Podcasts about hdl c

ไลฟ์ #85: ข้อบกพร่อง Lipid Energy Model & Lean Mass Hyper Responder ของ Dave Feldman จาก paper The Lipid Energy Model: Reimagining Lipoprotein Function in the Context of Carbohydrate-Restricted Diets ในปี 2565 Dave Feldman และคณะ ให้คำจำกัดความว่า Lean Mass Hyper Responder phenotype คือคนที่ lean BMI ต่ำ ออกกำลังกายสม่ำเสมอ เมื่อรับประทานไดเอ็ทที่คาร์บต่ำยิ่งยวด ไขมันสูง แล้วเกิดปรากฎการณ์ที่ระดับ LDL-C สูงเกิน 300 มก/ดล ไตรกลีเซอไรด์ต่ำ (47 มก/ดล) และ HDL-C สูง (99 มก/ดล) key point ที่สำคัญของ Lipid Energy Model (LEM) กับ Lean Mass Hyper Responder (LMHR) ที่ Dave ตั้งสมมุติฐานคือ 1. ในคนที่มี LMHR phenotype นั้น LDL-C ที่สูงกระฉูด เป็น Physiological adaptive response ของการกินคาร์บต่ำอย่างยิ่งยวด และ ไขมันสูงลิ่ว ที่เกิดจากกลไกสำคัญ 2 ประการคือ 1.1 ตับสร้าง VLDL สูงมาก เพื่อขนส่ง Triglyceride และ มีการทำงานของเอ็นไซม์ Lipoprotein Lipase สูง จึงนำไปสู่การมีระดับไตรกลีเซอไรด์ต่ำ และนำไปสู่การมีระดับ LDL-C สูงลิ่วตามมา 1.2 มีการทำงานของ Cholesteryl Ester Transfer Protein (CETP) ต่ำ นำไปสู่การมีระดับ HDL-C สูง Dave เชื่อว่าการกินไขมันอิ่มตัวสูง มีอิทธิพลน้อยกว่า BMI ในการทำให้เกิดปรากฎการณ์ LDL-C สูงลิ่ว และ LEM เป็น Physiological adaptation ใน LMHR phenotype 2. Dave เชื่อว่า สิ่งที่เกิดขึ้นใน LMHR เป็น Physiological adaptation ไม่ใช่ Pathological state ดังนั้นคนกลุ่มนี้ทนทานต่อการเกิด plaque ในหลอดเลือด มากกว่าคนที่มี Metabolic Syndrome จากการที่มี TG/HDL น้อยกว่า 2 บัดนี้โคนันยอดนักสืบหญิงพร้อมแล้วที่จะอธิบายข้อบกพร่องของ Lipid Energy Model & Lean Mass Hyper Responder ของพี่ Dave Feldman ตามสมมุติฐาน 2 ข้อของเขา พบกันวันเสาร์ 26 ต.ค. เวลา 19.00 น.ค่ะ #หาคำตอบสุขภาพจากงานวิจัยไม่ใช่จากเรื่องเล่า #FatOutHealthspans

Zaburzenia gospodarki lipidowej są najbardziej rozpowszechnionym czynnikiem ryzyka sercowo-naczyniowego. A częstość występowanie dyslipidemii wśród Polaków jest szacowana na 60–80% w populacji powyżej 18. roku życia. To dane, które budzą niepokój, a z drugiej strony temat ten często jest bagatelizowany. Dla wielu osób jest również kontrowersyjny, ale czy powinien? Czy podwyższony cholesterol ma negatywny wpływ na zdrowie? Czy istnieje ‘dobry' i ‘zły' cholesterol? Czy dieta ketogeniczna podwyższa cholesterol? Czy jajka podwyższają cholesterol? Na te i inne pytania odpowiemy w dzisiejszym odcinku. Gościem tego odcinka jest mgr Anna Gudan - dietetyk praktyk, specjalizujący się w diecie ketogenicznej i jej klinicznym zastosowaniu, a także popularyzuję model diety ketogenicznej śródziemnomorskiej w Polsce. Jest właścicielką Poradni Dietetycznej “Chodź na Keto” – miejsca, gdzie w skutecznym odchudzaniu pomagają wyszkoleni przez nią dietetycy w Metodzie – Diety Ketogennej Śródziemnomorskiej.Ponadto jest autorką ebooków oraz kursu o diecie ketogenicznej: https://kursy.annagudan.consulting/ Ania jest obecnie w trakcie doktoratu na Pomorskim Uniwersytecie Medycznym oraz jest autorką lub współautorką licznych publikacji i monografii naukowych. Anię znajdziecie na instagramie pod nickiem @annagudan_dietetyk oraz stronie internetowej: www.annagudan.consulting Odcinek podcastu jest wspierany przez markę Kogen, która czerpie inspirację z japońskiej filozofii troski o zdrowie oraz łączy naturę z osiągnięciami nauki. Marka Kogen tworzy zaawansowane nutraceutyki, które skutecznie wspierają organizm w radzeniu sobie z wyzwaniami współczesnego życia. Z kodem DRKARABIN otrzymasz 10% zniżki na produkty w sklepie Kogen: https://kogen.pl/sklep/ Lista publikacji o których wspominamy w podcaście: https://docs.google.com/document/d/1GpHB_Vppe2mZR4VVcM4yULuEPYsjw3GhMEIr4VMqU2E/edit?usp=sharing Ten materiał nie stanowi zamiennika wizyty lekarskiej. Nie jest też poradą zdrowotną, ani nie służy do diagnozowania ani leczenia chorób. Materiał ma charakter wyłącznie edukacyjny. Autorka nie ponosi odpowiedzialności za sposób wykorzystania przedstawionych informacji. 0:00 Intro 0:37 - Wstęp 4:12 - Choroby sercowo-naczyniowe - czym są i jak często występują? 6:21 - Czy podwyższony cholesterol ma negatywny wpływ na zdrowie? 8:19 - Dlaczego temat cholesterolu jest taki kontrowersyjny? 10:51 - Jakie czynniki zwiększają ryzyko chorób sercowo-naczyniowych? 14:58 - Czy czynniki genetyczne mają znaczenie w powstawaniu chorób sercowo-naczyniowych? 18:12 - Jak powstaje blaszka miażdżycowa? 23:40 - Jaką rolę pełnią czynniki ryzyka w powstawaniu blaszki miażdżycowej? 26:55 - Czy istnieje “dobry” i “zły” cholesterol? 38:13 - Jak możemy zbadać ryzyko chorób sercowo-naczyniowych? 47:02 - Czy warto badać stosunek trójglicerydów do HDL-C? 51:15 - Czym jest lipoproteina (a) i jakie jest jej znaczenie w ocenie ryzyka chorób sercowo-naczyniowych? 56:27 - Jak często warto badać lipidogram? 57:27 - Dlaczego na diecie ketogenicznej cholesterol rośnie? 1:06:18 - Tłuszcze nasycone w diecie - czy warto je ograniczać? 1:09:08 - Jak za pomocą diety obniżyć Apo B 1:11:44 - Czy jajka naprawdę podwyższają cholesterol? 1:17:16 - Jak aktywność fizyczna wpływa na poziom cholesterolu? 1:22:16 - Czy potrzeba restrykcyjnych diet, by utrzymać cholesterol w ryzach? 1:25:55 - Wpływ polifenoli na zdrowie układu sercowo-naczyniowego 1:28:55 - Suplementacja a zdrowie układu sercowo-naczyniowego

ไลฟ์#72 : สรุปเล็คเชอร์ The Evolving Narrative of HDL-C หลังจากความล้มเหลวของงานวิจัยยา CSL112 ของบริษัท biotech CSL Behring ซึ่งเป็น Human Apolipoprotein A1 (apolipoprotein สำคัญบน HDL Particle) CSL112 ทำหน้าที่ผลักคอเลสเตอรอลออกจาก macrophage ของ plaque หลอดเลือด (Cholesterol Efflux Enhancer) และส่งเสริมเอ็นไซม์ LCAT ซึ่งหน้าที่สำคัญนี้ของ ApolipoproteinA1 บนผนัง HDL เป็นหน้าที่ที่นักวิจัยให้ความสนใจเป็นอย่างมาก และเป็นความหวังสำคัญในการสร้างกลยุทธ์เพื่อลดความเสี่ยง/รักษาโรคหลอดเลือดหัวใจอุดตันให้ดียิ่งขึ้น งานวิจัยสำคัญที่ล้มเหลวนี้ทำให้ความเข้าใจบทบาทของ HDL เหมือนกลับไปตั้งต้นใหม่ เพราะงานวิจัยสารพัดในอดีตที่ทดสอบการเพิ่มปริมาณคอเลสเตอรอลที่อยู่ใน HDL และทดสอบหน้าที่ของ HDL (functionality of HDL) ต่อการลดความเสี่ยงของโรคหลอดเลือดหัวใจดูเหมือนจะล้มเหลวไปหมด ไม่ว่าจะเป็น Niacin, Fibrate, Gemfibrozil, Hormone Replacement และ CETP inhibitors พี่ปุ๋มโชคดีที่ได้มีโอกาสฟังเล็กเชอร์เรื่อง The Evolving Narrative of HDL-C: Contemporary Insights on Quality vs Quantity for Targeting Cardio Protection เมื่อวันที่ 2 มิ.ย. 2566 จัดโดย National Lipid Association เป็นเล็คเชอร์ที่ดีมาก (กอไก่ล้านตัว) โดยศาสตราจารย์ผู้ทรงคุณวุฒิในด้านโรคหลอดเลือดหัวใจและ Lipidology 3 ท่าน หัวข้อเป็นดังนี้ค่ะ 1. Rethink the HDL Hypothesis: Then and Now โดย Professor Vera A. Bittner MD, MNLA University of Alabama 2. More than a Number: Functional Role of HDL for Atheroprotection โดย Professor Robert S. Rosenson MD, FNLA, Mount Sinai New York 3. Restoring confidence in HDL: Does CEC hold a promising as a potential therapeutic target? โดย Professor Christie M. Ballantyne MD, Baylor College of Medicine, Houston Texas (คนนี้เป็น Editor texbook สำคัญ Clinical Lipidology) แม้เนื้อหามันจะยาก แต่มันก็ท้าทายพี่ในการจะนำมาสรุปเป็นไลฟ์ #72 โพสต์นี้ไฮไลท์ประเด็นสำคัญจากเล็คเชอร์ HDL ที่พี่ได้ฟัง ให้อ่านเป็นน้ำจิ้มกันก่อน 1. HDL Nomenclature: HDL =/= HDL-C แต่เกี่ยวข้องกับขนาดของ particle ความหนาแน่น รูปร่าง ประจุ จำนวน ที่สำคัญมากคือ ประเภทของ Apolipoprotein (AI, AII, CIII, E) โปรตีน มากกว่า 300 ชนิด ไขมัน มากกว่า 300 ชนิด micro RNA ที่อยู่บน HDL Particle ส่งผลต่อหน้าที่ของ HDL ที่แตกต่างกันในคนแต่ละคน (wow!!) 2. ดังนั้น ความเชื่อฝังหัวที่มาจาก Classic Epidemiological Study อย่าง Framingham Study ว่า HDL เป็น good cholesterol การมีระดับ HDL-Cholesterol ที่สูง จะลดความเสี่ยงของโรคหลอดเลือดหัวใจนั้น เราควรจะลืมมันไปได้แล้ว 3. Low HDL-C predicts poor outcomes, high HDL-C is not protective for ASCVD (Atherosclerotic Cardiovascular Disease) 4. เราควรจะมุ่งความสนใจไปที่หน้าที่ของ proteins และ Lipid ที่อยู่บน HDL ซึ่งส่งผลให้ทำหน้าที่แตกต่างกัน ไม่ใช่สนใจปริมาณคอเลสเตอรอลที่อยู่ใน HDL พี่หวังว่าไลฟ์นี้ จะทำให้น้องๆที่มีความเชื่อว่า ไม่ต้องสนใจระดับ LDL-Cholesterol ที่สูง ตราบใดที่ระดับไตรกลีเซอไรด์ต่ำ และระดับ HDL-Cholesterol สูง เพราะ LDL particle จะมีขนาดใหญ่ ไม่เป็นอันตรายต่อหลอดเลือดหัวใจ และ HDL-C ที่สูงจะช่วยปกป้องหัวใจ จะได้เข้าใจเสียใหม่ว่า HDL-C ที่สูงไม่ได้มีฤทธิ์ในการปกป้องหัวใจแต่อย่างใด และ LDL particle size ก็ไม่ได้สำคัญมากไปกว่าจำนวน LDL particle #หาคำตอบสุขภาพจากงานวิจัยไม่ใช่จากเรื่องเล่า#FatOutHealthspans#ApoBgirl

¡Hola! En el episodio del podcast de hoy os cuento todo lo que querías saber (y alguna cosita extra de regalo) sobre los lípidos en sangre. Al terminar de escuchar el podcast vas a saber cómo una autentic@ profesional:-Qué hay que pedir en unos análisis de sangre para valorar de manera completa nuestro perfil lipídico.-Cuáles son los valores OPTIMOS (que es diferente a valores dentro del “rango de la normalidad”) de colesterol, triglicéridos y Lp(a)-El colesterol bueno ¿Cuánto más alto mejor?-¿Cuál puede ser la causa de tener el colesterol “bueno” (HDLc) bajo si me alimento adecuadamente?-¿Como saber si tu colesterol elevado es por la dieta o por “genética”?-¿Si tomas estatinas, hay que tomar CoQ10? ¿Por qué?-Hay alternativas a las estatinas para conseguir bajar el colesterol?-¿Cómo bajar el colesterol en el embarazo y lactancia?Como os he dicho, todos los suplementos de los que os hablo en el podcast están en mis stories destacados “favoritos”. ¡Espero que os guste, acordaos de suscribiros y valorar mi trabajo en el podcast así me consigo llegar a más gente!VALORES DE OBJETIVOS DE COLESTEROL OPTIMOSColesterol HDL “bueno”: 50-90mg/dLColesterol NO-HDLc: 80-130 mg/dLColesterol LDLc: 50-70 mg/dLTriglicéridos: por debajo de 150 mg/dLLp(a): < 30-50 mg/dL o < 100-125 nmol/LCualquier duda extra, mira mi INSTAGRAM @isabelvina Allí tengo muchas más dudas de hormonas y metabolismo resueltas! Además, tenéis mi web https://ivbwellness.com para consultas, suscribiros a la newsletter para ver los blogs y como no, para poder adquirir mi línea de suplementos de alta calidad destinados a trabajar con tu cuerpo y sistema hormonal de manera natural para devolverte la calidad de vida y bienestar que mereces. Nos vemos el próximo sábado

On this episode, we go over a pharmacotherapy plan for a patient with sickle cell disease, HFrEF, DM2, dyslipidemia, hypertension, POAG, dry eye disease, constipation, GERD, and OSA. Episode 227 Patient Case Information 57-year-old male with sickle cell disease, HFrEF, DM2, dyslipidemia, hypertension, POAG, dry eye disease, constipation, GERD, and OSA comes to your clinic to establish care. His primary concern is the number of sickle cell crisis he has been experiencing (3 ER visits in the last 5 months). He is having significant constipation daily due to his maintenance opioid regimen.  He also reports difficulty controlling his blood glucose. He has experienced 6 hypoglycemic events (BG range between 65 and as low as 42) and is confused as to what he is doing wrong with managing his diabetes. He is also concerned because he is having vivid nightmares almost every night. He also asks about the best artificial tears to get OTC because his Refresh Optive (carboxymethylcellulose) doesn't seem to be working anymore. Medication List: Losartan 100 mg daily, atenolol 50 mg daily, torsemide 20mg – 4 tabs daily, metolazone 2.5 mg 2 times per week, amlodipine 5 mg daily, simvastatin 40 mg daily, fenofibrate 160 mg daily, lantus 40 units twice daily, humalog 5 units with meals if his pre-meal BG is > 150 mg/dL, metformin ER 500 mg twice daily, hydroxyurea 500 mg – two capsules daily (admits to limited adherence), latanoprost 0.005% nightly, esomeprazole 40 mg twice daily, famotidine 40 mg daily, MiraLax 17 grams daily, and bisacodyl 5 mg daily He has a CPAP at home but admits to using it very infrequently. BMP BP – 165/89 HR – 82 Na – 137 K – 3.6 Cl – 102 CO2 – 26 Glucose – 253 eGFR – 95 mL/min Ca – 8.9 Mg – 1.9 Lipid Profile Chol – 162 LDL-C – 99 HDL-C – 49 Triglycerides  - 242 Echo with EF – 32% B-Type Natriuretic Peptide – 56.2 Vitamin B12 – 367 Hemoglobin – 7.2 Hematocrit – 20.8 MCV – 98.6 Ferritin – 1491.6 (received blood transfusion 2 weeks ago) Thanks for listening! If you want to support the podcast, check out our Patreon account. Subscribers will have access to all previous and new pharmacotherapy lectures as well as downloadable PowerPoint slides for each lecture. You can find our account at the website below:  www.patreon.com/corconsultrx If you have any questions for Cole or me, reach out to us on any of the following: Text - 415-943-6116 Mike - mcorvino@corconsultrx.com Cole - cswanson@corconsultrx.com Instagram and other social media platforms - @corconsultrx                  

A new research paper was published in Aging (Aging-US) Volume 15, Issue 9, entitled, “Exogenous exposures shape genetic predisposition to lipids, Alzheimer's, and coronary heart disease in the MLXIPL gene locus.” In this new study, researchers Yury Loika, Elena Loiko, Fan Feng, Eric Stallard, Anatoliy I. Yashin, Konstantin Arbeev, Allison L. Kuipers, Mary F. Feitosa, Michael A. Province, and Alexander M. Kulminski from Duke University, University of Pittsburgh and Washington University School of Medicine examined associations of single nucleotide polymorphisms (SNPs) of the MLXIPL lipid gene with Alzheimer's (AD) and coronary heart disease (CHD) and potentially causal mediation effects of their risk factors, high-density lipoprotein cholesterol (HDL-C) and triglycerides (TG) in two samples of European ancestry from the United States (US) (22,712 individuals 587/2,608 AD/CHD cases) and the United Kingdom Biobank (UKB) (232,341 individuals; 809/15,269 AD/CHD cases). “Our results suggest that these associations can be regulated by several biological mechanisms and shaped by exogenous exposures.” Two patterns of associations (represented by rs17145750 and rs6967028) were identified. Minor alleles of rs17145750 and rs6967028 demonstrated primary (secondary) association with high TG (lower HDL-C) and high HDL-C (lower TG) levels, respectively. The primary association explained ~50% of the secondary one suggesting partly independent mechanisms of TG and HDL-C regulation. The magnitude of the association of rs17145750 with HDL-C was significantly higher in the US vs. UKB sample and likely related to differences in exogenous exposures in the two countries. rs17145750 demonstrated a significant detrimental indirect effect through TG on AD risk in the UKB only (βIE = 0.015, pIE = 1.9 × 10−3), which suggests protective effects of high TG levels against AD, likely shaped by exogenous exposures. Also, rs17145750 demonstrated significant protective indirect effects through TG and HDL-C in the associations with CHD in both samples. In contrast, rs6967028 demonstrated an adverse mediation effect through HDL-C on CHD risk in the US sample only (βIE = 0.019, pIE = 8.6 × 10−4). This trade-off suggests different roles of triglyceride mediated mechanisms in the pathogenesis of AD and CHD. “Finally, the results of this study suggest that genetic associations of SNPs from the MLXIPL gene locus with lipids, AD, and CHD are shaped by exogenous exposures. Further study of the related biological mechanisms can help to elucidate the related, modifiable risk factors.” DOI - https://doi.org/10.18632/aging.204665 Corresponding authors - Yury Loika - yury.loika@duke.edu, and Alexander M. Kulminski - alexander.kulminski@duke.edu Keywords - aging, MLXIPL, lipids, triglycerides, coronary heart disease, Alzheimer's disease About Aging-US Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways. Please visit our website at https://www.Aging-US.com​​ and connect with us: SoundCloud - https://soundcloud.com/Aging-Us Facebook - https://www.facebook.com/AgingUS/ Twitter - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@AgingJournal LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Media Contact 18009220957 MEDIA@IMPACTJOURNALS.COM

The following question refers to Section 4.6 of the 2021 ESC CV Prevention Guidelines. The question is asked by Student Dr. Shivani Reddy, answered first by Johns Hopkins Cardiology Fellow Dr. Rick Ferraro, and then by expert faculty Dr. Eileen Handberg. Dr. Handberg is an Adult Nurse Practitioner, Professor of Medicine, and Director of the Cardiovascular Clinical Trials Program in the Division of Cardiovascular Medicine at the University of Florida. She has served as Chair of the Cardiovascular Team Section and the Board of Trustees with the ACC and is the President for the PCNA. The CardioNerds Decipher The Guidelines Series for the 2021 ESC CV Prevention Guidelines represents a collaboration with the ACC Prevention of CVD Section, the National Lipid Association, and Preventive Cardiovascular Nurses Association. Question #22 Mr. HC is a 50-year-old man presenting for a routine clinic visit. He is not sure the last time he had a lipid panel drawn, and would like one today, but ate lunch just prior to your appointment – a delicious plate of 50% fruits and vegetables, 25% lean meats, and 25% whole grains as you had previously recommended. True or False: Mr. HC should return another day to obtain a fasting lipid panel. TRUE FALSE Answer #22 Answer choices TRUE FALSE Explanation  This statement is False. A non-fasting lipid panel is appropriate for risk stratification and lipid evaluation in most patients per the ESC guidelines. While no level of evidence in provided in the ESC guidelines, this recommendation is consistent with AHA/ACC cholesterol guidelines, which have also largely moved away from fasting lipid panels for most patients and give a Class 1 (LOE B) recommendation to obtaining a fasting or nonfasting plasma lipid profile for ASCVD estimation and baseline LDL-C in adults 20 years of age or older. The ESC recommendation is based upon large trials showing that results of fasting and non-fasting panels are largely similar. This is similar to the AHA/ACC guidelines, which note non-fasting and fasting LDL-C change minimal over time following a normal meal, while HDL-C and tryiglycerides appear to have similar prognostic significance with cardiovascular outcomes in fasting or nonfasting states. A fasting lipid panel should be considered in those with hypertriglyceridemia, metabolic syndrome, and diabetes mellitus, as consumption of food or drink can have direct and immediate effects on TG and blood glucose values. Main Takeaway A non-fasting lipid panel is appropriate for the majority of patients undergoing lipid evaluation and cardiovascular risk stratification.  Guideline Loc. Section 4.6.1 CardioNerds Decipher the Guidelines - 2021 ESC Prevention Series CardioNerds Episode Page CardioNerds Academy Cardionerds Healy Honor Roll CardioNerds Journal Club Subscribe to The Heartbeat Newsletter! Check out CardioNerds SWAG! Become a CardioNerds Patron!

