the efficacy of icosapent ethyl, that's been used previously for primary or secondary prevention of cardiovascular events. And next listeners, we are going to move to our second feature discussion and review some data pertaining to microbleeds in the central nervous system, during and after TAVR procedures. Welcome listeners, to our second feature discussion on this August 2nd. And we are going to explore some of the world of TAVR and its potential complications. And we have with us today, Dr. Eric Van Belle, from Lille, France. And also, Dr. Manos Brilakis, from Minneapolis, Minnesota. Welcome gentlemen. And Eric, we'll start with you. Can you describe for us a little, the background information that you use to assemble and construct your study, and describe, or list for us, the hypothesis that you wanted to address? Dr. Eric Van Belle:           Yes. Thanks a lot for the question. So we knew for many years, that some of the complication of the TAVR procedure relate to the brain. And it has been described by many others, that there were some complication in the brain of patient undergoing TAVR. And there was no previous investigation on potential bleeding or microbleeding in this population. And on the other side, there are previous publication on, of course, initially chronic microbleeding, in patient with some of, let's say, disease in the brain, but also, a possibility of acute microbleeding. And especially, in some interesting population relating to the TAVR feed, that is patient with valve disease, patient with endocarditis, or patient with assist device. In this population, microbleedings, acute microbleeding, have been described. And what is interesting, if you look at all these populations, these are population in which the Von Willebrand factor has been impacted and modified, and could be one of the reason of the microbleeding. And one of the similar feature of the patient with aortic stenosis that undergo TAVI, or TAVR, that are patient with indeed also, this kind of Von Willebrand disease. So if we put everything together that is previously, we only looked at antibody complication in those population, and that Von Willebrand disease, which is present in patient with aortic valve stenosis, could promote a bleeding, in particular, bleeding in the brain. We decided to look at the potential appearance of microbleeding, in patient undergoing TAVR procedure. Dr. Greg Hundley:           Very nice. And Eric, can you describe for us, your study design, and who was your study population? Dr. Eric Van Belle:           Yes. So basically, the study population is a basic population of patient undergoing TAVI. Just to make sure that one of the difficulty of this study, was to conduct and perform an MRI, a brain MRI, before the procedure, and as short as possible after the procedure, within three days, which is logistically challenging. And also, to make sure that we keep most of the population to undergo the MRI, we had to exclude patient with a high risk of pacemaker, or patient with pacemaker that could not undergo the MRI. But basically, without this, it's just a regular population. And if we indeed, compare to some of the previous work I was mentioning, about describing the acute MRI, it was important for us to make sure, or to be as sure as we could get, that indeed, this microbleeding, if we observe them, could be related to the procedure. And it means that, the MRI, after the procedure, should be done as short as possible. And also, that an MRI, a baseline MRI, should be performed. Because we know, that in this population, you could have some microbleedings also observed before starting the procedure. Dr. Greg Hundley:           So a cohort study design where MRIs are performed before, and then very soon after, TAVR procedures. So Eric, what did you find? Dr. Eric Van Belle:           So what we observed, the first thing that we confirmed was indeed, that in this population of that age, that is patient around 80 years old, when we do the baseline MRI, you find in about one out of four patients already, some microbleedings. And this was expected, and it is very similar to what is expected in this kind of population. But what was indeed more striking, that when we repeated the MRI after three days, we observed another 23% of patient with a new microbleedings that were observed. This is indeed the most important observation. What was also important that, the patient with microbleedings, and the location of the microbleedings, were not related to the cerebellum brain, because indeed we could observe some cerebellum arise in this population, as it is expected. And there was no relation between the two. So it's also, an important observation, suggesting that this microbleeding are not hemorrhagic transformation of cerebellum brain, for instance. And we also observed that, the risk of microbleeding, or the chance to observe the microbleeding, was increased when the procedure was longer. And also, when the total duration of anticoagulation was longer, we also observed that, when the procedure was, when we used protamine at the end of the procedure, the risk of microbleeding was less. And also, importantly, the status of the Von Willebrand factor, and indeed, an alteration of the multimer of Von Willebrand factor, was also associated with the risk of microbleeding in this population. Dr. Greg Hundley:           Very nice. So in this cohort of 84 individuals, average age around 80, undergoing TAVR procedure, and about 50/50 men and women, you had several factors. Prior history of bleeding, amount of heparin, absence of protamine, all indicating a higher risk of these microbleeds. So very practical information. Well, Manos, you have many papers come across your desk. What attracted you to this particular paper? And then secondly, how do we put these results really, in the context of maybe other complications that can occur during or after TAVR procedures? Dr. Emmanouil Brilakis: Yes, thanks so much, Greg. And also, congratulations Eric, for a wonderful paper, and thanks for sending it to circulation. I think, with increasing the number of targets, as you know, TAVR now is becoming the dominant mode for treating severe aortic stenosis. Safety is of paramount importance. And even though there's been a lot of progress, we still have issues with the safety of the procedure. So understanding how can make it safer is very important. And I think, what was unique in this paper, again, congratulations for creating this study, is that it opens a new frontier. We worry about stroke. We're all very worried about the stroke, and having the patient have a permanent neurologic damage during the procedure. But there may be more to it than the classic embolic stroke. And I think, this study opens actually, a new frontier with the micro cerebral bleeds. Now we don't completely understand, despite the study, we don't understand the functional significance from this. And I think, that's one of the areas that will need further research. But I think, trying to understand what causes them, and preventing those microbleeds, would have a very important role in the future, for making TAVR even safer than it