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In today's episode we preview our brand-new pod: Queer Life Crisis: the stories, struggles and successes of the LGBTQ+ community (available on most podcast players). We also start out the new year right with a FUMPOTD to help kick off our first LDL broadcast of 2022. Happy new year, everybody!Music provided by Purple Planet: https://purple-planet.com.
For Simon Hill, the proof is in the plants. This physiotherapist-turned-celebrity-nutritionist roots everything in science, and he's established a brand that helps to educate and empower people to live their best lives through an active and plant-based lifestyle. Simon has coached stars such as Chris Hemsworth and worked with professional Australian football teams, but today, this serial entrepreneur and nutritionist is sharing his best tips and explaining the science behind them. Motivated by a love for sport and watching his dad have a heart attack at 15 years old, Simon is passionate about helping everyone achieve better health. Listen in for an educational and practical seminar on plant-based nutrition. What we discuss in this episode: - Simon's realization of what he didn't know about nutrition - Changing gears from physiotherapist to getting a masters in nutrition - Watching his Dad experience a heart attack as a teenager - How genes load the gun but lifestyle pulls the trigger - How his vegan brother helped him realize he didn't have to sacrifice anything as a vegan - Protein sources and individualized nutrition - Omega-3 index test - LDL and HDL cholesterol and cardiovascular risk - How our environment normalizes unhealthy foods - Government influence in the foods we eat - How to ease into plant-based eating - Simon's website: https://plantproof.com/ - Follow Simon on Instagram @plant_proof - Get your BOGO B12 deal at: puralityhealth.com/SwitchB12 Connect with Switch4Good - YouTube - https://www.youtube.com/channel/UCQ2toqAmlQpwR1HDF_KKfGg - Facebook - https://www.facebook.com/Switch4Good/ - Instagram - https://www.instagram.com/switch4good/ - Twitter - https://twitter.com/Switch4GoodOrg - Website - https://switch4good.org/
Monologue Dr. Joel Wallach begins the show today outlining the COVID 19 numbers of infections and deaths in the U.S. and worldwide numbers. Stating that people who are eating gluten and not supplementing with all 90 essential nutrients will be in trouble if the get the virus. Contending people need keep their bone marrow healthy as this where the immune system is located. Pearls of Wisdom Doug Winfrey and Dr. Wallach discuss a news article regarding a study from Tunissian study. Finding that rats fed a high fat diet were exposed to oxidative stress. Giving some rats apple cider vinegar which lowered their cholesterol, triglyceride and LDL. Also normalizing oxidative stress and metabolic changes brought on by the high-fat diet. Callers Barabara has osteoporosis and wants avoid the drugs her doctor is recommending. David asks Doc's opinion of fasting. Tanesha's father has Alzheimer's and is losing his memory. Sean has a friend with a connective tissue disorder affecting several body functions. Dee's father is in the ICU with a bad case of the COVID 19 virus. Eddie has a friend had prostate surgery and is now experiencing chronic pain. Call Dr. Wallach's live radio program weekdays from noon until 1pm pacific time at 831-685-1080 or toll free at 888-379-2552.
Today, I am blessed to have here with me Dr. Saladino. He is the leading authority on the science and application of the carnivore diet. He has used this diet to reverse autoimmunity, chronic inflammation and mental health issues in hundreds of patients, many of whom had been told their conditions were untreatable. In addition to his personal podcast, Fundamental Health, he can be found featured on numerous podcasts including The Minimalists, The Model Health Show, Bulletproof Radio, The Dr. Gundry Podcast, The Ben Greenfield Podcast, Dr. Mercola, Health Theory, Mark Bell's Power Project, and many others. He has also appeared on The Doctors TV show and will release his first book in 2020 titled, “The Carnivore Code: Unlocking the Secrets to Optimal Health by Returning to our Ancestral Diet.” In this episode, Dr. Paul Saladino first speaks about his appearance on the Doctors and how it was a complete hit job. Then, Dr. Saladino reveals the reason he started incorporating more carbohydrates into his diet. We talk about why insulin resistance isn't the best term to describe what is going on with people's health. Later, we dive into the importance of lowering your linolic acid intake. Tune in as we chat about omega-3s, why Dr. Paul doesn't eat any vegetables, and if there is a connection between eating meat and colon cancer. Get Heart & Soil Supplements here: https://shop.heartandsoil.co/discount/AFFILIATE10?rfsn=6331076.ba6cb5 90 Day Detox Program: http://www.ketokampdetox.com Order Keto Flex: http://www.ketoflexbook.com -------------------------------------------------------- / / E P I S O D E S P ON S O R S PureForm Omega Plant Based Oils (Best Alternative to Fish Oil): http://www.purelifescience.com Use ben4 for $4.00 off. Paleo Valley beef sticks, apple cider vinegar complex, organ meat complex & more. Use the coupon code KETOKAMP15 over at https://paleovalley.com/ to receive 15% off your entire order. Upgraded Formulas Hair Mineral Deficiency Analysis & Supplements: http://www.upgradedformulas.com Use KETOKAMP15 at checkout for 15% off your order. Text me the words "Podcast" +1 (786) 364-5002 to be added to my contacts list. [00:50] Dr. Paul Saladino Talks About His Appearance on The Doctors Before Dr. Paul's appearance on The Doctors, he was told it would be a debate. They had five doctors and one lawyer. Plus, they had a vegan doctor to argue against Dr. Paul. There was a lot of yelling, and Dr. Paul was barely given a chance to say what he needed to say. Paul invited them to his podcast to have an honest and genuine debate. None of them showed up. If you want to watch it on YouTube, check it out here: https://www.youtube.com/watch?v=uaPrrg4tytE [09:50] Why Dr. Paul Started To Eat More Carbohydrates Ketosis at the beginning for Dr. Paul without carbohydrates in his diet seemed fine. Eventually, Dr. Paul was getting a lot of muscle cramps, and he was getting heart palpitations at night. So, Dr. Paul started to reintroduce carbohydrates into his diet. First, he started to introduce honey into his lifestyle. After incorporating honey, Dr. Paul started to feel better. Blood sugar will spike when you include carbohydrates in your diet, especially honey. However, Dr. Paul's blood glucose tracing was very low. [22:50] Why Dr. Paul Doesn't Like The Term Insulin Resistance Paul doesn't like the term insulin resistance. He thinks metabolic dysfunction is a more precise term. He doesn't like to say insulin resistance because two types of insulin resistance are often confused and conflated. The first type of insulin resistance is physiologic insulin resistance. Humans have evolved a state known as ketosis, which goes hand in hand with physiologic insulin resistance. Then, there is pathological insulin resistance. Many people who exclude carbohydrates will see improvements in their physiology. [34:50] The Importance of Decreasing The Amount of Linoleic Acid In Your Diet Many people should decrease the amount of linoleic acid in their diet. We have to understand how much linoleic acid is in the foods we eat as humans. Soybean oil has 45 to 50% linoleic acid. Butter and tallow, which has rendered animal fat from cows, will have much lower levels of linoleic acid, around 2%. The composition of our cell membranes takes a long time to change. So, breaking down the linoleic acid will take a great deal of time. A low carbohydrate approach will help lower the linoleic acid in your diet. [40:00] What Happens When We Consume Too Much Linoleic Acid When we eat more linoleic acid, we can find more oxidized LDL. The oxidation and the instability of linoleic acid is one of the problems. There could be some potentially hormonal roles for linoleic acid that are negative as well. The underlying thing to consider here is an evolutionarily appropriate diet for humans. We consume much more linoleic acid than we ever have. [47:25] Should You Be Taking Fish Oils on The Ketogenic Diet? Fish oil spoils extremely fast. These oils are so fragile, and we're putting them in capsules, and we're presuming that they're not oxidized. The only place Dr. Paul is getting omega-3 is essentially from ruminant animal fat. Paul is not convinced that omega-3s are that beneficial or that we should be pumping ourselves full of them. There have been millions and millions of humans that have no access to coastal foods; they did just fine from eating land animals. [64:35] You Want To Push Your Linoleic Acid Consumption As Low As Possible Paul says to keep your linoleic acid consumption as low as possible. The human body can't make omega-6, but there's omega-6 in everything. The linoleic acid composition of a mother's breast milk changes based on their dietary consumption. If you look at the hunter-gatherers, their linoleic acid in the breast milk is much lower because they're eating so little linoleic acid in their diet. [70:10] Thirty Days To Radical Health Paul is doing an animal-based 30-day challenge. In fact, Dr. Paul challenges you to try an animal-based diet for 30 days and NOT flourish! Learn more about the challenge here: https://animalbased30.com/ When you sign up, he will send you a free infographic and an eBook. [75:55] Are There Any Vegetables That You Should Be Eating? If you think canonically about what a vegetable is, it's the part of a plant that it doesn't want you to eat. Vegetables don't have a role in human health unless you want to go to great lengths to detoxify them. If you want to do vegetables, ferment the heck out of them and maybe do something like sauerkraut. Even some fruit can be problematic for humans. [88:10] Is There Really A Connection Between Eating Meat and Colon Cancer? We've been cooking meat for more than a million years. Calcium is an essential part of every human diet, whether you're getting it from bones or you're getting it from good sources of dairy. When you have more calcium in the diet, you tend to see lower rates of colon cancer. Overall, we should go back to the idea of what's evolutionarily consistent, and we try to understand that as best as possible to inform our behaviors. AND MUCH MORE! Resources from this episode: Check out Carnivore MD: https://carnivoremd.com Follow Dr. Paul Saladino Instagram: https://www.instagram.com/carnivoremd2.0/ Twitter: https://twitter.com/carnivoremd Facebook: https://www.facebook.com/carnivoreMD/ YouTube: https://www.youtube.com/c/paulsaladinomd Get The Carnivore Code: https://carnivoremd.com/my-book/ Listen to Dr. Paul Saladino, Benefits of Eating Meat on The Carnivore Diet, Dangers of Lectins in Food: KKP 87: https://poddtoppen.se/podcast/1470779784/the-keto-kamp-podcast-with-ben-azadi/dr-paul-saladino-benefits-of-eating-meat-on-the-carnivore-diet-dangers-of-lectins-in-food-kkp-87 The Fundamental Health Podcast: https://carnivoremd.com/podcast/ Get Heart & Soil Supplements here: https://shop.heartandsoil.co/discount/AFFILIATE10?rfsn=6331076.ba6cb5 Join theKeto Kamp Academy: https://ketokampacademy.com/7-day-trial-a WatchKeto Kamp on YouTube: https://www.youtube.com/channel/UCUh_MOM621MvpW_HLtfkLyQ 90 Day Detox Program: http://www.ketokampdetox.com Order Keto Flex: http://www.ketoflexbook.com -------------------------------------------------------- / / E P I S O D E S P ON S O R S PureForm Omega Plant Based Oils (Best Alternative to Fish Oil): http://www.purelifescience.com Use ben4 for $4.00 off. Paleo Valley beef sticks, apple cider vinegar complex, organ meat complex & more. Use the coupon code KETOKAMP15 over at https://paleovalley.com/ to receive 15% off your entire order. Upgraded Formulas Hair Mineral Deficiency Analysis & Supplements: http://www.upgradedformulas.com Use KETOKAMP15 at checkout for 15% off your order. Text me the words "Podcast" +1 (786) 364-5002 to be added to my contacts list. *Some Links Are Affiliates* // F O L L O W ▸ instagram | @thebenazadi | http://bit.ly/2B1NXKW ▸ facebook | /thebenazadi | http://bit.ly/2BVvvW6 ▸ twitter | @thebenazadi http://bit.ly/2USE0so ▸clubhouse | @thebenazadi Disclaimer: This podcast is for information purposes only. Statements and views expressed on this podcast are not medical advice. This podcast including Ben Azadi disclaim responsibility from any possible adverse effects from the use of information contained herein. Opinions of guests are their own, and this podcast does not accept responsibility of statements made by guests. This podcast does not make any representations or warranties about guests qualifications or credibility. Individuals on this podcast may have a direct or non-direct interest in products or services referred to herein. If you think you have a medical problem, consult a licensed physician.
Why You Should Listen: In this episode, you will learn about Integrative Cardiology. About My Guest: My guest for this episode is Dr. Jack Wolfson. Jack Wolfson, DO, FACC is a board-certified cardiologist and a fellow of the American College of Cardiology. He has emerged as one of the world's leading holistic natural cardiologists and was a Natural Choice Award Winner in the Holistic MD category from Natural Awakenings Magazine. His ideas have been featured by NBC and CNN and covered in publications like USA Today and The Wall Street Journal. Prior to opening Wolfson Integrative Cardiology, Dr. Jack was Chairman of the Department of Medicine and Director of Cardiac Rehabilitation at Paradise Valley Hospital in Arizona. He was also a partner in Arizona's largest cardiology practice. As a trusted leader in heart health and natural heart health, Dr. Jack has taught more than 10,000 physicians his natural heart health best practices. His book, The Paleo Cardiologist: The Natural Way to Heart Health, was an Amazon #1 best seller. He is an in-demand lecturer about natural healthy living without Big Pharma pills and invasive procedures. Key Takeaways: - Why is cholesterol not the cardiovascular risk factor once thought to be? - How might one mitigate the impact of statin medications? - How important is LDL particle size and LP(a)? - What is the role of sugar in higher levels of cholesterol? - Should salt be avoided? - Is aspirin beneficial for minimizing heart attacks and strokes? - Can supplemental calcium lead to systemic calcification? - How might the Carnivore diet be helpful? - Might reverse osmosis or distilled water be a healthy option? - What is the role of food allergy in systemic inflammation? - What are the primary causes of high blood pressure? - Is POTS a cardiovascular problem or an autonomic nervous system problem? - What is the role of nitric oxide in optimizing circulation? - Does poor dentition contribute to cardiovascular issues? - What infections or toxicants may contribute to heart issues? - Can EMFs impact the electrical system of the heart? - What are some tools that can be helpful in supporting optimal cardiovascular health? Connect With My Guest: https://NaturalHeartDoctor.com Related Resources: Book: Paleo Cardiologist: The Natural Way to Heart Health - https://FreeHeartBook.com https://WolfsonIntegrativeCardiology.com https://TheDrsWolfson.com Interview Date: January 5, 2022 Transcript: To review a transcript of this show, visit https://BetterHealthGuy.com/Episode159. Additional Information: To learn more, visit https://BetterHealthGuy.com. Disclaimer: The content of this show is for informational purposes only and is not intended to diagnose, treat, or cure any illness or medical condition. Nothing in today's discussion is meant to serve as medical advice or as information to facilitate self-treatment. As always, please discuss any potential health-related decisions with your own personal medical authority.
Levels Chief Medical Officer, Dr. Casey Means, talks with Levels advisor and author of Metabolical to discuss how to interpret your cholesterol panel in order to better understand your metabolic health. Dr. Lustig walks through what HDL, LDL, triglycerides, and total cholesterol mean, how fasting insulin tests relate to your cholesterol panel, and how to improve your cholesterol numbers. This episode dives into how to interpret ratios of your cholesterol numbers like triglyceride-to-HDL ratio to learn more about your metabolic health. Grab a pen, your recent cholesterol panel, and this episode to work through your numbers! This is a companion episode to this article: https://www.levelshealth.com/blog/the-ultimate-guide-to-understanding-your-cholesterol-panel-and-metabolic-blood-tests This episode DOES NOT CONSTITUTE MEDICAL ADVICE. Please talk to your doctor about all diagnostic testing. Become a Levels Member – levelshealth.com Learn about Metabolic Health – levelshealth.com/blog Follow Levels on Social – @Levels on Instagram and Twitter
I had the pleasure of sitting down with Dr. Eric Westman. We talked about all things related to the ketogenic diet and what he's observed from the decades he's been practicing, researching and teaching.. Dr. Westman is an Associate Professor of Medicine at Duke University. He is Board Certified in Obesity Medicine and Internal Medicine, and co-founded the Duke Keto Medicine Clinic with Dr. William S. Yancy Jr. in 2006 after 8 years of clinical research regarding low carbohydrate ketogenic diets.Dr. Westman is a New York Times best-selling author of such books as The New Atkins for a New You, Cholesterol Clarity, and Keto Clarity. He is also a co-founder of Adapt Your Life, an education and product company based on low carbohydrate concepts.We discuss the following:2:09 All about Dr. Eric Westman3:33 Keto Clarity and Cholesterol Clarity book4:28 Cholesterol and the belief that it's causing cardiovascular disease7:32 Risk of eating too many carbohydrates with fats and proteins9:22 Thoughts on keto causing ketoacidosis and that carbs are essential for optimal health11:50 End Your Carb Confusion book14:50 Thoughts on PUFAs22:32 Thyroid health and keto24:30 Can insulin be too low?26:02 The power of food30:44 Food addiction element32:28 Testosterone health and keto37:10 Thoughts on being in and out of ketosis40:58 Simple rules are needed to achieve success43:45 Internet-based keto vs. evidence-based keto video46:10 Tips and thoughts on low energy after doing keto for a while50:08 Cholesterol class55:14 Thoughts on LDL going up 1:01:17 Where to find Dr. Eric Westman_____RESOURCES- Dr. Eric Westman: https://ericwestmanmd.com/- Adapt Your Life Academy: https://adaptyourlifeacademy.com/- Facebook: https://www.facebook.com/AdaptYourLife- Instagram: https://www.instagram.com/AdaptYourLife/- YouTube: https://www.youtube.com/c/AdaptYourLife- New Book: End Your Carb Confusion: https://amzn.to/32nRm8q - Book: Cholesterol Clarity: https://amzn.to/3Fn1NI0 - Keto: Science-Based Versus Internet-Based: https://www.youtube.com/watch?v=qH_DyjphfpU ____CHECK OUT MY BOOK, Carnivore CureSIGN UP FOR MY WEEKLY NEWSLETTER_____ ADDITIONAL RESOURCESNutrition with Judy ArticlesNutrition with Judy ResourcesCutting Against the Grain Podcast_____ FIND ME
If you have high cholesterol levels and searching for evidence-based ways to reduce it, in this episode - a replay from 2019- I discuss several supplements and lifestyle changes that may help lower your total cholesterol and LDL bad cholesterol levels. I also review a weird report of a tapeworm causing muscles to grow larger (hypertrophy) like a bodybuilder. Support The Podcast Here's how you can support the podcast Click Here to contribute any amount to PayPal: Venmo: @ Joe-Cannon-38 (any amount) ==================================== Order My Rhabdo Book Rhabdomyolysis is the painful and serious side effect of exercise you need to know about. I've been teaching about rhabdo for over 10 years. If you are in the US, you can order them directly from me. I'll even autograph it if you like. Purchase My Rhabdo Book Order on Amazon ==================================== Connect with me: Joe-Cannon.com com My YouTube Channel My books: All my books on Amazon ====================== Disclaimer: Episodes are for information only. I'm not a medical doctor. No medical advice is given or implied. Always consult your doctor for the best health advice for you. I participate in the Amazon Associates program.
Jay is speaking publicly about his high LDL cholesterol.Every 40 seconds someone in the U.S. has a heart attack or stroke.Lowering your LDL cholesterol (the "bad" cholesterol) is considered the most modifiable risk factor. However, many people do not understand the connection between having high levels of “bad” cholesterol and their risk of cardiovascular disease. With cholesterol, there's no warning sign. You don't feel it, but it could lead to a heart attack and hit you out of nowhere.Jay Leno has teamed up with Amgen on Cholesterol 911, a national campaign that is aiming to raise awareness of and sound the alarm on high LDL-C, also known as “bad” cholesterol, and its link to heart attack and stroke.Jay is speaking publicly about his high LDL and urging patients with high bad cholesterol who are at increased risk for a heart attack or stroke to see the emergency in high bad cholesterol and to visit Cholesterol911.com to learn more about their risks and how to talk to their doctor about new treatment options.Listen as Jay joins Dr. Friedman in this encore episode from March 2019 to discuss more on the campaign and share his own efforts to lower his LDL-C. The two also chat about cars, Last Man Standing, The Tonight Show, Rodney Dangerfield, and more.
Jay is speaking publicly about his high LDL cholesterol.Every 40 seconds someone in the U.S. has a heart attack or stroke.Lowering your LDL cholesterol (the "bad" cholesterol) is considered the most modifiable risk factor. However, many people do not understand the connection between having high levels of “bad” cholesterol and their risk of cardiovascular disease. With cholesterol, there's no warning sign. You don't feel it, but it could lead to a heart attack and hit you out of nowhere.Jay Leno has teamed up with Amgen on Cholesterol 911, a national campaign that is aiming to raise awareness of and sound the alarm on high LDL-C, also known as “bad” cholesterol, and its link to heart attack and stroke.Jay is speaking publicly about his high LDL and urging patients with high bad cholesterol who are at increased risk for a heart attack or stroke to see the emergency in high bad cholesterol and to visit Cholesterol911.com to learn more about their risks and how to talk to their doctor about new treatment options.Listen as Jay joins Dr. Friedman in this encore episode from March 2019 to discuss more on the campaign and share his own efforts to lower his LDL-C. The two also chat about cars, Last Man Standing, The Tonight Show, Rodney Dangerfield, and more.