Fasting may have some general health benefits. It helps in weight loss, lowers bad cholesterol (Triglycerides, LDL-Cholesterol) and increases good cholesterol (HDL-C) and helps improve your blood sugar level. People with diabetes (PWD) should practice smart fasting .During Ramadan, PWD should have protein rich, high fiber meals at Sehari and should avoid high fat, high carb meals at Iftar. Instead of sharbat and juices opt for buttermilk, soups, lime water, jaljeera to keep yourself hydrated. During Navratri, try to eat at regular intervals and instead of fried food & sweets choose low fat foods, bhagar , kuttu ka aata, fresh fruits and vegetables, nuts and oilseeds. Avoid Vigorous exercises during fasting but be physically active. Monitor blood glucose frequently while fasting and also watch for low blood sugar. Recorded on 24th March 2023 at Akashwani Nagpur.

Nurse Doza presents an informative podcast about heart disease, the leading cause of death in the United States. It discusses how heart disease can be both expensive to manage and preventable. It emphasizes the importance of making healthy lifestyle choices such as quitting smoking to reduce the risk of heart disease by 50%. 00:00 The heart should be dear to everyone because everyone is affected by heart disease 04:30 Prevent heart disease. 10:59 Reduce heart disease risk: Exercise. 14:09 Take Omega 3 fish oil. 20:06 Lower cholesterol with supplements.   RESOURCES INTRO: Today we are talking about the HEART! The heart is so important to care about because _ Heart disease is the leading cause of death in the US (1) https://www.cdc.gov/heartdisease/facts.htm 1 in 3 people americans have at least 1  (cvd) heart disease condition (1)_____________. https://www.cdcfoundation.org/pr/2015/heart-disease-and-stroke-cost-america-nearly-1-billion-day-medical-costs-lost-productivity (1) I want to encourage you to take charge and be your most optimized self! BODY: The 1st reason: heart disease is one of the most expensive diseases to manage, sometimes more than cancer over the long run.    “Can cost a person $2000-$5000/year (new meds, screening/tests, cardiac rehab,etc). According to goodrx, heart meds can be anywhere from $10 to $500/month.(1) insurance may or may not cover all of this. Remember pre existing conditions. “ (2)   https://www.cdcfoundation.org/pr/2015/heart-disease-and-stroke-cost-america-nearly-1-billion-day-medical-costs-lost-productivity   Surgeries: Cardiac bypass: $55,694 nationwide and by state Cardiac catheterization: Can be used for diagnosis but also to perform different procedures and averages more than $100,000 (2) https://www.goodrx.com/health-topic/heart/reducing-risk-for-heart-disease (2)   The 2nd reason you want to care about the heart is  that even If you do have genetic risks, you can reduce your risk of heart disease by almost 50% by doing the following (3): Not smoking  Having a healthy weight Following a heart-healthy diet Doing regular exercise ***you control your heart health through diet, exercise, and managing stress___________.(1)   The biggest risk factors for heart disease that you may be able to control include: (3) Smoking High blood pressure High cholesterol Overweight or obesity Diabetes  A diet high in saturated or trans fats Lack of exercise  Heavy alcohol use Poor oral health (*) https://www.heart.org/en/news/2021/03/19/how-oral-health-may-affect-your-heart-brain-and-risk-of-death “These diets also promote a non-atherogenic lipid profile, and reduce liver volume, blood pressure, and insulin resistance, with an improvement in blood glucose and insulin levels”   “Ketones cross the blood–brain barrier and represent a more efficient glucose fuel, confirming the beneficial effects on cognitive functions obtained in patients with Alzheimer's disease [11,12]. Although the effects of ketosis on the cognitive functions of healthy subjects are still poorly investigated, significant biochemical evidence suggests, however, that ketones may have a positive impact on brain functions. “ (2)   “In summary, these ambulatory patients were able to make and maintain comprehensive changes in diet and lifestyle for 5 years and showed even more regression of coronary atherosclerosis after 5 years than after 1 year as measured by percent diameter stenosis. In contrast, patients following more conventional lifestyle recommendations showed even more progression of coronary atherosclerosis after 5 years than after 1 year, and had more than twice as many cardiac events as patients making comprehensive lifestyle changes.” (4)   “it could be deduced that the ketogenic diet may have effects on the increase in antioxidant capacity [31] and heart rate variability (HRV).” (2)   Supplements for heart health: Omega 3 (1-4G/DAY) TG Coq10 100-200mg (HDL) Taurine (TG) Resveratrol (NOS, BP) Red yeast rice: lowers LDL…TC , CRP too 5-MTHF B9 “ lower serum homocysteine levels are associated with lower incidence of cardiovascular disease (CVD)” (*) “Our meta‐analysis indicated a 10% lower risk of stroke and a 4% lower risk of overall CVD with folic acid supplementation.”   _______________________________________________________________   Omega 3  “For people with existing coronary heart disease, such as a recent myocardial infarction, the AHA recommends approximately 1 g/day EPA plus DHA, preferably from oily fish; however, supplements could also be considered under the direction of a physician “ “Omega-3s from fish and fish oil have been recommended by the American Heart Association (AHA) for the past 20 years to reduce cardiovascular events, like heart attack or stroke, in people who already have cardiovascular disease (CVD). “   Omega 3 lowers TG “4 grams a day of prescription omega-3 can lower triglyceride levels by 20% to 30% in most people.” Omega-3 Fatty Acids for the Management of Hypertriglyceridemia: A Science Advisory From the American Heart Association https://www.ahajournals.org/doi/10.1161/CIR.0000000000000709   Omega-3 fatty acids and the heart: New evidence, more questions https://www.health.harvard.edu/blog/omega-3-fatty-acids-and-the-heart-new-evidence-more-questions-2021032422213 (3) Omega 3 fatty acids https://ods.od.nih.gov/factsheets/Omega3FattyAcids-HealthProfessional/ (4) “Alzheimer's disease, dementia, and cognitive function Some, but not all, observational studies suggest that diets high in LC omega-3s are associated with a reduced risk of cognitive decline, Alzheimer's disease, and dementia [136,137]. Because DHA is an essential component of cellular membrane phospholipids in the brain, researchers hypothesize that LC omega-3s might protect cognitive function by helping to maintain neuronal function and cell- membrane integrity within the brain [137]. This hypothesis is supported by findings from case-control studies indicating that patients with Alzheimer's disease have lower serum levels of DHA than cognitively healthy people [138,139]. Lower serum DHA levels are also associated with more cerebral amyloidosis (build-up of protein deposits called amyloids) in healthy older adults, whereas higher DHA is correlated with preservation of brain volume [140].” ___________________________________________________   Coq10   Recent studies show that CoQ10 supplements can significantly increase HDL-C and ApoA1 levels, even in people taking statins, and may help reduce risk for CVD.  CoQ10 supplementation also lowers levels of inflammatory biomarkers shown to be risk factors for CVD, such as high-sensitivity C-reactive protein.  Finally, low CoQ10 levels have been associated with greater tissue damage to the heart during a heart attack and the brain during stroke. https://www.clevelandheartlab.com/blog/horizons-coq10-what-are-the-heart-health-benefits/ Coq10 might be benefical after MI https://pubmed.ncbi.nlm.nih.gov/12841346/ *Supplemental CoQ10 alters the natural history of cardiovascular illnesses and has the potential for prevention of cardiovascular disease through the inhibition of LDL cholesterol oxidation and by the maintenance of optimal cellular and mitochondrial function throughout the ravages of time and internal and external stresses.Overview of the use of CoQ10 in cardiovascular disease https://pubmed.ncbi.nlm.nih.gov/10416041/   TAURINE **It is clear that long-term taurine supplementation or continual taurine supplementation improves heart function, is anti-hypertensive, shows promise as a treatment in pre-hypertensive patients, and has beneficial effects in patients with type-2 diabetes  The Anti-Inflammatory Effect of Taurine on Cardiovascular Disease https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7551180/ TAURINE REDUCES Triglycerides : https://pubmed.ncbi.nlm.nih.gov/15221507/   Resveratrol (*) Reduces vascular oxidative stress Reduces arterial stiffness Increases endothelial nitric oxide production Helps blood vessels dilate and constrict Promotes healthy blood pressure levels Resveratrol and vascular function: https://www.mdpi.com/1422-0067/20/9/2155 (*) Red yeast rice: The effects of red yeast rice dietary supplement on blood pressure, lipid profile, and C-reactive protein in hypertension: A systematic review https://www.tandfonline.com/doi/abs/10.1080/10408398.2015.1018987?journalCode=bfsn20   **5-MTHF Folic Acid Supplementation and the Risk of Cardiovascular Diseases: A Meta‐Analysis of Randomized Controlled Trials https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5015297/ Study to reference: 28 amazing facts about the heart: Cleveland Clinic: https://health.clevelandclinic.org/facts-about-the-heart/ (1)   ___________________________________ DIET   Heart Rate Variability and Sympathetic Activity Is Modulated by Very Low-Calorie Ketogenic Diet https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8872337/(2)   https://www.goodrx.com/health-topic/heart/reducing-risk-for-heart-disease (3)   December 16, 1998 Intensive Lifestyle Changes for Reversal of Coronary Heart Disease https://jamanetwork.com/journals/jama/fullarticle/188274 (4) The 3rd reason you want to care about the heart is HEALTHY HEART, HEALTHY BRAIN_(1)__________. Stroke, vascular dementia** EKG/EEG stress response (2)   “Based on data gathered from many people, if the system is in more of a fight-or-flight mode, the variation between subsequent heartbeats tends to be lower. If the system is in more relaxed state, the variation between beats may be higher.” Study to reference: Brain Health Is Connected to Heart Health https://www.cdc.gov/heartdisease/brain_health.htm (1) Heart rate variability: How it might indicate well-being https://www.health.harvard.edu/blog/heart-rate-variability-new-way-track-well-2017112212789 (2)   CLOSING: Supplement to try _MEGA O's __________ Use code NURSEDOZA ENCOURAGEMENT Class has concluded! Facts:   Heart disease is the leading cause of death for men, women, and people of most racial and ethnic groups in the United States.1 One person dies every 34 seconds in the United States from cardiovascular disease.1 About 1 in 5 heart attacks are silent—the damage is done, but the person is not aware of it. https://www.cdc.gov/heartdisease/facts.htm Heart attacks happen most on christmas day: https://www.ahajournals.org/doi/10.1161/01.cir.0000151786.03797.18   The more education you have, the lower the risk of heart disease:: https://health.clevelandclinic.org/facts-about-the-heart/   Sitting is an independent risk factor for heart disease https://www.hopkinsmedicine.org/health/wellness-and-prevention/5-heart-facts-that-may-surprise-you   ​​Heart cells stop dividing, which means heart cancer is extremely rarehttps://www.healthline.com/health/fun-facts-about-the-heart  (6) Forms of heart disease: Coronary artery disease: This is when the arteries to the heart build up with plaque and become narrowed. This can make it hard for your heart muscle to get enough oxygen.  Heart attack: This is when blood flow to your heart is blocked. The heart muscle does not get enough oxygen, and it begins to die. Heart failure: This is when your heart does not pump blood very well, and your body can't get the oxygen it needs.  Arrhythmia: This is when the heart has an irregular heartbeat.  High blood pressure: This is when there is increased pressure against the walls of your blood vessels. Valvular heart disease: This is when a heart valve is damaged or not working properly. https://www.goodrx.com/health-topic/heart/reducing-risk-for-heart-disease

View the Show Notes Page for This Episode Become a Member to Receive Exclusive Content Sign Up to Receive Peter's Weekly Newsletter Dan Rader is a Professor at the Perelman School of Medicine at the University of Pennsylvania, where he conducts translational research on lipoprotein metabolism and atherosclerosis with a particular focus on the function of high-density lipoproteins (HDLs). In this episode, Dan goes in-depth on HDL biology, including the genesis of HDL, its metabolism, function, and how this relates to atherosclerotic cardiovascular disease (ASCVD). He explains why having high HDL-C levels does not directly translate to a low risk of cardiovascular disease and reveals research pointing to a better way to measure the functionality of HDL and predict disease risk. He also goes into detail on the role of HDL in reverse cholesterol transport and the benefits this has for reducing ASCVD. Additionally, Dan discusses the latest thinking around the association between HDL cholesterol and neurodegenerative diseases and ends the conversation with a discussion of how the latest research on HDL provides a promising outlook for ongoing trials and future therapeutic interventions. We discuss: The lipidology of apoB and apoA [4:00]; A primer on the high-density lipoprotein (HDL): genesis, structure, and more [9:30]; How the lipoprotein system differs in humans compared to other mammals [20:00]; Clarifying the terminology around HDL and apoA [25:30]; HDL metabolism [31:45]; CETP inhibitors for raising HDL-C: does it reduce CVD risk? [34:45]; Why it's so important to have hard outcome trials in the field of cardiovascular medicine [42:30]; SR-B1: an HDL receptor important for cholesterol efflux [48:00]; The association between HDL levels and atherosclerosis: are they causally linked? [53:15]; How insulin resistance is impacting HDL, and how HDL-C provides insights into triglyceride metabolism [58:00]; Disappointing results from the studies of niacin—a drug that raises HDL-C and lowers apoB [1:08:15]; HDL lipidation, dilapidation, and reverse cholesterol transport [1:12:00]; Measuring the cholesterol efflux capacity of HDL: a better predictor of ASCVD risk than HDL-C? [1:22:00]; A promising new intervention that may promote cholesterol efflux and reverse cholesterol transport [1:32:45]; The association between HDL cholesterol and neurodegenerative diseases [1:34:00]; Challenges ahead, a promising outlook, and the next frontier in lipidology [1:44:45]; and More. Connect With Peter on Twitter, Instagram, Facebook and YouTube

In this episode you'll learn what a healthy blood insulin level is, and how to interpret your blood results.At Zivli, we advocate prevention before prescription and think it's wise to reverse risk factors before they become disease.To help you become aware of your risk factors for cardiometabolic diseases such as insulin resistance, diabetes, and heart disease, we've partnered with a lab to offer an at-home fasting insulin test, and a more comprehensive cardiometabolic panel.Our Cardiometabolic test kit measures fasting insulin, HDL-C, Triglycerides, Hemoglobin A1c, hsCRP, VLDL-C, LDL-C, and total cholesterol.To order one of these tests go to www.zivli.com/testing. You can also use blood work obtained from your doctor, but you may not have all the values discussed here.Highlights From This EpisodeWhy “normal” bloodwork numbers are not optimal. How to check your insulin levels at home. How to download a free health assessment tracker form. Optimal levels for fasting insulin, fasting glucose, glucose after a meal, hsCRP, Hemoglobin A1c, Triglycerides, VLDL, HDL, waist circumference, HOMA-IR, and Triglyceride/HDL ratio. How to calculate your HOMA-IR for insulin resistance.How to learn more about joining Zivli. Subscribe & ReviewSubscribing and leaving a rating and review are important factors in helping the Reshape Your Health Podcast and the YouTube Channel reach more people. If you haven't already subscribed, please do that today.We would also be grateful if you left a rating and review, too. In your listening app, scroll to the “Ratings and Reviews” section, then click “Write a Review” and let us know what you enjoy about our show. We appreciate you taking the time to show your support. Thank you!Resources From This Episode>> Join Zivli>> Book a Free Zivli Discovery Call>> Freebie: Weight Loss Mindset Audio Training>> Freebie: The Ultimate Food Guide>> Test Your Insulin At Home>> Health Assessment Tracker Form

Niacin, also known as nicotinic acid and vitamin B3, is essential for health. At higher levels, it can cause important improvements in cholesterol particles like raising HDL-C, lowering LDL-C, and lowering Lipoprotein(a). This week Dr. Kahn discusses what niacin does, how it has been shown to reverse atherosclerosis, and how it has fallen out of favor unfairly. He shares his favorite brand of niacin products and how he uses them at the Kahn Center.

T16-E03 HDL: ¿Cómo influyen las emociones en el líder? / Lina Arrieta --- This episode is sponsored by · Anchor: The easiest way to make a podcast. https://anchor.fm/app Support this podcast: https://anchor.fm/aiccapellania/support

Broccoli Reduces Your Risk of Four Major Diseases University of Illinois, June 23, 2022   It's one of the most advantageous veggies you can eat, and love it or hate it, broccoli offers an array of health benefits. University of Illinois researchers have identified candidate genes controlling the accumulation of phenolic compounds in broccoli. Consumption of phenolic compounds, including certain flavonoids, is associated with a lower risk of coronary heart disease, type II diabetes, asthma, and cancer.   Sulforaphane in broccoli can also help to prevent or slow the progress of one of the most common forms of arthritis. Scientists have also discovered that broccoli protects the skin against the sun's harmful ultraviolet rays.  Many studies have shown that a diet rich in vegetables -- particularly brassica vegetables such as broccoli -- is linked to decreased risk of heart disease and stroke. The researchers crossed two broccoli lines and tested their progeny in terms of total phenolic content and their ability to neutralize oxygen radicals in cellular assays. They then used a genetic technique called quantitative trait locus analysis to search for the genes involved in generating phenolics in the most promising progeny.   By identifying the genes involved in accumulating these compounds, the researchers are one step closer to breeding broccoli and related Brassica vegetables like kale and cabbage with mega-doses of phenolic compounds.   The good news is that phenolic compounds are flavorless and stable, meaning the vegetables can be cooked without losing health-promoting qualities.   Once these vegetables are consumed, the phenolic compounds are absorbed and targeted to certain areas of the body or concentrated in the liver. Flavonoids spread through the bloodstream, reducing inflammation through their antioxidant activity.   "These are things we can't make ourselves, so we have to get them from our diets," Juvik says. "The compounds don't stick around forever, so we need to eat broccoli or some other Brassica vegetable every three or four days to lower the risk of cancers and other degenerative diseases."       Can Chronic Cellphone Use Hinder your Infant's Development? Environmental Health Trust, June 23, 2022   The two most important communicative mechanisms a newborn innately has to navigate his world are eye gaze and crying. From birth, newborns are constantly developing speech, language and communication skills with every response they command from their caregiver. As early as 5 days old, an infant can tailor his cries to reflect hunger, wetness, or discomfort as well as differentiate between mother and caregiver. Additionally, very early on newborns and infants develop prelinguistic skills: eye gaze (signaling a cue for communication) and joint attention – the ability of an infant to rest his or her gaze on a object at the same time the caregiver is looking at the same object. It is speculated that eye gaze between baby and mother is one of the most important prelinguistic skills to occur before verbal communication develops.   However, excessive cell phone usage can work to hinder the communicative rhythm and bonding experience that new mothers and infants work to establish, especially within the first six months. Communicative cues can be easily missed and trying to decode differences in newborn cries (hunger vs wet diaper) can become very difficult. As it is so important for new mothers to pay attention to different cries, constant distraction from a cell phone can alter the way the other perceives the cry, thus making it more difficult to decode.    Infants are so intuitive early on, that even the slightest delay in response to a coo or a cry can alter the way they perceive their world. Additionally, if a mother is perusing high-emotion content that is so pertinent in Facebook and social media, the overflow of emotion may inadequately color her response to the infant.   Breastfeeding can also be affected by a constant need to search the web or pursue Facebook, taking away from a significant bonding period for mother and baby, according to Erin Odom.    Physically, the mother may be present but mentally they are “somewhere else”. Many mothers use the cellphone to pass the time during the long nursing/feeding sessions of early infancy. However, infants are highly communicative during feeding, and texting and social media, when so engrossing, can distract a mother from the needs of the infant.   Chronic cell phone usage such as texting and social media usage could absolutely hinder infant development as a result of missed cues on the part of the mother.    The early months of a newborn who continuously has to wait for mother while looking at the cellphone before responding, to cry initiation for communication or other cues, the brain's connections will actually reorganize around this delay, later dampening the development of instinctual communication between mother and infant.         Yoga And Meditation Could Potentially Reverse The Genetic Effects Of Stress Coventry University (UK), Antwerp University (Belgium), Radboud University (Netherlands), June 21, 2022 A review of multiple studies focusing on the effects of mindfulness practices like yoga and meditation has found that these efforts may have the potential to reverse genetic expressions of stress. As the analysis, published in the journal Frontiers in Immunology, explains: While some MBIs, such as yoga, Tai Chi, and Qigong, have a strong physical component, others like meditation and mindfulness, breath regulation techniques, and the relaxation response (RR) are mainly sedentary. Despite the variability in these techniques, they all seem to produce various psychological benefits on healthy and clinical populations, such as the reduction of perceived stress , the alleviation of depression, decreases in anxiety, or to help in coping with a chronic medical disease. However, it is less clear what are the mechanisms underpinning the self-reported benefits of MBIs. Noting that there is some speculation that “MBIs increase gray matter in the brain regions related to emotion regulation, learning, memory, self-referential processes, and perspective taking,” they acknowledged the evidence is not conclusive and set out to delve deeper into the genetic expressions of stress and how MBIs may affect them. The review analyzed 18 studies “that used gene expression analysis in research on meditation and related MBIs [mind-body interventions].” Ultimately, they found that “meditation and related MBIs [were associated with] downregulation of NF-κB-targeted genes, which can be understood as the reversal of the molecular signature of the effects of chronic stress.”h useful information unless the relationship between gene expression and psychological variables is directly explored.”   Curcumin-piperine combo may support heart health for diabetics: Study  Baqiyatallah University of Medical Science (Iran), June 25, 2022 A combination supplement containing curcuminoids plus piperine from black pepper may support heart health for diabetics by improving the levels and functionality of cholesterol, says a new study. The combination reduced total cholesterol and non-HDL cholesterol levels, and improved levels of Lp(a) [Lipoprotein(a)], a structural component of LDL. “Although elevated Lp(a) has been considered as an important risk factor for premature atherosclerotic CVD for quite a long time independently of LDL-C and non-HDL-C levels, until very recently, the possibilities of influencing Lp(a) were extremely limited,” wrote scientists from Iran, Croatia and the USA in Complementary Therapies in Medicine . “Hence, this finding that curcuminoids as naturally occurring dietary supplements can decrease elevated Lp(a) in patients with [type 2 diabetes] is very important since such supplements are becoming more and more popular and attractive to the patients.” On the other hand, the curcumin-piperine combination significantly increased HDL levels by 1.56 mg/dL, compared to only 0.2 mg/dL in the placebo group.   Parkinson's is partly an autoimmune disease, study finds Columbia University, June 21, 2022 Researchers have found direct evidence that autoimmunity—in which the immune system attacks the body's own tissues—plays a role in Parkinson's disease, the neurodegenerative movement disorder. The findings raise the possibility that the death of neurons in Parkinson's could be prevented by therapies that dampen the immune response. The study, led by scientists at Columbia University Medical Center (CUMC) and the La Jolla Institute for Allergy and Immunology, was published in Nature. "The idea that a malfunctioning immune system contributes to Parkinson's dates back almost 100 years," said study co-leader David Sulzer, PhD, professor of neurobiology (in psychiatry, neurology and pharmacology) at CUMC. "But until now, no one has been able to connect the dots. Our findings show that two fragments of alpha-synuclein, a protein that accumulates in the brain cells of people with Parkinson's, can activate the T cells involved in autoimmune attacks. "These findings, however, could provide a much-needed diagnostic test for Parkinson's disease, and could help us to identify individuals at risk or in the early stages of the disease." Scientists once thought that neurons were protected from autoimmune attacks. However, in a 2014 study, Dr. Sulzer's lab demonstrated that dopamine neurons (those affected by Parkinson's disease) are vulnerable because they have proteins on the cell surface that help the immune system recognize foreign substances. As a result, they concluded, T cells had the potential to mistake neurons damaged by Parkinson's disease for foreign invaders. The new study found that T cells can be tricked into thinking dopamine neurons are foreign by the buildup of damaged alpha-synuclein proteins, a key feature of Parkinson's disease. "In most cases of Parkinson's, dopamine neurons become filled with structures called Lewy bodies, which are primarily composed of a misfolded form of alpha-synuclein," said Dr. Sulzer.   Vegetarian diets produce fewer greenhouse gases and increase longevity, say new studies  Loma Linda Health University, June 25, 2022 Consuming a plant-based diet results in a more sustainable environment and reduces greenhouse gas emissions, while improving longevity, according to new research from Loma Linda University Health. Based on findings that identified food systems as a significant contributor to global warming, the study focuses on the dietary patterns of vegetarians, semi-vegetarians and non-vegetarians to quantify and compare greenhouse gas emissions, as well as assess total mortality. The mortality rate for non-vegetarians was almost 20 percent higher than that for vegetarians and semi-vegetarians. On top of lower mortality rates, switching from non-vegetarian diets to vegetarian diets or even semi-vegetarian diets also helps reduce greenhouse gas emissions. The vegetarian diets resulted in almost a third less emissions compared to the non-vegetarian diets. Modifying the consumption of animal-based foods can therefore be a feasible and effective tool for climate change mitigation and public health improvements, the study concluded. "The takeaway message is that relatively small reductions in the consumption of animal products result in non-trivial environmental benefits and health benefits," said Sam Soret, Ph.D., MPH, associate dean at Loma Linda University School of Public Health and co-author of the studies. "The study analyzed more than 73,000 participants. The level of detail we have on food consumption and health outcomes at the individual level makes these findings unprecedented,” Soret said. 