is. Dr. Greg Hundley:           Very nice. Well, Manos, you really lead us into the kind of the next question. So Eric, what do you see as the next study to be performed in this sphere of research? Dr. Eric Van Belle:           Again, to me, and to follow with the comment of Manos, we need to include, I would say, to solve two questions. We have to solve the question of, what could really impact these microbleedings. And what would be the impact of this microbleeding on the long term outcome of this patient? So it's means that we have to set, as part of the studies that we will design, potentially studies on aortic immolation. Or let's say for instance, we could investigate the role of protamine. It has been suggested that protamine could be something interesting, so it could be tested as part of a randomized study. But this means that, as part of such randomized study on the use of protamine, for instance, you would include a last cohort of patients with MRI after the procedure. And also, a long term follow of the neurological complication, which indeed, is the missing part of our current study. We would need to have a much larger cohort of patients, to be able to reconnect the neurological outcome to the MRI outcome, and also to include this. So let's say, for me, one of the studies we would be interested to perform, is to conduct a study on the use of protamine, which is very simple, randomized, yes or no, and includes brain MRI in this population, as a systematic investigation, which is difficult to conduct. You have to know that it's difficult to do, but it will be very important. And then, to look at the long term neurological outcome. Dr. Greg Hundley:           And I see, Eric, you mentioned the long term, because really in the short term, so within six months, you really didn't see any changes in neurological functional outcome or quality of life. So Manos, just coming back to you. What do you see is the next study that should be performed in this space? Dr. Emmanouil Brilakis: Yeah, I agree actually, with Eric. The next step is, this was an 80 patient study. Right? It's a very small preliminary data, all that opens a new system for evaluation, we're still a very small number of patients. So having a larger number of patients, I think for me, the key thing is to understand the connection. Does this actually cause neurologic symptoms? What does it mean having a microbleed? I think right now, we're still confused on the study. There was not really much impact on the neurologic status of the patient. So for me, the number one thing is, to understand how it impacts the patient's quality of life, the neurologic status. Perhaps more sensitive studies, neurocognitive studies, to understand exactly how it impacts. And then after doing that, I agree with Eric, if this is a bad, something really bad, then we can find different ways to prevent them from happening. Protamine is one of them during the procedure time, and not be a very feasible one. Or it could be interesting to see if different valves, for example, have different propensity for causing those microbleeds. Dr. Greg Hundley: Very nice. Well listeners, we want to thank Dr. Eric Van Belle, from Lille, France, and also, our own associate editor, Dr. Manos Brilakis, from Minneapolis, Minnesota for bringing this very important study, highlighting that one out of four patients undergoing TAVR has cerebral microbleeds before the procedure. And then, after the procedure, one in four patients develop new cerebral microbleeds. And then, procedural and antithrombotic management, and persistence of acquired Von Willebrand factor defects, were associated with the occurrence of these new cerebral microbleeds. Well, on behalf of Carolyn and myself, we want to wish you a great week, and we will catch you next week On the Run. Dr. Greg Hundley:           This program is copyright of the American Heart Association 2022. The opinions expressed by speakers in this podcast are their own, and not necessarily those of the editors, or of the American Heart Association. For more, please visit ahajournals.org.

For more information, contact us at 859-721-1414 or myhealth@prevmedheartrisk.com. Also, check out the following resources:  ·Jubilee website·PrevMed's website·PrevMed's YouTube channel·PrevMed's Facebook page·PrevMed's Instagram·PrevMed's LinkedIn·PrevMed's Twitter ·PrevMed's Pinterest

WE APPRECIATE OUR PARTNERS. CHECK THEM OUT!Sleep Better on Natural Memory Foam: https://myessentia.com, use code DAVEVIP to get an exclusive discountControl Blood Glucose: https://pendulumlife.com, sign up for membership to get monthly supply delivery, use code DAVE20 to save $20 on your first shipmentSubscription Box for Biohackers: Each season (and limited editions, too!) discover and enjoy innovative wellness products, hand-curated by Dave Asprey, that you may not find anywhere else. https://daveaspreybox.comSPECIAL OFFER FOR THE HUMAN UPGRADE LISTENERSVisit https://getmyphoenix.com/dave and use code DAVE100 to save $100.IN THIS EPISODE OF THE HUMAN UPGRADE™… …urologist, surgeon and age medicine specialist Dr. Paul Thompson discusses the challenges men can experience with their sexual health, energy and performance. Erectile dysfunction happens to men at all ages and is actually quite normal. Causes can be physical, and hormones play a role. Nutrition or exercise habits may be culprits. And state of mind factors in.Dr. Thompson shares his clinical expertise on how getting to the root of what's going on with men's sexual functioning will not only improve erectile dysfunction but also support other critical areas of men's health. The conversation looks at the pros and cons of eating meat, what your cholesterol numbers really mean, and why cardiovascular health matters at every age.Guys, listening to this, if your doctor isn't asking you for Lp-PLA2, which is an enzyme that's expressed when there's damage to your arteries, then you have a problem. If they aren't looking at C-reactive protein, you have a problem; and if they're not looking at homocysteine, you have a problem. So, you could ask your doctor for them or you could ask your doctor, “Hey, what do you know about these?”You'll also find out why oral health is so important and why you have to pay attention to your nitric oxide production.Dr. Thompson talks about the at-home device he helped develop at Launch Medical (he's chief medical officer there) that's pioneering a solution for erectile dysfunction. It's based on clinical acoustic wave therapy treatment. “Acoustic wave is really simple and it works, and it has to do with the growth of blood vessels,” he explains. The Phoenix device helps men improve and/or restore their sexual functioning.Guys and women who love guys or guys who love guys, this thing is real technology. It does work, it is not too good to be true, and it's worth talking about.This conversation takes any embarrassment or shame out of the ED equation and gets into the details of plaque, blood flow and how you can find a fix and reclaim your sexual health.See Privacy Policy at https://art19.com/privacy and California Privacy Notice at https://art19.com/privacy#do-not-sell-my-info.