Alzheimer's disease and dementia prevalence and deaths are on the rise, claiming over 6,000 lives in the USA every week! Yet many people don't even know their APOE genotype, which arguably has the biggest impact on future Alzheimer's disease and dementia as well as cardiovascular disease risk. In this show we dive deeper into what the APOE gene does and how knowing this info can help tweak your nutrition and lifestyle helping to reduce risk of future disease—especially if you have one or two copies of the APOE ε4 gene. Save on your Omega-3 Index Test by MYOXCIENCE Nutrition: http://bit.ly/omega-3-index Use code Podcast at checkout Link to Video + Show Notes: https://bit.ly/apoe-gene-alzheimers Eat Like Your Life Depends on it Tee Shirt: http://bit.ly/myoxcience Enroll in the Blood Work MasterClass: https://bit.ly/blood-work-masterclass Time Stamps: 0:00 Intro 00:53 APOE is a gene that makes proteins that are involved in lipid binding. 01:10 APOE and Immunity 01:39 APOE 4 alleles and Alzheimer's disease risk 03:13 3 different APOE isoforms: APOE2, APOE3, APOE4 allele. 03:44 Having the gene does not mean that you will get the disease. 04:35 APOE is involved in lipid metabolism 05:30 Lipoproteins and lipids transport 06:05 APOE can redistribute lipids across tissues and cell types. 07:40 APOE is secreted by the liver with VLDL and bile acids 08:00 Lipoprotein lipase facilitates your metabolic deposits. Hormone sensitive lipase facilitates your metabolic withdrawals. 09:42 Your omega 3 index and APE 4 isoform. 11:35 APOE4 and cholesterol 11:45 ApoB VS ApoE 12:09 APOE2 carriers tend to have a less atherogenic lipid profile. 12:15 APOE4 carriers are associated with decreased levels of APOE triglycerides and increased levels of APOB in lipoproteins 13:12 APOE4 puts genotype carriers at increased risk for heart disease. This is likely due to the association with APOE4 and elevated LDL and Apolipoprotein B. 14:07 APOE4 primes your microglia to be more inflammatory. Microglia are brain immune cells. They are involved in synaptic processing, pruning of cells, shaping neurons, and removing inflammatory debris. APOE4 carriers have decreased cerebral glucose metabolism and increased levels of beta amyloid and tau protein. 15:50 With APOE4, there are changes and increase of tau protein within the neurons. There are also alterations in the blood brain barrier integrity. 16:00 To preserve the integrity of the brain, moderate alcohol consumption, increase exercise, incorporate sauna therapy and sauna bathing, as it effects cerebral blood flow. 16:45 APOE is expressed in astrocytes, microglia and other vascular cells within the brain. Blood brain barrier prevents toxins and metabolic waste from going into your brain. Increased expression of APOE is detected in stressed neurons. 17:42 APOE isoforms affect lipid transport, glucose metabolism, mitochondrial function, synaptic plasticity, beta amyloid protein expression, tau protein and cerebral vascular function within the brain. 18:18 Ratio of APOE4 allele correlates with loss of gray matter volume and abnormal glucose metabolism, a hallmark of Alzheimer's and dementia. 19:00 APOE4 is the greatest genetic risk factor for late onset Alzheimer's disease. It also influences the risk and outcomes for stroke, MS, Parkinson's disease, and frontotemporal dementia. 22:11 A low carb diet, high in wild caught fish, is protective for APOE4 carriers. It impacts brain metabolism and lipid levels favorably. Drive your glycemic load down. 24:05 If you are over the age of 50 and have one or two copies of the APOE4 allele, consider microdosing with rapamycin. Rapamycin is an mTOR inhibitor. It may delay the onset of Alzheimer's and dementia.
: Episode 2003 - On this special Sunday episode, we play a best-of featuring Dr. Jeffry Gerber. Dr. Gerber joins Vinnie to talk about the triglyceride to HDL ratio, insulin resistance, good medical studies, Dr. Gerber's book with Ivor Cummins, , and more! https://vinnietortorich.com/2021/12/best-of-insulin-resistance-cholesterol-jeffry-gerber-episode-2003 PLEASE SUPPORT OUR SPONSORS DR. JEFFRY GERBER Dr. Gerber has appeared on this show before! https://jgerbermd.com/ He is friends and colleagues with another one of Vinnie's favorites, Ivor Cummins. Dr. Gerber's been at this now for 28 years. For the first 10 years, he was clueless about diet and the like, but since, he's educated himself and is now a leading expert in nutrition and diet and the like. DOCTORS AND HEALING Doctors are using medications to stop fires. For many doctors, it's hard to realize just giving medication is not the right course of action. It must be more holistic. Dr. Gerber struggled with weight issues, and tried dietary modifications. He saw LCHF worked for a patient, then did his studies and homework. Once he tried it for himself and had success, he expanded it for his patients. Non-doctors were the ones who ID'd sat fats creating cholesterol as the problem. A relatively new paper in Lancet challenges Ancel Keys's 7 Country Study. This is the real science. People trust their doctors -- but sometimes, people need to be more investigative, and not just accept one answer -- listen to many experts, like Dr. Gerber! INSULIN RESISTANCE .HDL and triglyceride ratio is a marker for insulin This will go down if you eat LCHF most of the time because your metabolic issues will lessen. LDL not the problem, your ratio is a bigger issue. The ratio also demonstrates your insulin resistance which is the indicator of risk for bad health including cardiac health. PRE-ORDER BEYOND IMPOSSIBLE Vinnie's new documentary is now available for pre-order on Apple TV (iTunes). This is his third documentary in just over three years. It will be available on January 11th. Here is the link to the pre-order: Share this link with friends, too! Gina loves the film. She says "it's so Vinnie!" FAT DOC 2 IS AVAILABLE ON iTUNES and AMAZON Please also share it with family and friends! Buy it and watch it now on iTunes to get it to the top of the charts. We need it to get big for people to see it. Here's the (BLUERAY, DVD, PRIME) (MAY NOT BE AVAILABLE YET ACROSS THE POND). And the And the https://amzn.to/3rxHuB9 PLEASE DON'T FORGET TO REVIEW the film AFTER YOU WATCH! FAT DOC 1 IS ALSO OUT Go watch it now! We need people to buy and review for it to stay at the top of iTunes pages. Available for both rental and purchase. You can also buy hardcopy or watch online at Amazon. YOU CAN NOW STREAM FOR FREE ON AMAZON PRIME IF YOU HAVE IT! RESOURCES Https://www.vinnietortorich.com Https://www.purevitaminclub.com Https://www.purevitaminclub.co.uk Https://www.purecoffeeclub.com Https://www.bit.ly/fatdocumentary
Standard lipid panels are actually mathematical approximations. Emerging data suggests using the very affordable ApoB to ApoA1 ratio more accurately assess cardiometabolic disease risk. Save on your Omega-3 Index Test by MYOXCIENCE Nutrition: https://bit.ly/omega-3-index Use code Podcast at checkout Download the bloodwork cheatsheet: https://bit.ly/3dyy4zM Enroll in the Blood Work MasterClass Time Stamps 0:45 ApoB why it's more accurate 1:30 High LDL on a ketogenic diet 2:24 Heart disease deaths increase in the winter 2:59 High LDL after fasted exercise 4:50 What ApoB means and why it matters 7:15 Why Omega-6 seed oils are bad if your LDL is high 9:11 Request your ApoB to A1 ratio instead 9:38 Standard cholesterol tests are a mathematical estimate 12:06: HDL and ApoA-1, how it's cardioprotective 12:45 Harvard case study of LDL increases on a Keto diet 19:25 Advanced lipoprotein particle testing overview
Nella mattinata di mercoledì 22 dicembre, ai microfoni di Laura Basile è intervenuto Giulio Stefanini, cardiologo dell'istituto clinico Humanitas, per parlarci di colesterolo. Il colesterolo non è niente altro che il grasso che circola nel sangue. È normale che ci sia, l'importante è che non abbia una concentrazione eccessiva. Abbiamo due tipi di colesterolo: in particolare il colesterolo LDL è quello da tenere sotto controllo. Se supera una certa soglia rappresenta un'importante funzione di rischio cardiovascolare. Per evitare di aumentare il livello di colesterolo cattivo bisogna evitare un eccesso di grassi di origine animale. Spesso è consigliabile fare attività fisica, ma non è l'attività fisica a bruciare il colesterolo. Per evitare un Natale al colesterolo non eccedere coi grassi di origine animale, non dimenticarsi di mangiare la verdura e bere alcool con moderazione.
Dr. Jellinger joins the podcast to discuss the lipid section of the DCRM Multispecialty Practice Recommendations, as well the role of combination therapies and other concepts to lower LDL and what is coming next for the field of diabetes in 2022.
Procarenow.com for free samples. Use Code: Susan10 to save 10%Every holiday season several of my friends and my husband ask…”Hey, are you going to make that chocolate peanut treat? I want some.” In this episode I'll share my favorite, fast, go-to chocolate recipe. You won't believe how easy it is.Did you already ask yourself…can I have chocolate? I hope you answered yourself YES and remembered when I'm down the track from surgery, according to Dr. Susan, I can have small amounts of the foods I love. Video on how to make Chocolate Peanut Butter Crunch ClustersHere's what you need:1/2 cup natural peanut butter, creamy or crunchy2 cups dark chocolate chips or chunks2 cups unsalted or lightly salted, dry roasted peanuts Combine the peanut butter and the chocolate chips in a large microwavable bowl and microwave 30-40 seconds at a time on medium power until melted. Stir to blend the chocolate and the peanut butter.Stir in the chopped peanuts.Spoon the mixture onto parchment paper or wax paper about a tablespoon at a time. Chill in the fridge until firm. Listen to the episode for all the deets.Chocolate has health benefits. There are several you'll be happy to know. The naturally found flavonoids in chocolate may improve blood flow, reduce blood pressure and lower lousy or LDL cholesterol. I bet you never thought that chocolate is a source of fiber. The undigested fiber in cocoa is broken down in the gut and can be combined with prebiotics to produce anti-inflammatory compounds. There's a lot more information in episode #40 if you missed it: 3 Surprising Health Benefits of Chocolate. It goes in depth on dumping syndrome, ingredients you don't want in your chocolate, etc.We're just a few weeks away from a fresh new year. Be sure and sign up now for my weekly Breaking Down Nutrition newsletter. You'll be the first to know about new freebies, upcoming courses, tips, product discounts and of course, the latest podcast episode. It's super easy to sign up on my home page https://www.breakingdownnutrition.com While you're on the homepage, join me in the private Facebook group, the Bariatric Surgery Success community. You'll see the JOIN button on the homepage.If you need a festive meal plan for the holidays, go get this freebie. The meal plan comes complete with appetizer, entree, side and dessert plus the recipes and color photos of each recipe. It's available now to the end of December and you can find it on my homepage too.
Monologue Dr. Joel Wallach begins the show today discussing the tornadoes in Kentucky and other states. Also citing the COVID 19 numbers of infections and deaths. Stating people with pre-existing health challenges will be in trouble if the contract the virus. Asserting people should support their immune systems by supplementing with all 90 essential nutrients. Pearls of Wisdom Doug Winfrey and Dr. Wallach discuss a news article regarding the health benefits of eating foods with quercetin. A flavonoid antioxidant that can support proper blood pressure, blood sugar and lowers LDL. Neutralizing free radicals preventing the cell damage they cause. Experts recommend dosages between 500 and 1000 mg per day. Callers Madrew has a friend that has high blood pressure and is recovering from breast cancer. Bruce has two questions first asks Doc if oats have gluten. Second he has questions for his brother that has an abdominal hernia and low back pain. Ken asks Doc about an 80 pound dog diagnosed with Cushings disease. John has excessive ear wax and asks how best to clear it out. Call Dr. Wallach's live radio program weekdays from noon until 1pm pacific time at 831-685-1080 or toll free at 888-379-2552.
Those with genetic mutations that leave them with an LDL cholesterol of 30 live exceptionally long lives. Can we duplicate that effect with drugs?
Please join Guest Host Mercedes Carnethon along with first author Connie Hess and Guest Editor Gregory Lip as they discuss the article "Reduction in Acute Limb Ischemia With Rivaroxaban Versus Placebo in Peripheral Artery Disease After Lower Extremity Revascularization: Insights From VOYAGER PAD." 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 Poly Heart Center at VCU Health in Richmond, Virginia. Dr. Carolyn Lam: Greg, our feature discussion is on a really important topic, peripheral artery disease. So important, so rampant, not talked about enough. And it's really insights from the VOYAGER-PAD trial telling us about the reduction in acute limb ischemia with Rivaroxaban versus placebo in peripheral artery disease after lower extremity revascularization. But before we get into all that, I want you to get your coffee while I tell you about my picks of today's issue. Should I start? Dr. Greg Hundley: Very good. Dr. Carolyn Lam: Okay. So the first paper deals with the residual ischemic risk following coronary artery bypass grafting surgery. We know that despite advances, patients following CABG still have significant risk. So this paper refers to a subgroup of patients from the REDUCE-IT trial with a history of CABG, which was analyzed to evaluate the efficacy of icosapent ethyl treatment in the reduction of cardiovascular events in this high risk patient population. Now, as a reminder, the REDUCE-IT trial was a multicenter, placebo controlled, double blind trial, where statin treated patients with controlled LDL cholesterol and mild to moderate hypertriglyceridemia were randomized to four grams daily of icosapent ethyl or placebo. They experienced a 25% reduction in risk of a primary efficacy endpoint, which was cardiovascular death, MI, stroke, coronary revascularization, or hospitalization for unstable angina. Now the current report tells us about the subgroup of patients from the trial with a history of CABG. Dr. Greg Hundley: Ah, Carolyn. So what did they find in this subgroup of patients? Dr. Carolyn Lam: So of the 8,179 patients randomized in REDUCE-IT, 22.5% had a history of CABG with 897 patients randomized to icosapent ethyl and 940 to placebo. Baseline characteristics were similar between the treatment groups and randomization to icosapent ethyl was associated with a significant reduction in the primary endpoint, as well as in key secondary endpoint and in total ischemic events compared to placebo. This yielded an absolute risk reduction of 6.2% in first events with a number needed to treat of 16 over a median follow up time of 4.8 years. So, Greg, I think you'll agree, icosapent ethyl may be an important pharmaco-therapeutic option to consider in eligible patients with a history of coronary artery bypass grafting surgery. Dr. Greg Hundley: Very nice, Carolyn. What an excellent summary. So Carolyn, for my first paper... And this study comes to us from Professor Judith Haendeler from the Leibniz Research Institute for Environmental Medicine. So Carolyn, this is a new type of quiz question. And as you listen to the presentation, help us predict the clinical implications. Okay, here we go. Dr. Greg Hundley: All right. So Carolyn, telomerase, also called terminal transferase, is a ribonuclear protein that adds a species dependent telomere repeat sequence to the three prime end of telomeres. And Carolyn, just to refresh our memories, a telomere is a region of repetitive sequences at each end of the chromosomes of most eukaryotes. And telomerase was discovered interestingly by Carol Greider and Elizabeth Blackburn in 1984. And together with some others, including Jack Szostak, they were awarded the 2009 Nobel Prize in physiology and medicine for discovery. Dr. Greg Hundley: So Carolyn, telomerase is active in gamuts and most cancer cells, but is normally absent from or at very low levels in most somatic cells. And the catalytic subunit of telomerase called telomerase reverse transcriptase or trt has protective functions in the cardiovascular system, particularly in regard to ischemia reperfusion injury. And interestingly trt or telomerase reverse transcriptase is not present in the nucleus, but also in mitochondria. However, for us in cardiovascular medicine, it is unclear whether nuclear or mitochondrial trt is responsible for the observed protection. Dr. Carolyn Lam: Wow, fascinating. So what did today's paper find? Dr. Greg Hundley: Right, Carolyn. So it was mitochondrial, but not nuclear telomerase reverse transcriptase that was found critical for mitochondrial respiration during ischemia reperfusion injury. And mitochondrial telomerase reverse transcriptase improves complex 1 subunit composition. And trt is present in human heart mitochondria and remote ischemic preconditioning increases its level in these organelles. Also, Carolyn TA65 was found to have comparable effects ex vivo and improved migratory capacity of endothelial cells and myofibroblast differentiation. So Carolyn, with this summary, can you help speculate on the clinical implications of this paper? Dr. Carolyn Lam: Oh, Greg. You set it up so nicely. So I would speculate that the clinical implications are that an increase in the mitochondrial telomerase reverse transcriptase or trt would be able to help with cardioprotection in ischaemic reperfusion injury, or at least that's what we hope and that's where we should be going with this. Am I right? Dr. Greg Hundley: Absolutely, Carolyn. So in the future, this research showing that trt and cardioprotection... Maybe we increase this and it could serve as a therapeutic strategy. Excellent job, Carolyn. Dr. Carolyn Lam: Thank you, Greg. All right. My next paper is a preclinical paper. I will spare you of difficult quizzes and maybe... This is just so neat. Let me tell you about it. So the study really provides novel insights into the mechanisms underlying smooth muscle cell phenotypic modulation that contributes to the development of vascular diseases like renal atherosclerosis and restenosis after angioplasty. So very important. Dr. Jiliang Zhou from Medical College of Georgia and colleagues basically used an in silico approach to probe unbiased, proprietary, and diverse, publicly available bulk RNA-Seq and scRNA-Seq datasets to search for smooth muscle cell specific long non-coding RNAs or lncRNAs. Dr. Carolyn Lam: The search ended up identifying CARMN, which stands for cardiac mesoderm enhancer-associated non-coding RNA, CARMN. As a highly abundant, highly conserved smooth muscle cell specific lncRNA, CARMN was recently reported to play roles in cardiac differentiation and was initially annotated as a host lncRNA for the microRNA, the MIR143145 cluster, which is the best characterized microRNAs in regulating smooth muscle cell differentiation and phenotypical modulation. Dr. Carolyn Lam: But in the current study, the authors confirmed the expression specificity of CARMN using a novel GFP knock-in reporter mouse model, and discovered that CARMN is downregulated in various vascular diseases. They further found that CARMN is critical for maintaining vascular smooth muscle cell contractile phenotype, both in vitro and in vivo by directly binding to the smooth muscle cell specific transcriptional cofactor known as myocardit. Dr. Greg Hundley: Okay. Carolyn, what a beautiful summary here. So what's the take home message here? Dr. Carolyn Lam: So these findings collectively suggest that CARMN is a key regulator of vascular smooth muscle cell phenotype, and therefore represents a potential therapeutic target for the treatment of smooth muscle cell related proliferative diseases. Dr. Carolyn Lam: Well, Greg, thanks for letting me to tell you about that one. But let me tell you also about other papers in today's issue. There's an exchange of letters between Dr's Lee and Chew on high rates of coronary events in the rapid troponin T0 one hour protocol. Is it a reality or illusion? There's an ECG Challenge by Dr. Liu on “Acute Inferior Wall Myocardial Infarction. What is the Culprit Artery? In Cardiology News, Bridget Kuehn writes on persistent heart effects of COVID-19 and how that emphasizes the need for prevention. Dr. Greg Hundley: Very nice, Carolyn. Well, I've got a Research Letter to tell you about from Professor Huang, entitled “High Prevalence of Unrecognized Congenital Heart Disease in School-Age Children in Rural China: A Population-Based Echocardiographic Screening Study.” Well, Carolyn, what a fantastic issue. And how about we get onto that feature discussion now and learn more out lower extremity revascularization and insights from the VOYAGER-PAD study? Dr. Carolyn Lam: Let's go, Greg. Dr. Mercedes Carnethon: Good morning, everyone. Welcome to this episode of Circulation on the Run podcast. I'm Mercedes Carnethon, Professor and Vice Chair of Preventive Medicine at the Northwestern University Feinberg School of Medicine and associate editor of the journal. Really excited today to hear from one of our authors of a particularly interesting piece that we'd like to discuss today about peripheral artery disease after lower extremity revascularization. Dr. Mercedes Carnethon: And we have with us today, the lead author, Dr. Connie Hess from the division of cardiology at the University of Colorado School of Medicine in Aurora. And we have Dr. Gregory Lip with us. So welcome to the both of you. Professor Gregory Lip: Hello there. Dr. Connie Hess: Thank you for having me. Dr. Mercedes Carnethon: Thank you both for joining us. This is really exciting. I know that when I read this piece, I was really excited to think about the implications that these study findings from this clinical trial will have for a very important clinical problem of peripheral arterial disease and those complications. So, Connie, would you be willing to start by telling us a little bit about what you found in this study? Dr. Connie Hess: Yeah, absolutely. I think maybe a good place to start first is, if that's okay, is just a little bit of the background and why we looked at this and thought to look at this. I think as you're both probably aware, peripheral artery disease is a very highly prevalent condition. It affects a lot of people, but there's not a lot of awareness about it. It's in some ways the forgotten manifestation of atherosclerosis. And so acute limb ischemia in particular is a very feared complication of peripheral artery disease. And unlike things like ST elevation, myocardial infarction, and stroke about which patients and providers have a lot of knowledge and understanding, many people don't know about acute limb ischemia. And in particular ALI, acute limb ischemia, is a complication of peripheral revascularization that many of us as proceduralists are very concerned about. Dr. Connie Hess: And so what we wanted to do was use this very unique clinical trial and dataset to look at acute limb ischemia, to describe it, to better understand it, especially after a peripheral revascularization. And then also to look at the effect of Rivaroxaban plus aspirin versus aspirin alone on this feared outcome. We're lacking therapies to effectively prevent ALI. Dr. Connie Hess: And so if I just briefly review the trial, VOYAGER-PAD randomized 6,564 patients undergoing peripheral revascularization, both surgical or endovascular to Rivaroxaban, 2.5 milligrams twice daily versus placebo on top of aspirin. And then providers could use prochidagril for up to six months per their discretion. Now, the primary outcome for VOYAGER-PAD was very unique. This was a five point composite that looked at acute limb ischemia, major amputation of vascular etiology, myocardial infarction, ischemic stroke, or cardiovascular death. Dr. Connie Hess: And so in this trial in the primary results, Rivaroxaban plus aspirin versus aspirin alone was highly effective in reducing the primary endpoint, that five point composite I just described. And so we were excited to look specifically at the effect of this combination therapy on acute limb ischemia alone. What we found to begin with, I think in terms of describing acute limb ischemia is important. So the three year cumulative incidence in the patients assigned a placebo was about 8% for ALI. So this is not an uncommon problem. And in fact, we found that there was incidents of ALI occurring quite early after the procedure and that the risk persisted, even three years out. Dr. Connie Hess: And Rivaroxaban plus aspirin versus aspirin alone was very effective in reducing ALI by about 33%. Beyond that, we also looked at ALI in terms of severity of these complications. And we found that about a third of patients had a very severe ALI event that we defined as ALI followed by death, major amputation, or requiring a prolonged hospitalization with time in the intensive care unit. And for those patients, Rivaroxaban plus aspirin was even more effective with almost a 55% reduction. Dr. Connie Hess: Lastly, I think we also looked at just the patients who are at risk for ALI after peripheral revascularization. And we did identify some patient and procedural factors that might help us identify these patients. For example, having a prior lower extremity revascularization, having more severe PAD as indicated by a low ankle brachial index, undergoing surgical revascularization, and having longer target lesions. So I think we were able to describe ALI in a way that some other trials and datasets have not been able to do. And then also beyond that to provide some evidence for effective therapy to prevent this complication. Dr. Mercedes Carnethon: All of that is so exciting. And for somebody coming to this outside of the initial field, I can certainly see a lot of innovations that you describe in what you've done and the importance to the population of people who experience this very debilitating illness. So it's really wonderful to see this in print. So tell me, Greg, what excited you as the editor about this particular paper? So what made it really stand out in your mind? Professor Gregory Lip: Thanks, Mercedes. And firstly, congratulations to Dr. Hess for a really nice paper. And I think that it's really important because many cardiologists tend to neglect looking at and managing peripheral artery disease, especially with the medical therapies. And I think VOYAGER-PAD was an important advancement of how we can have... You could say, dual blockade, both with low dose anticoagulation plus antiplatelets should improve the outcomes. Professor Gregory Lip: So I think it really brings to the forefront how we should optimize medical therapy and peripheral disease. It's not simply a matter of surgery or just intervention with stenting. And I think maybe the other important aspects in regard to this study, this trial is when you combine an antiplatelet with an anticoagulant, it's worth flagging up the potential for added risk of bleeding. And it's therefore the fact that your analysis included to identify the patients at high risk of acute limb ischemia, then we will actually facilitate risk stratification so that we can perhaps target the very high risk patients where that balance in terms of the net benefit for the combination therapy compared to aspirin alone would be there because you're balancing the thrombotic and limb ischemic outcome versus the potential for bleeding. Professor Gregory Lip: We are also using of course, in VOYAGER-PAD low dose Rivaroxaban, which is not the stroke prevention dose of Rivaroxaban in everyday clinical practice. And that's worth emphasizing. So we