It is said that 50% of what is taught in medical school is wrong, but no one knows which 50%! For 50 years it has been taught that a low HDL cholesterol is a danger while a high HDL-C is protective.   This week, Dr. Kahn discussed new data that completely changes that simple formula and turns it on its head. Before that, Dr. Kahn discussed how vitamin K plays a role in certain proteins, including Matrix Gla Protein, to prevent calcification of arteries and valves.   A study using high dose Vitamin K2/M7 to prevent valve calcium has been published and it has mixed finding. The heart artery findings are hidden and provocative. 

Global diets are harming human and planetary health   University of Sao Paulo (Brazil) and Harvard School of Public Health, March 29, 2022   A global diet that increasingly includes ultra-processed foods is having a negative impact on the diversity of plant species available for human consumption while also damaging human and planetary health, according to a commentary published in the journal BMJ Global Health. Ultra-processed foods such as sweetened or salty snacks, soft drinks, instant noodles, reconstituted meat products, pre-prepared pizza and pasta dishes, biscuits and confectionery, are made by assembling food substances, mostly commodity ingredients, and 'cosmetic' additives (notably flavors, colors and emulsifiers) through a series of industrial processes. These products are the basis of a 'globalized diet' and are becoming dominant in the global food supply, with sales and consumption growing in all regions and almost all countries. Currently, their consumption is growing fastest in upper-middle-income and lower-middle income countries.   (NEXT)   People with fibromyalgia are substituting CBD for opioids to manage pain   The cannabis-derived substance provides fewer side effects, with less potential for abuse University of Michigan, March 24, 2022   As the ravages of the opioid epidemic lead many to avoid these powerful painkillers, a significant number of people with fibromyalgia are finding an effective replacement in CBD-containing products, finds a new Michigan Medicine study. Previous research shows that some people substitute medical cannabis (often with high concentrations of THC) for opioids and other pain medications, reporting that cannabis provides better pain relief and fewer side effects. Kevin Boehnke, Ph.D., a research investigator in the Chronic Pain and Fatigue Research Center surveyed people with fibromyalgia about their use of CBD for treatment of chronic pain. The U-M team found that more than 70% of people with fibromyalgia who used CBD substituted CBD for opioids or other pain medications. Of these participants, many reported that they either decreased use or stopped taking opioids and other pain medications as a result.   (NEXT)   Sleep Increases Chromosome Dynamics that Clear Out DNA Damage Accumulated During Waking Hours   Bar-Ilan University (Israel), 03-28-22   In a new study, published in the journal Nature Communications, researchers at Bar-Ilan University in Israelbreveal a novel and unexpected function of sleep that they believe could explain how sleep and sleep disturbances affect brain performance, aging, and various brain disorders. Using 3D time-lapse imaging techniques in live zebrafish, the researchers were able to define sleep in a single chromosome resolution and show that single neurons require sleep to perform nuclear maintenance. DNA damage can be caused by many processes including radiation, oxidative stress, and even neuronal activity. DNA repair systems within each cell correct this damage. The current work shows that during wakefulness, when chromosome dynamics are low, DNA damage consistently accumulates and can reach unsafe levels. The role of sleep is to increase chromosome dynamics, and normalize the levels of DNA damage in each single neuron. Apparently, this DNA maintenance process is not efficient enough during the online wakefulness period and requires an offline sleep period with reduced input to the brain in order to occur. Their discovery was achieved thanks to the characteristics of the zebrafish model. With their absolute transparency, and a brain very similar to humans, zebrafish are a perfect organism in which to study single cell within a live animal under physiological conditions. Using a high resolution microscope, the movement of DNA and nuclear proteins within the cell—inside the fish—can be observed while the fish are awake and asleep. The researchers were particularly surprised to find that chromosomes are more active at night, when the body rests, but this increased activity enables the efficiency of the repair to DNA damage.   (NEXT)   Tai chi can mirror healthy benefits of conventional exercise   University of Hong Kong and University of California at Los Angeles, March 21, 2022   A new study shows that tai chi mirrors the beneficial effects of conventional exercise by reducing waist circumference in middle-aged and older adults with central obesity. Central obesity is a major manifestation of metabolic syndrome, broadly defined as a cluster of cardiometabolic risk factors, including central obesity, dyslipidemia, hyperglycemia, low high-density lipoprotein cholesterol (HDL-C) level, and high blood pressure, that all increase risk for type 2 diabetes and cardiovascular disease. 543 participants were randomly assigned in a 1:1:1 ratio to a control group with no exercise intervention (n= 181), conventional exercise consisting of aerobic exercise and strength training (EX group) (n= 181), and a tai chi group (TC group) (n= 181). Interventions lasted 12 weeks.   (NEXT)   Improvement of vitamin D levels linked to longer life   Second Medical Centre & National Clinical Research Centre (China), March 28 2022.   The investigation included 1,362 participants aged 60 to 113 who had their serum vitamin D levels measured in 2012 and 2014. Mortality data was collected in 2018. Deficient vitamin D levels of less than 20 ng/mL were detected among 67.5% of the participants in 2012 and 68.4% in 2014. During follow-up, 420 deaths occurred. Men and women who were deficient in vitamin D in 2012 and 2014 had a 2.33 times greater risk of mortality than those who maintained nondeficient levels. Among participants who maintained sufficient vitamin D or were deficient in 2012 and not deficient in 2014, the risk of dying was 30% and 53% lower than participants who were deficient at both time points. Women and participants who among the oldest old at 80 years of age or older experienced the greatest benefit.

Join Jimmy today for a brand new Jimmy Makes Science Simple as he tackles the often misunderstand concept of why LDL cholesterol goes up for some people when they start eating low-carb.   “Is high LDL-C cholesterol harmful in lean mass hyper-responders?”  - Jimmy Moore In this episode, Jimmy features a study that was published in the November 2021 issue of the journal Current Developments in Nutrition entitled “Elevated LDL-Cholesterol with a Carbohydrate-restricted Diet: Evidence for a ‘Lean Mass Hyper-responder' Phenotype'.” One of the contributing researchers on this paper is Dr. David Ludwig along with Dr. Nicholas Norwitz, Adrian Soto-Mota, Dr. Tro Kalayjian, and science-minded layperson Dave Feldman who was the one who came up with the lean mass hyper-responders hypothesis with low-carb diets that noticed the pattern of excessively high LDL-C levels despite high HDL-C, low triglycerides, and low BMI. It's a truly fascinating paper for those of you who have experienced significant elevations in your LDL cholesterol despite spectacular numbers across the board in the rest of your lipid panel. Get the full details on this study in today's episode! Got a new study you want Jimmy to feature on his @jimmymakessciencesimple Instagram page and on a future podcast? Email him the link to livinlowcarbman@charter.net. NOVEMBER 2021 STUDY: Elevated LDL-Cholesterol with a Carbohydrate-restricted Diet: Evidence for a ‘Lean Mass Hyper-responder' Phenotype: https://academic.oup.com/cdn/advance-article/doi/10.1093/cdn/nzab144/6446805?login=false

Guest: Monique A. Freund, M.D. Host: Darryl S. Chutka, M.D. (@ChutkaMD) Hyperlipidemia is one of the major risk factors for cardiovascular disease. It's known that a combination of lifestyle changes and pharmacologic therapy has proven effective in reducing the complications of cardiovascular disease. Despite this, it's estimated that less than 35% of those patients with hyperlipidemia are adequately managed. Why aren't we doing a better job at managing this major public health problem? In this podcast, we'll be speaking with Monique A. Freund, M.D., a cardiologist at Mayo Clinic. We'll discuss how to optimize management of hyperlipidemia, which lifestyle changes are beneficial, when to use pharmacologic therapy and how to manage patients with statin intolerance. Specific topics: Relative importance of elevated LDLc, low HDLc and elevated triglycerides Effective non-pharmacologic therapy for treating elevated LDLc, low HDLc and elevated triglycerides When to consider starting a patient on a statin Benefits of fish oil Mechanism of action of statins Statin intolerance When to use ezetimibe When to use one of the PCSK9-inhibitors Connect with the Mayo Clinic's School of Continuous Professional Development online at https://ce.mayo.edu/ or on Twitter @MayoMedEd.

T10-E03 HDL: ¿Cómo ganar energía vital? / Omero Rojas --- This episode is sponsored by · Anchor: The easiest way to make a podcast. https://anchor.fm/app Support this podcast: https://anchor.fm/aiccapellania/support

T9-E08 HDL: ¿Cómo atraer Jóvenes a Dios? / Abinel Roldan --- This episode is sponsored by · Anchor: The easiest way to make a podcast. https://anchor.fm/app Support this podcast: https://anchor.fm/aiccapellania/support

The Gary Null Show Notes – 08.25.21 American Medical Association Calls for Covid-19 Vaccine Mandates China, 2049 The Leak That ‘Exposed the True Afghan War' Fauci Dismisses “Freedom” In Call For Vaccine Mandates: “The Time Has Come. Enough Is Enough.” A New Low for the FDA Eight Key Points on America's Defeat in Afghanistan 2 Things Mainstream Media Didn't Tell You About FDA's Approval of Pfizer Vaccine America in an Age of Faucism Today's Videos 1.  Dave Cullen Video on Mandating Vaccines: ” Vaccination: They're Becoming Desperate” 2. The Dunning-Kruger Effect – Cognitive Bias – Why Incompetent People Think They Are Competent 3. Dr. Malone Sounds Alarm On Liability Coverage Of Pfizer Vax Start this clip at 5.00 in when Dr. Malone begins to speak. 4. Dr. Ryan Cole #StoptheMandate (start at 1:25) Study suggests vitamin D supplementation may serve as part of strategy for autoimmune and infectious diseases associated with leaky gut MacKay Children's Hospital (Taiwan), August 15, 2021 According to news reporting from Taipei, Taiwan, research stated, “Vitamin D (VD) plays an important role not only in mineral balance and skeletal maintenance but also in immune modulation. VD status was found correlated with the pathophysiology and severity of inflammatory bowel diseases and other autoimmune disorders. Epithelial barrier function is primarily regulated by the tight-junction (TJ) proteins.” The news reporters obtained a quote from the research from MacKay Children's Hospital: “In this study, we try to establish an animal model by raising mice fed VD-deficient diet and to investigate the effects of VD-deficient diet on gut integrity and zonulin expression. Male C57BL/6 mice were administered either VD-deficient [VDD group, 25(OH)2D3 0 IU/per mouse] or VD-sufficient [VDS group, 25(OH)2D3 37.8 IU/per mouse] special diets for 7 weeks. Body weight and diet intake were recorded weekly. Serum VD levels were detected. After sacrifice, jejunum and colon specimens were collected. The villus length and crypt depth of the jejunum as well as mucosa thickness of the colon were measured. Various serum pro-inflammatory cytokines and intestinal TJ proteins were assessed. The serum level of zonulin and the mRNA expression of jejunum zonulin were also investigated. We found that mice fed a VDD diet had a lower serum level of VD after 7 weeks (p < 0.001). VDD mice gained significant less weight (p = 0.022) and took a similar amount of diet (p = 0.398) when compared to mice raised on a VDS diet. Significantly decreased colon mucosa thickness was found in VDD mice compared with the VDS group (p = 0.022). A marked increase in serum pro-inflammatory cytokine levels was demonstrated in VDD mice. All relative levels of claudin (CLD)-1 (p = 0.007), CLD-3 (p < 0.001), CLD-7 (p < 0.001), and zonulin-1 (ZO-1, p = 0.038) protein expressions were significantly decreased in the VDD group when compared to the VDS group. A significant upregulation of mRNA expression of jejunum zonulin (p = 0.043) and elevated serum zonulin (p = 0.001) were found in the VDD group.” According to the news editors, the research concluded: “We successfully demonstrated that VDD could lead to impaired barrier properties. We assume that sufficient VD could maintain intestinal epithelial integrity and prevent mucosal barrier dysfunction. VD supplementation may serve as part of a therapeutic strategy for human autoimmune and infectious diseases with intestinal barrier dysfunction (leaky gut) in the future. To our knowledge, this is the first study to demonstrate that VDD could lead to a significant upregulation in mRNA expression of the jejunum zonulin level and also a marked elevation of serum zonulin in a mouse model.” Investigating the anti-hypertensive effects of pumpkin seed oil Marymount University (US) and University of Guilan (China), August 24, 2021 In a study, researchers from Iran and the U.S. found that pumpkin seed oil can potentially treat hypertension in postmenopausal women. Their report was published in Complementary Therapies in Clinical Practice. Postmenopausal women are more likely to develop hypertension than men of the same age. In vivo studies reveal that pumpkin seed oil has anti-hypertensive activity. The team investigated the effects of pumpkin seed oil supplementation on vascular function and heart rate variability in postmenopausal women with elevated blood pressure. Participants were assigned to take either a pumpkin seed oil supplement or a placebo for the six-week study. Those in the experimental group took 3 grams of pumpkin seed oil every day. Brachial and central blood pressure, wave reflection (augmentation index, AIx), arterial stiffness (SI) and various HRV parameters were measured at baseline and at the end of the study. Those who took pumpkin seed oil had significantly lower AIx, brachial and systolic blood pressure after treatment. SI and HRV parameters remained unchanged for the treatment group and the placebo group at the end of the study. In sum, taking pumpkin seed oil may improve arterial hemodynamics in postmenopausal women.   Lack of exercise and poor nutrition could increase the risk of diseases like dementia Kings College London, August 23, 2021 New research from the Institute of Psychiatry, Psychology & Neuroscience (IoPPN) at King's College London has found that both diet and exercise can influence the risk of cognitive decline (CD) and dementia by potentially influencing hippocampal neurogenesis (the process by which the brain produces new brain cells) long before their onset. The study, published in Alzheimer's & Dementia: The Journal of the Alzheimer's Association, suggests that altered neurogenesis in the brain could potentially represent an early biomarker for both CD and dementia. The investigation studied how the blood of participants with and without CD and dementia could influence hippocampal neurogenesis in laboratory settings and whether diet and exercise were important factors. Specifically, blood samples of 418 French adults over the age of 65 were collected 12-years prior to CD and dementia diagnosis and tested on human hippocampal stems cells. Additionally, information on each participant's sociodemographic, lifestyle, and clinical data were collected and incidence cognition status and dementia were measured every two to three years over a 12-year period. Over the course of the study, the researchers established that 12 years prior to diagnosis, both CD and Alzheimer's were associated with levels of neural stem cell death. The team also found that exercise, nutrition, vitamin D levels, carotenoid and lipid levels are all associated with the rate at which cells die off. Furthermore, physical activity and nutrition were key factors that then also determined CD status. Specifically, researchers found that reduced physical activity and increased malnutrition both increased cell death which in turn increased the risk for future CD. While previous studies have established that diet and exercise have some protective effects against CD and dementia, these roles have been poorly understood at the neurobiological level. To date, studies on animals have shown how diet and exercise can directly influence hippocampal neurogenesis, potentially explaining how exercise and diet may biologically exert their effects, but this study sheds further light on this in the context of a human model. Dr. Sandrine Thuret, the study's lead investigator said, “Our study has demonstrated not only that there are individual markers of hippocampal neurogenesis associated with CD and dementia 12 years later, but also that there is some degree of specificity with respect to diagnoses of dementia subtypes. If an individual displays an increase in their levels of cell death during differentiation (when neural stem cells are becoming neurons), we can look at this as a potential warning sign of CD. Conversely, a decrease in levels of cell death during proliferation (the process by which a single cell divides into a pair) and reduced hippocampal progenitor cell integrity could be viewed as a predictor for Alzheimer's Disease and Vascular dementia, respectively.” According to Alzheimer's Research UK, there were a total of 525,315 people living with a dementia diagnosis in the UK in 2020. Rates of cognitive decline and dementia are expected to triple in prevalence by 2040. Dr. Andrea du Preez, the study's first author from King's IoPPN said, “While more work is undoubtedly needed to fully understand how diet and exercise might modulate hippocampal neurogenesis, our findings may represent an effective early preventative strategy against CD and dementia.” Mindfulness may improve cognition in older adults University College London, August 23, 2021 Mindfulness may provide modest benefits to cognition, particularly among older adults, finds a new review of evidence led by UCL researchers. The systematic review and meta-analysis, published in Neuropsychology Review, found that, while mindfulness is typically geared towards improving mental health and well-being, it may also provide additional benefits to brain health. The study's lead author, PhD student Tim Whitfield (UCL Psychiatry) said that “the positive effects of mindfulness-based programs on mental health are already relatively well-established. Here, our findings suggest that a small benefit is also conferred to cognition, at least among older adults.” The researchers reviewed previously published studies of mindfulness, and identified 45 studies that fit their criteria, which incorporated a total of 2,238 study participants. Each study tested the effects of a mindfulness-based intervention delivered by a facilitator in a group setting, over at least four sessions, while excluding mindfulness retreats in order to have a more homogenous set of studies. The majority of studies involved a certified instructor teaching participants techniques such as sitting meditation, mindful movement and body scan, generally on a weekly basis across six to 12 weeks, while also asking participants to continue the practices in their own time. The researchers found that overall, mindfulness conferred a small but significant benefit to cognition. Subgroup analysis revealed that the effect was slightly stronger for people over 60, while there was not a significant effect for people under 60. Tim Whitfield commented that “executive function is known to decline with age among older adults; the improvement in people over 60 suggests that mindfulness may help guard against cognitive decline, by helping to maintain or restore executive function in late adulthood. It might be easier to restore cognitive functions to previous levels, rather than to improve them beyond the developmental peak.” When they investigated which aspects of cognition were affected, the researchers found that mindfulness was beneficial only to executive function, and more specifically, there was strong evidence of a small positive effect on working memory (which is one facet of executive function). The researchers also analyzed whether mindfulness outperformed other ‘active interventions' (such as brain training, relaxation, or other health or educational programs) or only when compared to people who were not offered any alternative treatment. They found that cognitive benefits of mindfulness were only significant compared with an ‘inactive' comparison, which means they cannot rule out that the benefits may have been at least partly derived from an expectation of treatment benefits, or social interactions. The researchers say that more research is needed into which characteristics of mindfulness training may be more likely to confer cognitive benefits, or whether delivering interventions over longer periods, or in intensive retreat settings, might yield greater cognitive benefits. Senior author Dr Natalie Marchant (UCL Psychiatry) said that they “know mindfulness-based programs benefit mental health, and our paper now suggests that mindfulness may also help to maintain cognitive faculties as people age. Mindfulness practices do not share much in common with cognitive test measures, so it is notable that mindfulness training's impact appears to transfer to other domains. While our review only identified a small benefit to executive function, it remains possible that some types of mindfulness training might deliver larger gains.” Major Depression Symptoms Improved with Chlorella University of Western Australia, August 23rd 2021    The symptoms of depression are often treated with drugs that can have long-term adverse side effects. A new study finds chlorella significantly reduces symptoms of major depression. Research from the University of Western Australia in Perth has found that chlorella can significantly improve symptoms of depression. The researchers tested 92 patients with major depressive disorder – a disorder that affects millions of people around the world. The researchers split the patients into two groups. They gave 42 of the patients 1,800 milligrams of Chlorella vulgaris extract per day. The other 50 patients continued their standard care. The researchers used a scale called the Hospital Anxiety and Depression Scale (HADS) to test the patients' symptoms of depression, along with the Beck Depression Inventory II (BDI-II) scale. Both of these have been used in clinical settings to establish the range of depressive symptoms and the severity of the diagnosis. After six weeks of treatment with either the standard pharmaceutical treatment or chlorella extract, the researchers found that those patients who had taken the chlorella had significantly reduced scores in both depression tests. The BDI-II scores went down by over four points and the HADS scores went down by 3.71 points. To give some reference, the HADS scale consists of 21 points, and anything over an 8 is considered symptomatic of anxiety or depression. In addition to reduced total scores, the researchers also saw significant reductions in some of the subset scores. For example, physical and cognitive symptoms were significantly improved in the chlorella group, and subscales for depression and anxiety were significantly lower among the chlorella group. The researchers concluded: “This pilot exploratory trial provides the first clinical evidence on the efficacy and safety of adjunctive therapy with CVE in improving physical and cognitive symptoms of depression as well as anxiety symptoms in patients who are receiving standard antidepressant therapy.” Chlorella is a microalga. It is a single-celled algae that is typically grown in controlled growth medium tanks. It is significantly high in protein, with over 40 percent protein, with all of the essential amino acids. It also contains proteins that stimulate growth hormone and brain neurotransmitters. Concentrated extract was used in this study due to the fact that whole chlorella can be difficult for the body to break down the cell wall. An extract provides the contents of the cell after the cell wall has been broken. Greater adherence to Mediterranean diet associated with decreased cardiometabolic risk during pregnancy University of Granada, August 20, 2021 According to news reporting out of Granada, Spain,research stated, “Studies regarding dietary patterns and cardiometabolic risk markers during pregnancy are scarce. The aim of the present study was to analyse whether different degrees of adherence to the Mediterranean diet (MD) and the MD components were associated with cardiometabolic markers and a clustered cardiometabolic risk during pregnancy.” Our news journalists obtained a quote from the research from the University of Granada, “This study comprised 119 pregnant women from the GEStation and FITness (GESTAFIT) project. Dietary habits were assessed with a food frequency questionnaire at the 16th and 34th gestational weeks (g.w.). The Mediterranean Diet Score was employed to assess MD adherence. The following cardiometabolic markers were assessed: pre-pregnancy body mass index (BMI), systolic blood pressure (SBP), diastolic blood pressure (DBP), fasting glucose, triglycerides and high-density lipoprotein cholesterol (HDL-C). A greater MD adherence was associated with a better cardiometabolic status in cross-sectional (16th g.w. and 34th g.w.) and prospective analyses (MD adherence at the 16th g.w. and cardiometabolic markers at the 34th g.w.; SBP, DBP and HDL-C; all, p< 0.05). Participants with the highest MD adherence (Tertile 3) had a lower clustered cardiometabolic risk than those with the lowest MD adherence (Tertile 1) at the 16th and 34th g.w. (both, p< 0.05). A higher intake of fruits, vegetables and fish and a lower intake of refined cereals and red meat and subproducts were associated with a lower cardiometabolic risk during pregnancy (all, p< 0.05).” According to the news editors, the research concluded: “A higher MD adherence, a greater intake of fruits, vegetables and fish and a lower intake of refined cereals and red meat and subproducts showed a cardioprotective effect throughout gestation.” Unhealthy diet during pregnancy could be linked to ADHD King's College London and the University of Bristol , August 20, 2021   New research led by scientists from King's College London and the University of Bristol has found that a high-fat, high-sugar diet during pregnancy may be linked to symptoms of ADHD in children who show conduct problems early in life. Published in the Journal of Child Psychology and Psychiatry, this study is the first to indicate that epigenetic changes evident at birth may explain the link between unhealthy diet, conduct problems and ADHD. Early onset conduct problems (e.g. lying, fighting) and attention-deficit/hyperactivity disorder (ADHD) are the leading causes of child mental health referral in the UK. These two disorders tend to occur in tandem (more than 40 per cent of children with a diagnosis of conduct disorder also have a diagnosis of ADHD) and can also be traced back to very similar prenatal experiences such as maternal distress or poor nutrition. In this new study of participants from the Bristol-based ‘Children of the 90s' cohort, 83 children with early-onset conduct problems were compared with 81 children who had low levels of conduct problems. The researchers assessed how the mothers' nutrition affected epigenetic changes (or DNA methylation) of IGF2, a gene involved in fetal development and the brain development of areas implicated in ADHD – the cerebellum and hippocampus. Notably, DNA methylation of IGF2 had previously been found in children of mothers who were exposed to famine in the Netherlands during World War II. The researchers from King's and Bristol found that poor prenatal nutrition, comprising high fat and sugar diets of processed food and confectionary, was associated with higher IGF2 methylation in children with early onset conduct problems and those with low conduct problems. Higher IGF2 methylation was also associated with higher ADHD symptoms between the ages of 7 and 13, but only for children who showed an early onset of conduct problems. Dr Edward Barker from King's College London said: ‘Our finding that poor prenatal nutrition was associated with higher IGF2 methylation highlights the critical importance of a healthy diet during pregnancy. These results suggest that promoting a healthy prenatal diet may ultimately lower ADHD symptoms and conduct problems in children. This is encouraging given that nutritional and epigenetic risk factors can be altered.' Dr Barker added: ‘We now need to examine more specific types of nutrition. For example, the types of fats such as omega 3 fatty acids, from fish, walnuts and chicken are extremely important for neural development. ‘We already know that nutritional supplements for children can lead to lower ADHD and conduct problems, so it will be important for future research to examine the role of epigenetic changes in this process.' Green tea may help protect against sunburn Taiyo Kagaku Co (Japan), August 24, 2021 A systematic review and meta-analysis published in a recent issue of Molecules found an association between oral intake or topical application of green tea catechins and a reduction in ultraviolet (UV) radiation-induced sunburn, which is an inflammatory reaction of the skin to UV exposure, clinically known as erythema.* Catechins are a type of flavonoid that occur in plants such as Camellia sinensis (tea). Green tea catechins include (-)-epigallocatechin-3-gallate (EGCG), well known for its anti-cancer and health-promoting effects, (-)-epicatechin, and many other similar molecules. These compounds have been recognized as having anti-inflammatory, antioxidant and photo-protective properties. “To our knowledge, this is the first meta-analysis to assess the effectiveness of green tea catechins specifically on measures of ultraviolet radiation-induced erythema and related pro-inflammatory mediators,” authors Mahendra P. Kapoor and colleagues wrote. “Regular intake of as low as 540 mg of green tea catechins per day could be beneficial for the protection against ultraviolet radiation-induced erythema, wherein green tea catechin metabolites are bioavailable at the dermis and epidermis levels of the skin, and thus increase the minimal dose of radiation (MED) required to induce erythema.” Dr Kapoor added that the study “suggests that green tea catechins can strengthen the skin's tolerance to ultraviolet radiation-induced skin damage from radiation through the prevention of the ultraviolet radiation-induced perturbation of epidermal barrier functions.” Study details: 12 weeks of green tea intake yields benefits The meta-analysis included three randomized, double-blind, placebo-controlled trials and one non-double-blind, non-placebo-controlled study that examined potential protective effects of orally administered capsules containing green tea catechins against sunburn (clinically known as erythema) induced by solar-simulated UV radiation. Two additional studies that involved a single dose of topically administered catechins were separately analyzed. Pooled analysis of data from three studies that evaluated erythema in skin exposed to UV radiation before and after 12 or more weeks of green tea catechin intake revealed a favorable effect in association with catechin intake. Both low and high doses of the green tea capsules were effective at decreasing low-dose UV radiation-induced erythema. It was also noted that a significant favorable effect was seen in the one study which assessed UV radiation-induced erythema after green tea intake for only six weeks, but as none of the other studies assessed this shorter duration of intake, further analysis was not performed. When green tea catechins' effects compared to a placebo were analyzed, pooling the data of two placebo-controlled trials confirmed their effectiveness against low-intensity UV radiation-induced erythema. Pooling data from participants in the studies involving topical green tea catechins revealed significant benefit for green tea at higher UV radiation doses.