I'm covering David Sinclair's new book, "Lifespan: Why We Age—and Why We Don't Have To." Contained here are some interesting theories and discussions about aging and age-related diseases.  I also touched on the topics of Valter Longo's Prolon FMD (fasting-mimicking diet), vitamin K2 carboxylation and vitamin K2-dependent enzymes, inflammation tests (Hs-CRP, MPO, Lp-PLA2, and MACR), the secret life of fat cells, and niacin. For more information, contact us at 859-721-1414 or myhealth@prevmedheartrisk.com. Also, check out the following resources:  ·PrevMed's website·PrevMed's YouTube channel·PrevMed's Facebook page

Inflammation panel (CRP, MPO, MACR, Lp-PLA2), OGTT (oral glucose tolerance test), and Kraft insulin survey—these are definitive tests to check whether you got insulin resistance and/or cardiovascular inflammation. If you want them done but don't know how where to get them, we have a new program for lab screening plus free webinars.For more information, contact us at 859-721-1414 or myhealth@prevmedheartrisk.com. Also, check out the following resources:  ·PrevMed's website·PrevMed's YouTube channel·PrevMed's Facebook page

I tell the story of a friend that had a slightly positive Lp-PLA2 test. He was very worried about CV inflammation. I was able to put him at ease by describing the rest of his cardiovascular inflammation panel. This focus on CV inflammation started, and is still being researched, by Paul Ridker MD at Harvard. Here are the other tests we review: myeloperoxidase (MPO), high-sensitivity C-reactive protein (hsCRP), and microalbumin creatinine ratio (MACR). You can find a lot of this at the following link from Cleveland Heart Labs (CHL), which was recently purchased by Quest. For more information, contact us at 859-721-1414 or myhealth@prevmedheartrisk.com. Also, check out the following resources: PrevMed's article on inflammation testsPrevMed's websitePrevMed's YouTube channelPrevMed's Facebook page

Researchers at the Karolinska Institute found that a protein called CARD8 is somewhat connected to cardiovascular inflammation. In this podcast, let's have a brief look at CARD8 then have a deep discussion about inflammation and the sure things that drive it. What causes cardiovascular inflammation? A brief look at CARD8 (Caspase activation and recruitment domain 8);What is cardiovascular inflammation? The inflammation tests - MACR, myeloperoxidase, Lp-PLA2, C-reactive protein.For more information, contact us at 859-721-1414 or myhealth@prevmedheartrisk.com. Also, check out the following resources: PrevMed's article on cardiovascular inflammationPrevMed's websitePrevMed's YouTube channelPrevMed's Facebook page

Many people focused more on LDL cholesterol as being the cause of heart attacks and strokes. While plaque consists of oxidized LDL cholesterol, having a high LDL level isn't the problem. Recent studies showed that it's actually inflammation that is the culprit here.In this podcast, let's discuss:Inflammation and heart disease;How cardiovascular inflammation leads to heart attack and stroke;How to test & detect cardiovascular inflammation (CRP, MACR, Lp-PLA2, myeloperoxidase, IL-6);Prediabetes and cardiovascular inflammation;Can we delay atherosclerosis & cardiovascular inflammation?For more information, contact us at 859-721-1414 or myhealth@prevmedheartrisk.com. Also, check out the following resources: PrevMed's inflammation postPrevMed's websitePrevMed's YouTube channelPrevMed's Facebook page

We’re back for another info-packed episode of Keto Talk! In this episode, Jimmy and Dr. Will Cole answer your questions about Overwhelming Carb Cravings On Keto, Deposits Of Cholesterol On Face, Genetic Liver Cirrhosis, Bloating On Keto, Diabetic Neuropathy Treatment, and more! “It’s not the ketogenic diet that failed them, it’s how they prepared for it and what they were eating that was not working for them.” Dr. Will Cole People can so easily psyche themselves into doing keto badly and then blame keto for not working: Tried the Keto Diet, and I Hated Each Second of It Paid advertisement HOT TOPICS: Do people with Celiac disease need to eat more fat due to poor absorption? Does keto lead to an elevated level of bilirubin in the urine? Should I be concerned about my LP PLA2 being elevated (over 200) after starting keto? Why is my fasting insulin so high at 7.3 despite being strict keto without cheating at all? What if any impact does your blood type have on your body’s ability to be in ketosis? Paid advertisement HEALTH HEADLINES: Nutritionists Reveal Why People Listen To Low Carb Gurus Instead Of Science “Keto Diarrhea” Is Just One of the Many Gnarly Truths About the Keto Diet Best way to lose weight fast is to SWITCH between keto and low-carb diets Meatless meat is having a moment. Will eggless eggs be next? Low carb diet leads to “clinical remission” in three case studies of adults with type 1 diabetes STUDY:  Train your brain with computer game to eat less sugar “I think the best ketogenic approach in the world will become unraveled if you aren’t sleeping and are stressed.” Jimmy Moore Your Questions: What can I do to help get rid of the persistent and overwhelming carb cravings that hit me even while eating keto? Hey Jimmy and Will,  I recently joined in on Jimmy’s 7-day fasting challenge on Instagram and they were so incredibly helpful. I was really hoping that would be a reset for me and a springboard into eating clean keto. I’ve been struggling for years with on again off again low-carb eating, but I just have super intense carb cravings. I ended up going through my time of the month and struggling through that last day of the fast and then crashed and burned back into eating tons of carbage afterwards. I caught your emotional eating JIMMY RANTS episode and I just need some help with figuring out how to conquer the craving insanity that I just can’t always willpower through. I want to be successful once and for all, but I’m feeling like a failure here, yo-yoing at very high weights, with Type 2 diabetes. I know that the answer to this lies within eating a keto template and I’m not afraid to put in the hard work to make it happen. But I definitely feel controlled by food.  I refuse to believe that I have to have a dangerous weight loss surgery to conquer this problem, but I’ve been winning some battles but losing the war for years. What do you recommend for the obsessive, overwhelming cravings, and persistent thoughts about food? How do I get actual control over this? Thanks so much, Rhonda If cholesterol isn’t a bad thing, then why did keto lead to these permanent deposits of cholesterol underneath my eyelids? Hey Jimmy and Dr. Cole, Thanks for this podcast. I started reading Jimmy’s book Cholesterol Clarity recently because I developed these yellow bumpy lines under my eyes and was told it’s because I have high cholesterol.  