translate peripheral disease dosages or regimes versus what we see in other prothrombotic situations like atrial fibrillation, which leads to stroke. And that's probably worth emphasizing. And I think really what is most important is that we can hopefully identify the high risk subset of patients with peripheral artery disease at risk of acute limb ischemia, where they're going to particularly benefit from combination therapy. So an important advance for medical therapy for peripheral disease. So congratulations on this paper as well. Dr. Mercedes Carnethon: Yeah. I really echo that. One of the things that when we write original research papers, we are always encouraged not to speculate beyond the data that we're presenting. But one of the values of this podcast is that we get a chance to really needle the authors and challenge them to speculate about what does this mean? What does this mean for the field? And Connie in particular, what do you think the next steps are for patients and providers based on what you found today in this excellent study? Dr. Connie Hess: Mercedes, that's a great question. Certainly we always want to know what next? What are the implications of these findings? And so to me, I echo both of you. I'm personally very excited as someone in the field. And as a proceduralist, I'm very excited that for the first time, we actually have data to support a medical therapy post intervention. Although there's a lot of use of things like dual antiplatelet therapy and even anticoagulation, there's not a lot of data to support it after peripheral revascularization. So this really is the first large scale, high quality data to support a strategy. And so I do think that this is something that we should adopt. Dr. Connie Hess: I think what I didn't mention before is that actually, when you look at the cumulative incidence curves for ALI in the Rivaroxaban versus placebo groups, not only do you see that there is early risk for ALI after the procedure... And typically we think of this as potentially technical failure that we can't modify, but you saw a very early benefit for Rivaroxaban plus aspirin versus aspirin alone here, suggesting that the sooner you start, the better. Of course, it has to be when it's safe from a bleeding perspective and when the proceduralist feels comfortable with this. But I do think that the implications are that we should... We proceduralists, especially in this population and as professor Lip mentioned the high risk patients in particular, should be starting this therapy as soon as we feel safe. And so I think the data are there. The next step to me is really increasing awareness, in particular among providers who are treating these patients, but even among our other colleagues or cardiovascular colleagues who may not treat these peripheral artery disease patients primarily, but do see them in their clinic. Dr. Connie Hess: A lot of them have cardiovascular disease and other cardiovascular problems, but to increase awareness that this dual pathway inhibition with low dose factor 10, anticoagulation inhibition and low antiplatelet therapy is a viable and favorable combination and to continue this so that when they see this, they're not surprised and not questioning whether to stop it. Dr. Connie Hess: I think also of course now that we are getting more data to understand how morbid and bad ALI is, I do think we also need to educate patients. You both probably recall all the tremendous efforts that were made to increase awareness in the patient population about myocardial infarction and stroke. You have all those campaigns and understanding the importance of timely intervention and reperfusion. I think that actually should be done for acute limb ischemia as well. We need to have providers aware about this complication and understanding emergent treatment. We also need patients to understand it so they can come in sooner so that they're not having delayed presentation for which primary amputation is the only treatment option. So I think there's a lot of work to be done, but certainly very excited that we have a better understanding of ALI as well as preventive therapy. Dr. Mercedes Carnethon: I really appreciate that final word. And I really can't think of a better way to wrap up than the final words that you provided, Connie. Both the context that you provided around this piece and your thoughts as well, Greg, about what makes it innovative and exciting for our readership at Circulation are really invaluable. So I just really want to thank you for joining us as an author and thank you for selecting this, Greg. This is a really great piece. I've learned a good deal. Dr. Mercedes Carnethon: This is me, Mercedes Carnethon, wrapping up this addition of Circulation on the Run, following an outstanding discussion with Dr. Connie Hess from the University of Colorado and Greg Lip, the handling editor for the piece. Dr. Greg Hundley: This program is copyright of the American Heart Association, 2021. 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, visit ahajournals.org.
A new study scientifically defines the group of people whose LDL cholesterol rises dramatically after starting a low-carb diet — so-called lean mass hyper-responders. But what does this mean if you are in this group, and what does it mean for the broader topic of cholesterol?
In this AHA 2021 episode of Parallax, Dr Ankur Kalra's guest is Dr Amit Khera, Professor and Director of Preventive Cardiology at UT Southwestern Medical Center, Dallas and Vice Chair of the Scientific Sessions. For this week's show, Dr Khera selected three thought-provoking late-breaking trials that will inform or change clinical practice. Ankur and Amit discuss how the AVATAR trial will influence guidelines, and whether these findings could be translated to TAVR. Most importantly, they discuss how AVATAR's results could inform patient decisions. Next, Dr Khera highlights a randomized trial that was designed to address the needs of a larger population. The China Rural Hypertension Control Project offers exciting insights and an innovative framework for relying on social healthcare work. Lastly, Dr Kalra and Dr Khera discuss a trial that investigated the LDL-cholesterol lowering efficacy of MK-0616. This oral PCSK9 Inhibitor may open the door for more patients in the future. What were the key findings? What are the take-home messages? How will these 3 trials foster new opportunities for patients? Trials covered in detail include: • Aortic Valve Replacement versus Watchful Waiting in Asymptomatic Severe Aortic Stenosis: The Avatar Trial • A Cluster Randomized Trial of a Village Doctor-Led Intervention on Blood Pressure Control: China Rural Hypertension Control Project • The Clinical Safety, Pharmacokinetics, and LDL-Cholesterol Lowering Efficacy of MK-0616, an Oral PCSK9 Inhibitor Questions and comments can be sent to “podcast@radcliffe-group.com” and may be answered by Ankur in the next episode. Guest @dramitkhera hosted by @AnkurKalraMD. Produced by @RadcliffeCARDIO. Brought to you by Edwards: www.edwardstavr.com
As many as 1 in 4 of us inherit a high cholesterol particle called Lipoprotein(a). Less common but also risky is a high LDL cholesterol or FH. This week, Dr. Kahn reviews the 3 gene problems that cause FH. He discusses when and how to do genetic testing. Finally, current and future testing are discussed. FH matters!
Why would the foundation matter on a building or a person? We delve into that and how to create a strong long lasting foundation today on LDL. Enjoy!
Thank you for joining us for another episode of the Low Carb MD Podcast. In this special episode, Dr. Tro is joined by Dave Feldman, Dr. Nick Norwitz, and Dr. Adrian Soto Mota. In this podcast, Doctor Tro interviews these guests, who are also his co-authors, on their new paper published in the journal Current Developments in Nutrition. The paper found that there may be ways to predict which people will experience a rise in their LDL on a low carb diet and those who won't. Furthermore, they showed in a case series of patients from Doctor Tro's office that this high cholesterol may be reversible with the re-introduction of carbohydrates. In this conversation, Tro, Nick, Adrian, and Dave talk about the fruits of their research and years of labor. Among the topics discussed are the elimination of biases from research findings and observations, the lean mass hyper responder phenotype, how to determine individual likelihood of risk for various diseases, observations on fluctuations in LDL cholesterol and its relationship to dietary saturated fat, current research projects in the works, and the psychology of Twitter hate. For more information, please see the links below. Thank you for listening! Links: View the paper here: https://doi.org/10.1093/cdn/nzab144 Dr. Nick Norwitz: Twitter Dr. Adrian Soto Mota: Twitter Dave Feldman: Twitter Citizen Science Foundation Dr. Brian Lenzkes: Website Twitter Dr. Tro Kalayjian: Website Twitter Instagram
Please join first author Cecilia Bahit and Associate Editor Graeme Hankey as they discuss the article "Predictors of Development of Atrial Fibrillation in Patients With Embolic Stroke Of Undetermined Source: An Analysis of the RE-SPECT ESUS Trial." 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 and Director of the Pauley Heart Center at VCU Health in Richmond, Virginia. Well, Carolyn, this week's feature, we're going to analyze the RE-SPECT ESUS trial. What does that pertain to? Well, you're going to have to wait and find out, but it relates to atrial fibrillation and embolic stroke. But before we get to that, how about we grab a cup of coffee and go through some of the other articles in the issue? Would you like to go first? Dr. Carolyn Lam: I sure would. Greg, we know that Chronic kidney disease is associated with adverse outcomes among patients with established cardiovascular disease or diabetes. The question is: What are the effects of Icosapent Ethyl across the range of kidney function in patients with established cardiovascular disease or diabetes from the REDUCE-IT trial? Dr. Greg Hundley: Ah, Carolyn, can you remind us what was the REDUCE-IT trial? What did it encompass there? Dr. Carolyn Lam: The REDUCE-IT trial was a multicenter double-blind, placebo-controlled trial that randomized statin treated patients with elevated triglycerides, who had cardiovascular disease or diabetes, and one additional risk factor, two treatment with icosapent ethyl at 4g daily versus placebo. After a median follow up period of 4.9 years, the study drug demonstrated a 25% relative risk reduction in the primary composite endpoint of cardiovascular death, myocardial infarction, stroke, coronary revascularization, or unstable angina. Dr. Greg Hundley: Ah, great summary of the original paper, but now this is sort of a follow-up paper. What did this paper research? Dr. Carolyn Lam: Well first, remember they focused on renal function and the median baseline GFR was 75 ml/min with a range of 17 to 123 mL/min/1.73 m2. Treatment with Icosapent Ethyl led to consistent reduction in both primary and secondary composite endpoints across the baseline GFR categories. Patients with the GFR >60 treated with Icosapent Ethyl had the largest absolute, but similar relative risk reduction for the primary composite endpoint. And while patients with GFR >60 treated with Icosapent Ethyl had the highest numerical rates of atrial fibrillation of flutter and serious bleeding. The hazard ratios for atrial fibrillation flutter and serious bleeding were similar across GFR categories. In summary Icosapent Ethyl reduced cardiovascular events among patients with elevated triglycerides in a well-controlled LDL on statin therapy across a wide range of baseline renal function. Dr. Greg Hundley: Oh, Carolyn. Beautiful presentation. That presentation was so good that I know you are ready for a quiz. We haven't had Carolyn's quiz in a week, so we've got to get right back to that. Dr. Carolyn Lam: No, we don't (laughs). Dr. Greg Hundley: Can you describe the primary sequelae of Hutchinson-Gilford progeria syndrome? Dr. Carolyn Lam: Oh wow. Okay. So this is the syndrome where there's premature aging, there's a lot of vascular stiffening, calcification. I'm going to guess some sort of atherosclerotic consequence (laughs). Dr. Greg Hundley: Very nicely done Carolyn. Oh my goodness. I need to get you to take my ABIM recertification- Dr. Carolyn Lam: (laughing) Dr. Greg Hundley: Beautifully done. So Carolyn, this paper comes to us from Dr. Vicente Andrés from Centro Nacional De Investigaciones Cardiovasculares Carlos III, and Hutchinson-Gilford progeria syndrome is a rare disorder characterized, just like you said, Carolyn by premature aging and death, mainly due to myocardial infarction, stroke or heart failure. The disease is provoked by progerin, a variant of lamin A expressed in most differentiated cells. Carolyn, these patients look healthy at birth and symptoms typically emerge in the first or second year of life. In assessing the reversibility of progerin induced damage, and the relative contribution of specific cell types is critical to determining the potential benefits of late treatment and to developing new therapies. Dr. Carolyn Lam: Wow, you've really, really piqued my interest. So what did these investigators do and what did they find? Dr. Greg Hundley: Oh Carolyn, very clever design. So the authors use CRISPR-Cas9 technology to generate mice engineers to ubiquitously express progerin while lacking lain A and allowing progestin suppression in lain A restoration in a time and cell type specific manner upon CRE recombinase activation. They characterize the phenotype of these engineered mice and cross them with CRE transgenic lines to assess the effects of suppressing progestin and restoring lain A ubiquitously at different disease stages, as well as specifically in vascular smooth muscle cells and cardiomyocytes. So Carolyn, what did they find? Well, number one, like Hutchinson-Milford progenia syndrome patients, their engineered mice appeared healthy at birth, and progressively developed Hutchinson-Milford progenia syndrome symptoms, including failure to thrive, Lipodystrophy, vascular smooth muscle cell loss, vascular fibrosis, electric cardiographic anomalies and early death. Their median lifespan was 15 months versus 26 months in the wild types. Dr. Greg Hundley: Second, ubiquitous progestin suppression in lain A restoration significantly extended lifespan, when induced in six month old, mildly symptomatic mice, and even in severely ill animals aged 13 months, although the benefit was much more pronounced upon the early intervention. And then finally, Carolyn remarkably major vascular alterations were prevented and lifespan normalized in engineered Hutchinson-Milford progenia syndrome mice when progestin suppression and lain A restoration were restricted to: just Vascular smooth muscle cells and Cardiomyocytes. Dr. Carolyn Lam: Wow, just fascinating, but, okay. What is the clinical take home message? Dr. Greg Hundley: Right, Carolyn. So these authors findings suggest that it is never too late to treat Hutchinson-Milford progenia syndrome, although the benefit is much more pronounced when progestin is targeted early in mice with mild symptoms. Also, restricting its suppression to Vascular smooth muscle cells in Cardiomyocytes is sufficient to prevent Vascular disease and normalize lifespan in mice, and therefore these data suggest that strategies to treat Hutchinson-Milford progenia syndrome through gene therapy or RNA therapy should consider targeting Vascular smooth muscle cells and Cardiomyocytes. Dr. Carolyn Lam: Oh wow. Very, very cool. Well, my next paper is a basic science paper that's significant for both its methods and its results. Dr. Greg Hundley: Oh wow, Carolyn, I can't wait. So tell us about this novel methodology. Dr. Carolyn Lam: Well, this paper is from Dr. Chang from Westlake University in Hangzhou, China, and colleagues who use a gene editing approach to efficiently institute Exon Skipping without introducing DNA double-strand breaks. So harnessing a fusion of a nuclease defective Case protein, and a cytidine deaminase, which is, we're going to abbreviate it as Targeted AID-induced mutagenesis (TAM) or base editor three (BE3), their approach precisely edited conserved guanines at splice sites, thus abrogating Exon recognition resulting in a programmable skipping of the targeted Exons. Isn't that neat? Dr. Greg Hundley: Yeah, it really is sophisticated Carolyn, wow. So what did they do using these methods? Dr. Carolyn Lam: A novel mirroring model of Duchenne muscular dystrophy was generated, which recapitulated many cardiac defects observed in the human form of the disease, including dilated cardiomyopathy, reduced left ventricular function and extensive cardiac fibrosis. Using this model, they examined the feasibility of using a cytidine base editor to install Exon Skipping and rescue the dystrophic cardiomyopathy in vivo. A single dose administration of an Adenovirus 9EtAm, instituted over 50% targeted Exon Skipping in the Chengdu muscular dystrophy transcripts and restored up to 90% dystrophin in the heart. And as a result, early ventricular remodeling was prevented and cardiac and skeletal muscle function were improved, leading to an increased lifespan of the mice. Despite gradual decline of the Adenovirus vector and base editor expression, the dystrophin restoration and pathophysiological rescue of muscular dystrophy lasted for at least a year. And so this technique really has the potential to be applied to monogenic human diseases, to modulate Exon Skipping or inclusion. Isn't that cool? Dr. Greg Hundley: Absolutely, Carolyn. Beautifully explained. Dr. Carolyn Lam: Well, let me end by sharing what else is in today's issue. There's a Perspective piece by Dr. Alexander on “Chest Pain Redux: Updated and Patient Centered.” There is an In Depth paper by Dr. Kroemer on NAD plus metabolism in cardiac health, aging and disease. And there's a Research Letter by Dr. Shepherd on sudden death in female athletes, with insights from a large regional registry in the United Kingdom. Dr. Greg Hundley: Very good, Carolyn. What a great issue. Now, how about we get to that feature discussion? Dr. Carolyn Lam: Let's go, Greg. Dr. Greg Hundley: Welcome listeners to our feature discussion today on this November 30th. And we have with us Dr. Cecilia Bahit from Rosario, Argentina and our own associate editor, Dr. Graeme Hankey from Perth, Australia to talk to us about a paper pertaining to Atrial Fibrillation. Welcome to you both, and Cecilia, we'll start with you. Could you describe for us a little bit of the background information that went into formulating your study, and then what hypothesis did you want to address? Dr. Cecilia Bahit: Thank you for the invitation. So we all know that embolic stroke of undetermined source, which is called ESUS isn't just a subset of cryptogenic stroke, and is associated with stroke recurrence about 3-6% per year. And on the other hand, we know that continuous cardiac monitoring in this patient population shows that atrial fibrillation can be detected between 10% at six months or 30% at three years. So the underlying atrial fibrillation may be a mechanism for the recurrent thromboembolic stroke in this patient population. So we know that prior studies have identified some predictors of atrial fibrillation in these patients. And if we are able to identify which patients could benefit from cardiac monitoring and have a higher yield to detect atrial fibrillation, we could do a better job at treating them. So, that was our idea behind the paper. So using the RE-SPECT ESUS trial, which was a trial that included patient with ESUS stroke and were randomized to the bigger trend versus Aspirin, we look at predictors of atrial fibrillation unassociated regarding stroke. Dr. Greg Hundley: Very nice. And so, now was this a sub-study here and maybe define for us a little bit, your study design and specific study population. Dr. Cecilia Bahit: So this was a secondary analysis of a randomized clinical trial that as mentioned it was not a sub-study, it was a secondary analysis. We thought all along to do it because of the interest of the clinical question. We look at the total patient population was 5,390 patients. And we looked at those patients who developed atrial fibrillation during the 19 months of follow-up. And it was 7.5%, 403 patients developed atrial fibrillation. Dr. Greg Hundley: Very good. And what were your results? Dr. Cecilia Bahit: So, as I mentioned, we saw that 7.5% of our patient population developed atrial fibrillation during the follow-up. And we know those patients were older, were like, have higher morbidities, and we assessed, we did an one variable analysis and then a multi-variable analysis, trying to identify predictors for atrial fibrillation. And for our model, we identified different predictors, older age, hypertension, lack of diabetes, and higher body mass index, were independent predictors of atrial fibrillation. So the patients who have atrial fibrillation have a higher recurrence of stroke, it was 7.2 versus four, compared to those that did not have atrial fibrillation. Dr. Cecilia Bahit: So I think there's an important part, that 20% of the patient population of the overall trial, this is a little more than a thousand patients, had NT-prob measure at baseline. And when we included this biomarker into the model, only older age and NT-prob were independent predictors of atrial fibrillation. In addition, even though this was not the objective of this analysis, we look at the treatment effect of the bigger trend. And even though we saw that there was a statistical benefit of the bigger trend versus Aspirin in the higher group of these in our score, the overall treatment effect was not there. So we couldn't assess the fact that the bigger trend was better compared to Aspirin in patient with atrial fibrillation, but of course the numbers were very small. Dr. Greg Hundley: Very good. Thank you so much for that wonderful description. And Graeae, now we'll turn to you as associate editor for us at Circulation, and also the editorialist on this particular paper. What caught your attention about this particular study and the results from the many papers that really come across your desk. Dr. Graeme Hankey: Thank you, Greg. And congratulations to Cecilia and her RE-SPECT ESUS colleagues. I mean, this is a landmark study, the RE-SPECT ESUS study, and just to go back, embolic stroke of undetermined source is really common. About one in four ischemic strokes, we don't know the cause of, and it's one of the major subtypes of cryptogenic stroke is an embolic ischemic stroke in which the source could have come from the heart or the aortic arch or the carotids. And we're not really sure. And we think that some of these patients have occult atrial fibrillation, but we can't pick it up at the time. So one way is to try and monitor them with prolonged ECG monitoring. And another way is to actually treat them with anticoagulation because we know that, that's more effective in people with cardio embolic stroke. And so RE-SPECT ESUS and NAVIGATE ESUS used the latter strategy and said, let's see if treating people with ESUS with anticoagulation is more effective than antiplatelet therapy. Dr. Graeme Hankey: And both studies were not significant in terms of showing that Dabigatran or Parovarian for NAVIGATE ESUS was more effective than antiplatelet therapy. So we're left now with this default that all patients with ESUS just get Aspirin, but we have a hunch that some of them actually have cardiogenic embolism and are being undertreated with Aspirin and need anticoagulation. So it's a heterogeneous entity, but we're treating it homogeneously with a sort of weak antiplatelet. So we want to try and find out who's going to get AF or who's already got it that is occult. And this study is a really great and prospective study with 5,000 patients as Cecilia said, who of whom 7% did develop AF just through annual ECG reporting and just with symptom reporting. And that's probably an under report. You know, if they'd had monitoring, they probably would've found about 20 or 30% would've developed AF during that time of 19 months follow up. Dr. Graeme Hankey: And it's the first study to really then show that not just the AF people had a higher stroke rate, but in that group who they predicted to be at high risk of AF with older age and the NT-prob, that the high risk group had a significant reduction with Dabigatran versus Aspirin in that high risk group. It's just, when you look for hetero homogeneity or heterogeneity across the risk groups, it wasn't quite significant. And that might be because it's not significant or it might be that study was underpowered to look at those three, across those three risk subgroups. And also it might be a bit confounded because of it, the patients weren't randomized according to their risk status for AF, they were just randomized, whether they had ESUS, so it's further excited us that there might be a subgroup who needs anticoagulation. And that's why the ARCADIA trial is ongoing now, looking at where the people with ESUS who have high risk of AF benefit from a apixaban versus aspirin. Dr. Greg Hundley: Very nice. And so, with these results that we have here, maybe come back to Cecilia, what do you think would be the next series of studies that needs to be performed in this area of research? Dr. Cecilia Bahit: Well, there's one side that's ongoing as Dr. Hankie mentioned, but I think we should be able to identify which patients have a higher risk of atrial fibrillation and those patients who use cardiac monitoring for long term to identify atrial fibrillation and to treat properly. So I think that would be key in this area. Dr. Greg Hundley: Very nice. And Graeae, what are your thoughts? Dr. Graeme Hankey: Yes. Well, one way is to have our ESUS patients have prolonged ECG monitoring by implantable loop recorders, for example, and then those who develop AF randomizing them to anticoagulation versus antiplatelet therapy. Although if they declare themselves with AF they're usually just go straight onto anticoagulation therapy. So the burning question is, in these people with ESUS who haven't declared themselves as AF, but have predictors of AF like those shown in RESPECT ESUS, like older age, high blood pressure, high BMI ,prob, and perhaps echo features, like left atrial size or ECG features like lots of premature atrial contractions or P wave of abnormalities. Dr. Graeme Hankey: Are these, the subgroups or even LV dysfunction, are these subgroups who need to be more specifically targeted in a randomized trial rather than the whole group of ESUS. And also with longer follow up. NAVIGATE ESUS stopped after 11 months. The bigger RESPECT ESUS stopped after a median follow up of 16 months and the curves were diverging. Maybe with five years follow up, a lot of these people would've developed AF and would've benefited from longer term anticoagulation, but the trials were stopped early, because there wasn't a signal of benefit and there was an early risk of bleeding with anticoagulation. Dr. Greg Hundley: Very good. Well listeners, this has been a really interesting study and we want to thank Cecilia and Graeme for sharing results of the RESPECT ESUS study, highlighting that, in patients with embolic stroke of undetermined source, atrial fibrillation occurs and is a possible source of this stroke, and then also older age, and elevation of NT-prob can be associated with development of atrial fibrillation, subsequent to that stroke event. Dr. Greg Hundley: Well listeners, we want to wish you a great week. And on behalf of Carolyn and myself, look forward to catching you next week on The Run. This program is copyright of the American Heart Association, 2021. 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 visit ahajournals.org.