Certifícate con Nosotros como Entrenador de Liderazgo. Visita: www.liderazgoELAI.org Síguenos: @LiderazgoELAI /// @HablemosDeLiderazgo La palabra desierto siempre se termina relacionando con algo malo, los procesos son etapas dónde experimentaremos el dolor y nos asusta entrar en ellos. Nuestras fallas y fracasos pueden hacernos sentir menos y no merecedores de su gracia, pero tu padre te ama, confía y va a usar tu vida para bendecir a muchos. Juntos aprenderemos: ✅ ¿Cómo es el desierto? ✅ ¿Cómo es mi identidad en a Cristo? ✅ ¿Cómo puedo ayudarte? De esto es que te vamos a hablar en este nuevo episodio de #HablemosDeLiderazgo donde tendremos como invitado especial a Beto Figueroa @beto.figue Content Manager Enlace+. Tema: De tanta gente que hay en el mundo, ¿Cómo Dios te fue a buscar?

Watch the episode on YouTube at @ https://youtu.be/R5kY2fYCxFIOn this episode of the podcast, I discuss how the bloodstream carries molecules like glucose and triglycerides to provide energy for the body. I introduce what lipoproteins are and their important role in specifically carrying triglycerides (which are hydrophobic molecules) and cholesterol through the bloodstream. After that introduction, I present a scientific paper from the Journal of American Medical Association about how a fasting blood lipid profile of low triglycerides and high HDL-C are associated with low risk of heart disease even with the presence of other traditional risk factors such as high LDL-C, high blood pressure, low physical activity or even smoking. Near the end of the podcast I synthesize some practical conclusions about heart disease, blood markers, diet and other lifestyle choices trying to tie in everything that has been discussed on the podcast about this topic in the previous 3 episodes and this one. Read the whole article for yourself:https://jamanetwork.com/journals/jamainternalmedicine/fullarticle/647239If any of what I'm saying does not make sense and you need clarification, please leave a comment or send me a message atnewsletter@jmartfit.comIf you want to make a commitment to mastering your body then get a free copy of my Body Basics training program at -- https://subscribepage.com/bodybasicsConnect with J-Mart on Social MediaInstagram - https://www.instagram.com/jmartfit/​Facebook page - https://fb.me/jmartmoves​Medium page - https://jmartwrites.medium.com/Newsletter - newsletter@jmartfit.comTime codes0:00 - Intro1.49 - Start of Podcast4:03 - Glucose, Triglycerides and Lipoproteins8:55 - Low Triglycerides + High HDL-C and Risk of Ischemic Heart Disease Paper Introduction11:30 - Subjects and Methods14:09 - Results16:40 - Discussion and Biological Plausibility19:55 - My Practical Takeaways27:01 - OutroSupport this podcast at — https://redcircle.com/state-of-health/donationsMusic: https://www.bensound.comSupport this podcast at — https://redcircle.com/state-of-health/donations

Leo's channel: https://www.youtube.com/c/LeoandLongevity Derek's channel: https://www.youtube.com/channel/UCoR7CHkMETs3ByOv74OAbFw Steve's channel: https://www.youtube.com/user/VigorousSteve TIMESTAMPS: 0:00 intro 0:29 Connor Murphy/ Ayahuasca and DMT 1:36 Kenny KO and Connor 2:10 Leo on psychedelics/ his friend 3:38 Steve on psychedelics 5:29 Marijuana and schizophrenia/ More on Connor 7:45 Man cutting his genitals off on drugs 9:30 Screen sharing on Zoom 9:58 Leo's manic Canadian friend 10:47 Derek will avoid psychedelics 12:13 Derek on being ambitious 13:29 Losing your ego 14:12 How Leo hurt his finger 16:42 Antoine's Vaillant bicep and Olympia placing 19:06 Derek's bodybuilding genetics 20:13 Why Derek stopped doing steroids/ Making money as a bodybuilder 23:16 GH15, Antoine, and Frank Mcgrath 24:44 Bodybuilding, dieting, and tren 26:25 Recovery from injury Beta-blockers either before or after a surgery Nebivolol, collagen and gelatin protein, Propranolol, 29:03 Angiogenesis BPC 157, TB500, erythropoietin 31:06 Growth factors and hair loss/ Icing and cooling injuries 32:06 MK677, ghrelin  and surgeries/ MK677, GH, and IGF1 34:05 MK677, Ghrelin, PTSD, and Insulin 39:22 Jujimufu and Greg Ducette/Canadian accents 43:34 People being hyper-critical of people in the fitness industry. 44:49 Jujimufu, arm wrestling, and stomach distension 47:53 Leo's GH experience 49:31 Jujimufu's genetics 51:06 Looking like you work out while wearing a shirt 52:25 Anabolic pathways 53:30 Dallas McCarver autopsy/ Anthony Roberts ban 58:20 Dallas McCarver organs 1:00:21 Leo's friend taking large sums of steroids/ Derek on the autopsy 1:07:00 Derek and Steve on blood and urine drug tests/ Tren cough 1:11:10 What steroids do to your heart Dislipidemia, HDL goes down, HDLC decreases by approx 50%, APO A1 decreases by 33-41%, increases LDLC by approx 36% Reduce lipoprotein [a] 1:12:41 Homocysteine blood tests/ Chris Masterjohn  Creatine, Choline, B vitamins 1:13:50 More on Lipoprotein [a] Niacin, Repatha, and steroids 1:15:01 Derek's client with strange test results 1:15:54 Hypercholesterolemia  Homozygous APOCIII, CETP, and APOE4 1:17:33 Steroids, left ventricular systolic function, left ventricular diastolic function, and heart hypertrophy. 1:19:15 Heart FMRI 1:20:28 Impaired tonic cardiac autonomic regulation, and Clenbuterol 1:22:32 Leo's list of tests and genetics 1:23:25 Statins, Ezetimibe, and cholesterol 1:25:00 Automated gene searches 1:26:09 Statins and natural status 1:27:24 Lowering LDL and extending life PCSK9 inhibitors, Bempedoic acid, Ezetimibe, and Statins 1:28:41 Steve on Ezetimibe 1:29:32 Leo on Statins (the good and the bad) Pitavastatin, Rosuvastatin crestor ,livalo, lipitor 1:33:56 Telmisartan, Valsartan, Azilsartan and Irbesartan 1:39:17 Diuretics, bloating, and Estrogen 1:41:28 Hyperkalemia, Potassium and drug interactions 1:43:20 Minoxidil as a potassium channel opener and microneedling 1:45:49 Steve doesn't like hair 1:47:40 Leo's hypothesis on hair loss/ Derek on hair loss 1:54:25 Topical dutasteride 1:55:35 70-year-old women and balding 1:56:45 Steve on being secure with hair loss 2:00:40 Men and size 2:02:04 Pre-workout androgens Anadrol, Dianabol, Superdrol and Anadrol 2:08:26 Taking short-acting compounds around your workout 2:10:00 How steroids cause liver cancer and why Anavar doesn't cause it 2:11:56 Dianabol back pumps 2:13:19 Egyptian bodybuilders 2:14:52 Steve's fasting protocols 2:18:15 Reasons to fast 2:20:44 Leo's reasons to fast/ Satchin Panda's book/Valter Longo's fasting-mimicking diet and Prolon 2:23:47 Proper fasts on PEDs Allopurinol 2:27:36 How Steve and Leo prepare salads 2:30:35 The discord group 2:34:19 Unhealthy relations to Youtubers 2:39:58 Epigenetics and children 2:43:14 IVF and metabolic profiles 2:45:35 Coming off of testosterone and getting back to baseline 2:46:37 Having kids at an older age (epigenetic damage over time to sperm) 2:49:42 Steve and Leo on TV 2:50:15 Past downloading services 2:54:06 Unusual pre workout supplements for more strength or a better pump 2:56:40 Why the hell are people taking Phenibut and Kratom pre workout 2:58:00 Low dose Naltrexone therapy 3:00:16 Getting over addiction 3:02:34 Gynecomastia 3:05:43 Removing your glands before you take steroids/ Problems with Nolvadex 3:08:02 Derek and Steve on their gyno experiences 3:10:45 How to deal with gyno if you don't want the surgery 3:11:56 Steve on growing your gyno, to get the surgery JOIN OUR COMMUNITY: Reddit ▶ https://www.reddit.com/r/TheLongLived/ FOR GENETIC ANALYSIS & COACHING: Website ▶ https://www.leoandlongevity.com TO READ MY ARTICLES: Blog ▶ https://www.leoandlongevity.com/blog TO FOLLOW ME ON SOCIAL MEDIA:  Instagram ▶ https://www.instagram.com/leoandlongevity Twitter ▶ https://www.twitter.com/leoandlongevity

Certifícate con Nosotros como Entrenador de Liderazgo. Visita: www.liderazgoELAI.org Síguenos: @LiderazgoELAI /// @HablemosDeLiderazgo La procrastinación es el arte de dejar todo para después, o de tener mil razones para posponer desde cosas importantes hasta cosas que son irrelevantes. Es como irte engañando por la vida, encontrando qué hacer por el camino, que, de hecho, son cosas que te producen más placer realizar. En esta charla quiero que juntos: ✅ Conozcamos realmente que es la procrastinación para poder vencerla. ✅ Identifiquemos las fases que nos detienen y alejan de nuestros objetivos. ✅ Reconozcamos los beneficios que se obtienen cuando decidimos ser una persona altamente productiva. De esto es que te vamos a hablar en este nuevo episodio de #HablemosDeLiderazgo donde tendremos como invitada especial a Yamily Ortiz @yamilyortizcoach Conferenciante Internacional, Coach Empresarial y Autora. Tema: Dejar de procrastinar.