I went to the doctor and immediately they wanted to put me on statins. I hate going to the because of this kinda thing. They didn’t even go over the results with me. They had the front desk call me and tell me I had a high cholesterol number and that there was a prescription for statins waiting for me at the pharmacy.  I didn’t take them, of course, and I retested after a three-month, 30l-pound keto weight loss and it was even higher. The doctor again insisted I take a statin and I again refused.  My question for you guys is if cholesterol isn’t bad, then why do these permanent deposits of cholesterol end up on my face? They look horrible and I’m told they will never go away on their own. How and why does this happen? I wanted to show you these yellow things on my face and I wondered if you had any knowledge about them. Thank you for answering my question. Louise Would a genetic liver cirrhosis condition be hindered or helped by eating a low-carb, high-fat, ketogenic diet? Greetings Jimmy and Will, My boyfriend was recently diagnosed with liver cirrhosis which developed as en effect of a genetic disorder he was not aware of. He’s never been much a drinker and he definitely doesn’t drink now. He works out regularly and eats somewhat “healthy” according to his doctors. He’s in great shape especially for someone with only 20% liver function. I read somewhere that a hepatic diet is made up of primarily carbs since protein breakdown is impaired and fat is bad for the liver. I by no means consider myself an expert on nutrition and metabolism, but this sounds like total BS to me. It doesn’t make sense to feed your liver carbs which turn into sugar. In my mind, it just makes sense that a keto diet is the way to go in conjunction with coffee enemas perhaps. What do you think? I want to learn and do as much as I can to help my boyfriend have the best life and the best health possible.  Thank you, Brenda Why do I have bloating when I eat keto foods? Why won’t my Ketonix breath ketone analyzer show the presence of ketosis with anything I do? Hi Jimmy and Dr. Cole, I love your show and never miss an episode because it really helps keep me on track. I’m a 31-year old breastfeeding female and have been eating keto since January 2017. When I transitioned to keto, I had already been breastfeeding my daughter for 10 months and I was starting to struggle with weight gain and hunger that was much worse than when I was pregnant. I ate whole organic foods and took probiotics for years but still consumed far too much sugar (honey, coconut sugar, and grains) and I knew I had to make a change when I started gaining more weight than I ever had in my life and having an insatiable appetite for sugar.  My transition was rough and I had keto flu and lightheadedness for weeks despite consuming plenty of water, salt loading, and taking a multimineral supplement. Urine test strips at the time showed that my ketones were off the charts high. At the beginning of my pregnancy my hemoglobin A1C was prediabetic, but after a few months on keto it was down to normal. My fasting blood sugar in the morning is now 83, and it drops to 76 after my 25 minute beginner’s strength training workout and 59 two hours after my usual breakfast of scrambled eggs. In the evening, 2 hours after dinner, it is around 80. I lost about 30 pounds in the first months and my milk supply never dropped (I’m still breastfeeding now, almost a year on keto later, with no problems.)  I love the ketogenic way of eating and am so thankful to be off carbs, but I have two main concerns: the first one is constant bloating. When I still ate carbs I had stomach pain every morning that improved after eating breakfast. Now that I’m keto I tend to feel very bloated after meals. I eat dairy and nuts, but temporarily cutting them out of my diet and it doesn’t seem to make a difference. Sometimes my worst bloating is after eating something like riced cauliflower with bacon. It seems like everything sits in my stomach too long. And I really can’t handle seltzer water! I once had a UGI endoscopy in my stomach for the stomach pain years ago and it showed everything normal except for low stomach acid. Could that be the problem? How do I increase stomach acid? I also sometimes have nausea and an acid taste, like reflux symptoms, although I’ve never had heartburn.  My other concern is with testing my ketones. I use the Ketonix breath analyzer and no matter what I do, I blow green. If I have a glass of dry champagne the night before and keto treats full of almond flour and cheese, I blow green the next day. If I intermittent fast for three days and eat very strict keto, I still blow green! How is this possible? Am I truly in ketosis? Thank you so much for your help! Rachel KETO TALK MAILBOX: Paid advertisement Would the inevitable diabetic neuropathy be rectified more effectively with IF and keto than with Gabapentin? Hey guys, My boyfriend’s mother was just diagnosed with Type 2 diabetes. Unfortunately, she suffers from horrible neuropathy and finds it very difficult to sleep at night which is very common. I have read on the Internet that people with neuropathy most of the time are prescribed a drug called Gabapentin. To my surprise, they are also prescribes to patients as antidepressants. The more I think about it, long-term use of these drugs has to be very difficult on the kidneys and liver which is a double whammy for diabetics who already have issues with both of these organs. To me, it seems intermittent fasting and keto can help solve this neuropathy without the need for any risky medications. In your functional medicine practice, Dr. Cole, have you found this to be true in your patients? Sincerely,  Emi 

In this five-part series, Thomas Dayspring, M.D., FACP, FNLA, a world-renowned expert in lipidology, and one of Peter's most important clinical mentors, shares his wealth of knowledge on the subject of lipids. In Part V, Peter and Tom talk about inflammation, endothelial health, and oxidative stress as they pertain to cardiovascular disease, and our attempts to monitor them using biomarkers. They also discuss a couple of very important risk factors that too few people (and doctors) know about. Tom closes the five-part series with a tragic story about his good friend that is likely all-too-common for many practicing physicians, that both haunts and motivates Dr. Dayspring to learn as much as he can about the number one killer in the United States. We discuss:     Lp(a) [2:30];     Inflammation [17:15];     Oxidative stress markers: Lp-PLA2 and oxLDL [20:45];     Endothelial health markers: ADMA and SDMA [34:30];     Remnants [43:45];     Omega-3 fatty acids (EPA and DHA) and apoC-III [55:30];     Red blood cells and cholesterol transport [1:07:45];     Tom's friend Earl [1:10:00];     Peter's friend JP [1:18:15]; and     More. Learn more at www.PeterAttiaMD.com Connect with Peter on Facebook | Twitter | Instagram.