Today, I am lucky to have here with me, a specialist in Weight Management and Bariatric Surgery for adults and adolescents, Dr. Robert Cywes. He has been doing bariatric surgery for 18 years, performing over 8,000 surgeries. This is an episode that originally aired on March 2020, and it was so good we decided to re-release it here today. Dr. Cywes' medical training began in Cape Town, South Africa, where he received his medical degree from The University of Cape Town. In 1989, Dr. Cywes moved to North America and completed a year-long residency in Pediatric Surgery at Ohio State University's Columbus Children's Hospital. After completing his pediatric surgery fellowship at the University of Michigan's C.S. Mott Children's Hospital, Dr. Cywes was appointed as an Assistant Professor of Pediatric and Fetal Surgery at Vanderbilt University in Nashville, Tennessee where he did hepatic stem cell research. During this time, Dr. Cywes became increasingly interested in adolescent obesity and the impact of the liver and metabolic syndrome on young patients. Dr. Cywes' research led to a comprehensive understanding of the toxicity of chronic excessive carbohydrate consumption as the primary cause of obesity and so-called obesity-related co-morbidities, and he became interested in developing a clinical program to treat obese patients using this knowledge. Dr. Cywes relocated to Jacksonville, Florida where he joined the Department of Pediatric Surgery at the Nemours Children's Clinic and Wolfson Children's Hospital. This led to a national meeting in Jacksonville where guidelines for adolescent obesity surgery were established. Dr. Cywes established JSAPA to continue his work in both adolescent and adult obesity treatment and surgery, and in 2013 opened a practice in Palm Beach County, Florida. He now works with a highly experienced team of professionals from a variety of medical sub-specialties to better care for obese patients. He has developed the practice into an internationally recognized Center of Excellence for obesity surgery. The practice uses a cognitive behavioral therapy approach that addresses carbohydrate addiction, along with bariatric surgery, to help patients manage their obesity long term. In this episode, Dr. Cywes opens the show discussing the correlation between carbohydrates and toxic drugs. Our bodies do not need to run on sugar; our bodies prefer a keto lifestyle. Also, Dr. Cywes explains effective methods of treating diabetes and what's wrong with conventional treatments. Stay tuned, as Dr. Cywes discusses dopamine fasting, serotonin loading, and how our feedback controls for survival work. BiOptimizers Special November Deal: www.magnesiumbreakthrough.com/ketokamp and use code ketokamp to get your discount and free gifts today!
Chadi re-invites Dave Feldman (@DaveKeto), senior software engineer and entrepreneur, and Ethan Weiss (@ethanjweiss), MD, cardiologist at UC San Francisco, to rehash a Twitter argument on secondary prevention for heart attacks for patients with high LDL. Should patients receive statins or should they not? What does the data show and where is the controversy, if any? How does diet play a role? What about the infamous KETO diet? The guests discuss a couple of realistic hypothetical scenarios with different LDL receptor and metabolism variables. Dave shares an IRB-approved trial that he is leading to better understand high LDL that emerges from Keto and its impact on cardiac atherosclerotic disease. This was a high-spirited debate where the host said so little and the guests were arguing respectfully about various views. Will there be a common ground? You must listen to find out. Check out Chadi's website for all Healthcare Unfiltered episodes and other content. www.chadinabhan.com/ Watch all Healthcare Unfiltered episodes on Youtube. www.youtube.com/channel/UCjiJPTpIJdIiukcq0UaMFsA
Every week, Dr. Roizen discusses the latest health headlines YOU need to know.In this episode, Dr. Roizen talks about the latest health headlines that YOU need to know. Does exercise lower your LDL cholesterol? What do you do after a heart attack? Coffee linked metabolites linked to chronic kidney disease Natural diuretics in food A study about the importance of folates and folate-rich foods Obesity bias in healthcare PLUS so much more...
Hyperbaric oxygen therapy may alleviate symptoms of Alzheimer's Disease Tel Aviv University (Israel) A new Tel Aviv University study reveals that hyperbaric oxygen treatments may ameliorate symptoms experienced by patients with Alzheimer's disease. "This revolutionary treatment for Alzheimer's disease uses a hyperbaric oxygen chamber, which has been shown in the past to be extremely effective in treating wounds that were slow to heal," says Prof. Uri Ashery of TAU's Sagol School of Neuroscience and the Faculty of Life Sciences, who led the research for the study. "We have now shown for the first time that hyperbaric oxygen therapy can actually improve the pathology of Alzheimer's disease and correct behavioral deficits associated with the disease. (NEXT) Scientists discover that CoQ10 can program cancer cells to self-destruct A promising study shows that this nutrient causes cancer cells to self-destruct before they can multiply – giving rise to hopes that it can be utilized as an important integrative therapy for cancer patients. Let's take a closer look at this wonderful scientific work. CoQ10 “reminds” cancer cells to die Coenzyme Q10 (CoQ10) – which supports many indispensable biochemical reactions – is also called “ubiquinone.” This is due to its ubiquitous nature – CoQ10 is found in nearly every human cell, with particularly high concentrations in the mitochondria, the powerhouses of the cell. Researchers report that the out-of-control replication characteristic of cancer cells is a result of the cells' lost capacity to respond to programmed cell death, or apoptosis. (NEXT) Study suggests hot flashes could be precursor to diabetes Analysis of Women's Health Initiative data demonstrates effect of severity and duration of hot flashes on risk of developing diabetes The North American Menopause Society Hot flashes, undoubtedly the most common symptom of menopause, are not just uncomfortable and inconvenient, but numerous studies demonstrate they may increase the risk of serious health problems, including heart disease. A new study suggests that hot flashes (especially when accompanied by night sweats) also may increase the risk of developing diabetes. Results are being published online today in Menopause, the journal of The North American Menopause Society (NAMS). "This study showed that, after adjustment for obesity and race, women with more severe night sweats, with or without hot flashes, still had a higher risk of diabetes," says Dr. JoAnn Pinkerton, NAMS executive director. "Menopause is a perfect time to encourage behavior changes that reduce menopause symptoms, as well as the risk of diabetes and heart disease. Suggestions include getting regular exercise and adequate sleep, avoiding excess alcohol, stopping smoking, and eating a heart- healthy diet. For symptomatic women, hormone therapy started near menopause improves menopause symptoms and reduces the risk of diabetes." (NEXT) Garlic extract may help obese adults combat inflammation University of Florida Aged garlic extract may help obese people ward off painful inflammation and lower cholesterol levels, a new University of Florida study shows. In the UF/IFAS study, scientists divided 51 obese people who were otherwise healthy into two groups ? those who took the aged garlic extract for six weeks and those who took a placebo. Researchers encouraged participants to continue their regular diet and exercise routine during the experiment. Research showed the garlic extract helped regulate immune-cell distribution and reduced blood LDL ? or "bad" ? cholesterol in the obese adults. Aged garlic extract modified the secretion of inflammatory proteins from immune cells, Percival said. (NEXT) Having children can make women's telomeres seem 11 years older George Mason University A recent study by George Mason University researchers in the Department of Global and Community Health found that women who have given birth have shorter telomeres compared to women who have not given birth. Telomeres are the end caps of DNA on our chromosomes, which help in DNA replication and get shorter over time. The length of telomeres has been associated with morbidity and mortality previously, but this is the first study to examine links with having children. (NEXT) Scientists uncover why sauna bathing is good for your health UNIVERSITY OF EASTERN FINLAND Over the past couple of years, scientists at the University of Eastern Finland have shown that sauna bathing is associated with a variety of health benefits. Using an experimental setting this time, the research group now investigated the physiological mechanisms through which the heat exposure of sauna may influence a person's health. Their latest study with 100 test subjects shows that taking a sauna bath of 30 minutes reduces blood pressure and increases vascular compliance, while also increasing heart rate similarly to medium-intensity exercise. (OTHER NEWS NEXT) Biden's Bounty on Your Life: Hospitals' Incentive Payments for COVID-19 By Elizabeth Lee Vliet, M.D. and Ali Shultz, J.D. – ASSOCIATION OF AMERICAN PHYSICIANS AND SURGEONS. November 17, 2021 Upon admission to a once-trusted hospital, American patients with COVID-19 become virtual prisoners, subjected to a rigid treatment protocol with roots in Ezekiel Emanuel's “Complete Lives System” for rationing medical care in those over age 50. They have a shockingly high mortality rate. How and why is this happening, and what can be done about it? As exposed in audio recordings, hospital executives in Arizona admitted meeting several times a week to lower standards of care, with coordinated restrictions on visitation rights. Most COVID-19 patients' families are deliberately kept in the dark about what is really being done to their loved ones. The combination that enables this tragic and avoidable loss of hundreds of thousands of lives includes (1) The CARES Act, which provides hospitals with bonus incentive payments for all things related to COVID-19 (testing, diagnosing, admitting to hospital, use of remdesivir and ventilators, reporting COVID-19 deaths, and vaccinations) and (2) waivers of customary and long-standing patient rights by the Centers for Medicare and Medicaid Services (CMS). In 2020, the Texas Hospital Association submitted requests for waivers to CMS. According to Texas attorney Jerri Ward, “CMS has granted ‘waivers' of federal law regarding patient rights. Specifically, CMS purports to allow hospitals to violate the rights of patients or their surrogates with regard to medical record access, to have patient visitation, and to be free from seclusion.” She notes that “rights do not come from the hospital or CMS and cannot be waived, as that is the antithesis of a ‘right.' The purported waivers are meant to isolate and gain total control over the patient and to deny patient and patient's decision-maker the ability to exercise informed consent.” Creating a “National Pandemic Emergency” provided justification for such sweeping actions that override individual physician medical decision-making and patients' rights. The CARES Act provides incentives for hospitals to use treatments dictated solely by the federal government under the auspices of the NIH. These “bounties” must paid back if not “earned” by making the COVID-19 diagnosis and following the COVID-19 protocol. The hospital payments include: A “free” required PCR test in the Emergency Room or upon admission for every patient, with government-paid fee to hospital. Added bonus payment for each positive COVID-19 diagnosis. Another bonus for a COVID-19 admission to the hospital. A 20 percent “boost” bonus payment from Medicare on the entire hospital bill for use of remdesivir instead of medicines such as Ivermectin. Another and larger bonus payment to the hospital if a COVID-19 patient is mechanically ventilated. More money to the hospital if cause of death is listed as COVID-19, even if patient did not die directly of COVID-19. A COVID-19 diagnosis also provides extra payments to coroners.