This week, join author authors John J.V. McMurrary and Milton Packer, and Associate Editor as they discuss their Perspective article "How Should We Sequence the Treatments for Heart Failure and a Reduced Ejection Fraction? A Redefinition of Evidence-Based Medicine." TRANSCRIPT BELOW Dr. Carolyn Lam: Welcome to Circulation on the Run, your weekly podcast summary and backstage pass to the journal and its editors. We're your co-hosts. I'm Dr. Carolyn Lam, associate editor from the National Heart Center and Duke National University of Singapore. Dr. Greg Hundley: And I'm Dr. Greg Hundley, associate editor, director of the Pauley Heart Center at VCU Health in Richmond, Virginia. Dr. Carolyn Lam: Greg, this feature discussion is going to knock you off your seat, because it did me. It's about treatment sequencing in HFrEF and discussing it with some luminaries on the field, Dr. John McMurray and Dr. Milton Packer. You are going to love it. I loved it. But I'm going to make you wait. How about you grab some coffee and let's start with some of the other papers in today's issue first. Dr. Greg Hundley: All right, Carolyn. How about if I go first? I'm going to start with a paper from Dr. Liam Brunham from the University of British Columbia. Well, Carolyn, the high density lipoprotein or HDL hypothesis of atherosclerosis has been challenged by clinical trials of cholesterol ester transfer protein, or CETP inhibitors, which failed to show significant reductions in cardiovascular events. Plasma levels of HDL cholesterol, or HDL-C, declined drastically during sepsis. And this phenomenon is explained in part by the activity of CETP, a major determinant of plasma HDL-C levels. So Carolyn, these authors tested the hypothesis that genetic or pharmacologic inhibition of CETP would preserve HDL levels and decrease mortality in clinical cohorts in animal models of sepsis. Dr. Carolyn Lam: Huh. Interesting. And what did they find? Dr. Greg Hundley: Well, Carolyn, results from both the human UK Biobank and the mouse model experiments suggested that inhibiting CETP may preserve HDL levels and improve outcomes for individuals with sepsis. Dr. Carolyn Lam: Wow. So is this ready for clinical applications somehow? Dr. Greg Hundley: Well, Carolyn, two conclusions from this work. First, high density, lipoprotein cholesterol, a commonly used biomarker for cardiovascular risk assessment, may also predict risk of death from sepsis. And then second, cholesterol ester transfer protein inhibitors that have been tested in clinical trials of cardiovascular disease could be repurposed and studied in clinical trials of sepsis. Dr. Carolyn Lam: Ooh, exciting. Well, Greg, for my paper, I'm going to ask you a question. Have you ever thought about what the temporal changes in medical prevention and adverse outcomes are in patients with symptomatic peripheral artery disease after revascularization? Well, wait no longer. Our next paper addresses that. It's from Dr. Sogaard from Aalborg University Hospital in Denmark and colleagues who identified all patients with a first open surgical or endovascular revascularization procedure in the lower extremities or abdomen in Denmark from 2000 to 2016. And this is what they found. Dr. Carolyn Lam: First, the profile of patients with PAD who underwent lower extremity revascularization changed towards older age and a higher prevalence of comorbidity. Despite increases in age and co-morbidity, medical prevention of adverse events improved substantially over time, particularly in the first part of the study period and among patients who used medications chronically. Dr. Carolyn Lam: Now in contrast, initiating treatment after revascularization increased modestly among treatment-naive patients. Now concurrently, prognosis improved for almost all adverse outcomes in patients of both sexes, all age groups, and in all high-risk co-morbidities. In particular, the risks of myocardial infarction and cardiovascular death declined by more than 40%. Dr. Greg Hundley: Well, Carolyn, are there any other findings with clinical implications here? Dr. Carolyn Lam: Yes. So that was the good news earlier. But despite overall improvements, significant disparities remain. Less than 40% of treatment-naive patients initiated cardioprotective therapy after revascularization, underscoring the need for raising levels of awareness and education in the vascular community, general practitioners and patients of this. Major amputations also remained unchanged and thus more work is needed to understand relationships between the preventive measures, revascularization and amputation. Dr. Greg Hundley: Great summary, Carolyn. My next paper comes from Dr. Rachael Cordina from the Royal Prince Alfred Hospital, University of Sydney. Neurocognitive outcomes beyond childhood in people with a Fontan circulation are not well-defined. So the investigators here aim to study neurocognitive functioning in adolescents and adults with a Fontan circulation and associations with structural brain injury, brain volumetry and postnatal clinical factors. Dr. Carolyn Lam: Okay, you got our attention. What did they find, Greg? Dr. Greg Hundley: Thanks, Carolyn. So participants with a Fontan circulation, without a pre-existing major neurological disability, were prospectively recruited from the Australia and New Zealand Fontan registry. And the investigators found that neurocognitive impairment is common in adolescents and adults with a Fontan circulation and is associated with smaller grey and white matter brain volume. Understanding, therefore Carolyn, modifiable factors that contribute to brain injury to optimize neurocognitive function is paramount. Dr. Carolyn Lam: Indeed. Well, this next paper I want to talk about is the first detailed endothelial cell cysteine-S self-hydrome. Dr. Greg Hundley: Self? S self-hydrome? What is that, Carolyn? Dr. Carolyn Lam: Good. I needed to catch your attention. Let me tell you about it. So in vascular endothelial cells, cysteine metabolism by cystathionine gamma-lyase, or CSE, generates hydrogen sulfide- related sulfane sulfur compounds. And these exert their biological actions via cysteine-S self-hydration of target proteins. So the paper we're talking about today by Dr. Fleming from Goethe University in Germany and colleagues, they aimed to map the S self-hydrome, which is the spectrum of proteins targeted by this hydrogen sulfide-related sulfane sulfur compounds, or H2Sn, in human endothelial cells. And they did this using liquid chromatography and tandem mass spectrometry. Dr. Carolyn Lam: So here's what they found: vascular disease was associated with mark changes in the S self-hydration of endothelial cell proteins involved in mediating responses to flow. Integrins were most effected by S self-hydration and the modification of beta-3 integrin resulted in reshuffling of the intramolecular disulfite bonds to preserve its extended and open confirmation. Loss of beta-3 integrin self-hydration, on the other hand, inhibited endothelial cell adhesion, impaired mechanosensing and attenuated flow induced phase with dilation. Thus, short term H2Sn supplementation could improve vascular reactivity in humans, highlighting the potential of interfering with this possibly to treat vascular disease. Dr. Greg Hundley: Very nice, Carolyn. You know, just more from the world of hydrogen sulfide and endothelial function. Thanks so much. Well, the next paper I have comes to us from Dr. John McEvoy from Johns Hopkins University School of Medicine. So Carolyn, recent clinical guidelines support intensive blood pressure treatment targets. However, observational data suggests that excessive diastolic blood pressure lowering might increase the risk of myocardial infarction. Therefore reflecting, does a J or U-shaped relationship exist when we're following the treatment of diastolic blood pressure? So Carolyn, these authors analyzed 47,407 participants from five cohorts with a median age of 60 years. First to corroborate prior observational analysis, the authors used traditional statistical methods to test the shape of association between diastolic blood pressure and cardiovascular disease. Dr. Carolyn Lam: Okay. So was it J or U? Dr. Greg Hundley: Okay, Carolyn. So interesting, traditional observational analysis of the cohorts suggested a J-shaped association between diastolic blood pressure and myocardial infarction. However by contrast, linear MRI analyses demonstrated an adverse effect of increasing diastolic blood pressure increments on cardiovascular disease outcomes, including myocardial infarction. Furthermore non-linear MRI analyses found no evidence for a J-shaped relationship. Instead confirming that myocardial infarction risk decreases consistently per unit decrease in diastolic blood pressure, even among individuals with low values of baseline diastolic blood pressure. So Carolyn, in answer to you, no, the J or U-shaped curve does not exist. Dr. Carolyn Lam: I suppose depending which way you look at it. Very interesting. Well, let's finish up with what else is in today's issue. There's an AJ update by Dr. Elkin on COVID-19 at one year, the American Heart Association president reflect on the pandemic. A white paper by Dr. Zannad on challenges of cardio kidney composite outcomes in large scale clinical trials. A research letter by Dr. Kass on  the reduced right ventricular sarcomere contractility in HFpEF with severe obesity. Another research letter by Dr. Messas on the feasibility and performance of non-invasive ultrasound therapy in patients with severe symptomatic aortic valve stenosis. A first in human study. Dr. Greg Hundley: Right, Carolyn. So I've got an exchange of letters from Dr. Vazgiourakis  addressing a prior publication entitled Right Heart Dysfunction in COVID-19 Patients: Does Mechanical Ventilation Play an Additional Role? And then finally, an exchange of letters from Drs. Carrizales-Sepúlveda and Topalisky regarding the prior paper, The Spectrum of Cardiac Manifestations in COVID-19. Well, Carolyn, I'm really excited to get to that feature that you explained to us right at the beginning. Very exciting. Dr. Carolyn Lam: So am I. So am I. Thanks, Greg. Dr. Carolyn Lam: Wow. Today's feature discussion could not be more star-studded in my point of view. We are talking about the very, very hot topic of how do we sequence treatments in heart failure with reduced ejection fraction now? A really hot topic because just last year in 2020, we suddenly got a bonanza of positive trials and everybody's grappling with how to put it all together. Dr. Carolyn Lam: Now who better than the two authors I'm going to talk to today, Professor John McMurray from University of Glasgow and Professor Milton Packer from Baylor University Medical Center in Texas. So welcome both. John, Milton, I'm almost tripping over myself to talk about this because this is an amazing perspective piece. Everybody must get your hands on it and even look at the figure while you're listening to this. We're going to divide today's discussion into just three simple questions. Why do we need a new sequencing approach? How in the world do you come up with a new sequencing approach? Based on what? And finally, what is that new approach that you're both proposing? So maybe I'll start off with you, John. What's wrong with what we've been doing? Dr. John McMurray: So Carolyn, I think we've maybe neglected the fact that while we think of, for example, cancer as something that's incredibly urgent to diagnose and to treat as fast as possible, to give the patient all those life-saving therapies, we haven't had the same urgency in our treatment with heart failure. And our existing approaches, as you know, being largely one of start with the first treatment that was ever tested in the trial, up titrate to the pill dose, take your time, then on the second, third and so on. And of course, what that means is that it takes months for patients to be treated with all of the fantastic life-saving options that we have available for them. And we know that that's failing. Dr. John McMurray: We've seen from numerous registries, CHAMP registry in particular springs to mind, where that's simply not happening. It's probably taking too long. It's too complicated for both the doctor and the patient, and we need to change it. And I suppose Milton will tell you his view, but I think my view and I think his as well, was that the SGLT2 inhibitor story really brought this question, I think, to the fore because here is our fourth life-saving drug that if we do things the same way might not get started for six months. And we really felt that we need to rethink what we're doing. Milton, I'm sure, will say whether he agrees with that. But I think that was sort of where the starting point was. Dr. Carolyn Lam: Great. But if I could interject a bit, so now we're talking about that left side of the panel, where in your beautiful article where you're showing, we start with ACE inhibitors and ARBs, and then go on to beta blockers and mineralocorticoid receptor antagonists, and so on. I would love to know, and Milton I'm sure you'll add, is it the sequence that's wrong? Or is it really just the timing? Or the fact that we're just all too lazy? What do you say to people who go, "But that's how the trials were done." Especially because you guys both led those amazing trials of ARNIs and SGLT2 inhibitors. It's just awesome. Dr. Milton Packer: So Carolyn, what's really amazing is that everyone assumes that that's how the trials were done. But two things, one, just because we did things in a certain way, developed things in a certain way, doesn't mean we have to prescribe them in a certain way. I mean, we developed digitalis before all of them and so does that mean we need to use digitalis in everyone? But a lot of the early trials, all the patients were, or most of the patients were, on cardiac glycosides. Dr. Milton Packer: There are four things that we've learned from the large-scale clinical trials. One is the order of drugs does not matter with respect to efficacy. The beta blockers work the same whether people are getting ACE inhibitors or not, MRAs are not effected by background therapy. Neither is neprilysin inhibitors. They work pretty much the same regardless of background therapy, so you don't have to sequence them in the order in which they were developed. Dr. Milton Packer: Two is low doses, low starting doses of these drugs seem to work amazingly well, perhaps surprisingly well. And the third thing is that they work very early. So in a lot of the clinical trials, nearly all the trials that were carried out, there was a meaningful separation of the curves and in effect size in the first 30 days of all of these trials. And in many of the trials, in the first 30 days, patients were still on the starting dose. Hadn't been uptitrated. Dr. Milton Packer: The last point is that these drugs can influence each other's safety profiles. So the result of all of this was for us to rethink what the sequence should be based not on how the drugs were developed, but how they might be most logically used with respect to relative efficacy, safety and ease of use. Dr. John McMurray: So, Carolyn, to go back to your question then is sort of what Milton is saying is that it's a bit of both of the things you asked about. It is about timing, but it's also about the order of the drug. And that last point Milton made is very important about the potential synergies in terms of making it easier to use treatments, but timing is critically important as well. I mean, we do tend in the conventional approach to therapy recommended in the guidelines to perhaps spend too much time trying to reach that target dose, and then doing that before moving on to the second drug. So again as Milton pointed out, if you're getting early benefit from all of these treatments, fundamentally what you want is as many of these treatments started as quickly as possible as you can do safely. And that may be facilitated by some of the synergies between treatments as we, I think, rather provocatively suggested in the new algorithm, might even be possible to start two treatments at once. Dr. Carolyn Lam: Okay. Now I know everybody's really, really wondering what that new algorithm is, but I'm going to lengthen the pain a little bit more because this is critically important. You've already started discussing the how did you come up with an algorithm. It seems a lot of, yeah, very reasonable approaches, but could you give us specific examples of actual scientific interrogation of the data from the trials that you've led, frankly, to show us these points, that maybe support that we can come up with a reasonable new approach? Those points that Milton very rightly put, the treatment benefit of each class is independent. Give us some examples of that. The dose issue, the side effects, how one could help in that too. Could you give us some examples? Dr. Milton Packer: Oh, my God. So let me say that there's so many pieces of evidence and please read the article. We try to summarize as much of them as possible. But in all of the major clinical trials, there was a separation that occurs within 30 days. That's true across every single major trial. Anyone who thinks that the treatment effects of these drugs are delayed, that it takes months to evolve, we're getting statistical significance within two to four weeks across all of the drugs. Dr. Milton Packer: Second is, in many of the trials, for example, COPERNICUS trial with carvedilol, the trials with MRAs, even the trials with ACE inhibitors, during that first 30 days when the curves were separating, patients hadn't been uptitrated. They started on low doses and remained on relatively low doses and the curves were separating. So we knew that the drugs had early effects at low doses, low starting doses. And we also have randomized trials that really tell us that if you go to high doses for some of these drugs, you get a little bit more benefit, but you don't get as much benefit as starting another drug with a different mechanism at a low dose. Dr. Milton Packer: And lastly, we know that some of these drugs actually prevent the side effects of others. There's evidence that neprilysin inhibitors and SGLT2 inhibitors mitigate the hyperkalemia produced by spironolactone and aplerno. So these are just a few examples. Dr. John McMurray: Sorry, Carolyn. To add a couple more, we obviously know that the treatments work independently. We primarily knew that from subgroup analyses, but also from trials like RALES for example, where spironolactone was tested in addition to an ACE inhibitor, but very, very few patients were on a beta blocker. Subsequently we tested different a MRA in patients who were taking both an ACE inhibitor and a beta blocker, and the benefit was essentially the same. And of course, our very first trial with an ACE inhibitor, the CONSENSUS trial, was actually done in a population where more than half of the patients were on a very large dose of an MRA. So you can sort of put all the trials together in a type of jigsaw and figure out that these drugs all clearly work independently. Dr. John McMurray: And then maybe the only other thing I would mention, because it's perhaps relevant to the new algorithm, is that we do have another key trial, which is, a trial I think often forgotten about, the CIBIS III, which was a study that tested whether or not you could start treatment with either a beta blocker or with and ACE inhibitor in patients with HFrEF, showing that you could start with a beta blocker in patients who had not yet received an ACE inhibitor and do that safely and efficaciously. So there's a lot of material out there that you can sort of put together to answer all of these questions. Dr. Carolyn Lam: Great. And now drum roll. Okay. What is the new algorithm? John, you want to introduce it? Or Milton? Up to you. Dr. Milton Packer: John can start. That's fine. Dr. Carolyn Lam: Well, which one, Carolyn? I suppose the one in the Circulation article is a three-step algorithm. It starts with the combination of a beta blocker, based as I mentioned, so there's three plus an SGLT2 inhibitor. So again, thinking about synergies, thinking about tolerability, thinking about size of effect and thinking about repetity of onset of benefit. So I think most of us would agree, beta blockers are incredibly effective treatments, life-saving treatments, reduce the risk of sudden death. We know that you can start a beta blocker safely as first-line therapy. We do know that there may be more intolerance in patients who are volume overloaded. So why not give a treatment that has a modest, initial diarrhetic effect when you're starting the beta blocker? In other words, the SGLT2 inhibitor. SGLT2 inhibitors work extremely quickly. There's no dose up titration needed. So they seem like the perfect combination to start with. Dr. Carolyn Lam: In step two, we suggested moving then to sacubitril valsartan, which in itself is two more drugs combination of an angiotensin receptor blocker and their prolines inhibitor. And then there's the third and final step. We suggested using a mineralocorticoid receptor antagonist. But Milton and I have had a lot of discussion about this. I think we're not saying that all those are necessarily the three steps for all patients. There may be different approaches in different people depending on patient's characteristics. But really the point here was, the provocative statement was we should be able to do this quickly in all patients. And this in fact was an approach to get all four of those drugs started potentially within four weeks. Dr. Milton Packer: So Carolyn, the mantra here, our motto going forwards, is four drugs in four weeks. Dr. Carolyn Lam: Okay. Dr. Milton Packer: An angiotensin receptor blocker, a beta blocker, an MRA, an SGLT2 inhibitor. Four drugs in four weeks. And if you're going to start all four drugs in four weeks, in all honesty, the order probably doesn't matter that much. John and I happen to think that if you have to define a first step, a combination of a beta blocker and an SGLT2 inhibitor simultaneously as step one makes a lot of sense. And then you can follow up with sacubitril valsartan and an MRA. Dr. Milton Packer: But here's the thing that's really important: do not take months to follow up. What we're proposing in this algorithm is you start a beta blocker and an SGLT2 inhibitor on day one, and you then follow through with sacubitril valsartan and an MRA within the next couple of weeks. But here's what's really important and we really need to emphasize this: this is a algorithm that assumes that someone's not on any of these drugs already. And of course, most of these patients are taking some of these drugs already. But the other thing that's really important is that we're also assuming that physicians are being very meticulous about background use of diuretics, so that patients really have to be maintained in a clinically euvolemic state in order to make this algorithm work. Dr. Carolyn Lam: Okay, well, I'm picking myself off the floor because it certainly was provocative. I love it. I love it for that. It's the first time I've ever seen any algorithm start with a beta blocker and SGLT2 inhibitor. You first go, "Where's the ACE and how come the new kid on the block is right on top?" So I really like that because it must challenge our current thinking. In other words, if we just look at the data for what it is, let's see how we could think it over. So salute you for that. But let me just press on a little bit. So four drugs in four weeks. That's really great. Are there any particular patients you may say the ARNIs come on top or the MRAs? Specific situations or...? Dr. Milton Packer: Well, Carolyn, as John has already said, the physicians need to understand the principles, but the application of those principles have to be individualized. So if a patient has a borderline blood pressure, you would probably be well advised to put the MRA before sacubitril valsartan. Depending on renal function, you may decide to advocate one drug a little bit earlier or preferentially compared to another. There are hundreds of individualized nuances, but to get tied up in these is to miss the point of our paper. The point of our paper is that we need to do things quickly... Four drugs, four weeks... And we need to not rely on our historical testing in order to determine the optimal sequence. If you embrace those conclusions, then patients and physicians can individualize their care to the greatest optimal degree. But our current approach, which is a historically-driven algorithm that takes six months to execute, it doesn't work. Dr. John McMurray: Carolyn, we obviously did give a lot of thought to the initial treatments, and we did realize that it would potentially be a surprise to people. But just to reiterate, I don't think there's much debate about the incredible benefits of beta blockers, the size of that benefit. We know that the benefit is apparent within 30 days. So Milton and we had Henry Krum's very nice paper about that in JAMA from the COPERNICUS trial, but we're seen it in the other trials. You know that SGLT2 inhibitors have had early benefit. You think about these two drugs being used in a newly presenting patient with HFrEF, probably don't even need to do any electrolyte monitoring, provided your patients not volume overloaded or recently decompensated. That patient's very unlikely to have any significant intolerance to these two treatments. Dr. John McMurray: They don't, in those sorts of patients, substantially reduced blood pressure in either drug, beta blockers certainly don't affect kidney function. SGLT2 inhibitors have minimal effect on kidney function. If your GFR is relatively normal, you probably don't even need to check it. And of course, there's no effect on potassium. So in terms of getting two treatments onboard quickly that will have a rapid benefit, are likely to be well-tolerated in the type of patient that we just described, and where they might have monitoring necessary is minimal, then this seemed to be the best option. And as Milton said thereafter, it's maybe less important what order you do it in as opposed to the speed with which you do it. And you're right, you would definitely probably tailor this approach according to the patient characteristics, but this was a general starting point to stimulate debate, which it seems to have done. Dr. Milton Packer: So Carolyn, there's something important. If you believe in what we've proposed, then at the end of four weeks, every patient with heart failure and reduced ejection fraction would be on low starting doses or four foundational drugs. Our estimate is if doing that would provide them with a substantial benefit, maybe 70, 75% of the benefit of bringing all of those doses to target doses. And if you can do that, you can do all four drugs at starting doses at four weeks and provide that magnitude of benefit really quickly? That has a big impact on patients. And that has a big impact on public health. Dr. Carolyn Lam: Wow. Just thank you so much for igniting this debate. I wish we could go on forever. I just had to share that when we editors looked at this paper, it did spur a very robust debate. But as you can see, we're publishing it as you've proposed it because we do see where you're coming from. It is very interesting. And I just want to reiterate what you both just said, to listeners out there, remember this is referring to a patient who is compensated. Diuretics are still part of it. Remember that the key message is to get everyone on the four foundational therapies within four weeks. And I just love the way you pushed the boundaries with this. Really, really appreciate it. Milton, you look like you want to say something else. If you'd like closing words, I'd love to... Dr. Milton Packer: We really thank Circulation for having the courage to do this. And please understand, John and I strongly feel that this is the start of a debate. This is the start of a discussion. This algorithm is a proposal to get people to start thinking differently. This is not the final word on the subject by far. We think this is the beginning of a very important discourse that will evolve over the next year or more. And we just wanted to remind people what the clinical trial evidence actually shows about these drugs, because we think it has been frequently misunderstood much to the detriment of patients with heart failure. Dr. Carolyn Lam: Yes. And John, any last words? Dr. John McMurray: I would go back to where I started, Carolyn. In a way, what's important here is to inject a sense of urgency back into the way in which we treat patients with heart failure and reduced ejection fraction. It deserves that sense of urgency, as I mentioned that, for example, cancer does. And also thank you for summarizing, I think, what we tried to get across absolutely accurately. Dr. Carolyn Lam: Okay. So John, Milton, so far I take it. I take your points well, but as a practitioner, what I would do, frankly, is if I have a patient that I'm starting a beta blocker and an SGLT2 inhibitor, I would surely just start an ACE inhibitor perhaps, or ARNI, at the same time. I don't see why I need to delay it. How about that? Even faster? Dr. John McMurray: Okay, well, I'll let Milton answer the faster, but I would say one thing, Carolyn, the new algorithm doesn't mention ACE inhibitors or angiotensin receptor blockers as a monotherapy. Because I think those days are gone. I really do think that we shouldn't go through that cycle of starting a RAS blocker, uptitrating it, then switching to an ARNI because that's a waste of time. You're delaying the introduction of life-saving therapy. And this is the whole point to, again, get that sense of urgency across in implementing all of these treatments as quickly as possible. Dr. Milton Packer: And Carolyn, if you want to go faster, that would be fine. Maybe we shouldn't have proposed four drugs in four weeks. We should have proposed four drugs in four days. But Carolyn, I think that changing the way people think is a gradual process. Perhaps four drugs in four weeks is a good starting point. If everyone feels comfortable with that and understands why we are proposing that, then in another six months or so, Circulation can invite John and I to come back and propose four drugs in four days. But let's see what happens. Dr. Carolyn Lam: Kudos. Thank you so much. Well, thank you once again, John and Milton. That was an incredible discussion. A beautiful paper. Dr. Carolyn Lam: Thank you so much, listeners. I'm sure you enjoyed that as much as I have or probably more. But thank you and please don't forget to tune in again next week. From Greg and I, here's Circulation on the Run. Dr. Greg Hundley This program is copyright of the American Heart Association, 2021.  

A. Estratégia Low Carb para Controle e Gerenciamento da Diabetes Tipo 1 Diferença entre DM1 e DM2 Os trabalhos do Dr. Bernstein A Lei dos Pequenos Números Por que os médicos temem a restrição de carboidratos - A Cetoacidose. A Nota Técnica liberada pela SBD (http://bit.ly/2LxMwgh) SBD não recomenda Ultraprocessados, mas ainda se vale daquela máxima: de tudo um pouco, com moderação Live polarizada sem profissionais que usam a Low Carb na DM1 (https://bit.ly/34gWWYp) Se os estudos envolvendo Low Carb no DM1 são escassos, quais são os estudos que mostram que comer carboidratos e consertar a glicemia com insulina exógena é melhor para o paciente? O viés pró carboidratos. Nós nunca seremos superiores a um pâncreas! Ausência de Evidência não significa Evidência de Ausência O profissional deve seguir as diretrizes e guidelines de forma cega? B. Dieta Cetogênica e Diabetes Tipo 2 (https://bit.ly/37iu9EL, https://bit.ly/3qXk5Zu) Dieta Cetogênica é superior a Low Carb para DM2 (https://bit.ly/3gN9fR4) Perigo das CVD para o diabético (https://bit.ly/2K6yqlN) Picos de Glicemia são piores do que constância da glicose (https://bit.ly/3mlVSIE) LDL como preditor do risco cardiovascular Tipos de LDL: sdLDL e lbLDL O Fenótipo de Lipoproteínas Aterogênico: Triglicerídeos altos, Baixo HDL e maior número de sdLDL Efeitos da Dieta Cetogênica: Diminuição de peso, aumento do HDL-C, diminuição dos Triglicerídeos e melhora do perfil de LDL (de sdLDL para lbLDL) Sem progresso no CIMT Seriam esses efeitos dependente da perda de peso? Ou aconteceriam mesmo que o peso fosse mantido? Há estudos com intervenção cirúrgica (Bandagem ajustável do Estômago) onde o LDL melhorou, mesmo sem perda de peso significativa C. Nutrição Bizarra O que são óleos de Sementes? Qual a origem dos óleos de semente: Crisco e a substituição da manteiga A substituição da gordura saturada pela polinsaturada (https://bit.ly/2NcGr6z) Ácido Linoleico (Omega 6 altamente oxidável com subprodutos tóxicos) Nós não fabricamos e não temos tanta gordura polinsaturada em nosso corpo (https://bit.ly/3e7px4S) O excesso de ácidos graxos polinstaurados e as disfunções mitocondriais (https://bit.ly/37l5TC0) Os ácidos graxos polinsaturados e o câncer (https://bit.ly/3oUh8qG) Afirmação não científica: Qualquer toxina presente na banha de porco comum será menos tóxica a longo prazo do que óleo de girassol

¿Quieres mis libros? amazon.com/author/jccalderonn Certifícate con Nosotros como Entrenador de Liderazgo Visita: www.liderazgoELAI.org Síguenos: @LiderazgoELAI /// @HablemosDeLiderazgo #HablemosDeLiderazgo Quiero hablarte de algunas cosas profundas que he aprendido. Cosas que quizás no sean muy agradables y que seguramente cuando las leas no te sentirás muy bien, ya que no son de esas frases que motivan. Sin embargo, atrévete a leerlas. Quiero darte algunas ideas que, en momentos de preguntas claves, pueden ser la respuesta a muchas decisiones futuras y puedan hacerte arribar de forma certera hacia quién debes llegar a ser. Para tomar una decisión difícil es necesario tener cuatro elementos funcionales entrelazados los unos con los otros: ✅ Información. ✅ Carácter. ✅ Intimidad. ✅ Determinación. De esto es que te vamos a hablar en este nuevo episodio de #HablemosDeLiderazgo donde tendremos como invitado a @jccalderonn quién es Presidente y CEO de ELAI Leadership International Academy. TEMA: ¿Cómo tomar decisiones difíciles?

Certifícate con Nosotros como Entrenador de Liderazgo  Visita: www.liderazgoELAI.org  Síguenos: @LiderazgoELAI /// @HablemosDeLiderazgo  #HablemosDeLiderazgo Durante muchos años he visto a personas con un deseo ardiente por ser llamados líderes, pero esta responsabilidad va más allá de llevar dicho título. Ser líder realmente amerita una serie de responsabilidades que sí no te preparas para enfrentar puedes morir en el intento de desarrollar tu liderazgo. Quiero que juntos podamos desglosar el panorama completo de lo que debes enfrentar como líder y a su vez compartir contigo 3 pasos que te ayudarán a ¿Cómo sobrevivir en el liderazgo y no morir en el intento? . ✅ Confía en Dios creyendo que el presente y el futuro no serán determinados por tu pasado. ✅ Nuestros carácter siempre se antepondrá a nuestras emociones. ✅ Tú brújula y mapa serán claros siempre y cuando te mantengas conectado a tu fuente de sabiduría. . De esto es que te vamos a hablar en este nuevo episodio de #HablemosDeLiderazgo donde tendremos como invitada @nidiamilano quién es entrenadora y Directora comercial de nuestra escuela. . TEMA: ¿Cómo sobrevivir en el liderazgo y morir en el intento?