In over half of all cases of hospitalization for a cardiovascular event, the first symptom is the event itself. So anything we can do to get any early indicator that something is going wrong in the cardiovascular system can have a huge impact. Erectile dysfunction is one such early signal. According to cardiovascular health expert Daniel Chong, ND, identifying sexual dysfunction is essential for improving cardiovascular outcomes.  Approximate listening time: 30 minutes About the Interview It may seem counterintuitive to interview a cardiologist, and not a urologist, on the topic of erectile dysfunction (ED). But we now know that ED is a result of endothelial cell dysfunction and ED can be an early warning sign of systemic atherosclerosis. Looking at ED from a cardiovascular perspective is essential. That’s why we invited cardiovascular expert Daniel Chong, ND, to talk to us about ED’s connection to heart health. In this interview, Natural Medicine Journal’s editor-in-chief, Tina Kaczor, ND, FABNO, asks Chong about the complex interplay between vascular function and sexual function. According to Chong, cardiovascular disease always has some degree of contribution—potentially a major one—in ED. That’s in part because blood flow is the key facet to obtaining a full erection. Cardiovascular dysfunction, including plaque in the arteries that regulate that blood flow, can therefore have an impact on ED. Even before plaque development becomes a problem, endothelial dysfunction in the inside walls of the arteries can play a role in erectile function. In this enlightening interview, Chong explains the different issues that can contribute to ED, including anatomical, physiological, and psychological problems. It’s an important listen for any practitioner who sees men, since beyond being a problem in and of itself ED can be an early signal of other serious health concerns. About the Expert Daniel Chong, ND, has been a licensed naturopathic physician, practicing in Portland, Oregon, since 2000 and focusing on risk assessment, prevention, and drug-free treatment strategies for cardiovascular disease and diabetes, as well as general healthy aging, and acute and chronic musculoskeletal injuries. Chong has also completed certificate training in cardio-metabolic medicine from the American Academy of Anti-Aging Medicine and is an active member of the Society for Heart Attack Prevention and Eradication (SHAPE). In addition to his clinical work, Chong serves as a clinical consultant for Boston Heart Diagnostics Lab. Transcript Tina Kaczor, ND, FABNO: Hello. I’m Tina Kaczor for the Natural Medicine Journal. Today, we’re going to be talking about erectile dysfunction and cardiovascular disease with Dr Daniel Chong. Dr Chong is a naturopathic physician with a private practice in Portland, Oregon for the past 17 years. He specializes in what he likes to call "vascular wellness optimization." He’s also the founder of the web-based consulting company, the Healthy Heart Project which offers a number of educational and direct consulting options for both the general public as well as healthcare practitioners on how best to assess and reduce risk for cardiovascular disease. Dr Chong also lectures and serves as a clinical consultant for Boston Heart Diagnostics Lab. Thanks so much for joining me today, Dr Chong. Daniel Chong, ND: You're welcome, Tina. Good to be here. Kaczor: As I mentioned, our topic today is erectile dysfunction. At first, it may seem odd to our listeners that I’m talking to a cardiology expert and not a urologist or men’s health expert but we now know that erectile dysfunction is a result of dysfunction of endothelial cells and in fact, this can be an early warning sign of systemic atherosclerosis. Dr Chong, can you start us out with a brief overview of how erectile dysfunction and cardiovascular disease are related? Chong: Sure. I can do my best there. There’s definitely going to be different circumstances that can contribute to erectile dysfunction. Some of which may not be actually anatomical, so to speak, or physiological from the cardiovascular perspective but I would say the majority is at least indirectly affected because even if we’re talking, for example, about a psychological contributor which we may touch on later, if somebody has dysfunctional arteries down there in the penis, they’re going to be more vulnerable to effects from psychological aspects than they would be otherwise. In other words, a young teenager may get stressed out in an early sexual experience but that’s not going to affect function as much as it could a 50-year-old man. Anyways, in general, we could just say that cardiovascular disease is going to have some degree of contribution and potentially major. Obviously, blood flow is the key facet to obtaining a full erection and certain arteries are going to be more vulnerable to impacts from the development of cardiovascular disease but even so, the arteries in the penis may or may not actually have plaque in them but they can still dysfunction. Typically, we know, and we’re going to talk about this later, in cardiovascular disease, the preceding step prior to actual anatomical change or plaque development is endothelial dysfunction or dysfunction in the inside wall of the arteries and even that going on without any actual plaque having developed yet can affect erectile function and not to be noticeable by the person. All in all, I guess you could say they’re intimately intertwined because you have to have good blood flow. It may or may not have plaque. Plaque may or may not be actually playing a role yet but it will in some cases and cause really significant dysfunction, but even minor dysfunction is going to be at least the partial result of the arteries starting to misbehave for various reasons that hopefully we’ll touch on. Kaczor: Yeah. I actually came across some mention of erectile dysfunction in that whole idea of plaque formation. One author said that it could signify in some patients, or at least it should be followed up to see if it signifies subclinical atherosclerosis. Chong: Correct. Kaczor: Yeah. Atherosclerosis being pretty much asymptomatic in people until there’s larger consequences. On that note- Chong: Right. Yeah. Sorry to cut you off. Sadly, it’s been shown that in over 50% of cases of hospitalization for a cardiovascular event, the first symptom is the event and that’s over half of all of them, so anything we can do to get any early indicator of something in this, so to speak, before, for example, erectile dysfunction, is hugely important for us because we are not doing a very good job at least conventionally in identifying early on what’s going on with people. Kaczor: Yeah. I look forward later in this discussion to talk to you about how to assess it, to find early markers besides just the symptom of erectile dysfunction but let’s start with the larger picture in conventionally recognized erectile dysfunction and cardiovascular disease risk factors. Can you talk a little bit about like when we’re, as clinicians, who walk into our office, who we should suspect it in