Please join first author Yuan Lu and Guest Editor Jan Staessen as they discuss the article "National Trends and Disparities in Hospitalization for Acute Hypertension Among Medicare Beneficiaries (1999-2019)." Dr. Carolyn Lam: Welcome to Circulation on the Run: your weekly podcast, summary and backstage pass to the journal and it's 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, and director of Pauley Heart Center at VCU health in Richmond, Virginia. Dr. Carolyn Lam: Greg, today's feature discussion is about the national trends and disparities and hospitalizations for hypertensive emergencies among Medicare beneficiaries. Isn't that interesting? We're going to just dig deep into this issue, but not before we discuss the other papers in today's issue. I'm going to let you go first today while I get a coffee and listen. Dr. Greg Hundley: Oh, thanks so much, Carolyn. My first paper comes to us from the world of preclinical science and it's from professor Christoff Maack from University Clinic Wursburg. Carolyn, I don't have a quiz for you, so I'm going to give a little break this week, but this particular paper is about Barth syndrome. Barth syndrome is caused by mutations of the gene encoding taffazin, which catalyzes maturation of mitochondrial cardiolipin and often manifests with systolic dysfunction during early infancy. Now beyond the first months of life, Barth syndrome cardiomyopathy typically transitions to a phenotype of diastolic dysfunction with preserved ejection fraction, one of your favorites, blunted contractile reserve during exercise and arrhythmic vulnerability. Previous studies traced Barth syndrome cardiomyopathy to mitochondrial formation of reactive oxygen species. Since mitochondrial function and reactive oxygen species formation are regulated by excitation contraction coupling, these authors wanted to use integrated analysis of mechano-energetic coupling to delineate the pathomechanisms of Barth syndrome cardiomyopathy. Dr. Carolyn Lam: Oh, I love the way you explained that so clearly, Greg. Thanks. So what did they find? Dr. Greg Hundley: Right, Carolyn. Well, first defective mitochondrial calcium uptake prevented Krebs cycle activation during beta adrenergic stimulation, abolishing NADH regeneration for ATP production and lowering antioxidative NADPH. Second, Carolyn, mitochondrial calcium deficiency provided the substrate for ventricular arrhythmias and contributed to blunted inotropic reserve during beta adrenergic stimulation. And finally, these changes occurred without any increase of reactive oxygen species formation in or omission from mitochondria. So Carolyn what's the take home here? Well, first beyond the first months of life, when systolic dysfunction dominates, Barth syndrome cardiomyopathy is reminiscent of heart failure with preserved rather than reduced ejection fraction presenting with progressive diastolic and moderate systolic dysfunction without relevant left ventricular dilation. Next, defective mitochondrial calcium uptake contributes to inability of Barth syndrome patients to increase stroke volume during exertion and their vulnerability to ventricular arrhythmias. Lastly, treatment with cardiac glycosides, which could favor mechano-energetic uncoupling should be discouraged in patients with Barth syndrome and left ventricular ejection fractions greater than 40%. Dr. Carolyn Lam: Oh, how interesting. I need to chew over that one a bit more. Wow, thanks. But you know, I've got a paper too. It's also talking about energetic basis in the presence of heart failure with preserved ejection fraction, but this time looking at transient pulmonary congestion during exercise, which is recognized as an emerging and important determinant of reduced exercise capacity in HFpEF. These authors, led by Dr. Lewis from University of Oxford center for clinical magnetic resonance research sought to determine if an abnormal cardiac energetic state underpins this process of transient problem congestion in HFpEF. Dr. Carolyn Lam: To investigate this, they designed and conducted a basket trial covering the physiological spectrum of HFpEF severity. They non-invasively assess cardiac energetics in this cohort using phosphorous magnetic resonance spectroscopy and combined real time free breathing volumetric assessment of whole heart mechanics, as well as a novel pulmonary proton density, magnetic resonance imaging sequence to detect lung congestion, both at rest and during submaximal exercise. Now, Greg, I know you had a look at this paper and magnetic resonance imaging, and spectroscopy is your expertise. So no quiz here, but could you maybe just share a little bit about how novel this approach is that they took? Dr. Greg Hundley: You bet. Carolyn, thanks so much for the intro on that and so beautifully described. What's novel here is they were able to combine imaging in real time, so the heart contracting and relaxing, and then simultaneously obtain the metabolic information by bringing in the spectroscopy component. So really just splashing, as they might say in Oxford, just wonderful presentation, and I cannot wait to hear what they found. Dr. Carolyn Lam: Well, they recruited patients across the spectrum of diastolic dysfunction and HFpEF, meaning they had controls. They had nine patients with type two diabetes, 14 patients with HFpEF and nine patients with severe diastolic dysfunction due to cardiac amyloidosis. What they found was that a gradient of myocardial energetic deficit existed across the spectrum of HFpEF. Even at low workload, the energetic deficit was related to a markedly abnormal exercise response in all four cardiac chambers, which was associated with detectable pulmonary congestion. The findings really support an energetic basis for transient pulmonary congestion in HFpEF with the implication that manipulating myocardial energy metabolism may be a promising strategy to improve cardiac function and reduce pulmonary congestion in HFpEF. This is discussed in a beautiful editorial by Drs. Jennifer Hole, Christopher Nguyen and Greg Lewis. Dr. Greg Hundley: Great presentation, Carolyn, and obviously love that MRI/MRS combo. Carolyn, these investigators in this next paper led by Dr. Sara Ranjbarvaziri from Stanford University School of Medicine performed a comprehensive multi-omics profile of the molecular. So transcripts metabolites, complex lipids and ultra structural and functional components of hypertrophic cardiomyopathy energetics using myocardial samples from 27 hypertrophic cardiomyopathy patients and 13 controls really is the donor heart. Dr. Carolyn Lam: Wow, it's really all about energetics today, isn't it? So what did they see, Greg? Dr. Greg Hundley: Right, Carolyn. So hypertrophic cardiomyopathy hearts showed evidence of global energetic decompensation manifested by a decrease in high energy phosphate metabolites (ATP, ADP, phosphocreatine) and a reduction in mitochondrial genes involved in the creatine kinase and ATP synthesis. Accompanying these metabolic arrangements, quantitative electron microscopy showed an increased fraction of severely damaged mitochondria with reduced crystal density coinciding with reduced citrate synthase activity and mitochondrial oxidative respiration. These mitochondrial abnormalities were associated with elevated reactive oxygen species and reduced antioxidant defenses. However, despite significant mitochondrial injury, the hypertrophic cardiomyopathy hearts failed to up-regulate mitophagic clearance. Dr. Greg Hundley: So Carolyn, in summary, the findings of this study suggest that perturbed metabolic signaling and mitochondrial dysfunction are common pathogenic mechanisms in patients with hypertrophic cardiomyopathy, and these results highlight potential new drug targets for attenuation of the clinical disease through improving metabolic function and reducing myocardial injury. Dr. Carolyn Lam: Wow, what an interesting issue of our journal. There's even more. There's an exchange of letters between Drs. Naeije and Claessen about determinants of exercise capacity in chronic thromboembolic pulmonary hypertension. There's a "Pathways to Discovery" paper: a beautiful interview with Dr. Heinrich Taegtmeyer entitled,"A foot soldier in cardiac metabolism." Dr. Greg Hundley: Right, Carolyn, and I've got a research letter from Professor Marston entitled "The cardiovascular benefit of lowering LDL cholesterol to below 40 milligrams per deciliter." Well, what a great issue, very metabolic, and how about we get onto that feature discussion? Dr. Carolyn Lam: Let's go, Greg. Dr. Greg Hundley: Welcome listeners to our feature discussion today. We have a paper that is going to address some issues pertaining to high blood pressure, or hypertension. With us, we have Dr. Yuan Lu from Yale University in New Haven, Connecticut. We also have a guest editor to help us review this paper, Dr. Jan Staessen from University Louvain in Belgium. Welcome to you both and Yuan, will start with you. Could you describe for us some of the background that went into formulating your hypothesis and then state for us the hypothesis that you wanted to address with this research? Dr. Yuan Lu: Sure. Thank you, Greg. We conducted this study because we see that recent data show hypertension control in the US population has not improved in the last decades, and there are widening disparities. Also last year, the surgeon general issued a call to action to make hypertension control a national priority. So, we wanted to better understand whether the country has made any progress in preventing hospitalization for acute hypertension. That is including hypertension emergency, hypertension urgency, and hypertension crisis, which also refers to acute blood pressure elevation that is often associated with target organ damage and requires urgent intervention. We have the data from the Center for Medicare/Medicaid, which allow us to look at the trends of hospitalization for acute hypertension over the last 20 years and we hypothesize we may also see some reverse progress in hospitalization rate for acute hypertension, and there may differences by population subgroups like age, sex, race, and dual eligible status. Dr. Greg Hundley: Very nice. So you've described for us a little bit about perhaps the study population, but maybe clarify a little further: What was the study population and then what was your study design? Dr. Yuan Lu: Yeah, sure. The study population includes all Medicare fee-for-service beneficiaries 65 years and older enrolled in the fee-for-service plan for at least one month from January 1999 to December 2019 using the Medicare denominator files. We also study population subgroups by age, sex, race and ethnicity and dual eligible status. Specifically the racial and ethnic subgroups include Asian, blacks, Hispanics, North American native, white, and others. Dual eligible refers to beneficiary eligible for both Medicare and Medicaid. This study design is a serial cross sectional analysis of these Medicare beneficiaries between 1999 and 2019 over the last 20 years. Dr. Greg Hundley: Excellent. Yuan, what did you find? Dr. Yuan Lu: We actually have three major findings. First, we found that in Medicare beneficiaries 65 years and older, hospitalization rate for acute hypertension increased more than double in the last 20 years. Second, we found that there are widening disparities. When we look at all the population subgroups, we found black adults having the highest hospitalization rate in 2019 across age, sex, race, and dual eligible subgroup. And finally, when we look at the outcome among people hospitalized, we found that during the same period, the rate of 30 day and 90 day mortality and readmission among hospitalized beneficiaries improved and decreased significantly. So this is the main findings, and we can also talk about implications of that later. Dr. Greg Hundley: Very nice. And did you find any differences between men and women? Dr. Yuan Lu: Yes. We also looked at the difference between men and women, and we found that actually the hospitalization rate is higher among females compared to men. So more hospitalizations for acute hypertension among women than men. Dr. Greg Hundley: Given this relatively large Medicare/Medicaid database and cross-sectional design, were you able to investigate any relationships between these hospitalizations and perhaps social determinants of health? Dr. Yuan Lu: For this one, we haven't looked into that detail. This is just showing the overall picture, like how the hospitalization rate changed over time in the overall population and by different population subgroups. What you mentioned is an important issue and should definitely be a future study to look at whether social determine have moderated the relationship between the hospitalization. Speaker 3: Excellent. Well, listeners, now we're going to turn to our guest editor and you'll hear us talk a little bit sometimes about associate editors. We have a team that will review many papers, but when we receive a paper that might contain an associate editor or an associate editors institution, we actually at Circulation turn to someone completely outside of the realm of the associate editors and the editor in chief. These are called guest editors. With us today, we have Dr. Jan Staessen from Belgium who served as the guest editor. He's been working in this task for several years. Jan, often you are referred papers from the American Heart Association. What attracted you to this particular paper and how do you put Yuan's results in the context with other studies that have focused on high blood pressure research? Dr. Jan Staessen: Well, I've almost 40 years of research in clinical medicine and in population science, and some of my work has been done in Sub-Saharan Africa. So when I read the summary of the paper, I was immediately struck by the bad results, so to speak, for black people. This triggered my attention and I really thought this message must be made public on a much larger scale because there is a lot of possibility for prevention. Hypertension is a chronic disease, and if you wait until you have an emergency or until you have target organ damage, you have gone in too late. So really this paper cries for better prevention in the US. And I was really also amazed when I compared this US data with what happens in our country. We don't see any, almost no hospitalizations for acute hypertension or for hypertensive emergencies. So there is quite a difference. Dr. Jan Staessen: Going further on that, I was wondering whether there should not be more research on access to primary care in the US because people go to the emergency room, but that's not a place where you treat or manage hypertension. It should be managed in primary care with making people aware of the problem. It's still the silent killer, the main cause of cardiovascular disease, 8 million deaths each year. So this really triggered my attention and I really wanted this paper to be published. Dr. Greg Hundley: Very nice. Jan, I heard you mention the word awareness. How have you observed perhaps differences in healthcare delivery in Belgium that might heighten awareness? You mentioned primary care, but are there any other mechanisms in place that heighten awareness or the importance? Dr. Jan Staessen: I think people in Belgium, the general public, knows that hypertension is a dangerous condition. That it should be well treated. We have a very well built primary care network, so every person can go to a primary care physician. Part of the normal examination in the office of a primary care physician is a blood pressure measurement. That's almost routine in Belgium. And then of course not all patients are treated to go. Certainly keeping in mind the new US guidelines that aim for lower targets, now recently confirmed in the Chinese study, you have to sprint three cells. And then the recent Chinese study that have been published to the New England. So these are issues to be considered. I also have colleagues working in Texas close to the Mexican border at the university place there, and she's telling me how primary care is default in that area. Dr. Jan Staessen: I think this is perhaps part of the social divide in the US. This might have to be addressed. It's not only a problem in the US, it's also a problem in other countries. There is always a social divide and those who have less money, less income. These are the people who fell out in the beginning and then they don't see primary care physicians. Dr. Jan Staessen: Belgium, for instance, all medicines are almost free. Because hypertension is a chronic condition prevention should not only start at age 65. Hypertension prevention should really start at a young age, middle age, whenever this diagnosis of high blood pressure diagnosis is confirmed. Use blood pressure monitoring, which is not so popular in the US, but you can also use home blood pressure monitoring. Then you have to start first telling your patients how to improve their lifestyle. When that is not sufficient, you have to start anti hypertensive drug treatment. We have a wide array of anti hypertensive drugs that can be easily combined. If you find the right combination, then you go to combination tablets because fewer tablets means better patient adherence. Dr. Greg Hundley: Yuan we will turn back to you. In the last minutes here, could you describe some of your thoughts regarding what you think is the next research study that needs to be performed in this sphere of hypertension investigation? Dr. Yuan Lu: Sure. Greg, in order to answer your question, let me step back a little bit, just to talk about the implication of the main message from this paper, and then we can tie it to the next following study. We found that the marked increase in hospitalization rate for acute hypertension actually represented many more people suffering a potential catastrophic event that should be preventable. I truly agree with what Dr. Staessen said, hypertension should be mostly treated in outpatient setting rather than in the hospital. We also find the lack of progress in reducing racial disparity in hospitalization. These findings highlight needs for new approaches to address both the medical and non-medical factors, including the social determinants in health, system racism that can contribute to this disparity. When we look at the outcome, we found the outcome for mortality and remission improved over time. Dr. Yuan Lu: This means progress has been made in improving outcomes once people are hospitalized for an acute illness. The issue is more about prevention of hospitalization. Based on this implication, I think in a future study we need better evidence to understand how we can do a better job in the prevention of acute hypertension admissions. For example, we need the study to understand who is at risk for acute hypertensive admissions, and how can this event be preempted. If we could better understand who these people are, phenotype this patient better and predict their risk of hospitalization for acute hypertension, we may do a better job in preventing this event from happening. Dr. Greg Hundley: Very nice. And Jan, do you have anything to add? Dr. Jan Staessen: Yes. I think every effort should go to prevention in most countries. I looked at the statistics, and more than 90% of the healthcare budget is spent in treating established disease, often irreversible disease like MI or chronic kidney dysfunction. I think then you come in too late. So of the healthcare budget in my mind, much more should go to the preventive issues and probably rolling out an effective primary care because that's the place where hypertension has to be diagnosed and hypertension treatment has to be started. Dr. Greg Hundley: Excellent. Well, listeners, we've heard a wonderful discussion today regarding some of the issues pertaining to hypertension and abrupt admission to emergency rooms for conditions pertaining to hypertension, really getting almost out of control. We want to thank Dr. Yuan Lu from Yale New Haven and also our guest editor, Dr. Jan Staessen from Louvain in Belgium. On behalf of Carolyn and myself, we want to wish you a great week and we will catch you next week on the run. This program is copyright of the American Heart Association, 2021. The opinions express by speakers in this podcast are their own and not necessarily those of the editors or of the American Heart Association for more visit aha journals.org.
If you've followed the NBT podcast for a while you probably heard Dr. Malcolm Kendrick talking about the tenuous connection between cholesterol levels and cardiovascular disease. Malcolm has published with The International Network of Cholesterol Skeptics on this topic, including a recent review paper entitled LDL-C does not cause cardiovascular disease. In the paper, they include both total cholesterol and LDL-C in their discussions, and if you look at epidemiological data, I think they make a good point. For instance, total cholesterol had almost no effect on mortality in the HUNT-2 study in Norway, and higher levels were associated with lower mortality risk in women. Or the ESCARVAL-RISK study, where higher LDL-C is associated with lower all-cause mortality until it's well above 200 mg/dl. Or the In-Chianti study, where people over 64 had the lowest mortality rates if they had an LDL-C greater than 130mg/dl. The question then becomes, if not cholesterol, then what? To answer that we must resist monomania and acknowledge the very notion of causation in a complex system is suspicious. Ask not what but how. Malcolm argues in his new book The Clot Thickens that if you maintain metabolic health, manage stress, and mind your endothelial function, cholesterol levels become largely irrelevant. Simple enough, but as you'll discover in this interview, the devil is in the details. Here's the outline of this episode with Malcolm Kendrick: [00:00:24] Previous NBT podcasts with Malcolm Kendrick: Why Cholesterol Levels Have No Effect on Cardiovascular Disease (And Things to Think About Instead) and A Statin Nation: Damaging Millions in a Brave New Post-health World. [00:00:42] Book: The Clot Thickens: The enduring mystery of heart disease, by Malcolm Kendrick. [00:03:04] 5-part series with lipidologist Thomas Dayspring (Part 1, 2, 3, 4, 5); 2-hour interview with Ron Krauss on The Drive Podcast. [00:04:23] Book: Braunwald's Heart Disease: A Textbook of Cardiovascular Medicine. [00:06:12] LDL Cholesterol - challenging mainstream thought. [00:17:16] Fatty streaks never become atherosclerotic plaques; Review: Velican, C., M. Anghelescu, and D. Velican. "Preliminary study on the natural history of cerebral atherosclerosis." Medicine interne 19.2 (1981): 137-145. [00:18:54] Genetic influences; familial hypercholesterolemia (FH) and high clotting factors; Case study of patient with untreated FH but no presence of atherosclerosis: Johnson, Kipp W., Joel T. Dudley, and Jason R. Bobe. "A 72-year-old patient with longstanding, untreated familial hypercholesterolemia but no coronary artery calcification: a case report." Cureus 10.4 (2018). [00:21:22] Clotting factors more important than high LDL; Paper: Ravnskov, Uffe, et al. "Inborn coagulation factors are more important cardiovascular risk factors than high LDL-cholesterol in familial hypercholesterolemia." Medical hypotheses 121 (2018): 60-63. [00:25:03] UK Biobank Study: Mora, Samia, Seth S. Martin, and Salim S. Virani. "Cholesterol Insights and Controversies From the UK Biobank Study: Three Take-Home Messages for the Busy Clinician." (2019): 553-555. [00:25:51] Machine learning used to predict cardiovascular disease; Study: Weng, Stephen F., et al. "Can machine-learning improve cardiovascular risk prediction using routine clinical data?." PloS one 12.4 (2017): e0174944. [00:30:54] FOURIER PCSK9-inhibitor study: More deaths in the treatment group; Study: Sabatine, Marc S., et al. "Evolocumab and clinical outcomes in patients with cardiovascular disease." New England Journal of Medicine 376.18 (2017): 1713-1722. [00:31:26] Evolocumab also reduces Lp(a); Study: O'Donoghue, Michelle L., et al. "Lipoprotein (a), PCSK9 inhibition, and cardiovascular risk: insights from the FOURIER trial." Circulation 139.12 (2019): 1483-1492. [00:34:02] APOA-1 Milano and HDL cholesterol. [00:38:45] Lp(a) and Vitamin C, plasminogen and clotting. [00:47:02] Rudolf Virchow, the father of the cholesterol hypothesis. [00:48:42] So what causes CVD? [00:49:53] Biomechanical stress; High blood pressure. [00:52:16] Endothelial and glycocalyx damage. [01:02:19] Steroids, immunosuppressants. [01:03:52] Avastin (bevacizumab) increases the risk of CVD; Study: Totzeck, Matthias, Raluca Ileana Mincu, and Tienush Rassaf. "Cardiovascular adverse events in patients with cancer treated with bevacizumab: a meta‐analysis of more than 20 000 patients." Journal of the American Heart Association 6.8 (2017): e006278. [01:06:07] Clotting disorders. [01:10:41] Sickle cell anemia - 50,000% increased risk of CVD. [01:11:36] Case study of 14-year old boy: Study: Elsharawy, M. A., and K. M. Moghazy. "Peripheral arterial lesions in patient with sickle cell disease." EJVES Extra 14.2 (2007): 15-18. [01:13:25] Air pollution, smoking, lead. [01:15:57] Biggest risk factors for CVD. [01:20:09] Supplements that strengthen the glycocalyx; Chondroitin Sulfate. [01:22:12] Malcolm's blog.
Dr. Michael Greger of NutritionFacts.org explains the difference, nutrition-wise, between whole coconuts and coconut milk or coconut oil. Please take a moment to rate & review the podcast here. Thank you!