Abnormal blood lipids—such as alterations in total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), triglycerides (TG), and high-density lipoprotein-cholesterol (HDL-C)—are major risk factors for cardiovascular disease (CVD). Known collectively as dyslipidemia, these abnormal lipid fractions have a prevalence of 38.6% among individuals aged 40 and above—with alterations of one out of five US children and adolescents aged 8 to17 years—according to research—Ubiquinol (CO Enzyme Q10) Ameliorates Endothelial Dysfunction in Subjects with Mild-to-Moderate Dyslipidemia: A Randomized Clinical Trial, which appeared in the August 2020 issue of the journal Nutrients.The endothelium is the largest organ in the body—composed of a layer of cells that lies between the wall of blood vessels and the bloodstream. It is a living shield that keeps the arteries clear of build-up and blockage, so that essential oxygen and nutrients can get to the vital organs of the body.In addition, endothelial cells are involved in many aspects of vascular structure—acting as a barrier between the vessel lumen and surrounding tissue, while controlling the passage of materials and the transit of white blood cells into and out of the bloodstream.The authors of the Nutrients study from South Africa and Italy state that, "The impairment of endothelial function (EF) predates the morphological changes of atherosclerosis and can mechanistically contribute to atherosclerosis-related diseases."Endothelial function can be assessed by flow mediated dilation (FMD), which, "assumes that endothelial dysfunction (ED) is a systemic process involving the coronary arteries, as well as, the peripheral circulation."Using ultrasound technology, FMD estimates, "the dilation of a large peripheral conduit artery, typically the brachial artery, in response to the increased blood flow resulting from the removal of a transient ischemic stimulus." FMD has proved effective in evaluating the impact of several interventions on ED.The researchers point out that coenzyme Q10 (CoQ10)—especially in its reduced form known as ubiquinol—"has improved endothelium-dependent vasodilation, as measured by FMD, in patients with type 2 diabetes, or coronary artery disease (CAD). However, the evidence of its effect on ED in subjects without clinical manifestations of atherosclerosis-related disease is limited."Mayoclinic.org states that CoQ10, "is an antioxidant that your body produces naturally. Your cells use CoQ10 for growth and maintenance. Levels of CoQ10 in your body decrease as you age. CoQ10 levels have also been found to be lower in people with certain conditions, such as heart disease."CoQ10 is found in meat, fish and whole grains. The amount of CoQ10 found in these dietary sources, according to Mayo, isn't enough to significantly increase CoQ10 levels in your body.The Nutrient study authors sought to determine whether an 8-week ubiquinol supplementation period enhanced endothelium-dependent vasodilation in adults with moderate, untreated dyslipidemia and without evidence of CVD. The researchers recruited fifty-one subjects with low-density lipoprotein (LDL) cholesterol levels of 130-200 mg/dL, who were not taking statins or other lipid lowering treatments—with moderate (2.5%–6.0%) endothelial dysfunction, as measured by flow-mediated dilation (FMD) of the brachial artery, and no clinical signs of cardiovascular disease. During the study period, the participants were randomized to receive either ubiquinol (200 or 100 mg/day) or a placebo. The primary objective was to determine the effect of the ubiquinol supplementation on FMD by the end of the study period.Read the rest at Mackieshilstone.com

Dyslipidemia, the characteristic change of one or more blood lipid (fat) components – including total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), triglycerides (Trig), and high-density lipoprotein cholesterol (HDL-C) – is an established risk factor for cardiovascular disease (CVD).According to Italian research – Ubiquinol (co-enzyme Q-10) Ameliorates Endothelial Dysfunction in Subjects with Mild-to-Moderate Dyslipidemia: A Randomized Clinical Trail —dyslipidemia, “has a prevalence of 38.6% among individuals aged 40 years and above, and the alteration of TC, HDL-C, or non-HDL-C has been reported in one out of five US children and adolescents aged 8–17 years.”Stanfordhealthcare.org says, “endothelial dysfunction is a type of non-obstructive coronary artery disease (CAD) in which there are no heart artery blockages, but the large blood vessels on the heart’s surface constrict (narrow) instead of dilating (opening).”This condition, comments Stanford, “tends to affect more women than men and causes chronic chest pain. Because most clinics do not diagnose or treat endothelial dysfunction, people with this condition may feel frustrated and hopeless.”The vascular endothelium is critical in maintaining vascular balance – capable of sensing alterations in vessel walls and releasing a variety of autocrine (a substance secreted by a cell on its surface structure) and paracrine (stimulate cell regeneration) substances to protect the cell wall integrity.COQ-10 and its bioactive form ubiquinol, exert antioxidant protection by preventing the oxidation of LDL-C, while also improving endothelium-dependent vasodilation (opening). “CoQ10 has improved endothelium-dependent vasodilation, as measured by FMD (flow mediated dilation), in patients with type 2 diabetes, or coronary artery disease,” notes the study authors.The Italian researchers sought to determine, if an 8-week ubiquinol supplementation period enhances endothelium-dependent vasodilation in adults with moderate, untreated dyslipidemia and without evidence of CVD. The primary study outcome was to measure the effect of COQ-10 (ubiquinol) on FMD of an artery, when blood flow increases or not in that artery. A secondary outcome included the assessment FMD and changes in COQ-10 status at weeks 4 and 8 – along with changes in vasodilators nitrite and nitrate levels, and LDL-C oxidation at week 8. The Italian’s study participants included fifty-one subjects with low-density lipoprotein (LDL) cholesterol levels of 130–200 mg/dL, not taking statins or other lipid lowering treatments, moderate (2.5%–6.0%) endothelial dysfunction, as measured by FMD of the brachial artery, and no clinical signs of cardiovascular disease, who were randomized to receive either ubiquinol (200 or 100 mg/day) or placebo for 8 weeks. At the study completion, it was determined that, “ubiquinol significantly ameliorated (make more acceptable) dyslipidemia-related endothelial dysfunction. This effect was strongly related to increased nitric oxide bioavailability and was partly mediated by enhanced LDL antioxidant protection.”The take-away message is clear that COQ-10 is another option, with medical supervision, in the non-pharmaceutical tool kit to help address, along with diet and exercise, the negative health effects of dyslipidemia.Sign up for Mackie Mail, on mackieshilstone.com - my free, weekly wellness update with Fitness in Small Spaces 90-second videos on Monday, my Maximum Wellness podcast and script on Wednesday, and, on Friday, you’ll receive my WWL/WUPL TV 3-minute Workout Wednesday segment. You can also contact spencer@mackienutrition.com should you desire nutrition product to be shipped or locally delivered to your door. My 4 locally operated GNC franchise stores are open, regularly sanitized – with appropri

Al hacernos una analítica, el colesterol es el valor al que solemos prestar más atención, y también el que causa más confusión. Por un lado, algunos médicos se alarman si ven un colesterol por encima de 200 mg/dl, recomendando estatinas sin explorar nada más. Otros colectivos, por el contrario, asumen que el colesterol no tiene relación con el riesgo coronario. La realidad, una vez más, está en un punto intermedio. En el artículo de hoy entenderás lo siguiente: Diferencia entre colesterol, lipoproteínas y apolipoproteínas. Cómo se inicia realmente la aterosclerosis. Por qué el LDL que estiman las analíticas es un dato poco fiable en muchos casos. Qué valores son realmente más importantes y qué tipo de análisis realizar. De qué otros factores depende la enfermedad coronaria más allá del LDL. Colesterol, Lipoproteínas y Apolipoproteínas El colesterol es una molécula fundamental para la vida. Forma parte de las membranas celulares, participa en la producción de bilis y es precursor de las hormonas sexuales. Es clave también en la síntesis de vitamina D y en las vainas de mielina que recubren los axones neuronales. En resumen, sin colesterol no hay vida. Por suerte, las células son capaces de producir la mayoría del colesterol que necesitan, y cuentan además con el colesterol que reciben desde el hígado, bien producido por él mismo o absorbido a partir de los alimentos. Al ser una molécula hidrófobica (no se lleva bien con el agua), no puede viajar libremente por nuestro torrente sanguíneo, y debe unirse a unas partículas especiales, llamadas lipoproteínas. Como su nombre indica, estas lipoproteínas se componen de lípidos y proteínas. Dentro de su carga lipídica pueden transportar tanto colesterol como triglicéridos, todo unido por una membrana de fosfolípidos. La parte proteica se denomina apolipoproteína, y en breve entenderás su importancia a la hora de estimar tu riesgo cardiovascular. Ejemplo de Lipoproteína, con su carga lipídica (colesterol y triglicéridos) y su Apolipoproteína Las lipoproteínas HDL y LDL son las más conocidas, pero no son las únicas. Por ejemplo, el hígado genera inicialmente lipoproteínas VLDL (Very Low Density Lipoprotein), que van reduciendo de tamaño a medida que liberan su carga, convirtiéndose primero en IDL (Intermediate Density Lipoprotein) y finalmente en LDL (Low Density Lipoprotein). No todas las VLDL e IDL se convierten finalmente en LDL, muchas son captadas por receptores de LDL en el hígado y son recicladas. ¿A qué se refiere la densidad? Al ratio proteína/grasa. A medida que las lipoproteínas vacían su carga de triglicéridos y colesterol este ratio aumenta (misma proteína pero menos lípido). La lipoproteína HDL es la de mayor densidad (mayor ratio proteína/grasa), de ahí su nombre: High Density Lipoprotein. Su papel en la enfermedad cardiovascular es secundario, por lo que hoy no hablaré mucho de ella. Densidad y Diámetro de las principales Lipoproteínas Y el último concepto importante. La parte de proteína de cada una de estas partículas se denomina apolipoproteína, y simplificando existen dos tipos: ApoA: presente principalmente en las partículas HDL. ApoB: presente en las partículas VLDL, IDL y LDL. Lipoproteínas, Colesterol y Analíticas Como analogía, podríamos decir que las lipoproteínas son camiones y el colesterol (y los triglicéridos) la carga que transportan. Partícula LDL cargando colesterol y triglicéridos Las analíticas tradicionales no dan información sobre el número de lipoproteínas (camiones), sino simplemente sobre la carga total que transportan. Estos son los valores que se miden realmente: Colesterol total: Carga total de colesterol que transportan todas tus lipoproteínas. Su correlación con el riesgo cardiovascular es bastante baja (más detalle). HDL: Colesterol total que transportan tus lipoproteínas o partículas HDL. Se suele denominar a este valor HDL-C.

Dave Feldman is a software engineer and runs the Cholesterol Code website. In 2015 Dave adopted a low-carb high-fat diet, which improved his overall health. However, upon seeing his LDL-cholesterol skyrocket, he set out learn all he could about blood lipids and health. Dave has gained prominence as a “LDL-skeptic” and promoter of his “lipid triad” hypothesis. This lipid triad relates to a situation where one sees high LDL-C, high HDL-C and low triglycerides. Dave hypothesises that in such a context, the high LDL-C does not confer high risk of cardiovascular disease. This is counter to the current consensus position of the lipid hypothesis, where LDL plays a causal role in atherosclerosis development. Alan Flanagan is the Research Communication Officer here at Sigma Nutrition. Alan is currently pursuing his PhD in nutrition at the University of Surrey, UK, with a research focus in chrononutrition. Alan previuosly completed a Masters in Nutritional Medicine at the same institution. SHOW NOTES: https://sigmanutrition.com/episode321

Just like sugar and fat, cholesterol has really been trashed over the years and given such a negative connotation. What many of us are not aware of is that behind this negative halo and tremendous marketing effort by the food industry (i.e. food products that are low in cholesterol, food product that “sucks/absorbs” cholesterol) is more recent evidence. The current evidence shows that cholesterol from food is not associated with all the diseases we thought it was. In fact, cholesterol is a big part of being human- we simply need cholesterol to survive. In this episode, I talk about cholesterol and its association with HDL-C, LDL-C, and triglycerides in a fun way, using taxis (yes, I mean cabs) as an analogy. I also highlight what is more important in the food we consume- hint: it is not cholesterol!Connect with meInstagram: @celynngEmail: celyn.ng@gmail.comTowards a Greater Life websiteMusic from https://filmmusic.io"Carefree" by Kevin MacLeod (https://incomptech.com)License: CC BY (http://creativecommons.org/licenses/by/4.0/)

Metabolic Syndrome (MetS) - a cluster of conditions, such as increased abdominal obesity, pre-hypertension, dyslipidemia (triglycerides, HDL cholesterol), and pre-diabetes - predisposes that individual, who meets the criteria, to diabetes, cardiovascular disease, and even potentially to certain forms of cancer. It’s now a public health concern world-wide.According to research – Dietary Patterns and Metabolic Syndrome in Adult Subjects: A Systematic Review and Meta-Analysis – which appears in the September 2019 online journal Nutrients, “the diagnosis of MetS requires three or more of the following criteria: (i) waist circumference >102 cm in men (40 inches) and >88 cm in women (35 inches); (ii) HDL-C

Dr Carolyn Lam: Welcome to Circulation on the Run, your weekly podcast summary and backstage pass to the journal and its editors. I'm Dr Carolyn Lam, associate editor from the National Heart Center and Duke National University of Singapore. Dr Greg Hundley: And this is Dr Greg Hundley from VCU health, the Poly Heart Center in Richmond, Virginia. Well, Carolyn, this week's feature analyzed a pool cohort of all patients in partner one and partner two, both the trials and registries. Patients had severe aortic stenosis and were treated with TAVR or SAVR and then were analyzed with respect to the development of prosthetic valve endocarditis. But more to come on that later. Dr Carolyn Lam: Let me start by telling you about my picks from this week's journal. So the first one is a really interesting natural experiment. First, do you think that a short term visit to a location with severe air pollution increases the risk of cardiovascular disease? Dr Greg Hundley: Well, Carolyn, I would say yes. Dr Carolyn Lam: Greg, you're too smart. But let me tell you what these investigators did. So their co-corresponding authors, Dr Araujo from David Geffen School of Medicine and UCLA, Dr Zhu from UCLA Fielding School of Public Health, and Dr Qiu from College of Environmental Sciences and Engineering in Peking University. These co-corresponding authors and their colleagues did a natural experiment by collecting urine and blood samples from 26 healthy adult residents of Los Angeles before, during, and after they spent 10 weeks in Beijing during the summer of 2014 and 2015. Dr Greg Hundley: I am really excited to hear this. Carolyn, what did they find? Dr Carolyn Lam: So traveling from less polluted Los Angeles to more polluted Beijing induced pro oxidative and pro inflammatory effects, which reversed after returning to Los Angeles. This is also the first human study associating exposures to polycyclic aromatic hydrocarbons with changes in paraoxonase 1, enzymatic activity, and circulating levels of hydroxyeicosatetraenoic and hydroxyoctadecadienoic acids. Cool, huh? Dr Greg Hundley: Absolutely. Carolyn, you did an awesome job. Very nice. Well, my article comes from the world of basic science and it's from Dr Philip Shaul at the University of Texas Southwestern medical Center. So Carolyn, in recent studies of obesity induced insulin resistance in mice with corroborating findings in human type 2 diabetics, this group, Shaul’s group, previously made the surprising discovery that the insulin resistance is driven by an altered post-translational modification in IgG that leads to enhanced activation of FCYR2B in endothelial cells. And as a result, there is an attenuation of insulin transcytosis across endothelial cells and delivery to skeletal muscle myocytes where up to 80% of glucose disposal usually occurs. Dr Carolyn Lam: Oh. Interesting, Greg. So what did the authors find in the study and how did these findings equate with obesity and hypertension? Dr Greg Hundley: Well, they found that hyposialyation of the Fc glycan on IgG is identified as a key contributing factor in obesity induced hypertension. And therefore low levels of IgG Fc glycan sialylation may identify individuals at greater risk of developing hypertension. In addition, the degree of sialylation of IgG may predict the relative response of an individual to any hypertensive therapy. Dr Carolyn Lam: Nice. So my next paper is from Dr Al-Lamee from Imperial College, London, and colleagues who studied the ability of a pre-randomization stress echocardiographic score to predict the placebo-controlled efficacy of PCI within the ORBITA trial. Now as a reminder, the primary results of the ORBITA trial showed us smaller than expected effect size of PCI in comparison with placebo in single vessel stable coronary artery disease on the primary end point of change in treadmill exercise time. Now in the current study, 183 patients underwent dobutamine stress echo cardiography before randomization, and they found that the degree of ischemia assessed by dobutamine stress echo cardiography predicted the placebo-controlled efficacy of PCI on patient reported angina frequency. Dr Greg Hundley: Hmm. Very interesting. So help me out again, Carolyn. What's the clinical importance of this? Dr Carolyn Lam: Ah, so this study really provides the first placebo-controlled evidence of an association between stress echo cardiography, ischemia, and the magnitude of placebo-controlled benefit attributable to PCI. And the greater the downstream stress echo cardiography abnormality caused by the stenosis, the greater the reduction in symptoms from PCI. That's the take home. Dr Greg Hundley: Oh wow. Very interesting. You know, especially we perform so many stress echo cardiograms. What a great relationship to unfold and present. Well, Carolyn, I'm going to walk through several other important publications in this issue of the journal. The first is from Dr Peter Eckman from the Minneapolis Heart Institute, and he provides an In-Depth review of veno-arterial extra corporal membrane oxygenation, or VA-ECMO, for cardiogenic shock and it's beautifully written for the busy clinician. Robert Platt, PhD, and colleagues discuss in an On My Mind piece the fact that those with adverse cardiovascular sequelae during pregnancy may require development of new cardiovascular risk prediction models. The hypertension or the diabetes that occurs during pregnancy, perhaps we need to incorporate that into our prediction models. Next. Our own associate editor Torbjørn Omland provides results in a research letter from the peace trial relating the relationship between smoking and high sensitivity troponin T levels. Dr Allen Sniderman from McGill University Health Center writes a letter to Welsh and Associates regarding their study of the UK bio bank database and measures of HDLC. A paper we discussed just a few weeks ago. Dr Derek Chew from the DCRI and Durham North Carolina has another EKG challenge for us. And Dr Tracy Hampton provides an updated news report regarding cardiovascular disease from several recently published articles in the world of basic science. And then finally Dr Thomas Krieg from the University of Cambridge has a nice piece regarding clinical implications of targeting succinate metabolism in ischemia reperfusion injury. Well, Carolyn, what a great slate, but I can't wait to get to that feature discussion related to prosthetic valve endocarditis. Dr Carolyn Lam: Me too. Let's go. Our feature discussion today is really the first paper that describes adjudicated evaluation of prosthetic valve endocarditis in patients with transcatheter and surgical aortic valve replacement. Very unique and valuable data from the partner's trial. I'm so pleased to have with us the corresponding author, Dr Wael Jaber from Cleveland Clinic as well as our associate editor, Dr Manos Brilakis from UT Southwestern. So Wael, very unique question. Could you please tell us how you went about doing this? And I suppose in this setting, the first question on everyone's mind is how did you make this diagnosis of prosthetic valve endocarditis? Dr Wael Jaber: Actually we saw this as an opportunity that probably we should never miss. I think this is one of the rarer instances where we can objectively not only look at SAVR data but also TAVR data. And over the past maybe seven years, eight years, we started getting here as a referral center patients with TAVR endocarditis for surgery. And we never thought we'd start seeing these weird organisms, different bugs. Of course this is a population that's frail or elderly, but we never had any idea if they behave similarly to SAVR or differently than SAVR in our previous experience with SAVR endocarditis. So we planned this actually about maybe five years ago, but we didn't have the data because you know the partner trials were undergoing another evolution by going to lower and lower risk population. So we pose this question about a year and a half ago to CRS by asking them, can you provide us with the data on all the endocarditis in partner. The idea was not only to answer one question but to answer multiple questions. So the first question was in the modern era, what happens in SAVR? All the SAVR endocarditis information we have so far as you will know has been from mainly single center studies or even when we learn about it from multiple centers sites, usually IN European studies, the Swedish registry, the Danish registry, and these are usually limited by the fact that there are a multicenter. The adjudication is at the site what endocarditis happened. So that was the first question. Then the second issue for us was, does TAVR, because of the unusual access to the heart and the fact that we dilate the valve, post dilate the valve, their paravalvular AI, they could be micro-fractures of the refis. This is provide a different opportunity for these bugs to form on the valve, and do they behave differently? And the third question was, is there any difference between SAVR and TAVR incidence of endocarditis? And bugs. And the final question was what happens to patients when they develop endocarditis in the current decade. Do they do well? Especially for septic endocarditis or do they succumb to their illness? And also this is how we came up with a strategy to answer all these questions. Dr Carolyn Lam: Very nice. So Wael, could you just expand a little bit more about how the diagnosis or adjudication of prosthetic valve endocarditis was done? And then tell us please, what did you find? Dr Wael Jaber: All the partner patients, the records were sent to a central place. So the ECHOS first were educated at central places. We were one of those centers. Other places were Columbia University, MedStar and Quebec, the group in Quebec. So all the ECHOS were adjudicated centrally. So that's first, as far as from the echo side of calling it endocarditis or not. On the clinical side, again, all the records and the forms were sent to a central adjudication committee, CDC group. We served at the Cleveland Clinic as the CDC for most of these trials and actually even for the current trials. So they were sent and they were adjudicated according to the Duke criteria. Which is, you know, the most, probably, reliable way still today to adjudicate these. And then there was the CDC and the echo core labs were separate. So the people who have information from the CDC did not have access to what's going on in the core lab and vice versa. So these were independently adjudicated as far as echocardiographic evidence and clinical evidence. And then they were fed into it. So by the end, when you hold it on a Duke criteria endocarditis, the echo was fed after the fact, not before. So this is in general how it happened. So all the events were educated centrally, not at the site. And the ECHOS, the same thing, were adjudicated centrally. Dr Carolyn Lam: Fantastic. And I would love to hear the results. Dr Wael Jaber: The first question was, what's the incidence of endocarditis? And we decided because of the way these trials were done, to report the incidents as you would see in the results section, to report the incidents of endocarditis per 1000 person year because of the imbalances in follow up and the competing risk for death from other reasons. So we found in general that the incidents of endocarditis was 5.2 endocarditis events per 1000 patients per year in the TAVR side and 4.1 in the SAVR side with a non statistically significant difference. More importantly, we found out that once you develop endocarditis, unfortunately most of these patients succumb to the illness and are dead after the diagnosis. So the risk of dying after developing endocarditis is 4.4 times higher than patients who did not have endocarditis in the trials. In all the trials. Now there's some caveats here. First, these are trials with different patient populations, as you well know. Starting with partner with the inoperable patients moving on to the most modern S3 trial, which was on the lowest kind of side of population. So we have totally different population groups. Some of them had prolonged hospitalizations before and after, so this should be taken with a little bit of caution. However, if you look at some of the individual trial data, we found that incidents of endocarditis at least have a trend towards a reduction of incidence of endocarditis over time going from partner, the initial experience with partner, all the way to the modern era. Dr Carolyn Lam: That is so great. Manos, you know, as an interventional cardiologist yourself, could you tell us how important these results are? Does it affect your practice? Dr Emmanouil Brilakis: Thanks again, Carolyn. I would like to congratulate Wael for a phenomenal paper. I think it's a very timely study and addresses one of the common concerns there is about whether TAVR does predispose people to more risk for endocarditis. Although again, the opposite grade was kind of low at 0.5% a year. I think this may be a little more than people are commonly seeing in the setting of TAVR, and I think the paper is a good reminder that this is something we should always be mindful and watching. Although typically we'll discuss with the patient about the risk of stroke or access complications, but the risk of infection may not be as well emphasized. And based on this one question I would have is about what can we do if there is something that could potentially lower that risk? I understand the limitations of retrospective study, but are there any recommendations that you have based on the study? Should give more aggressive antimicrobial therapy? Any other biotic prophylaxis or anything else that can be done to reduce the risk of endocarditis in those patients? Dr Wael Jaber: Actually this is the question we raised. Unfortunately we did not. So the guidelines did not catch up with what we know. So if you look right now, like I was reviewing this paper that came up last month from the Swedish Registry for Endocarditis, it came out in Europe in the European Heart Journal, and one of the questions they raised is how to address, in the editorial, how to address the risk of endocarditis and prophylaxis in this population. There are no standards for that. This is one aspect of it. We need first an update of the guidelines of how to address this issue. The second question is we do not have any idea, unfortunately, about duration of antibiotics. How the antibiotics prophylaxis were given before the procedure, like as we do right now commonly in surgery, and after the procedure in these patients. We do not know that. Like right now, at least at our center, if you go in for aortic or mitral valve surgery or any valve surgery, you have to have a dental clearance before you start, before you go to surgery. I don't know if this was rigorously applied in the setting of TAVR, and I think it would be a good idea to apply it to make sure that there are no dental, phosphide or potential infections and things like that. So I think it's a multi-front battle to get these patients to the lowest risk possible. I don't think there's one single silver bullet here. Dr Emmanouil Brilakis: So thanks again, Wael for addressing this. I agree that there's a lot of information to be gained understanding the intricacies of endocarditis prophylaxis. And building on this, let's say another patient develops endocarditis as you've shown in your 170 patients in the study. It was fascinating that staph aureus was actually less common than it was for surgical valves, which has been shown in other studies as well. So you think this affects the choice of the biotic prophylaxis? And then also if the patient develops endocarditis, I understand many people who are not candidates for surgery, but from the ones who did actually undergo surgery, what are the outcomes encouraging? Dr Wael Jaber: This is a fascinating question actually. This is one of the reasons we had... There was a delay for us in getting the paper out from when we presented it as an abstract at TCT a year and a half ago, is we didn't know. We wanted to answer that question. The second part of the question is how many patients went to surgery? And unfortunately, very few patients. So less than a handful of patients end up going to surgery. And we do not know why. So this is the dilemma here. Is why the rate of referral to surgery for redo surgery was very low. Was it because these patients were the sickest of the sick? Maybe it is because we waited too long and we did not treat them the same way. We should have treated prosthetic valve endocarditis, which is surgery to be offered as soon as possible because there's no really antibiotic cure for that. So we do not have the answer for that because these very few patients went to surgery and actually I think of those who went to surgery, even the mortality there even was similar to people who did not go to surgery. But we cannot speculate on that because the very few patients. As far as the bug involved, I think this could be a reflection of the antibiotics given at the time of the procedure, so probably we're covering that very well. But if you notice from the paper, most of the infections happen more than 30 days after the procedure. Whether this is something that was acquired because these patients are more likely to end up in the hospital again for other reasons, whether these patients had endocarditis because they have more instrumentation down the road... Remember this is a population in general above the age of 65 which would require colonoscopies, frequent urinary tract issues, and other procedures. So we know that we're covering very well, at least I can speculate, we're covering very well for the first 30 days because very few patients had endocarditis right after the procedure, but we're not covering probably after the 30 days. And that remains to be studied. And the worrisome thing is to try to treat these patients with prophylactic antibiotics for a long time and then end up with bug resistance and things like that. Now the CDC issued a big warning about this yesterday. I am not comfortable to speculate from this small number of patients on how to treat for prophylaxis, but I'm comfortable to say probably patients should be sent to surgery as soon as possible after developing endocarditis, especially prosthetic valve endocarditis because the outcomes are dismal. Dr Emmanouil Brilakis: And do you think... Let's say patient is not a candidate for surgery and gets endocarditis, and I presume they get into prolonged therapy. There were some patients like this that did okay, right? So there is some hope even for those patients. Dr Wael Jaber: I feel like I'm the cup half full here because if you look at the mortality curves here, we're talking about north of 95% death in this population. So the people who survive this must be very few people survive. So probably about seven patients who survive. So the mortality was 96% at six months versus 46%. So there are very few people who survived that event. Maybe I should go back now and figure out what was the quality of life after survival. So I don't think the picture we have right now is very rosy as far as the way we're managing endocarditis. Dr Carolyn Lam: Manos, I'm going to give you the final parting words from this very interesting discussion. I mean what do you think are the take home messages and future directions from here? Dr Emmanouil Brilakis: I agree that this is a phenomenal landmark study and my key takeaways are the same ones that Dr Jaber presented before. But the main thing is, on the consent process, who can tell the patients there is about 0.5% per year. So it's not zero, but it's very high either. The second thing is that this choice between TAVR versus SAVR, that should not have to do with the risk of infection because as it was shown very convincingly, it was very similar to the two groups. And number three that everything possible should be done to prevent this because if you do get infection, the outcomes are not very good. Dr Carolyn Lam: Thank you so much Manos, Wael. Thank you so much audience for joining us today. You've been listening to Circulation on the Run. Tune in again next week. This program is copyright American Heart Association 2019.  