or at least engage in the conversation because many patients won’t bring it up themselves unless they're directly asked? Dr Chong: Yeah, absolutely, so, certainly age. The older a man gets, the more potential there's going to be for all kinds of different changes going on physiologically. Some people are well aware of testosterone production, how crucial that is and that certainly begins to change as a man ages. But certainly, very standard, interestingly enough, it’s the same standard risk factors you might consider for cardiovascular disease in general in terms of high blood pressure, diabetes, certainly, smoking. Conventionally, you're going to see high cholesterol as a stated contributor but we can certainly talk in more detail about that because I know that some people out there in the functional medicine world, naturopathic world, et cetera, consider high cholesterol as a past tense risk factor for cardiovascular disease which it really is and it’s just more complicated than that. Obesity, lifestyle factors in terms of exercise and then certainly, psychological factors, depression and anxiety, et cetera are all going to be key things. I also want to make a just brief mention even though this is kind of a topic in and of itself, when we talk about erectile dysfunction, obviously, we’re talking about men but it should be very clearly stated that the same potential processes are going on in women as they age. Women with difficulty with sexual activity or orgasm, et cetera, may in fact be having their own version of “erectile dysfunction” with the clitoris as essentially an analogous structure in a woman and all of these blood flow issues can occur in women as well. It’s important to really kind of make mention to that. I say men, I keep saying men, as men age, blah, blah, blah, but it really should be looked at as both sides of the coin, so to speak. Kaczor: That’s actually an important point. Thank you for mentioning that. Chong: Sure. Kaczor: I want to do a follow-up on that cholesterol thing that you just mentioned because I think that that’s kind of top of mind. I think it’s important to give voice to any new data on looking at cholesterol because I'm with you on it being much more complex and it’s more complex than I understand. I'm happy for you to kind of flesh it out for us. Chong: Yeah. I mean, I guess anybody that says that cholesterol has nothing to do with cardiovascular disease is not really thinking about the fine details of the situation. You can't have a plaque form without cholesterol and lipoprotein particles being involved because they are what are the sort of primary components to the development of the plaque. What I don’t agree with conventionally is the idea that high cholesterol, in and of itself, is just going to definitively contribute to cardiovascular disease because obviously, there are many people out there who have relatively “high cholesterol” who don’t get cardiovascular disease. There's certainly something else going on that’s playing a role as to whether or not high cholesterol is going to lead to that issue in some people versus others. Long story short, I consider cholesterol and related markers to be secondary factors. They are absolutely involved but they are not … There's going to be other things that help sort of determine the likelihood or lack thereof of the high cholesterol sort of turning into cardiovascular disease. That’s a really fun discussion in and of itself. It could be another hour or so by itself but hopefully, that kind of answers your question, at least preliminarily. Kaczor: Well, it brings up another question which is- Chong: Certainly, keep going with that. Yeah. Kaczor: Yeah. If cholesterol is considered a secondary factor, and I see what you're saying, cholesterol is not … needs to be present but can't be causative because there's not a cause and effect 100% of the time. Chong: Correct. Kaczor: If it’s secondary, what are you looking at as primary? Chong: Well, to me, the absolute most important thing that’s going to contribute to the potential or lack thereof of eventual cardiovascular disease development or i.e. plaque, development is the health and vitality of the walls of the artery and how well they're functioning. In other words, the healthier, more nutritionally replete the walls of the arteries are themselves and the better they're being sort of manufactured in the first place by the body, are going to be the primary factor that leads to vulnerability or not. If you imagine like … I would like to use analogies. On a coastline, you may have, let’s say, in Hawaii versus somewhere else on the mainland. Hawaii is made up of volcanic rock which is, tends to be a little bit more brittle and it can sort of erode more easily. If you have waves crashing into the wall, into a wall of rock in Hawaii, it may erode more quickly. Then, an analogous wall somewhere else in the world that’s made up of a different, harder, more resilient material, the waves are still crashing into them with the same potential force but one’s going to erode more quickly than another. If we then relate that to the vascular system, somebody who has poor nutrition and tons of inflammation, oxidative stress, et cetera, and especially long-term poor nutrition, they're not going to be able … especially if we’re talking about collagen production, they're not going to be able to manufacture the sort of strong, resilient vascular walls that they should which will inevitably be, if they are stronger, will inevitably be more resistant and resilient to the impact of the turbulence of the flow of blood. There are certainly other things that are going to impact that as well especially the turbulence itself and the viscosity of the blood. That’s going to make for essentially like stronger waves crashing in which obviously, the stronger the waves is crashing into the area, the more potential there is for erosion as well. To me, long story short, the primary situation that’s going to lead to the potential development of plaque is a combination of two primary factors. That’s the vulnerability of the wall of the artery and the stress that is being placed on the wall of artery. Kaczor: By- Chong: If you look at every single risk factor we know of, they are impacting one or both of those factors. Kaczor: Okay. When you say stress, you mean mechanical forces, as well as chemical? Chong: Chemical. Absolutely. Kaczor: As in oxidative stress? Chong: Correct. That would be one of them. I mean, even environmental toxins, different types of infectious organisms and certainly mechanical stress as well or what we call blood viscosity which is impacted by a variety of factors. Primarily, probably the main ones for blood viscosity would be hydration and like even iron levels or high sort of … basically, concentrated solid substances in the blood and then also, cloudiness of the blood, how high is fibrinogen levels and things like that are going to impact the viscosity of the blood. Then, the classic risk factor of high blood pressure is going to be too, more or less, stress on the wall of artery. Kaczor: Let’s- Chong: Sorry. One other thing. I mean, one of the ways that high cholesterol may be contributing to things is it’s known that the higher the cholesterol is, the stronger the impact on the vascular wall is. It actually causes … High cholesterol itself can contribute to endothelial dysfunction or stress on the function of the wall of the artery. Kaczor: Doing mechanical forces, you're saying, to the viscosity of the blood. Chong: Right, and more technical reasons, like it literally messes with certain aspects of how the wall, the endothelium is supposed to be functioning. It’s not just that it gets into and becomes part of the plaque. The higher your cholesterol goes, the potentially worse the endothelial function initially. Kaczor: Okay. Let’s switch gears a little bit. If we’re talking about endothelial dysfunction as the commonality between erectile dysfunction, atherosclerosis, cardiovascular disease, it’s all about a healthy endothelium. Chong: Right. Kaczor: It’s interesting, in that same paper I mentioned before, I came across a term that I had not seen before. It was the endothelium as a single organ which I thought was a really interesting concept like, “Oh,” thinking, “I'm sure it’s different, in different tissues,” but just the idea of overall health of it being a singular thing was interesting to me. Chong: Right. People look at the blood vessel as like these tubes that are just allowing for the passage of blood flow. There's so much going on at the wall of the artery physiologically. It is absolutely an entire organ. Kaczor: Let me ask you this. As far, for us as clinicians, what are either biomarkers or assessment tools, how do we gauge endothelial function in a patient? Chong: Well, technically, when we’re specifically talking about endothelial function, there's only a few ways to directly assess that. Clinically, they're going to involve some way, shape, or form of actually testing, in-office, the function of the arteries themselves. There's a general … There's a few … There's basically two main machines that I'm aware of. One is called an EndoPAT and one is called the EndoTherm that are designed to directly assess endothelial function. The way they basically work is they … You have your fingers in some type of device that’s monitoring either blood flow or temperature at the fingertips. Then, you basically occlude the artery and the arm like you would with the blood pressure cuff. You have to do that for about 5 minutes which is not enjoyable for the patient because, as you can imagine, it isn’t feel very good to have your blood occluded for 5 minutes. Then, prior to doing that though, you're doing a general assessment on blood flow and temperature of the fingers. Then, you occlude the blood flow and then you let it out all at once. When the blood comes, as you might imagine, rushing back into the extremities in the fingers, you should get some degree of expansion of the arteries. Normal function would lead to the arteries, as the blood really rushes in there, would lead to the arteries expanding to a certain extent. People that have endothelial dysfunction, their blood vessels will not expand appropriately. The machines are designed to sort of read that, sort of the tip, where your tips of your fingers are sitting, the machines is detecting, is there a significant enough change in temperature and or blood flow. There's also something called arterial pulse velocity which basically, there's a smaller device called an iHeart like an iPod but it’s iHeart. I'm not connected to any of these companies or anything like that but that is a newer device that’s being developed that checks sort of indirectly the same thing. It looks kind of like a pulse oximeter but it’s actually detecting arterial pulse wave velocity and literally how quickly a pulse rate is moving down the arterial tree. If you might imagine, the sort of left compliant and arterial, an artery is, the quicker the pulse rate is going to move down it. That’s generated by heart, a heartbeat. Those are the only ways that I'm aware that are … Those are the only things that I'm aware that are being used in-office to directly assess endothelial function. There is a lab test that can be measured with people called ADMA. It stands for asymmetric dimethylarginine. That is considered a surrogate or indirect assessment of endothelial function. The higher the ADMA is, the higher the potential for endothelial dysfunction because it’s a direct sort of inhibitor of nitric oxide production. Kaczor: All right. Well, that leads us into our next little piece, doesn’t it? Nitric oxide production being integral to the whole relaxation of the smooth muscle and the endothelium to allow for blood flow whether we’re talking about the fingertips or the penis. Can you talk a little bit about nitric oxide? Maybe briefly mention how an assessment can be made, the ADMA being one of the means of assessing that as far as the blood test and anything else that might be accessible to a general physician or clinician that might be seeing these patients. Chong: Well, I mean, endothelial function is, to me, the ideal way to get an assessment of that because I'm a big proponent of the idea that we want to check end of point factors as often as we can. Classic example of this is looking at the different impacts of certain dietary changes on cholesterol markers and making conclusions about whether or not that is good for the vascular system or not, certain changes like HDL going up, for example, after the implementation of a certain diet did not guarantee by any stretch of the imagination that you're having a positive effect on the vascular system so I like to use endpoint markers or end, sort of, functional markers as much as possible so far and away still, the best way to me to assess nitric oxide levels is via those endothelial function tests that we mentioned already. Other ways to sort of try to get an assessment of it, the only other way that I’m really aware of is if you've seen … You've been to enough conferences, I know. You’ve probably seen this company that has this little saliva test that you can use to check basically nitrate levels in the saliva. That’s going to be … Nitrate is a crucial factor, nitric oxide production as well, so some people are using these little saliva tests to check what a person’s typical nitrate intake is and then recommending dietary or supplement interventions based on that. Those are really the only ways that I’m aware of to sort of really truly get an assessment on that other than, obviously, history and talking to a person, seeing how well things are working, so to speak. Kaczor: Can I ask you a question? I don’t mean to put you on the spot and I do not know the company that’s offering nitrate levels in saliva but is this something that’s been validated or is it with any rigor or is this one of those early adoption things that happen? Chong: Right. You're asking me if something has been validated with scientific tests or research? Can you restate? Kaczor: Or at least … Yeah. Chong: You do that with everything which is great. That’s