Videos for Today: 1. DR Peter C. Gøtzsche Comments – 3 mins 2. PARENTS IN NY TAKE TO THE STREETS TO WARN IGNORANT PARENTS INJECTING THEIR CHILDREN WITH PFIZER SHOT 3, DANIEL NAGASE – EFFECTS OF CV VX ON THE IMMUNE SYSTEM DEVELOPMENT IN CHILDREN 4.The Great Narrative: A call to action speaker Freeke Heijman (start 3 min mark) 5. COMMERCIAL PILOT CODY FLINT: “I DON'T KNOW IF I WILL EVER BE ABLE TO FLY A PLANE AGAIN.” 6. Study, Experts: Vaccinated Are Spreading COVID-19 start 23 seconds in 7. RFK CLIP Start 50 seconds in Everyone missed this one… vaccinated people are up to 9X more likely to be hospitalized than unvaccinated people Australian War Propaganda Keeps Getting Crazier Are we seeing some new form of Covid-19 Vaccine induced Acquired Immunodeficiency Syndrome? – Official Government data suggests the Fully Vaccinated are on the precipice of disaster as their Immune Systems are being decimated $285 Billion Tax Cut for the Rich Is Now 2nd Most Expensive Piece of Build Back Better Wall Street's Takeover of Nature Advances with Launch of New Asset Class Court Deals New Blow to ‘Fatally Flawed' Biden Vaccine Mandates, But What Does That Mean? Study: Sustainable eating is cheaper and healthier Oxford University, November 11, 2021 Oxford University research has today revealed that, in countries such as the US, the UK, Australia and across Western Europe, adopting a vegan, vegetarian, or flexitarian diet could slash your food bill by up to one-third. The study, which compared the cost of seven sustainable diets to the current typical diet in 150 countries, using food prices from the World Bank's International Comparison Program, was published in The Lancet Planetary Health. It found that in high-income countries: Vegan diets were the most affordable and reduced food costs by up to one third. Vegetarian diets were a close second. Flexitarian diets with low amounts of meat and dairy reduced costs by 14%. By contrast, pescatarian diets increased costs by up to 2%. “We think the fact that vegan, vegetarian and flexitarian diets can save you a lot of money is going to surprise people,” says Dr. Marco Springmann, researcher on the Oxford Martin Programme on the Future of Food. “When scientists like me advocate for healthy and environmentally-friendly eating, it's often said we're sitting in our ivory towers promoting something financially out of reach for most people. This study shows it's quite the opposite. These diets could be better for your bank balance as well as for your health and…the planet.” Miguel Barclay, author of the bestselling “One Pound Meals” series of cookbooks, says, “I definitely agree that cutting down your meat, or cutting it out completely, will save you money. I've written seven budget cookbooks and have costed up hundreds of recipes, and without doubt vegan and vegetarian meals consistently come in at a much lower price than recipes with meat.” The study focused on whole foods and did not include highly-processed meat replacements or eating at restaurants or takeaways. The study also found that in lower income countries, such as on the Indian subcontinent and in sub-Saharan Africa, eating a healthy and sustainable diet would be up to a quarter cheaper than a typical Western diet, but at least a third more expensive than current diets. To analyze what options could improve affordability and reduce diet costs, the study looked at several policy options. It found that making healthy and sustainable diets affordable everywhere is possible within the next 10 years when economic development, especially in lower income countries, is paired with reductions in food waste and a climate and health-friendly pricing of foods. “Affording to eat a healthy and sustainable diet is possible everywhere, but requires political will,” according to Dr. Springmann. “Current low-income diets tend to contain large amounts of starchy foods and not enough of the foods we know are healthy. And the western-style diets, often seen as aspirational, are not only unhealthy, but also vastly unsustainable and unaffordable in low-income countries. Any of the healthy and sustainable dietary patterns we looked at are a better option for health, the environment, and financially, but development support and progressive food policies are needed to make them both affordable and desirable everywhere.” The study, “The global and regional costs of healthy and sustainable dietary patterns: a modeling study,” is published in The Lancet Planetary Health on 10 November 2021. Country-level results are available here. Green One Pound Meals by Miguel Barclay is published on 30 December. It features planet-friendly recipes and includes tips and ideas for shopping smart and avoiding food waste. Meta-analysis concludes resveratrol beneficially modulates glycemic control in diabetics Zagazig University and Suez Canal University (Egypt), October 29 2021. Findings from a meta-analysis of clinical trials published on October 16, 2021 in Medicina Clinica (Barcelona) revealed an association between supplementing with resveratrol and improvements in glycemic control. “Type 2 diabetes mellitus (T2DM) is a progressive meta-inflammatory disorder, which induces micro and macrovascular complications,” Ibrahim A. Abdelhaleem and colleagues wrote. “Resveratrol is a nutraceutical known to have antioxidant and anti-inflammatory properties.” “This systematic review and meta-analysis is the first to consider resveratrol's efficacy on glycemic and cardiometabolic parameters in patients with T2DM.” Sixteen randomized trials that included a total of 871 diabetic men and women were selected for the meta-analysis. The trials compared resveratrol to a placebo with or without concurrent antidiabetic medications or other drug treatment. Resveratrol doses of 500 milligrams or more were associated with lower fasting blood glucose, fasting serum insulin, insulin resistance, total cholesterol, LDL cholesterol and diastolic blood pressure in comparison with a placebo. Resveratrol was associated with a greater reduction in hemoglobin A1c (a marker of long-term glucose control) compared to a placebo in trials of three months duration. When HDL cholesterol levels were analyzed, resveratrol was superior to a placebo in trials of less than two months duration. Resveratrol was also associated with a reduction in systolic blood pressure compared to measurements obtained in the placebo group. Furthermore, triglycerides were lower in association with resveratrol in trials that lasted six to twelve months. “We concluded that resveratrol appropriately improved insulin sensitivity by decreasing insulin resistance, fasting blood glucose, fasting serum insulin, and hemoglobin A1c,” the authors concluded. “In addition, it improved other cardiometabolic parameters, including triglycerides, total cholesterol, LDL cholesterol, and systolic and diastolic blood pressure. The most appropriate glycemic control effect was fulfilled when consumed for at least one month with doses of 500 mg or more.” Exercise linked to better mental health Kaiser Permanente Research, November 11, 2021 Kaiser Permanente research published on November 11 in Preventive Medicine showed people who exercised more during the initial lockdown period of the COVID-19 pandemic experienced less anxiety and depression than those who didn't exercise. It also showed that people who spent more time outdoors typically experienced lower levels of anxiety and depression than those who stayed inside. More than 20,000 people participated in the survey-based study from 6 regions served by Kaiser Permanente across the United States, which included Hawaii, Colorado, Georgia, and the mid-Atlantic states, as well as Southern and Northern California. “What these study findings tell us is that even during an active pandemic or other public health crisis, people should be encouraged to be physically active to help maintain their physical and mental health,” said the study's lead author Deborah Rohm Young, PhD, the director of the Division of Behavioral Research for the Kaiser Permanente Southern California Department of Research & Evaluation. “Parks and other nature areas should remain open during public health emergencies to encourage outdoor physical activity.” In March 2020, COVID-19 developed into a worldwide pandemic. With no known treatment, public health officials attempted to reduce its spread by limiting human interactions through stay-at-home policies. Businesses temporarily closed or changed their practices to prevent the spread of the virus, affecting the economy and many people's jobs. These stressful factors, along with fewer opportunities to socialize with friends and family, increased symptoms of depression and anxiety for many people. Since it is known that physical activity and time spent in nature are associated with improved mental health, researchers at Kaiser Permanente in Southern California sought to determine how exercise and time outdoors was associated with people's mental health during the height of the pandemic. In April 2020, researchers sent a series of COVID-19 surveys to more than 250,000 participants in the Kaiser Permanente Research Bank — a collection of lifestyle surveys, electronic health record data, and biospecimens, which Kaiser Permanente members volunteered. People who reported COVID-19 symptoms were not included in this analysis, resulting in 20,012 respondents. They each completed at least 4 surveys between April and July 2020. White women older than 50 accounted for a high proportion of the respondents. Most respondents said they were retired and generally adhered to the “safer-at-home” orders during the period of the survey. The study found that: Reports of anxiety and depression decreased over time Anxiety and depression scores were higher for females and younger people, and lower for Asian and Black people compared with white respondents Participants who reported no physical activity reported the highest depression and anxiety compared to people who had exercised Spending less time outdoors was associated with higher depression and anxiety scores People who had increased their time outdoors the most reported the highest anxiety scores, but the research could not explain the finding “What we learned from these findings is that during future emergencies it will be important to carefully weigh the decisions to close parks and outdoor areas against the negative impact those closures may have on people's mental health,” said Dr. Young. Bedtime linked with heart health University of Exeter (UK), November 9, 2021 Going to sleep between 10:00 and 11:00 pm is associated with a lower risk of developing heart disease compared to earlier or later bedtimes, according to a study published today in European Heart Journal—Digital Health, a journal of the European Society of Cardiology (ESC). “The body has a 24-hour internal clock, called circadian rhythm, that helps regulate physical and mental functioning,” said study author Dr. David Plans of the University of Exeter, UK. “While we cannot conclude causation from our study, the results suggest that early or late bedtimes may be more likely to disrupt the body clock, with adverse consequences for cardiovascular health.” While numerous analyses have investigated the link between sleep duration and cardiovascular disease, the relationship between sleep timing and heart disease is underexplored. This study examined the association between objectively measured, rather than self-reported, sleep onset in a large sample of adults. The study included 88,026 individuals in the UK Biobank recruited between 2006 and 2010. The average age was 61 years (range 43 to 79 years) and 58% were women. Data on sleep onset and waking up time were collected over seven days using a wrist-worn accelerometer. Participants completed demographic, lifestyle, health and physical assessments and questionnaires. They were then followed up for a new diagnosis of cardiovascular disease, which was defined as a heart attack, heart failure, chronic ischaemic heart disease, stroke, and transient ischaemic attack. During an average follow-up of 5.7 years, 3,172 participants (3.6%) developed cardiovascular disease. Incidence was highest in those with sleep times at midnight or later and lowest in those with sleep onset from 10:00 to 10:59 pm. The researchers analyzed the association between sleep onset and cardiovascular events after adjusting for age, sex, sleep duration, sleep irregularity (defined as varied times of going to sleep and waking up), self-reported chronotype (early bird or night owl), smoking status, body mass index, diabetes, blood pressure, blood cholesterol and socioeconomic status. Compared to sleep onset from 10:00 to 10:59 pm, there was a 25% higher risk of cardiovascular disease with a sleep onset at midnight or later, a 12% greater risk for 11:00 to 11:59 pm, and a 24% raised risk for falling asleep before 10:00 pm. In a further analysis by sex, the association with increased cardiovascular risk was stronger in women, with only sleep onset before 10:00 pm remaining significant for men. Dr. Plans said: “Our study indicates that the optimum time to go to sleep is at a specific point in the body's 24-hour cycle and deviations may be detrimental to health. The riskiest time was after midnight, potentially because it may reduce the likelihood of seeing morning light, which resets the body clock.” Dr. Plans noted that the reasons for the observed stronger association between sleep onset and cardiovascular disease in women is unclear. He said: “It may be that there is a sex difference in how the endocrine system responds to a disruption in circadian rhythm. Alternatively, the older age of study participants could be a confounding factor since women's cardiovascular risk increases post-menopause—meaning there may be no difference in the strength of the association between women and men.” He concluded: “While the findings do not show causality, sleep timing has emerged as a potential cardiac risk factor—independent of other risk factors and sleep characteristics. If our findings are confirmed in other studies, sleep timing and basic sleep hygiene could be a low-cost public health target for lowering risk of heart disease.” Garlic compounds may boost cardio health indirectly via gut microbiota National Taiwan University, November 6 2021 Allicin from garlic may prevent the metabolism of unabsorbed L-carnitine or choline into TMAO, a compound linked to an increased risk of cardiovascular diseases, says a new study from the National Taiwan University. TMAO – or trimethylamine N-oxide – has been known to be generated from dietary carnitine through metabolism of gut microbiota, and was recently reported to be an “important gut microbiota-dependent metabolite to cause cardiovascular diseases,” explained Taiwanese researchers in the Journal of Functional Foods . While antibiotics have been found to inhibit TMAO production, concerns over side effects and resistance have limited their use. This has led researchers to examine the potential of natural alternatives. New data indicated that carnitine-fed lab mice showed a “remarkable increase in plasma TMAO levels”, compared with lab mice fed a control (no carnitine). However, when allicin supplements were provided with the carnitine diet, TMAO levels were significantly reduced. “Surprisingly, the plasma TMAO levels in the mice of ‘carnitine diet + allicin' treatment group were as low as that of chow diet [control] group,” wrote the researchers. “This result indicated that the metabolic capacity of mice gut microbiota to produce TMAO was completely inhibited by allicin supplement even though provided with carnitine-rich environment in the gut. “It means the functional alteration of gut microbiota induced by carnitine diet can be prevented by addition of another substance with antimicrobial potential derived from food, such as allicin.” Garlic and heart health The study adds to the body of scientific literature supporting the potential heart health benefits of garlic and the compounds it contains. Consumer awareness of the health benefits of garlic, mostly in terms of cardiovascular and immune system health, has benefited the supplements industry, particularly since consumers seek the benefits of garlic without the odors that accompany the fresh bulb. The benefits have been linked to the compound allicin, which is not found in fresh garlic: It is only formed when garlic is crushed, which breaks down a compound called diallyl sulphide. Study details “This may offer an opportunity to take advantage of plants' delicately designed defense system against microorganisms, to protect ourselves by modulating gut microbiota to a healthier status,” wrote the researchers The Taiwanese researchers divided male C57BL/6(B6) mice into four groups: One group received only the control chow diet; the second group received the carnitine diet (carnitine added to drinking water at a level of 0.02%); the third group received the carnitine diet with supplemental allicin; and the final group received the control diet plus the allicin supplement for six weeks. Results showed that the second group (carnitine diet) had TMAO levels 4–22 times greater than those observed in the control group. However, these increases were attenuated in the carnitine + allicin group, said the researchers. “Our study suggests that antimicrobial phytochemicals such as allicin effectively neutralize the metabolic ability of TMAO production of gut microbiota induced by daily intake of L-carnitine,” wrote the researchers. “It may offer an opportunity for us to take advantage of plants' delicately designed defense system against microorganisms, to protect ourselves by modulating gut microbiota to a healthier status. “Our research also suggested that allicin and dietary fresh garlic containing allicin might be used as functional foods for the prevention of atherosclerosis,” they concluded. Drug used to prevent miscarriage increases risk of cancer in offspring University of Texas Health Science Center, November 9, 2021 Exposure in utero to a drug used to prevent miscarriage can lead to an increased risk of developing cancer, according to researchers at The University of Texas Health Science Center at Houston (UTHealth Houston). The study was published today in the American Journal of Obstetrics and Gynecology. The drug, 17α-hydroxyprogesterone caproate (17-OHPC), is a synthetic progestogen that was frequently used by women in the 1950s and 1960s, and is still prescribed to women today to help prevent preterm birth. Progesterone helps the womb grow during pregnancy and prevents a woman from having early contractions that may lead to miscarriage. “Children who were born to women who received the drug during pregnancy have double the rate of cancer across their lifetime compared to children born to women who did not take this drug,” said Caitlin C. Murphy, PhD, MPH, lead author on the study and associate professor in the Department of Health Promotion and Behavioral Sciences at UTHealth School of Public Health in Houston. “We have seen cancers like colorectal cancer, pancreatic cancer, thyroid cancer, and many others increasing in people born in and after the 1960s, and no one really knows why.” Researchers reviewed data from the Kaiser Foundation Health Plan on women who received prenatal care between June 1959 and June 1967, and the California Cancer Registry, which traced cancer in offspring through 2019. Out of more than 18,751 live births, researchers discovered 1,008 cancer diagnoses were made in offspring ages 0 to 58 years. Additionally, a total of 234 offspring were exposed to 17-OHPC during pregnancy. Offspring exposed in the womb had cancer detected in adulthood more than twice as often as offspring not exposed to the drug – 65% of cancers occurred in adults younger than 50. “Our findings suggest taking this drug during pregnancy can disrupt early development, which may increase risk of cancer decades later,” Murphy said “With this drug, we are seeing the effects of a synthetic hormone. Things that happened to us in the womb, or exposures in utero, are important risk factors for developing cancer many decades after we're born.” A new randomized trial shows there is no benefit of taking 17-OHPC, and that it does not reduce the risk of preterm birth, according to Murphy. The U.S. Food and Drug Administration proposed in October 2020 that this particular drug be withdrawn from the market.
For nearly 70 years now, Americans have been bombarded with advice on how to lose weight. Countless diet books have become bestsellers. Some diets like Atkins keep coming back in sort of a recycled way. And there really hasn't been agreement, even among nutrition scientists, about which approach is best. Lots of attention has focused in recent years on carbohydrates, but over the years, protein and fat have had plenty of attention. In this podcast, our guest, Dr. David Ludwig of Harvard University, discusses this history and the reason for re-envisioning how best to lose weight – and for people to maintain the weight loss, perhaps the most important issue of all. Ludwig recently published a landmark, exquisitely designed and controlled study that tests whether limiting carbohydrates actually makes sense. This study, published in the "American Journal "of Clinical Nutrition 2021," has been generating lots of attention. Interview Summary Access the study: https://doi.org/10.1093/ajcn/nqab287 I'll begin by asking a question fundamental to this work. Why care so much about carbohydrates? Great question, Kelly. Carbohydrates amount to at least half the calories in a typical diet today, which is interesting from a historical and evolutionary perspective. Because of the three major nutrients we eat, protein, fat, and carbohydrate, carbohydrate is the only one for which humans have virtually no requirement. Think of Northern populations, especially in the Ice Ages but also up to recently, such as the Inuit, that had access to only animal products and could eat plant products like berries maybe one or two or three months a year at most. So for nine months a year, they were eating only fat and protein. And yet, those populations were healthy. The women were fertile; they could breastfeed. And children grew normally. So recognizing that there's no absolute requirement for carbohydrates, the question then becomes: How much carbohydrate and what kind would be optimal for health and allow for the greatest flexibility, diversity and enjoyment in our diets? So David, if the body doesn't have an innate need for these, presumably there's no biological driver to go out and seek these, why in the heck are people eating so much of this? Well, carbohydrates are delicious. And the food industry certainly knows that and has taken advantage of that. In fact, when you step back and ask: What are the foods that we tend to binge on? They may have a combination of key flavors and nutrients. Oftentimes, we hear sugar, salt and fat. But I'll argue that there are virtually no binge foods that are just fat. Do people actually binge on butter? I mean, butter is very tasty. You might enjoy an initial bite. But very few people, perhaps with the exception of a major eating disorder, would sit down and eat a quarter pound, a stick of butter. But there are all sorts of high-carbohydrate binge foods. Sugary beverages are 100% sugar. Bread, baked potato chips, popcorn, especially the low-fat versions, these are easy to binge. And from one perspective, the key difference is the hormone insulin. Fat does not raise insulin. And so fat is digested slowly, and doesn't get directly stored in large amounts into body tissue. It has to be metabolized more slowly. Whereas carbohydrates, especially the processed ones, when eaten in large amounts, raise insulin to high levels. That insulin directs those incoming calories into storage. And a few hours later, blood sugar crashes and we get hungry again and are ready to have another blood sugar surge by indulging the next time in those foods. So what question specifically was your study designed to address? We conducted a large feeding study that had two parts. The parent study had 164 young and middle-aged adults, who were at least a little bit overweight, ranging from overweight to having obesity. And the first thing we did was bring their weight down by providing them all of their foods, delivered foods to their home, in a calorie-restricted way. You know, you cut back calories, and of course you're going to lose weight for a while. It doesn't address why people get hungry, and why they regain weight. But in the short term, we cut their calories, and they lost 10% to 12% of their weight. Then we stabilized them at their new, lower body weight, and then randomly assigned them to one of three groups: low, moderate or high-carbohydrate diets. And we kept them on these three different diets for another five months. And during this time, we were again delivering all of the meals to the participants. This was over 100,000 prepared meals throughout this time, so it was a really major effort. And during this low, moderate, and high-carbohydrate diet period, we adjusted calories to keep their weight the same. We wanted to keep them at that weight-loss anchor, 10% to 12% below where they started. The first study looked at what happened to their metabolism and their energy expenditure. And we found that when people were on the low-carb diet at the same weight as the other groups, they were burning about 200 calories a day more. So the study raised an interesting possibility, that the kind of calories you eat can affect the number of calories you burn. That from a biological perspective, all calories are not alike to the body. David, this is fascinating work. I'd like to ask a strategy question. So this was an extremely intensive study of 164 people. And you mentioned the people were provided all their meals, very careful measurement and things like that. So the same amount of money, you could have studied many more people but just done a less intensive study with less supervision and fewer measurements of outcome. So why do the study in such an intensive way? Right, there's always going to be a trade-off in design considerations. And you've identified a classic trade-off. You can study fewer people more intensively, or more people less intensively. Most weight loss trials have chosen the second route. They take a lot of people, and they try to study them for a long period of time, or at least some of them do: a year or ideally two years or longer. The problem is that without an intensive intervention, so what are we talking about? These studies would oftentimes have participants meet with a nutritionist once a month. They would get written educational materials, and maybe other kinds of behavioral support. But that's about it. And without greater levels of support and intervention, people characteristically can't stick to these diets over the long term. Maybe they make changes for two, three or four months. But by six months or a year, they're largely back to eating what they were originally. And the different diet groups don't look much different. So if the groups didn't eat in much of a different way throughout most of the study, why would we expect to see any differences in outcomes, such as weight or energy expenditure, or cardiovascular disease risk factors? So these studies don't test a dietary hypothesis very well. It leads to the mistaken conclusion that all diets are alike. Really, what the conclusion of these studies has to mean is that we need more intensive intervention in our modern toxic environment, if you will, to promote long-term change. And it's only when we get that long-term change can we actually figure out which diet is better and for whom. So you've explained how the study was done and why you did it. What did you find? So the first leg of the study, which was published in "BMJ" late in 2018, so just before the pandemic, showed that the kinds of calories you're eating can affect the number of calories you burn. And, that by cutting back on the total and processed carbohydrates, you can increase your metabolic rate. And that could be a big help in the long-term management of a weight problem. You know, you want your body on your side rather than fighting you when you're trying to maintain weight loss. And a faster metabolism would be a tremendous help if this is a reproducible finding and applies to the general population. We recently published in the September "American Journal of Clinical Nutrition," a second part of the study. And that asks: How do these different diets, low, moderate and high carbohydrate, affect cardiovascular disease risk factors? It's one thing to lose weight. Maybe a low carbohydrate diet helps you lose weight. But if your cardiovascular disease risk factors go up, that might not be such a good trade-off. So that's the aim of the second study. Because low-carbohydrate diets are often very high in saturated fat. So we wanted to find out what were the effects of this low-carbohydrate, high-saturated-fat on a range of risk factors. So tell us specifically some of the cardiovascular risk factors that changed. And if you would, place the changes that you found in your participants in a context. Like are these big-deal changes? Are they small changes? Or put it in context, if you would? The big problem with saturated fat is that it clearly raises LDL cholesterol, low-density lipoprotein cholesterol, which is a classic cardiovascular disease risk factor. It's the main one that's targeted by many of the drugs, such as statins. Yeah, I think there's no question that on a conventional high-carbohydrate diet, a lot of saturated fat is harmful. So the combination of bread and butter is not a good one. But the question we wanted to ask was: What happens when you get rid of a lot of that bread? Does the saturated fat still comprise a major risk factor? And so our low-carbohydrate diet was exceptionally high in saturated fat, as is characteristic of how these low-carb diets are usually consumed. It had 21% saturated fat, which compares to the 7% saturated fat on the high-carb, low-fat diet that's oftentimes recommended to people at risk for heart disease. So what did we find? Well, the first thing we found was that LDL cholesterol was not adversely affected at all. There was no difference in LDL cholesterol between those getting 21% versus 7% saturated fat. Suggesting that when you substitute saturated fat for processed carbohydrates, from the standpoint of this key risk factor, it's pretty much a wash. However, the low-carbohydrate, high-saturated-fat diet benefited a range of other risk factors that go along with what we call the metabolic syndrome, the insulin resistance syndrome. Specifically, we saw strongly significant, from a statistical perspective, improvements in triglycerides, that's the total amount of fat in the bloodstream; HDL cholesterol, that's the good cholesterol that you want to be higher; and other lipids that indicate overall levels of insulin resistance. Suggesting that insulin resistance was improving. And we know that low-carbohydrate diets show promise for diabetes in other studies, in part because they do tend to improve insulin resistance and lower blood sugar. And so our study suggests that if you are pursuing a low-carbohydrate diet, and we can talk about the different degrees of restriction of carbohydrate, and at the same time you're reducing the processed carbohydrates, then the saturated fat might not really be such a problem. So then if you take all this information in this, as I said, exquisitely designed intensive study and distill it into what dietary recommendations would be, what do you think is a reasonable proportion of fat, carbohydrate and protein in the diet? And what sort of things should people think about as they want to lose weight and keep the weight off? One key qualification I need to mention is even though this was an intensive study with a relatively large number of people for a feeding study of this magnitude, we still don't know how generalizable these findings are to people at different ages, different body weights, different levels of susceptibility. So no one study can inform a change of clinical practice like this, especially in the world of nutrition where there's so many complicated and interacting factors. I will also venture to say that there's no one diet that's going to be right for everybody. We know that some people can do perfectly well on a high-carbohydrate, low-fat diet. I mean, think of the classic Asian agrarian societies where rates of obesity and diabetes are very low. But those societies tend to be highly physically active and the people insulin-sensitive. America is characterized by high levels of overweight and obesity, sedentary lifestyle. And these create insulin resistance as a highly prevalent problem. For societies such as ours, we think that high-carbohydrate diets that are raising insulin levels on the background of insulin resistance is a recipe for metabolic problems. And so for Americans, especially those struggling with weight, pre-diabetes, and even more so diabetes, a reasonable first step is to cut back on the processed carbohydrates. And I think that's an intervention that increasingly few experts would argue with. We're talking about concentrated sugars and refined grains. Where we start to get into the controversy is whether carbohydrates should be further reduced down to say 20% as in our study, which still leaves room for some unprocessed grains, beans, and a couple of servings of whole fruit a day, or even lower to what's called the ketogenic diet that's less than 10%. And that's where you really have to give up most carbohydrates and focus just on the proteins and fats. I think for people with diabetes, such a strict approach looks appealing in preliminary research studies. But again, this is going to need more research. And I would caution anybody with diabetes or anybody who's thinking about a ketogenic diet to discuss these kinds of dietary changes with their healthcare provider. I realize your study wasn't meant to address this issue that I'm about to raise, but I'd appreciate hearing your instincts. One key, of course, to any recommended nutrition plan or diet, if you'd like to call it that, is whether people will stick to it. What do your instincts tell you, or data if you have it, on how readily people can adhere to this sort of an approach over the long term compared to other kinds of approaches? Great question. And I'll approach that by saying: We all understand that if diet is a problem that's contributing to obesity, diabetes, heart disease, other chronic health problems, then we have to change our diet in one way or another regardless of what the mechanisms are. So I'll return the question to you by saying: Which do you think is going to be easier for most people over the long term: cutting back calories, getting hungry and trying to ignore that very intense drive to eat, or getting rid of certain kinds of foods that may be triggering hunger and making it so much harder to stick to a lower calorie intake? As a doctor, as a pediatrician, and as a researcher, and also myself, I try to do N of 1 experiments on myself with any kind of a nutrition approach I might use with patients or with research participants. I've found that it's so much easier to just give up the processed carbohydrates and enjoy a range of other very satisfying, delicious, higher fat foods. And oftentimes, in my experience personally and I hear as reported by patients that the cravings for these highly processed carbohydrates go down. And lastly, I'll just say, it's not that these processed carbohydrates are inherently so irresistibly delicious. I mean, white bread, these common binge foods, white bread, unbuttered popcorn, baked potato chips, even though these are almost 100% carbohydrate yet they're commonly binged on not because they're so incredibly tasty. But I would argue because they're producing changes in our body that are driving overeating. So it's not that they're so tasty and we're getting so much enjoyment. We're eating these foods because we're driven to metabolically. And once you come off that blood sugar rollercoaster, it becomes much easier to say no. When you mentioned before that with one approach, you're kind of fighting your body; and another approach, your body is becoming your ally in this process, I thought of going to the beach and, you know, you can go out and try to swim against the waves coming in, or you can ride the waves toward the beach. And one, of course, is a lot easier than the other. And it sounds that's kind of what you're talking about, isn't it? When you line up biology and behavior, and clearly behavior, psychology, and our food environment are all factors that are going to have to be addressed. We don't want to make it much harder for people. So we do need to think in systems dynamics: the food supply, the environment. But on a strictly individual level, when you line up biology with your behavior, the effort required to accomplish your goals becomes less. You know, this is characteristic of so many areas of medicine and research. This is why we aim to identify the cause of a problem when you treat a cause. So let's use the example of fever. Fever you could say is a problem of heat balance: too much heat in the body, not enough heat out. And so from that perspective, you could treat any fever by getting into an ice bath. Couldn't you, right? The ice would pull the excess heat out of your body. But is that an effective treatment for fever? No, of course not. Because your body's going to fight back violently with severe shivering, blood vessel constriction. And you're going to feel miserable and you're going to get out of that ice bath quickly. In the case of obesity, the timeframe is much longer, but similar kinds of responses occur. The body fights back against calorie restriction because calorie restriction, according to this way of thinking, is an effect. It's not the cause. If the cause is the body's been triggered to store too much fat, then we have to address that problem by lowering insulin levels and producing a more stable blood sugar pattern after eating. If that happens, then the effort that you put into cutting back calories goes a lot further. Bio: David S. Ludwig, MD, PhD is an endocrinologist and researcher at Boston Children's Hospital. He holds the rank of Professor of Pediatrics at Harvard Medical School and Professor of Nutrition at Harvard School of Public Health. Dr. Ludwig is the founding director of the Optimal Wellness for Life (OWL) program, one of the country's oldest and largest clinics for the care of overweight children. For 25 years, Dr. Ludwig has studied the effects of diet on metabolism, body weight and risk for chronic disease – with a special focus on low glycemic index, low carbohydrate and ketogenic diets. He has made major contributions to development of the Carbohydrate-Insulin Model, a physiological perspective on the obesity pandemic. Described as an “obesity warrior” by Time Magazine, Dr. Ludwig has fought for fundamental policy changes to improve the food environment. He has been Principal Investigator on numerous grants from the National Institutes of Health and philanthropic organizations totaling over $50 million and has published over 200 scientific articles. Dr. Ludwig was a Contributing Writer at JAMA for 10 years and presently serves as an editor for American Journal of Clinical Nutrition. He appears frequently in national media, including New York Times, NPR, ABC, NBC, CBS and CNN. Dr. Ludwig has written 3 books for the public, including the #1 New York Times bestseller Always, Hungry? Conquer Cravings, Retrain your Fat Cells, and Lose Weight Permanently.