Dr Carolyn Lam:                Welcome to Circulation On The Run, your weekly podcast summary and backstage pass to the journal and it's editors. I'm Dr Carolyn Lam, associate editor from the National Heart Center and Duke National University of Singapore. Dr Greg Hundley:             And I'm Greg Hundley, associate editor from the Pauley Heart Center in Richmond, Virginia at VCU Health.                                                 Well, Carolyn, we've got a great feature article to discuss later in our interview today. We're going to compare surgical versus percutaneous aortic valve replacement, but now with coronary artery revascularization. So, very exciting results from the SURTAVI trial.                                                 So, Carolyn, do you have a couple papers to discuss? Dr Carolyn Lam:                For sure. Actually, it's exactly a couple, and it's a couple of GWAS papers. The first is a GWAS of the cardiac magnetic resonance imaging derived left ventricular phenotypes of the UK bio bank. It comprises almost 17,000 European-UK bio bank participants without prevalent myocardial infarction or heart failure. So this was led by professors Petersen and Monroe from Queen Mary University of London, and colleagues who found that prognostically important left ventricular imaging phenotypes were highly heritable, with a heritability of 22 to 39%. A total of 14 genetic susceptibility low PSI, eight of which were unique, enriched in the cardiac developmental pathways and regulation of contractile mechanisms were discovered, and the polygenic risk scores of left ventricular phenotypes were predictive of heart failure events independently of clinical risk. Dr Greg Hundley:             Well, Carolyn, knowing me and MRI, something I really am interested in. So tell us a little about what are the clinical implications? Dr Carolyn Lam:                Well, the findings not only enhance our understanding of the genetic basis of prognostically important left ventricular phenotypes in the general population, but they also underscore the intricate genetic relationship between these endo phenotypes and the pathogenesis of heart failure. The prioritized genes in the genome whites significant load size should be followed up in the functional studies to aid the development of potential novel therapies in future. The polygenic risk scores of left ventricular phenotypes may have a role in personalized risk stratification. But this, of course, is dependent on further validation of the clinical robustness in future studies.                                                 I want to skip onto my second GWAS paper, and this time dealing with bicuspid aortic valve. So, first a little reminder that bicuspid aortic valve disease is a congenital defect that affects 0.5 to 1.2% of the population, and is associated with comorbidities including ascending aortic dilatation and calcific aortic stenosis. To date, while a few causal genes have been identified, the genetic basis for the vast majority of bicuspid aortic valve cases remains unknown. Today's paper from Dr Lipschultz from Medical University of South Carolina reports novel human genetic based models, which developed bicuspid aortic valve and aortic stenosis with high penetrance. Dr Greg Hundley:             Very interesting. So, how did the authors do this, Carolyn? Dr Carolyn Lam:                Yeah, it is interesting. What they did is they performed a GWAS and replication study using cohorts of more than 2,000 patients with bicuspid aortic valve and more than 2,700 controls, which identified the primary Celia genes as associated with the bicuspid aortic valve phenotype. Specifically the most associated snips were identified in or near genes that are important in regulating Ciliogenesis through the exocyst, which is a shuttling complex that chaperone Celia cargo to the membrane. Genetic dismantling of this exocyst resulted in impaired Ciliogenesis through the XO CIS, disrupted Ciliogenic signaling, and resulted in a spectrum of cardiac defects in zebra fish and aortic valve defects including bicuspid aortic valve, valve stenosis, and Velveeta calcification in murine models as well. So this data really supports that the exocyst is required for normal Ciliogenesis during aortic valve morphogenesis and really implicates the disruption of Ciliogenesis, and its downstream pathways may contribute to bicuspid aortic valve and its associated comorbidities. Dr Greg Hundley:             Wow. Very interesting. Learning more and more about bicuspid valves through our journal. I'm going to shift Carolyn and talk about an article from Dr Marc Sabatine from the TIMI study group at Brigham and Women's hospital. This study performed a systematic review and a trial level meta regression analysis of three classes of lipid lowering therapies that reduce triglycerides to a greater extent than they do LDLC. Fibrates, Niacin, and Marine derived Omega-three fatty acids and key inclusion criteria were a randomized, controlled trial that reported on major vascular events. The study also incorporated data from a previous Meta-regression of 25 Statin trials, and the main outcome measure was the risk ratio for major, vascular events associated with absolute reductions in lipid parameters. Dr Carolyn Lam:                Oh, very interesting. So did the study show that it was beneficial to lower triglycerides or not? Dr Greg Hundley:             Let me tell you a little more about it. The study encompass 374,358 patients that sustained 46,180 major cardiovascular events, and in their multi-variable Meta-regression model, that included terms for both LDLC and triglyceride surrogates for LDL and VLDL. The risk ratio was 0.8 per one millimole per liter reduction in LDLC, and 0.84 per one millimole liter reduction in triglycerides. Therefore, a reduction in non-HDLC, a measure of atherogenic LDL and VLDL particles, is strongly associated with lower risk of major vascular events regardless of the lipid lowering drug class, and triglyceride lowering is associated with a lower risk of cardiovascular events, but to a lesser extent per absolute amount of reduction then with LDLC. Interesting, Carolyn one study reduce it and impacted the study results, and nearly all non-statin trials did not achieve significant non-HDLC lowering to detect a clinical difference in major vascular events. Now how about in regards to Omega- three dose?                                                 Well, each one gram per day of EPA administered was associated with a 7% relative risk reduction in major vascular events, whereas there was no significant reduction in major vascular events with DHA. So the benefits of Marine-derived Omega-three fatty acids, particularly high dose EPA, appear to exceed their lipid lowering effects. Dr Carolyn Lam:                Wow. Interesting. So Greg, take it home for us. What should we do clinically about this information? Dr Greg Hundley:             Carolyn, developing drugs that achieve large reductions in VLDL and triglycerides and are targeting patients with high baseline levels of triglycerides would likely increase the probability of showing a meaningful clinical benefit, and fibrates could be considered in patients needing further non-HDLC lowering, being mindful of side effects, as they should offer clinical benefit proportional to the degree of non-HDLC lowering, and if a disproportionate relationship between lipid lowering and cardiovascular risk reduction is validated in ongoing high dose Omega-three fatty acid trials, it will support the hypothesis that confers a unique benefit of this class of agents beyond simply their lipid lowering.                                                 How about that? Dr Carolyn Lam:                Very nice Greg and I think very balanced and good clinical take home messages. Tell us what else is in the mailbag. Dr Greg Hundley:             We have so many interesting articles in Circulation and let me just run through a quick list of those that are also in this issue. First, Dr Jere Mitchell, from UT Southwestern, reviews the 50th anniversary of the Dallas Bedrest Study that involve five 20-year-olds that underwent several weeks of bedrest, and he discusses how this informs many of our thoughts regarding the benefits of activity today, and one of his major coauthors is Dr Ben Levine. Our own Josh Beckman reviews the ongoing efforts of physicians to understand the role of paclitaxel coated stents for those undergoing peripheral arterial interventions. Dr Berlinde von Kemp, in our case series, identifies that not all cardiomyopathy, after delivery, is simply postpartum cardiomyopathy. In another article, Dr Anurag Agrawal discusses what's on their mind regarding the use of spirometry as a cardiovascular disease risk assessment tool, should it be incorporated into existing cardiovascular disease risk models.                                                 Then, we have a great letter back and forth discussion from Dr Junfeng Wang, Dr Daxin Wang, and our own Naveed Sattar in three separate letters that discussed the relevance of age of onset for type two diabetes relative to cardiovascular risk. Then, finally our own Carolyn Lam reviews the role of biomarkers in heart failure and preserved ejection fraction. Dr Carolyn Lam:                Let's hop on to our feature discussion, shall we? Dr Greg Hundley:             Absolutely. Dr Greg Hundley:             Welcome everyone to the discussion of our featured article today where we're going to review an excellent study comparing TAVR versus SAVR in patients with aortic stenosis, but also now considering simultaneous coronary artery revascularization. Discussing our article today we have Dr Thomas Engstrøm and then our own associate editor, Dharam Kumbhani. Well Thomas, welcome to our podcast featured article discussion. I wonder if you could start us off with a little background regarding your study. What were your hypotheses, and then tell us a little about your study population and your methods. Dr Thomas Engstrøm:     Now, as you know, up to 50% of patients that are treated for aortic stenosis have coronary artery disease, and this may be considered as a bystander disease to develop disease, but definitely also adds to the prognosis for the patients. A priority guideline recommends that if you do SAVR, you'll also have significant coronary artery disease. What we don't know is if the complete percutaneous approach is as good as a surgical approach. Maybe do TAVR plus PCI comply with fiber plus CABG. That's the background for the study.                                                 Now, the population involved in this study is the population from the search TAVR trial, which as you know compared TAVR to SAVR in patients that were clinically at intermediate risk and in patients that had severe aortic stenosis. If patient had additional coronary artery disease with a syntax called Bob 22, they were excluded from the trial. We are talking about intermediate risk patients with low syntax score. Of the patients in the TAVR trial, 20% had additional coronary artery disease and were resterilized. In the paper, we compare TAVR plus PCI versus SAVR plus CABG in those patients with significant coronary artery disease. Dr Greg Hundley:             How did you define the presence or absence of coronary disease? Just real quickly before we get to your results. Dr Thomas Engstrøm:     This was at the discretion of your operator to define where the patients had coronary artery disease or not. In the paper, patients were defined as having significant diseases. More than 70% of stenotic lesions were present in one or more coronary arteries. Dr Greg Hundley:             And so can you tell us, Thomas a little about the results of your study? Dr Thomas Engstrøm:     First of all, the patients that had additional coronary artery disease had a poor prognosis than those that only had valve substitution, which is probably not a surprise. Within those that also had coronary artery disease, TAVR plus PCI appeared to be as good as CABG plus SAVR in terms of the primary endpoint, which was all because mortality or disabling stroke after two years. Then, if you dive more deeply into the endpoint and the number of secondary endpoints were pre-specified, there were no differences regarding any stroke myocardial infraction and in total no differences between what you could call major heart end points. If you look more into detail of the secondary endpoint, there are subtle differences. Patients that were in the SAVR plus CABG had more atrial fibrillation as they also had more acute kidney injury following that treatment. Whereas, in the TAVR plus PCR, more patients had vascular complications and of course had the need for pacemaker implantation. There are differences between the outcome in the two groups, but not in regard of pre-specified primary and more important secondary endpoints. Dr Greg Hundley:             Dharam, I was wondering if you could help us think about what this means for the field in terms of both from aortic valve replacement, and then also the concomitant management of coronary disease in patients that require aortic valve replacement. Dr Dharam Kumbhani:   As Thomas just pointed out, I think this is a very important question. This comes up all the time in patients with severe aortic stenosis, being evaluated for best options, and the guidelines have stayed true to this that if somebody has concomitant coronary artery disease, then the guidelines typically would recommend SAVR as the first option because then they can have CABG at the same time. This study really seeks to address a very important knowledge gap in the field, and as he very well pointed out, this does restrict itself a little in terms of the population, because they couldn't have a high syntax score, actually an intermediate or high syntax score, and they need in the trial...I think the main syntax score was eight or nine. I think that is important, but having said that, more than 50% of the patients had multi-vessel disease, and it was really impressive that nearly 15 or 17% still had three vessel PCI even in this arm.                                                 I think it's important for people to recognize that although this was the lowest syntax score, multivessel PCI was still pursued. I think that's definitely an important takeaway from the strike. It's a really important trial. It's one of the very few pieces of information that we have that is prospectively done under the auspices of a big trial like SURTAVI, and with low risk approval in and what this means for patients going forward I think will be very exciting to see how this few devolves.                                                 Thomas, as this field matures, could you walk us through, in terms of did you do the valve first and then the coronaries, or where the coronaries worked on first and then the valve? That's sort of the first question. Can you walk us through how you make those decisions? Dr Thomas Engstrøm:     It was up to the discretion of the operator whether to do a concomitant procedure, both PCI and TAVR, or to state the procedures in that way that PCI was done first, and this could be done up to seven days before the TAVR. If you compare those two groups, and now numbers become a little bit few, so we can't be conclusive here. It appears that patients that had stage procedures did poorer than those that had concomitant procedures done. Of course, it raises some questions. The prioritization as to do it in one way or the other was that through concomitant procedure, you may introduce too much of stress to the patient. Otherwise, if you do a stage procedure, it's best to do the PCI first, because the actual appearance of the valve may make it more difficult and cumbersome to address the coronary arteries. To sum this up, in the patients that we have, it appeared that a concomitant procedure is safe. Dr Greg Hundley:             Dharam, tell us, what do you think is the next step forward for this field? What do see as the next study moving forward here? Dr Dharam Kumbhani:   I think this study really sets the stage for, I think future trials where perhaps we would have... So I'm doing this in this trial. The stratification was done based on whether or not they need to revascularization. I think going forward, again with LOTUS approval here and proliferation of the number of TAVR procedures that are being offered everywhere, I think it will be helpful. This study would set the stage for future studies, where I think you would prospectively have patients with needing an aortic valve replacement and perhaps even complex revascularization, and how that was kind of actually the randomization, which is the stratification strategy, which again was very helpful. These are really among the first few data that we have of this, but I think this kind of sets the stage for future investigations in this space. And then as I briefly alluded to, I think this may help evolve or this may help in the evolution on the guidelines as well.                                                 Thomas, would you like to add anything to that? Dr Thomas Engstrøm:     Yeah, I completely echo that. Going back to the old syntax trial, it would be very interesting to see if PCI holds through, even in high tunes, syntax scores with newer drug eluting stents, and also of course the question of the diabetics is totally unsolved in this cohort. CABG plus SAVR may turn out to be the best solution, but we still are waiting to see data that can support any of the two strategies in those patient cohorts. Dr Greg Hundley:             We want to thank Thomas Engstrøm and also our own Dharam Kumbhani. We look forward to seeing you next week. Dr Carolyn Lam:                This program is copyright American Heart Association, 2019.  