why I like you so much but I don't know for sure. This is … In all honesty, I haven’t really looked too deeply into that method of assessment with people, so I wouldn’t be able to say with any certainty at all. I know that they’re quite widely used and it’s not a very complicated, technically complicated test so I think it’s pretty straightforward. I do recall seeing literature being made available by these companies but I have not looked that in-depth at that at this point. Kaczor: Well, I appreciate your honesty. When you're on the cutting edge, early adoption of new technologies is part of our … We get to do that. We get to be right there doing, instituting things but it’s important, I think, for us all to go at a pace that has some, at least reproducibility, if not rigor. Chong: Absolutely. The other thing that I would say to add to that is like using different angles of assessment is also crucial, not just relying on one piece of information whether it be cholesterol. That’s why the classic conventional mistake is like, “Okay, we’re going to check and see if you have a high risk for cardiovascular disease. Let’s check your lipid panel. There’s so much more beyond that that can be done to assess and evaluate people and get a much clearer picture. That’s a classic idea, just sort of not settling on one thing, not just using the newest thing, whatever it is. Use as many tools as you can within reason to get the clearest picture. Kaczor: Yeah. I want to continue on the molecular biology of this and specifically, we have just a few minutes left, really talk about- Chong: Time flies when you're talking about erectile dysfunction. Kaczor: What’s that? Chong: I said time flies when you're talking about erectile dysfunction. Kaczor: Well, oxidative stress, being something that you mentioned and it’s just something that we’re … That inflammation is kind of always at the forefront of anyone who’s doing integrative medicine or optimal wellness or however you want to term it. I guess my thought is this. In a concise way, can you tell me if you use any actual blood markers that are widely available and what are some of your favorite ways of, kind of across the board, addressing oxidative stress issues, which even beyond erectile dysfunction, it becomes part and parcel with that but it’s also just part of life and part of being alive, is creating oxidation? Chong: Right. In the realm of assessment, especially if we were going to so far as to separate out inflammation in oxidative stress because obviously, they aren’t exactly the same thing, when we’re talking inflammation, the primary markers that I’m measuring with people certainly are high sensitivity CRP as our sort of general global marker of inflammation or lack thereof. When we’re talking about the vascular system, I’m also typically going to be checking something called Lp-PLA2 or what’s also known as the PLAC test. That is more specifically an inflammation marker for the vascular system so it’s going to actually reveal immunoactivity and inflammation going on in the wall of the artery whereas a high CRP is not going to be able to definitively determine that or not. MPO or myeloperoxidase is a later stage, nonspecific but frequently correlated marker for late stage vascular inflammation for a vulnerable vascular system. In the realm of oxidative stress, the 2 primary markers that I might look at is actually … number 1 is actually oxidized LDL so it’s pretty hard to have moderately elevated LDL levels and a high amount of oxidative stress and not see a relatively increased level of oxidized LDL in the bloodstream. That is sort of a good, what you'd call extracellular oxidative stress marker, but we can also get intracellular oxidative stress for different reasons. For that, you can also check something called 8-oxoguanine which is an actual, actually a urinary test. Not too many labs run that. I’m not sure if we’re supposed to name names here but that is an … If you just Google 8-oxoguanine test or something like that, you can probably find the labs that run that but that’s going to give you more of an assessment of intracellular oxidative stress. Then, beyond that, you can, in all honesty, get a pretty good idea whether or not somebody is going to be a candidate for high oxidative stress just by talking to them and looking at them and that type of thing as well. Kaczor: Yeah. A lot of those other markers for cardiovascular disease like obesity, even the aging process, certainly smoking, all- Chong: Right. Absolutely. Kaczor: Obviously, we would take into account for oxidation. Can you let me know or let the listeners know your top three? Someone looks at you and they’re like, “Listen. I do everything right. I exercise. I eat well. My BMI is normal. I don’t drink. I don’t smoke. What are the three supplements you …” You only get to see them once. They’re going to leave your office. Chong: These people are eating well, you said, in my opinion? Kaczor: Okay. That brings up the point. What would that look like in your opinion? Chong: No, no. I’m sorry. I’m just- Kaczor: We only have 2 minutes left but what would be an ideal guy in your opinion and then- Chong: No, no, no, no, no. I’m sorry. I was just clarifying the question. If these people are already eating well like they’re eating lots of fruits and vegetables, et cetera and I’m just talking about supplements, the 3 main ones I’m going to recommend are going to be vitamin C, magnesium, and then probably some type of concentrated plant-based antioxidant. As a naturopath, herbal medicine trained, I have an affinity to hawthorn but also, I frequently recommend hibiscus tea to people. Kaczor: Nice. Hibiscus being, you're also from Hawaii so that’s- Chong: Good point. You could certainly go beyond that and complement it with things like arginine, citrulline, and then there are a number of nitric oxide precursor type of products that are high in dietary nitrates. Kaczor: Well, Dan, I really appreciate this. I feel like we could have a whole part 2 where we go into the therapeutics and more details into all of this but I think the listeners have gotten good overview today and I really do appreciate the time you've taken and your expertise, and best of luck with your Healthy Heart Project. Chong: Thank you, Tina. It was good to talk to you and happy to help as I can. Kaczor: All right. Take care. Chong: All right.

QUESTION: "My Lp-PLA2  bloodwork shows me at risk for arterial inflammation.  I understand there is a new drug being tested to reduce Lp-PLA2.  Should I take it as soon as it is available?" GENERAL BACKGROUND: Advanced tests measure blood levels of an enzyme called lipoprotein phospholipase A2 (Lp-PLA2). The Lp-PLA2 enzyme unleashes a chain of harmful events culminating in endothelial dysfunction, which is a pathological abnormality in the blood vessel wall that sets the stage for atherosclerosis, plaque accumulation, and rupture. An elevated level of Lp-PLA2 may signal that an arterial plaque is susceptible to rupture, which could cause a clot to break loose, precipitating a heart attack or stroke.