Grape consumption benefits gut microbiome and cholesterol metabolism University of California at Los Angeles, November 11, 2021 A new clinical study published in the scientific journal Nutrients found that consuming grapes significantly increased the diversity of bacteria in the gut which is considered essential to good health overall. Additionally, consuming grapes significantly decreased cholesterol levels, as well as bile acids which play an integral role in cholesterol metabolism. The findings suggest a promising new role for grapes in gut health and reinforce the benefits of grapes on heart health. In the intervention study], healthy subjects consumed the equivalent of 1.5 cups of grapes[2] per day – for four weeks. The subjects consumed a low fiber/low polyphenol diet throughout the study. After four weeks of grape consumption there was an increase in microbial diversity as measured by the Shannon index, a commonly used tool for measuring diversity of species. Among the beneficial bacteria that increased was Akkermansia, a bacteria of keen interest for its beneficial effect on glucose and lipid metabolism, as well as on the integrity of the intestinal lining. Additionally, a decrease in blood cholesterols was observed including total cholesterol by 6.1% and LDL cholesterol by 5.9%. Bile acids, which are linked to cholesterol metabolism, were decreased by 40.9%. Vitamin D supplementation associated with lower risk of heart attack or death during follow-up Kansas City VA Medical Center, November 8 2021. The October 2021 issue of the Journal of the Endocrine Society published findings from a retrospective study of US veterans that uncovered an association between supplementing with vitamin D and a lower risk of heart attack and mortality from any cause during up to 14 years of follow-up. The study included men and women treated at the Kansas City VA Medical Center from 1999-2018 who had low 25-hydroxyvitamin D levels of 20 ng/mL or less. Among 11,119 patients who were not treated with vitamin D supplements, follow-up vitamin D levels remained at 20 ng/mL or lower. For those who received the vitamin, levels improved to 21-29 ng/mL among 5,623 patients and to at least 30 ng/mL among 3,277 patients at follow-up. Men and women whose vitamin D levels improved to at least 30 ng/mL had a risk of heart attack that was 35% lower than patients whose levels improved to 21-29 ng/mL and 27% lower than the untreated group. The difference in risk between untreated individuals and those whose levels improved to 21-29 ng/mL was not determined to be significant. Patients whose vitamin D levels improved the most also experienced significantly greater heart attack-free survival during follow-up than the remainder of the patients. When mortality from any cause during follow-up was examined, men and women whose vitamin D levels improved to 21-29 ng/mL had a 41% lower risk, and those whose levels improved to 30 ng/mL or more had a 39% lower risk than the untreated group. “These results suggest that targeting 25-hydroxyvitamin D levels above 30 ng/mL might improve prognosis in the primary prevention setting among individuals with vitamin D deficiency,” authors Prakash Acharya of the University of Kansas Medical Center and colleagues wrote. Meditative practice and spiritual wellbeing may preserve cognitive function in aging Alzheimer's Research and Prevention Foundation and Thomas Jefferson University, November 12, 2021 It is projected that up to 152 million people worldwide will be living with Alzheimer's disease (AD) by 2050. To date there are no drugs that have a substantial positive impact on either the prevention or reversal of cognitive decline. A growing body of evidence finds that targeting lifestyle and vascular risk factors have a beneficial effect on overall cognitive performance. A new review in the Journal of Alzheimer's Disease, published by IOS Press, examines research that finds spiritual fitness, a new concept in medicine that centers on psychological and spiritual wellbeing may reduce multiple risk factors for AD. Research reveals that religious and spiritual involvement can preserve cognitive function as we age. Significantly, individuals who have a high score on a "purpose in life" (PIL) measure, a component of psychological wellbeing, were 2.4 times more likely to remain free of AD than individuals with low PIL. In another study, participants who reported higher levels of PIL exhibited better cognitive function, and further, PIL protected those with already existing pathological conditions, thus slowing their decline. Radiotherapy may explain why childhood cancer survivors often develop metabolic disease Rockefeller University, November 9, 2021 Decades after battling childhood cancer, survivors often face a new challenge: cardiometabolic disease. A spectrum of conditions that includes coronary heart disease and diabetes, cardiometabolic disease typically impacts people who are obese, elderly, or insulin resistant. For reasons yet unknown, young, seemingly healthy adults who survived childhood cancer are also at risk. Radiation therapy may be to blame. A new study finds that childhood cancer patients who were treated with abdominal or total body irradiation grow up to display abnormalities in their adipose (fat) tissue, similar to those found in obese individuals with cardiometabolic disease. "When physicians are planning radiation therapy, they are very conscious of toxicity to major organs. But fat is often not considered," says Rockefeller's Paul Cohen. "Our results imply that the early exposure of fat cells to radiation may cause long-term dysfunction in the adipose tissue that puts childhood cancer survivors at higher risk of cardiometabolic disease." Researchers discover link between dietary fat (palm oil) and the spread of cancer Barcelona Institute of Science and Technology (Spain), November 10, 2021 The study, published in the journal Nature and part-funded by the UK charity Worldwide Cancer Research, uncovers how palmitic acid alters the cancer genome, increasing the likelihood the cancer will spread. The researchers have started developing therapies that interrupt this process and say a clinical trial could start in the next couple of years. Newly published findings reveal that one such fatty acid commonly found in palm oil, called palmitic acid, promotes metastasis in oral carcinomas and melanoma skin cancer in mice. Other fatty acids called oleic acid and linoleic acid—omega-9 and omega-6 fats found in foods such as olive oil and flaxseeds—did not show the same effect. Neither of the fatty acids tested increased the risk of developing cancer in the first place. The research found that when palmitic acid was supplemented into the diet of mice, it not only contributed to metastasis, but also exerts long-term effects on the genome. Cancer cells that had only been exposed to palmitic acid in the diet for a short period of time remained highly metastatic even when the palmitic acid had been removed from the diet. The researchers discovered that this "memory" is caused by epigenetic changes—changes to how our genes function. The epigenetic changes alter the function of metastatic cancer cells and allow them to form a neural network around the tumor to communicate with cells in their immediate environment and to spread more easily. By understanding the nature of this communication, the researchers uncovered a way to block it and are now in the process of planning a clinical trial to stop metastasis in different types of cancer. Study finds consuming nuts strengthens brainwave function Loma Linda University, November 15, 2021 A new study has found that eating nuts on a regular basis strengthens brainwave frequencies associated with cognition, healing, learning, memory and other key brain functions. In the study titled "Nuts and brain: Effects of eating nuts on changing electroencephalograph brainwaves," researchers found that some nuts stimulated some brain frequencies more than others. Pistachios, for instance, produced the greatest gamma wave response, which is critical for enhancing cognitive processing, information retention, learning, perception and rapid eye movement during sleep. Peanuts, which are actually legumes, but were still part of the study, produced the highest delta response, which is associated with healthy immunity, natural healing, and deep sleep. The study's principal investigator, Lee Berk, DrPH, MPH, associate dean for research at the LLU School of Allied Health Professions, said that while researchers found variances between the six nut varieties tested (almonds, cashews, peanuts, pecans, pistachios and walnuts), all of them were high in beneficial antioxidants, with walnuts containing the highest antioxidant concentrations of all. Why Nitrates And Nitrites In Processed Meats Are Harmful – But Those In Vegetables Aren't University of Hertfordshire (UK), November 11, 2021 While there are many reasons processed meats aren't great for our health, one reason is because they contain chemicals called nitrates and nitrites. But processed meats aren't the only foods that contain these chemicals. In fact, many vegetables also contain high amounts – mainly nitrates. And yet research suggests that eating vegetables lowers – not raises – cancer risk. So how can nitrates and nitrites be harmful when added to meat but healthy in vegetables? The answer lies in how nitrates and nitrites in food get converted into other molecules. Nitrates and nitrites occur attached to sodium or potassium, and belong to a family of chemically related molecules that also includes the gas nitric oxide. Vegetables such as beetroot, spinach and cabbages are particularly good sources of nitrates. When we eat something containing nitrates or nitrites, they may convert into a related molecular form. For example, nitrate in vegetables and in the pharmaceutical form nitroglycerine (which is used to treat angina), can convert in the body into nitric oxide. Nitric oxide dilates blood vessels, which can reduce blood pressure. It's actually sodium nitrite – not nitrate – that's linked to cancer. But if consuming nitrites alone directly caused cancer, then even eating vegetables would be harmful to us. Given this isn't the case, it shows us that cancer risk likely comes from when the sodium nitrites react with other molecules in the body. So it isn't necessarily the nitrates and nitrites themselves that cause health issues – including cancer. Rather, it's what form they are converted into that can increase risk – and what these converted molecules interact with in our bodies. The main concern is when sodium nitrite reacts with degraded bits of amino acids – protein fragments our body produces during the digestion of proteins – forming molecules called N-nitroso compounds (NOCs). These NOCs have been shown to cause cancer. Obama Climate & Environment Record Seasoned environmentalists were very skeptical of obama from the very start n the 2008 campaign -- notably his coal to liquid technology he advocated and his great enthusiasm for ethanol Sold off 2.2 billion tons of coal from public land (Greenpeace report). The sales to private interests generated $2.3 billon but CO2 damage estimated between $52-530 billion His Clean Power Plan -- which Trump administration later trashed -- really had little to do with the plan's name -- had nothing to do with eradicating hazardous pollutants from power generation; it was primarily all based on a cap and trade system to regulate carbon dioxide Ran on campaign that by 2025, 25% of US energy would be renewable Was never anywhere close on being on track for that goal Promoted fracking as a move away from coal to natural gas -- this was a midst promises to have highest standards for fracking on federal land -- never happened Lowered natural gas export restrictions in order to sell more US natural gas to foeign customers Made efforts to weaken rules.on methane leaks from oil and gas operations -- leaks account or 3 percent of US gas emissions Also instrumental in pushing on behalf of pipeline companies and terminals to have major coastal terminals for gas exports (most notable example was Cove Point terminal in Maryland that Obama touted Flint Water crisis Sued the EPA over a dozen ties against the agency's effort to increase environmental regulations on corporations Opened more federal and land (18% increase between 2009-2014) for oil and gas drilling -- including "off limits" regions in the mid Atlantic coast, along Alaska's Arctic coast and Gulf of mexico, Completely failed on setting rules or clean disposal of coal ash byproduct -- US produces about 100 million tons of this crap annually and just dumps into holes in the ground Went soft on ozone pollution and smog rules -- did lower Bush's ozone threshold from 75ppb to 70 ppb, but his EPA was recommending 60-65 ppb Very insensitive to wood pellet development under the disguise as a renewable -- part of his clean power plan
It's important to know that fat is good for you and how avoiding it can actually hurt your health. Listen in for types you should focus on! My guest today is breaking it down for us and giving the true story when it comes to the what, why and how of fats! Rhyan Geiger is a registered dietitian and vegan author who specializes in vegan nutrition. She is the owner of Phoenix Vegan Dietitian where she helps others easily transition to vegan living. She has many years of experience in vegan nutrition and believes in positively impacting the world one bite at a time. Rhyan is an expert in this field and has been featured in Women's Health and Business Insider. You can connect with her on her website (where you can join her newsletter to get a free vegan smoothie book!) or on Instagram. You can also get 10% off her book, A Complete Guide to Grocery Shopping Vegan, with code REALFOOD! Types of Fats Fats are one of the macronutrients (protein, carb, fat) and are really important for your body. There are different types of fats: Monounsaturated and polyunsaturated fats are considered healthy fats or heart healthy and are predominately found in foods that come from plants.Trans fat and saturated fats can wreak havoc in your body and are predominately found in foods that come from animals and in fried foods. Why We Need Healthy Fats Because trans and saturated fats can raise your triglycerides and LDL cholesterol, which can lead to heart disease, you want to avoid them for the most part. However a little in an otherwise healthy individual isn't the end of the world. But unsaturated fats are needed in order for our bodies to function properly. Fats do a variety of things. They help build cell membranes and build the surroundings of our nerves, which keep our body moving and functioning. Also vitamins A, D, E, and K are fat soluble and they need fat in order to be absorbed. Without these vitamins you can experience a variety of health issues. Omega 3 fatty acids are a type of polyunsaturated fats. They are really important for brain function like building brain cells. These types of fat typically come from fish, but fish often get them from algae so there are ways to get Omega 3 fats from plants. Algae being one of them, however you can also get them from plant foods like flax seeds, chia seeds and walnuts. Unsaturated keep you heart healthy overall and can help prevent heart disease. But fat also keeps you feeling full, because it takes you longer to digest. This helps regulate your blood sugar, which in turn can help prevention of type 2 diabetes. How Much Fat You Need The dietary reference Intake (DRI) is 20-35% of the total calories you are eating. So this will vary with everyone. Because many of us do not calculate or track our food, another way to visually think about it is through your plate. The MyPlate Guidelines say that half of your plate should be comprised of fruit and/or veggies, one quarter grains and one quarter protein. With fat, you can think about the area in the middle being filled with about two tablespoons of healthy fat. This is simply a guideline and will vary with each meal. Food With Healthy Fats Here are some foods you can include in your diet so you can get in those healthy fats: AvocadoNuts like walnuts, macadamia and almondsSeeds like chia, hemp and flaxNut buttersBeansDark chocolateOlives Here are some ideas on how to use these foods for meals: Adding flax, hemp and chia with fruit into a smoothieMaking a chickpea scramble and adding flax, hemp and chia in with veggiesPutting walnuts in oatmealEating avocado in a sandwich, wrap or tacoEating apples or toast with nut butterMaking dairy free sauces with cashews Also, if you keep these foods eye level in the fridge and pantry you are more likely to grab for them when making meals. Signs You May Need More Fats Fats are so important for our body to function appropri...
Heart disease is the number one cause of death in the United States. Leading cardiologist, Dr. Joel Kahn, talks about how to reduce your risk of heart disease by changing your lifestyle. Eating a majority plant-based diet, stopping smoking, and getting enough sleep are key factors in heart health. Best Supplements for Optimal Heart Health Vitamin D CoQ10 Magnesium Melatonin Berberine About Dr. Joel Kahn Dr. Joel Kahn is a practicing cardiologist in Detroit, Michigan, and a Clinical Professor of Medicine at Wayne State University School of Medicine. He graduated Summa Cum Laude from the University of Michigan Medical School. Known as "America's Healthy Heart Doc", Dr. Kahn has triple board certifications in Internal Medicine, Cardiovascular Medicine, and Interventional Cardiology. He was the first physician in the world to certify in Metabolic Cardiology with A4M/MMI and the University of South Florida. He founded the Kahn Center for Cardiac Longevity in Bingham Farms, MI. Heart Health: The Leading Cause of Death Dr. Joel Kahn starts off by sharing exactly how serious heart disease is to the average American: very. Heart disease is the number one cause of death in the US. Dr. Kahn is on a mission to help the general population reduce their likelihood of developing heart disease in their lifetime. There are several lifestyle factors Dr. Kahn attributes to helping reduce the risk of heart disease. By stopping smoking, eating a majority plant-based diet, and improving the quality of your sleep, you have a lower chance of avoiding heart disease. Saying that, however, there are certain hereditary markers that can increase your development of the disease. So when this is the case for you, Dr. Kahn says it's even more important to keep your lifestyle factors to a minimum. Plants Based Eating for Optimal Heart Health Dr. Kahn is an advocate for a majority plant-based diet. A diet rich in plants is much healthier for the heart as it tends to be lower in cholesterol. But make sure you're supplementing on this type of diet, especially Vitamin B12. Certain nutrients are better for heart health. While most come from a healthy plant-based diet, some are more difficult to get naturally. Dr. Kahn shares the best supplements for optimal heart health and explains why we should all use supplements for our health. Finally, we talk about what lab and blood tests you should ask your doctor for to check your markers. In particular, it's important to keep an eye on your cholesterol, both LDL and HDL, as this has a massive impact on your heart health. How much of a plant-based diet are you eating? Are you worried you might have heart disease? Call the Integrative Health and Hormone Clinic today and schedule your first appointment at 319-363-0033. Quotes “Heart disease is the number one cause of death in America of men and women since 1918. 103 years in a row we have the champion's belt to show for heart disease. It's time to stop that.” [4:18] “The whole public should ensure that their diet is working for them in terms of vitamin and cholesterol levels.” [15:36] “If you are eating meat, follow your direction and go for better quality cuts.” [35:30] In This Episode How serious heart disease is [4:00] How to prevent heart disease [5:30] How we should be eating for heart disease prevention [8:30] Why we should reduce our consumption of animal products [10:30] What nutrient deficiencies someone on a plant-based diet might have [19:30] The top nutrients for optimal heart health [21:30] Sources of cholesterol on a plant-based diet [29:00] What percentage of your diet should be plant-based [30:00] What blood tests indicate heart disease [36:00] Links & Resources Use Code BERBERINE for 10% Off Berberine Support Use Code MAGNESIUM for 10% Off Magnesium Find Dr. Joel Kahn Online Find the Kahn Center for Cardiac Longevity Online Follow Dr. Joel Kahn on Instagram | Facebook | Twitter | YouTube Find Your Longevity Blueprint Online Follow Your Longevity Blueprint on Instagram | Facebook | Twitter | YouTube | LinkedIn Get your copy of the Your Longevity Blueprint book and claim your bonuses here Find Dr. Stephanie Gray and Your Longevity Blueprint online Follow Dr. Stephanie Gray on Facebook | Instagram | Youtube | Twitter | LinkedIn Integrative Health and Hormone Clinic Podcast Production by the team at Counterweight Creative Related Episodes Episode 69: Pluck Seasoning With James Barry Episode 67: A Different Kind Of Healing With Dr. Shiroko Sokitch Episode 11: Intermittent Fasting Truths With Cynthia Thurlow
If you are interested in lipids, you've probably heard of Dave Feldman and his work. If not, you've got some homework to do, and I think you'll be amazed at what you find. Dave's work can be found at cholesterolcode.com where he details his multiple, meticulous self-experimental projects. Prior to cholesterol adventures Dave was a senior software scientist and an engineer. He brings this “out of the box” thinking to the world of medicine and we are all better off for it. He began a low-carb, high-fat diet in April 2015 and has since learned everything he could about it with special emphasis on cholesterol. He saw his own lipid numbers spike substantially after going on the diet and spotted a pattern in the lipid system that's very similar to distributed objects in networks. Time Stamps: 0:09:20 Podcast begins with Dave Feldman 0:09:45 Responding to the common question: "I feel so good on Animal-Based, but my cholesterol is sky high. What's going on?" 0:20:05 The importance of context in regards to cholesterol 0:26:20 Just because cholesterol is involved in asc sclerosis, that does not mean it is the cause of asc sclerosis 0:33:50 Inflammation and it's role with asc sclerosis 0:36:00 Do we have any experiments that shows LDL is directly harmful to humans? 0:47:05 The more saturated fat you eat, the higher your LDL goes, but does this result in more chronic disease? 0:57:35 PUFA's are essential for humans, but if you're eating saturated fat from grass-fed ruminant animals, you will not become deficient 1:02:44 Familial hypercholesterolemia (FH) and healthy individuals 1:07:40 Macrophages of genetically characterized familial hypercholesterolaemia patients show up‐regulation of LDL‐receptor‐related proteins: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5323824/ 1:14:20 A 72-Year-Old Patient with Longstanding, Untreated Familial Hypercholesterolemia but no Coronary Artery Calcification: A Case Report: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5991918/ 1:15:20 Chimpanzee VS Human LDL 1:15:45 Chimpanzee serum lipoproteins. Isolation, characterisation and comparative aspects of the low density lipoprotein and apolipoprotein-BH: https://pubmed.ncbi.nlm.nih.gov/6477668/ 1:25:05 Distribution of glycosaminoglycans in the intima of human aortas: changes in atherosclerosis and diabetes mellitus: https://pubmed.ncbi.nlm.nih.gov/8477876/ 1:29:20 The importance of hemostasis and how it relates to blood clots 1:35:40 Xanthoma in lean-mass hyper responders who do not have FH 1:40:50 Low Triglycerides–High High-Density Lipoprotein Cholesterol and Risk of Ischemic Heart Disease: https://jamanetwork.com/journals/jamainternalmedicine/fullarticle/647239 1:44:00 Hyperlipidaemia does not impair vascular endothelial function in glycogen storage disease type 1a: https://linkinghub.elsevier.com/retrieve/pii/0021915094900728 1:47:35 If a patient has a rising LDL, but is otherwise healthy, what does Dave suggest? 1:53:00 https://citizensciencefoundation.org/ and where to find more of Dave's work 1:54:30 Dave's current diet Sponsors: Heart & Soil: www.heartandsoil.co White Oak Pastures: www.Whiteoakpastures.com, use code: CarnivoreMD for 10% off your first order Belcampo: www.belcampo.com use code: CarnivoreMD for 20% off your order Lets Get Checked: 20% off your order at www.TRYLGC.com/paul
¿Es el colesterol tan malo como dicen? ¿Cuál es el peligro de este tipo de grasa? Durante los últimos años se ha demonizado el colesterol, pero ¿es el único factor que hay que tener en cuenta cuando hablamos de salud cardiovascular?En este episodio del podcast, descubrimos toda la verdad sobre el colesterol de la mano del Dr. Jose Albellán, médico cardiólogo. Hablaremos de qué otros factores depende la enfermedad coronaria más allá del LDL, de qué valores son realmente importantes en una analítica, de alimentación y de cómo unos buenos hábitos de vida pueden ser una excelente forma de prevenir eventos cardiovasculares.
Repatha is a popular cholesterol-lowering medication. It's not a statin and must be injected and can dramatically reduce bad LDL cholesterol. Several people have reported intense muscle pains occurring soon after taking the drug. In this interview, I sit down with Robert, a physician and marathon runner who describes what happened soon after he took the Repatha drug. He also talks about how long the drug stays in the body which is important if you are taking the medication and now and having similar side effects. Repatha video podcast Does Repatha Cause Muscle Pain (written review) =================== Order my rhabdo book Everyone who works out or who is a fitness coach needs to know about exercise rhabdomyolysis. It's the serious side effect you've never heard about. I've been teaching about rhabdo for over 10 years. If you are in the US, order it directly from me. Purchase My Rhabdo Book Order on Amazon ================ My YouTube Channel ================== Support The Podcast Here's how you can support the podcast Click Here to contribute any amount to PayPal: Venmo: @ Joe-Cannon-38 (any amount) ============== I'm Joe Cannon. I have an MS degree in exercise science and a BS degree in biology & chemistry. I'm an authority on dietary supplements, personal fitness training, and the author of several books including Rhabdo, the first book about exercise-induced rhabdomyolysis. Connect with me: Joe-Cannon.com SupplementClarity.com My books: All my books on Amazon ================= Disclaimer: Episodes are for information only. I'm not a medical doctor. No medical advice is given or implied. Always consult your doctor for the best health advice for you. I participate in the Amazon Associates program.
I sit down with my friend Kori Meloy to discuss our opposing views with veganism versus animal foods. We cover nutrition, ethics, and planetary health. We also cover navigating friendships with opposing views centered around respect and open heartedness. If you've followed me for any amount of time you know that I l advocate for and live a whole foods plant-based vegan lifestyle. Kori advocates for a way of eating which includes plants and animal foods like raw dairy, organ meats, grass fed beef and eggs and is often called The Pro Metabolic lifestyle. In this episode we cover: Kori's reservations coming on the podcast and the types of messages she receives about having vegan friends Navigating friendships with differing views Nutrition: Where we find common and where we disagree Can we be healthy and get everything we need from a plant exclusive diet? the bioavailability of nutrition from plants versus animal foods Saturated fat, is significant consumption of animal foods healthy or not? LDL cholesterol and heart disease Beta carotene and Vitamin A/ Retinol Are nuts and seeds health promoting? PUFAS and processed seed oils Are all ethical vegans big animal lovers? Is there an ethical way to eat animals? Factory farming and animal exploitation Planetery health: plant-based diets versus animal foods Regenerative Grazing: Is it sustainable for the population? Deforestation, ocean dead zones, water pollution and habitat destruction WHERE TO FIND KORI: Instagram @korimeloy Website: https://www.rewildculture.com WHERE TO FIND ME: Get my ebooks My instagram WATCH these episodes on my podcast YouTube channel Family YouTube channel CLICK HERE FOR EPISODE SOURCE REFERENCES (in description box of the YT video launching Tuesday 5am HST)
Welcome back to Hunger Hunt Feast! Today Zane shes his technique for making insulin serve him rather than fear it. Get glims into what Zane's weeks look like and what lifestyle choices every day to maintain optimal health. NOTES FROM ZANE: If you are working to reverse insulin resistance or lose 20 or more pounds, this is not for you yet 12-16 hour fasted state going into an intense workout. Post workout shake with banana and half a sweet potato on the side, i.e. quick digesting protein and about 50-70g of carbs. Shift back to whole food animal-based protein and fat. Dinner to dinner fast once a week. LINKS: Effects of Intermittent Fasting on Health, Aging and Disease https://www.nejm.org/doi/full/10.1056/nejmra1905136 Intermittent metabolic switching, neuroplasticity and brain health https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5913738/ Zane's Links: Get organic keto meals delivered to your door!! https://trifectanutrition.llbyf9.net/zane ReLyte Electrolytes by Redmond Real Salt https://shop.redmond.life?afmc=Zane Follow me on Instagram: https://www.instagram.com/zanegriggsfitness QUICK EPISODE SUMMARY: The most vilified components of our bodies The effects of elevated insulin levels Clarity around LDL The importance of vitamin D and cholesterol LDL vs. VLDL Dietary factors that lead to small LDL particles The truth about fat and heart disease A healthy number of triglycerides What has changed over the last 120 years?
: Episode 1957 - BEST OF: On this Saturday show, we feature the esteemed Nina Teicholz's third appearance on the podcast from August, 2018. Nina joins Vinnie to talk her participation in the Fat Doc, the "come-from-behind" story, lies about saturated fat, and more. Https://www.vinnietortorich.com/2021/10/best-of-lies-about-saturated-fat-nina-teicholz-episode-1957 PLEASE SUPPORT OUR SPONSORS NINA TEICHOLZ Nina is one of Vinnie's favorite people She is a top luminary in the field. Vinnie likes to say the male version of her is Gary Taubes. She's been interviewed for the Fat Doc. Nina kindly took time off of her family vacation to shoot her part in Vinnie's living room. Check out the Fat Doc 3 when Vinnie's done with it, too! Nina's an accomplished author. LIES ABOUT SATURATED FAT Nina wrote a book on this - https://www.amazon.com/Big-Fat-Surprise-Butter-Healthy/dp/1451624433/ref=sr_1_1?ie=UTF8&qid=1535678281&sr=8-1&keywords=nina+teicholz Since the 1960s, people have been following the advice not to eat sat fats. In the last 50 years, scientists have looked at this data. There have been tons of meta analyses that show that even this data is BS. Not linked to your risk of heart disease or heart attack. Yes, they may raise LDL but that's not inherently bad. Many Harvard studies funded by vegetable oil industry --> biased. Coconut oil is NOT BAD for you. In fact, it is good! Entered US market in the 50s. Soybean and other vegetable oil corporations were angry about this. A stunt to keep out foreign competition. Case to be made that the sat fat lies are due to a trade war. Good to use in manufacturing and don't cause inflammation like many others do! It's awful because this trade war has made so many unhealthy. Many who have decided these are bad for you find they can't go back on it because of the psychology of going against your life's work. Effort to shore Ancel Keys' work up in an effort to make themselves feel better. Studies also use too small a sample size for those who are low carb. If people are still fat after 60 years of following these dietary guidelines, maybe it's the guidelines that are the problem. FAT DOC 2 IS AVAILABLE ON iTUNES and AMAZON Please also share it with family and friends! Buy it and watch it now on iTunes to get it to the top of the charts. We need it to get big for people to see it. Here's the (BLUERAY, DVD, PRIME) (MAY NOT BE AVAILABLE YET ACROSS THE POND). And the And the https://amzn.to/3rxHuB9 [the_ad id="17480"] PLEASE DON'T FORGET TO REVIEW the film AFTER YOU WATCH! FAT DOC 1 IS ALSO OUT Go watch it now! We need people to buy and review for it to stay at the top of iTunes pages. Available for both rental and purchase. You can also buy hardcopy or watch online at Amazon. YOU CAN NOW STREAM FOR FREE ON AMAZON PRIME IF YOU HAVE IT! RESOURCES Https://www.vinnietortorich.com Https://www.purevitaminclub.com Https://www.purevitaminclub.co.uk Https://www.purecoffeeclub.com Https://www.nsngfoods.com Https://www.bit.ly/fatdocumentary
Welcome to the Brain Biohacking Podcast, where we discuss all things optimal health, nutrition, high performance, cognitive excellence, biohacking, longevity and more! Today I had the honor of chatting with my friend and super-star doctor, Dr. James DiNicolantonio. This podcast is for informational purposes. The podcast host and guests are not responsible for any issues that may arise from using this information. When making any changes, please consult your medical provider. Dr. James J. DiNicolantonio, PharmD Dr. James DiNicolantonio, is a Doctor of Pharmacy and a cardiovascular research scientist. A well-respected and internationally known scientist and an expert on health and nutrition, he has contributed extensively to health policy and has testified in front of the Canadian Senate regarding the harms of added sugars. He serves as the associate editor of the British Medical Journal's Open Heart, a journal published in partnership with the British Cardiovascular Society, and is on the editorial advisory boards of several other medical journals. Dr. DiNicolantonio is the author or coauthor of over 250 publications in the medical literature. He also is the author of five bestselling health books, The Salt Fix, Superfuel, The Longevity Solution, The Immunity Fix and The Mineral Fix. You can follow him on Instagram and Twitter @drjamesdinic and on Facebook at Dr. James DiNicolantonio. Follow Dr. James on Instagram at https://www.instagram.com/drjamesdinic/ and visit his website at http://drjamesdinic.com. In this episode, you'll hear: - Why salt is essential to optimal health... - How our soil is depleted of minerals and what minerals are most impactful on our wellbeing.. - What minerals to take and how.. - What is Inositol, and why do we need it.. - What is metabolic syndrome and how to reverse it.. - Have the metrics on cholesterol changed? How much does LDL matter? - Dr. James' diet and favorite biohacks.. and much more!
In this episode of Revolution Health Radio, I answer frequently asked questions from our listeners, including topics such as LDL particle count and cardiovascular disease, a Functional Medicine approach to ADD/ADHD and long COVID, and the best diet for children. The post RHR: Community Q&A: Cholesterol, ADHD, Paleo for Children, and Long COVID appeared first on Chris Kresser.
Today we are joined by Simon Hill of the Plant Proof Podcast, to discuss the science behind why a plant-based diet really works. He talks in depth about studies and peer-reviewed literature that reveal the health benefits of eating plant-based. We also talk about saturated fat, LDL cholesterol, and common confusions around nitrates and leafy greens. Simon is extremely well-versed on all things plant-based eating, so we are so excited to talk to him today. === Simon Hill: Instagram Website === Make sure to subscribe so you don't miss future episodes! Please leave us a review to ensure that the Mastering Diabetes message reaches as many people living with diabetes as possible. Connect with us on Instagram and Facebook
Heart Disease is the number one killer of humans in modern history. The saddest part about this reality is these deaths are self-inflicted by lifestyle choices. Listen in as Zane shares the role of insulin and LDL's in heart disease and what the doctors aren't explaining to you. QUICK NOTES FROM ZANE: The prevalence of heart disease has increased over the last 100 years What changed to cause this Insulin and LDL are vital components of our health How insulin and LDL are corrupted leading to the formation of arterial plaques LINKS: Evidence from randomised controlled trials does not support current dietary fat guidelines: a systematic review and meta-analysis https://pubmed.ncbi.nlm.nih.gov/27547428/ LDL-C does not cause cardiovascular disease: a comprehensive review of the current literature https://www.tandfonline.com/doi/full/10.1080/17512433.2018.1519391 Saturated Fats and Health: A Reassessment and Proposal for Food-Based Recommendations: JACC State-of-the-Art Review https://www.jacc.org/doi/full/10.1016/j.jacc.2020.05.077 Low-Density Lipoprotein Size and Cardiovascular Disease: A Reappraisal https://academic.oup.com/jcem/article/88/10/4525/2845681 Zane's Links: Get organic keto meals delivered to your door!! https://trifectanutrition.llbyf9.net/zane ReLyte Electrolytes by Redmond Real Salt https://shop.redmond.life?afmc=Zane Follow me on Instagram: https://www.instagram.com/zanegriggsfitness QUICK EPISODE SUMMARY The most vilified components of our bodies The effects of elevated insulin levels Clarity around LDL The importance of vitamin D and cholesterol LDL vs. VLDL Dietary factors that lead to small LDL particles The truth about fat and heart disease A healthy number of triglycerides What has changed over the last 120 years?
Make your health an act of rebellion. Join The Healthy Rebellion Please Subscribe and Review: Apple Podcasts | RSS Submit your questions for the podcast here News topic du jour: https://mises.org/wire/how-fiat-money-made-beef-more-expensive L-Arginine: https://www.thelancet.com/journals/eclinm/article/PIIS2589-5370(21)00405-3/fulltext https://chrismasterjohnphd.com/blog/2021/10/01/the-one-amino-acid-that-cured-covid 1. Calculating How Much Protein For My Bodyweight [19:52] Gloria says: On your last show you talked about having 1 gram of protein for every pound of body weight. Other people say 1 gram for every kg of body weight. Which is it in your opinion? Thanks so much! Keep up the good work. I look forward to your show every week. 2. High Cholesterol and eating more protein [20:56] Kimberly says: Hi Love your show. I have been listening since the beginning. Please never stop recording. In the last couple years (since covid hit) I have lost 20 lbs. I have a muscular body type, I am 54 years young , 5'4", weigh 137lbs (post menopausal) workout 5 days a week with crossfit, 1 day Yoga, and walk the dog 2 miles a day. I attribute the weight loss with eating more protein. I now eat almost 120 gms a day where before I probably only got 50-70 if that (did not track) . My protein sources are usually chicken , smoked salmon, tuna, turkey, once a week red meat. I do add pure protein bars (20gms) towards the end of the day when protein levels aren't there yet. I went to the doctor and got bloodwork done and my cholesterol went up. It went from the total 226 to -244, LDL-101 to 131, to HDL-105 to 101, ratio-2.1 to 2.4, Triglycerides-61 to 62 from Sept of 2020 to Sept 2021. ugh I know I should probably ignore it because my ratio seems great and I feel great. For some reason its bugging the crap out of me, how can I lose weight and eat more protein and have the numbers go up? Should I be concerned? Thanks you both rock. 3. Butyrate and Tributyrin for Gut Health [25:37] Ruby says: Hi Robb! Long time listener here (yeah! #throwback to Greg days) and current LMNT lover. I came across a supplement that uses a combination of Tributyrin and Vitamin D, and supposedly promotes a healthy gut, aids in healing leaky gut, helps reduce bloating, improves digestion and vitamin absorption, boots immune system etc. etc. etc. What they say is that Tributyrin has been used in Spain for at least 3 years but is just starting to come to the US. There are some studies on mice but not a ton in humans yet. I'm just wondering if you've done research on Butyrate/Tributyrin and whether or not you'd suggest experimenting with something like this. I am mostly paleo for about a decade, but my belly pooches out a ton (granted, I've had 2 kids and I'm working on core function), I haven't had consistent bowel movements in months, and while my stress levels are somewhat high because I'm an entrepreneur, I get 7 hours of sleep a night and do my best to keep myself regulated. I've tried probiotics, drink kombucha, try to get resistant starches (hate fermented foods unfortunately) and am pretty well versed in diet/health (thanks in large part to you!). I'm interested in trying out this supplement but very wary of putting anything in my body that is unknown and I can't find much info from people I trust (like you) on this particular topic. So I guess my question is twofold - what do you know about Butyrate/Tributyrin and also, how to decide what is safe to experiment with? Thanks so much for dealing with all the BS out there to provide information to all of us. Tributyrin, a Stable and Rapidly Absorbed Prodrug of Butyric Acid, Enhances Antiproliferative Effects of Dihydroxycholecalciferol in Human Colon Cancer Cells 4. Strength/aerobic/flexibility targets after age 50 [33:26] Jen says: Hello Robb and Nicki, I'm currently working as a health coach in a small clinical study to reverse cognitive impairment with “integrative therapy and lifestyle rehabilitation”. Can you point us to any reliable strength, aerobic, and flexibility benchmarks for men and women over 50? Ideally, the fitness assessment could be done at home without special equipment. It could be useful for participants to develop greater awareness of their relative fitness. Some seniors feel great about their occasional walks in comparison to their physically-deteriorated, sedentary peers. But, outside of my health coaching sessions, the doctor will plainly state that just “walking isn't cutting it.” For brain health, it could me most therapeutic for them to engage in complex, cognitively challenging physical activities, such as dance, martial arts, or sports (at an appropriate level), and check to see what supplemental exercise is needed to meet cardio, muscular, and flexibility targets. The fitness assessments I found from the Mayo Clinic https://www.mayoclinic.org/healthy-lifestyle/fitness/in-depth/fitness/art-20046433 seem questionable in that both men and women at age 65 have the exact same target of 10 classic pushups. Does the upper body strength differential between the two sexes really disappear by age 65? I couldn't find an especially good resource for ages 50-90. For instance, the Fullerton Functional test/Senior Fitness test has arm curls as the best assessment of upper body strength. The presidents challenge at health.gov has assessments for students but not elders. If people want to be physically functional and free from chronic illness at a ripe old age, shouldn't they have be able to look for what needs attention at age 55, 60, 65, etc? I'd so appreciate your thoughts! With tons of respect and admiration!! https://moveskill.com/athletic-skill-levels/ 5. Itching after Jiu Jitsu Class [39:47] Ryan says: Hi Robb and Nicki, Big fan of your work! I've been training jiu jitsu (nogi) for about 6 years and absolutely love it… except for the fact that every morning after training I experience uncontrollable itching on my body, predominately my legs, but sometimes all over. I generally train in the evening, so the onset is about 10-12 hours after my session. This has been frustrating to say the least. I've read that this can be a problem for exercisers due to sweat… but that sounds iffy to me, plus I never had an issue with other forms of exercise, just jits. I've tried probiotics and different soap/laundry detergent to no avail. The only thing that semi helps is to shower immediately after the itching begins or sweat it out. Usually subsides after about 30-60 minutes… Any thoughts? Oss! Ryan Sponsor: The Healthy Rebellion Radio is sponsored by our electrolyte company, LMNT. Proper hydration is more than just drinking water. You need electrolytes too! Check out The Healthy Rebellion Radio sponsor LMNT for grab-and-go electrolyte packets to keep you at your peak! They give you all the electrolytes want, none of the stuff you don't. Click here to get your LMNT electrolytes Transcript: https://robbwolf.com/2021/10/08/fitness-targets-after-50-butyrate-for-gut-health-protein-and-cholesterol-thrr090/
Real Life Pharmacology - Pharmacology Education for Health Care Professionals
On this episode, I discuss rosuvastatin pharmacology, adverse effects, drug interactions and pharmacokinetics. Rosuvastatin is a hydrophilic statin which differs from some of the most commonly used statins like simvastatin and atorvastatin. Rosuvastatin is minimally affected by CYP3A4 drug interactions so that is a small potential advantage over simvastatin and atorvastatin. At dosages of 20-40 mg, rosuvastatin is considered a high intensity statin and can bring down LDL by over 50%.
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