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 cohosts. I'm Dr Carolyn Lam, associate editor from the National Heart Center and Duke National University of Singapore. Dr Greg Hundley:             And I'm Greg Hundley, associate editor from the Poly Heart Center at VCU health in Richmond, Virginia. Carolyn, oh, this is going to be an exciting featured article today, and we're going to discuss the combination of agents or their administration et al that are best suited for managing both anticoagulation and antiplatelet therapy and those with coronary disease, peripheral arterial disease and heart failure. And, we'll speak with Dr Kelley Branch from the University of Washington. Dr Carolyn Lam:                And me! Dr Greg Hundley:             Yes. How am I going to interview you? And, we'll discuss the utility of Rivaroxaban with or without aspirin in patients with heart failure or peripheral arterial disease from the compass trial. Dr Carolyn Lam:                Well, I'm not going to let you get there until I tell you about this first basic paper I've chosen because it focuses on the unfolded protein response. Dr Greg Hundley:             What's that? Dr Carolyn Lam:                Well, Greg, I was really hoping you'd ask. The unfolded protein response is a cellular adaptive process to cope with protein folding stress. Now, approximately 40% of human proteins are predicted to be either transmembrane or secretory. The synthesis, the folding, the cellular transportation and location of these proteins rely on proper functioning of this secretory pathway. Numerous studies have established that the unfolded protein response plays versatile roles during development and under physiologic and pathophysiologic conditions. However, the role of this unfolded protein response in the regulation of cardiomyocyte growth is unclear. Dr Greg Hundley:             That's fantastic, Carolyn. I've already learned something here. So, what did this paper show? Dr Carolyn Lam:                This is from Dr Wang and colleagues from UT Southwestern, and basically, they use both gain and loss of function approaches to genetically manipulate spliced X-box binding protein one or XBP1, which is the most conserved signaling branch of the unfolded protein response in the heart. In addition, primary cardiomyocyte cultures were employed to address the role of XBP1S in cell growth in a cell autonomous manner. They found that XBP1S expression was reduced in both human and Rhode and cardiac tissues with heart failure deficiency of XBP1S lead to decompensation and exacerbation of heart failure progression under pressure overload. On the other hand, cardiac restricted over expression of XBP1S prevented the development of cardiac dysfunction. Mechanistically, they found that XBP1S stimulated adaptive cardiac growth, your activation of mechanistic target of rapamycin or MTOR signaling which is mediated via the FK-506 binding protein 11, which is a novel transcriptional target of XBP1S. So in conclusion, this study really showed a critical role of the XBP1S FKB or FK-506 binding protein 11 and MTOR axis in coupling the unfolded protein response and cardiac cell growth regulation. Dr Greg Hundley:             Boy Carolyn, you explained that so well, and I learned a lot from that. I hope I can do as well with this next article from Professor Johann Backs from the University of Heidelberg. Now paradoxically, some glucose lowering drugs have been shown to worsen heart failure, raising the question of how glucose mediates protective versus detrimental cardiac signaling, and this study from his group focused on one of the class two histone deacetylases or HDAC's namely HDAC-4, which functions as an important epigenetic regulator by responding to upstream stress signals, and linking them to downstream gene regulatory programs involved in among other things, metabolic regulation. Dr Carolyn Lam:                Very interesting. So what did they find? Dr Greg Hundley:             What they found is that HDAC4 acts as an important maintenance factor of cardiac function in diabetes and O-glycine-N0acetylglucosamine of HDAC4 at searing 642 induces the production of cardio-protective HDAC F-end terminal fragment and attenuates cardio detrimental Cam kinase two mediated phosphorylation of HDAC4 at searing 632. Vice versa, Cam kinase two mediated phosphorylation of HDAC4 at searing 632 attenuates HDAC-4 n terminal production. Thus, these findings lay the ground for the development of novel therapeutic strategies for diabetic patients with heart failure by inhibiting Cam kinase phosphorylation at CIHR 632 or enhancing o-glycine and escalation at searing 642. Dr Carolyn Lam:                Fascinating, Greg. Well, my next paper is a subgroup analysis of EUCLID and is the first to assess acute limb ischemia in the context of a large-scale clinical trial studying a primary peripheral artery disease population. Dr Greg Hundley:             So Carolyn, reminded us what was the EUCLID trial. Dr Carolyn Lam:                Okay, so EUCLID stands for Examining Use of Ticagrelor in Peripheral Artery Disease, and this was a randomized clinical trial that included acute limb ischemia as an adjudicated outcome in a primary peripheral artery disease population randomized to ticagrelor versus clopidogrel. Now in EUCLID ticagrelor was not superior to Clopidogrel for the prevention of cardiovascular events in patients with stable peripheral artery disease. However, a EUCLID subgroup analysis of patients with and without prior limb revascularization demonstrated significantly higher risk for acute limb ischemia hospitalization in patients with prior low extremity revascularization. Dr Greg Hundley:             So Carolyn, that's interesting. So, what did they find related in this study that focused on the acute limb ischemia? Dr Carolyn Lam:                Right. So, today's paper is from Dr Hess and colleagues at University of Colorado School of Medicine and CPC, clinical research in Aurora, Colorado. And, they found that acute limb ischemia occurred in 1.7% of almost 13,900 randomized patients with a median time to hospitalization for acute limb Ischemia of 320 days after randomization. In this population, prior lower extremity revascularization, atrial fibrillation and lower ankle brachial index identified patients at higher risk for acute limb ischemia. Hospitalization for acute limb ischemia was associated with subsequent cardiovascular and limb ischemic events. So, the take home message is providers should monitor for signs and symptoms of acute limb ischemia in patients with stable symptomatic peripheral artery disease, particularly those with prior lower extremity revascularization, atrial fibrillation, and lower ankle brachial index. Dr Greg Hundley:             That's very instructive, Carolyn. Fantastic message. So, I'm going to ask you if you could select one lipid biomarker to forecast future adverse cardiovascular events, which would you select? Total cholesterol, HTLC, non-HTLC, direct and calculated LDLC, APO-A1, or APO-B? Dr Carolyn Lam:                Well, I'm traditional. I would have chosen LDL. Dr Greg Hundley:             Okay. Well, the authors of this study led by Dr Paul Welsh at the University of Glasgow attempted to answer this question by studying participants from the UK Biobank without baseline cardiovascular disease and not taking statins with relevant lipid measurements. They had 346,686 participants. An incident fatal or nonfatal cardiovascular event occurred in 6,200 participants of which 1,656 were fatal, and they occurred over a median time of 8.9 years. So, the associations of non-fasting lipid measurements, total cholesterol, HDLC, non HDLC, direct and calculated LDLC, APO-a1, and APO-B with cardiovascular disease were compared using Cox models, adjusting for classical risk factors and predictive utility was determined by the C-index and net reclassification index. Also, prediction was tested in 68,649 participants taking a statin with or without baseline cardiovascular disease, and that group experienced 3,515 cardiovascular events. Dr Carolyn Lam:                Okay, so drum roll. What did they find? Dr Greg Hundley:             So, measurement of total cholesterol and HDLC in the non-fasted state is sufficient or was sufficient to capture the lipid associated risk in the cardiovascular disease prediction with no meaningful improvement from addition of APO lipoproteins, direct or calculated LDLC. And, similar findings were reproduced in those taking a statin at baseline.                                                 As such, the authors feel like calls for widespread use of APO lipoproteins are not warranted given the negligible difference in risk prediction beyond total cholesterol in HDLC. And, direct LDLC is also not required for risk prediction. Non HDLC is a cheaper or equivalent predictor of risk on and off statins without the requirement of one of us being fasting. This is an excellent article for our listeners to review or download. Dr Carolyn Lam:                Wow, that is so cool. So, from one excellent paper to another excellent paper in our feature discussion. Let's go, shall we? Dr Greg Hundley:             Welcome everyone to discussion of our featured article. We have Dr Kelley Branch from the University of Washington and our own Carolyn Lam, and they're going to be discussing the compass trial. So Kelley, could you tell us a little bit about the rationale for compass as opposed to the previously published commander study? Dr Kelley Branch:              So, in order to understand compass and compare it to commanders, we're going to have to go back a little bit in time here. And recall, you know well over 20 years ago that when we used anticoagulants in coronary artery disease, that was actually shown to be more beneficial than aspirin alone, but because of the excess bleeding risk, warfarin or vitamin K antagonists not used, and aspirin won. Fast forward a number of years, and now we have the non-vitamin K anticoagulants, and the was potentially that we could find the goldilocks, if you will, the good balance of benefit as well as less bleeding maybe used to these new agents. So, the compass trial was really born from an atlas ACS one and Atlas ACS two, which found that a low dose of, in this case, Rivaroxaban 2.5 milligrams VAB as well as five milligrams VAB were shown to be beneficial in patients after acute coronary syndrome.                                                 And then, it was thought what happens if we treat these patients with now chronic coronary disease as well as arterial disease? And from this 27,000 patients, 47,395 patients were tested, and our study very specifically looked at patients with a baseline or a history of heart failure when they answered compass. Compass were shown to be beneficial with specifically the use of aspirin plus Rivaroxaban, 2.5 milligrams BAD. And, our idea was to test this in patients with this baseline or history of heart failure. Now, this is in real contradistinction to what the commander tried to do. And the reason why encompass, we actually excluded patients with severe heart failure. This was defined as a New York Heart Association class three or four or an ejection fraction less than 30%. Now if you looked at patients with commander, these patients had ejection fraction less than 40%. That was a criteria to get in. And of course, these patients had to have a recent hospitalization for heart failure. So, these are very different patient populations. Well, both of them, yes, they did have coronary artery disease, but really very different patient populations. Dr Greg Hundley:             Very good. So Kelley, tell us specifically, what were your treatment group assignments and the doses and the outcomes that you were going to follow, and then lead us into what did you find? What were the outcomes of your study? Dr Kelley Branch:              Sure, so compass was actually developed as a partial three by two factorial. The arm that we're going to be talking about is the rivaroxaban arm. There was also another arm that tested the use of Proton pump inhibitors, and that actually was shown to not be as beneficial as we thought to decreased bleeding. But specifically for rivaroxaban, the baseline was aspirin, and this was on top of guideline based medical therapy. And then patients were randomized to either aspirin alone plus placebo or Rivaroxaban, five milligrams BAD, plus placebo. So, no aspirin at all or aspirin, a hundred milligrams daily, plus Rivaroxaban, 2.5 milligrams BAD. Those were really the three treatments. Patients were going to be followed for about three to four years. That's what we expected to get our 2200 events , an event-driven trial. But, because of the overwhelming benefits at 23 months median follow up, this trial was actually stopped early, so we only had a little over 1300 events at that time.                                                 And with that we saw substantial reduction in major adverse cardiovascular events, about 24% mortality was reduced 18%, and there was a bleeding risk along with this, major bleeding, little different way of actually measuring major bleeding, but that was increased by about 70%, and that was the overall trial results. So, looking at the patients with heart failure, though, there was actually a relatively large proportion of patients, so 5,902 patients, about 22% of patients, actually had either baseline heart failure or had a history of heart failure coming in. Now, this was defined specifically by the PI's. These were not rigorously defined as compared to say commander, but these were patients where the PI said this patient has history or has chronic heart failure. So, with these 5,902 patients, we looked specifically at the outcomes of major adverse cardiovascular events similar to what we saw with compass and that is cardiovascular death, myocardial infarction, or any stroke, that combination. And then, looked at some others exploratory analysis like mortality.                                                 And, what we found is that in patients with heart failure, the baseline rate was substantially higher for a mate's. Not too surprising because this tends to be a higher risk patient population. But, what we found is that the hazard ratio was about 0.68, so pretty similar to what we've seen the 24% relative risk. In this case, this was a 32% relative risk reduction in those patients with heart failure. Now, if we looked at a patients without heart failure, the hazard ratio is 0.79, so fairly similar and the [conference intervals 00:16:33] overlap. No statistical heterogeneity or no difference between those, but what we did see if we looked at the absolute risk reduction, was an absolute risk reduction in heart failure of 2.4% reduction. That means a number needed to treat of about 42. If you look at the absolute risk reduction for those patients without heart failure, that was 0.9 to 1.0 depending on what the rounding was. We took 1.0 so that means the number needed to treat of 103. So, these were slightly different relative risks, but overall, what we saw is that the hazard ratio is very consistent with the overall effect of compass in the same direction.                                                 Interestingly, and actually I think even for me it was surprisingly, we actually looked at the hazard ratios for bleeding, and when we looked at the hazard ratios for bleeding, we fully expected that because it's the higher risk patient population, we actually expected that to go up. What we saw is that the bleeding actually was no difference at all, and if anything in the heart failure population was slightly lower. And, this was fairly surprising to us because we thought that the patients with heart failure, the bleeding would actually trend up because this was a higher risk patient population. So it looks like it's something can be used and really no substantial increase in bleeding. Dr Greg Hundley:             Very good. Well Carolyn, as someone that's managing patients with heart failure, what do you see are the clinical implications of this study? Dr Carolyn Lam:                That is a beautifully simple, direct question but is not as easy to answer as I may have thought. And, that's because the commander trial that Kelley did describe a bit earlier was neutral on its primary outcome. And, the commander trial is what we would traditionally think of as a heart failure trial. And why? Because those were patients that we rigorously define heart failure, including a naturally acid peptide inclusion criteria. And, because we really wanted these to be severe heart failure patients, we recruited them very close to their hospitalization or decompensation event. So, I just want to reiterate what Kelley has already so beautifully described that commander was neutral, whereas this heart failure subset of compass showed very impressive results that were consistent with the very impressive positive results of the overall compass trial.                                                 So, how do we reconcile all of it? Well, first of all, I have to humbly remind myself that this heart failure subset of compass, the entire subset was actually bigger in numbers than the entire of the commander trials. So, this is not a small little subgroup analysis. This is a huge subgroup analysis. And that's why a paper like this, we're so proud to be publishing in circulation.                                                 So, how do I apply it? Well, when I have a compass like patient, which means it's a stable coronary artery disease or peripheral artery disease patient who happens to have some mild heart failure. I think of this patient as a compass patient and I think that the combination of aspirin and low dose Rivaroxaban has been shown to be effective in these patients. So, in such a patient, I continue the aspirin rivaroxaban combination. However, if I have a new patient coming in with decompensated heart failure, a very low ejection fraction and has some coronary artery disease, by the way, I see that as a commander patient, and I just want to make sure that in such a patient I'm not trying to reduce their overall mortality by treating them with a combination of aspirin Rivaroxaban because commander has shown that I don't impact their overall survival with this combination, even though we may still have beneficial effects on their thromboembolic thrombotic events.                                                 Kelley, would you agree? Dr Kelley Branch:              I would completely agree. That was actually born out very, very well by Barry Greenberg who had a really a wonderful sub analysis which he looked at the thrombotic events published in Jama cardiology and really showing that yes, you can affect the thrombotic events, but I mean really what it comes down to is we want to save lives. We want people to be better. There's just an overwhelming risk for these patients with heart failure that is really non thrombotic, primarily. And so, you're really not going to move the needle very much. You may prevent a stroke here, you may prevent some cardiovascular death from a thrombotic problem, but overwhelmingly pump failure, arrhythmia, et cetera. Those are really going to be the drivers for the commander like population. Dr Carolyn Lam:                But Kelley, this comes up a lot when we've chatted, but if you have a compass patient who has heart failure and then gets admitted with heart failure, what would you do then? Dr Kelley Branch:              That's a really interesting question, right? It depends on what the overall goal is. So, if the patient gets admitted for heart failure, now has it decreased ejection fraction sick. So has an MI, now decreased the ejection fraction. What's the end game? Right? Well you know, you may not be affecting mortality in this case because there's now competing events. However, if the goal was to decrease stroke, we've seen that. Still this goal is to decrease MI to some extent than we see that also. So, it would be reasonable to continue in order to prevent those events. But, just knowing full well that there's many other medications which actually do much better for the patients with decreased ejection fraction. And, those would probably be considered first line, but it's reasonable to continue. But, I would never start it. Dr Carolyn Lam:                Kelley, I couldn't agree more. And here I think the, your data showing that the bleeding risk is not significantly increased in this patient matters a lot. So, if I had a patient, a compass patient who was already on the combination and then gets admitted with heart failure, I too, if there's no additional bleeding risk, I would continue the combination as well. Dr Kelley Branch:              Couldn't agree more. Dr Greg Hundley:             Well listeners, this was a fantastic discussion, and we look forward to seeing you next week. Have a great week. Dr Carolyn Lam:                This program is copyright American Heart Association 2019.  

「高脂血症のLDL-CとHDL-C比」について。（解説）群馬大学循環器内科教授・倉林正彦（ききて）防衛医科大学校教授・池脇克則氏

In Episode 37 I sit down for the second time with Dr Michelle McMacken (previous guest on Episode 2) to talk about where the science lies in terms of eating for longevity. We talk about a plethora of fascinating topics including: Michelle's project with Bellevue Hospital which is now offering out-patients with chronic disease the option of participating in a plant based food program Where the science lies in terms of saturated fat & cholesterol and their contributions to disease The particular type of fat & cholesterol we need to be worried about when it comes to atherosclerosis (narrowing of our arteries) and cardiovascular disease Sources of healthy fats The Paleo & Keto diets and where the science sits in terms of these diets being helpful or harmful from a longevity & disease point of view What Type 2 diabetes is and helpful nutritional information for managing and reversing this disease and much much more This is an absolute cracker of an episode, one of my favourites so far in terms of breaking down the science, clearing the confusion and helping us all understand what we should be eating more of and what we should be eating less of. Despite the headlines, the science is very clear and in this episode Michelle offers agenda free insight into exactly what it means. Grab a pen and paper...you're going to want to take notes and more than likely listen 2-3 times! To connect with Michelle you can find her on Instagram @veg_md- I strongly suggest following her page as she often posts really helpful information directly from the many lifestyle medicine conferences she attends and speaks at. For extra information from Michelle explaining Cholesterol, LDL-C & HDL-C please read here As always folks I hope you enjoy the episode and find it thought provoking. I definitely did! If you did enjoy it please share your feedback by leaving a review on iTunes or posting on social media and tagging Michelle and Myself (@plant_proof) (I re share a lot of the feedback posted on my own story). Simon Hill For agenda free information on plant based nutrition checkout my website plantproof.com

In Episode 37 I sit down for the second time with Dr Michelle McMacken (previous guest on Episode 2) to talk about where the science lies in terms of eating for longevity.We talk about a plethora of fascinating topics including:Michelle's project with Bellevue Hospital which is now offering out-patients with chronic disease the option of participating in a plant based food programWhere the science lies in terms of saturated fat & cholesterol and their contributions to diseaseThe particular type of fat & cholesterol we need to be worried about when it comes to atherosclerosis (narrowing of our arteries) and cardiovascular diseaseSources of healthy fatsThe Paleo & Keto diets and where the science sits in terms of these diets being helpful or harmful from a longevity & disease point of viewWhat Type 2 diabetes is and helpful nutritional information for managing and reversing this diseaseand much much moreThis is an absolute cracker of an episode, one of my favourites so far in terms of breaking down the science, clearing the confusion and helping us all understand what we should be eating more of and what we should be eating less of. Despite the headlines, the science is very clear and in this episode Michelle offers agenda free insight into exactly what it means. Grab a pen and paper...you're going to want to take notes and more than likely listen 2-3 times!To connect with Michelle you can find her on Instagram @veg_md- I strongly suggest following her page as she often posts really helpful information directly from the many lifestyle medicine conferences she attends and speaks at.For extra information from Michelle explaining Cholesterol, LDL-C & HDL-C please read hereAs always folks I hope you enjoy the episode and find it thought provoking. I definitely did! If you did enjoy it please share your feedback by leaving a review on iTunes or posting on social media and tagging Michelle and Myself (@plant_proof) (I re share a lot of the feedback posted on my own story).Simon HillFor agenda free information on plant based nutrition checkout my website plantproof.com

In this episode, Dave Feldman, discusses his journey from software engineer to n=1 experimenter, his experience with low-carbohydrate diets, and his hypothesis that cholesterol levels are influenced by energy metabolism.   We discuss: Peter’s synthesis of Dave’s energy model [5:00]; Dave’s journey from software engineer to cholesterol enthusiast [15:00]; Standard blood panels, sterol panels, and what moves the needle when it comes to particle numbers [18:30]; Hyper-responders [20:00]; Lipoprotein transport [33:45]; The lean mass hyper-responder phenotype [47:30]; The progression of atherosclerosis, CAC, and CIMT [52:30]; Testing for oxidized LDL [55:30]; All-cause mortality and clinical endpoints [1:01:15]; What does “LDL as causal” mean? [1:05:15]; Dave’s low carb cholesterol challenge and drug & genetic study qualifications [1:13:15]; If all other markers are in an healthy range, but LDL-P is high, is the patient at risk? A couple of case studies, and a self-experiment [1:27:30]; Peter’s three-day exercise and ketosis experiment [1:41:00]; What are remnant lipoproteins? [1:45:00]; What might cause lean mass hyper-responders to have higher LDL particle numbers? [1:53:30]; A case study from Dave of a lean mass hyper-responder [1:56:30]; Mass balance and cholesterol flux [2:05:30]; Can a higher degree of cholesterol explain the lean mass hyper-responder phenotype? [2:10:00]; Peter’s LDL during his keto-fast-keto experiment [2:13:30]; Does substituting saturated fats with monounsaturated fats lower LDL-P and LDL-C? [2:15:45]; Dave’s carb-swap experiments [2:22:15]; Dave’s carotid intima-media thickness tests [2:41:15]; Looking for studies that stratify for high HDL-C and low TG alongside low and high LDL-C [2:53:00]; and More Learn more at www.PeterAttiaMD.com Connect with Peter on Facebook | Twitter | Instagram.

Whenever I’m stumped on a patient case or in my thinking about lipids, Ron is one of the first people I turn to for insight. Ron is recognized globally for his research into lipidology and has worn many hats in his career, including clinician, lipidologist, nutrition, genetics, and drug research. In this episode, we explore heart disease at its origins before diving into the highly discussed, largely misunderstood, role of LDL and inflammation in atherosclerosis. Ron also shares his insights on the evidence for and against statins and other lipid-lowering therapies. My hope is that both the curious patient and the physician can get a lot out of this episode by being more informed about dyslipidemia and the interventions used to reduce the risk of atherosclerotic disease. We covered a lot of ground on this critically important topic.   We discuss: The pathogenesis of atherosclerosis [7:00]; How early atherosclerosis begins [12:40]; Ron’s motivation for getting into lipidology [43:00]; How reading an article series in the NEJM in 1967 had a profound impact on him and his career [43:30]; How PCSK9 inhibitors work and why they may be under-utilized [47:00]; Mendelian randomization: nature’s randomized trial [49:15]; The “battle” between particle size and particle number [52:00]; The use of statins [1:04:45]; The role of chronic inflammation in atherosclerosis [1:24:15]; Why niacin may have been unjustly dismissed as a therapeutic option [1:40:45]; The HDL paradox: why drugs that raise HDL-C seem to raise (or have little impact on) heart disease risk [1:43:00]; Lp(a) [1:47:45]; And more. Learn more at www.PeterAttiaMD.com Connect with Peter on Facebook | Twitter | Instagram

What is cholesterol? Cholesterol is a waxy, lipid in every cell’s membrane and our blood plasma, vital for life It insulates neurons Building cellular membranes Metabolizing fat soluble vitamins Produces bile to help digest food Synthesis if many hormones including sex hormones There are rare genetic disorders in which people cannot properly synthesize cholesterol.  Once such disease is Smith-Lemli-Opitz syndrome (also called “SLOS,” or 7-dehydrocholesterol reductase deficiency) which is a metabolic and congenital disorder leading to a number of problems including autism, mental retardation, lack of muscle, and many others. You get some cholesterol from the your diet and some your body makes. Cholesterol is different day to day All Cholesterol is NOT created equal. The tests your doctor runs do not tell the whole story Many (not all) people will have increase in cholesterol on a high fat diet but most studies show IMPROVED cholesterol profiles (inc in good cholesterol, decrease in bad) So the AHA is right. Saturated fat does increase cholesterol. But does this mean it increases heart attack?  Probably depends what you are eating the saturated fat with and your genetics. The good (HDL), The bad (TG) and The ugly (LDL) HDL (the Good) Transfers excess cholesterol that tissues don’t use back to liver Liver excreted through bile HDL is the one to naturally help get rid of excess cholesterol when the body’s done with it, You want it as high as possible Increased by LCHF / Keto Triglycerides: (THE BAD) (causes fatty liver and heart disease) TG are fuel for your body High TG in blood because your body is not using it Its using glycogen instead If fat adapted - you are using this up TG just sit  around and cause problems TG float around in circulation Because hard and dense and causes problems/ plaques It starts to get oxidized Damaged and clogged arteries Your body tries to clear it with local inflammation Cells responding to inflammation cause plaque and clog arteries Arteries are narrowed and less blood and less oxygen TG increase small dense LDL LDL: (the ugly) - because its complicated LDL delivers cholesterol to tissues. Large fluffy LDL does this SO IMPORTANT LDL-C (large and fluffy) and LDL-P (go to artery walls and clog) ApoB (a proxy for LDL-P which not many labs run) Apolipoprotein B (ApoB) is an important component of many lipoproteins that are involved in atherosclerosis and cardiovascular disease. Apo B containing lipoproteins are the ones that are most likely to enter the wall of the arteries. TAKE HOME If you are not going to change your lifestyle and eat high sugar diet and you have heart disease - you might want to take a statin If you eat low carb high fat your cholesterol panel will be different then someone on a SAD Make sure you get the break down of particles to get a better picture Currently, most people in the United States (and the world for that matter) undergo a “standard” lipid panel, which only directly measures TC, TG, and HDL-C.  LDL-C is measured or most often estimated HIGH Triglycerides is BAD HIGH HDL is GOOD LDL-C is large fluffy and healthy GOOD LDL-P vs ApoB is small and dense and bad LDL-P (or apoB) is the best predictor of adverse cardiac events, which has been documented repeatedly in every major cardiovascular risk study When looking for information look to lipidologists who have phDs in this stuff not correlational / drug company funded research (mostly what doctors are aware of) https://idmprogram.com/diet-heart-hypothesis-hormonal-obesity-xxxv/ https://peterattiamd.com/the-straight-dope-on-cholesterol-part-i/ http://eatingacademy.com/cholesterol-2/the-straight-dope-on-cholesterol-part-iii cbi.nlm.nih.gov/pubmed/27389628 https://www.marksdailyapple.com/cholesterol/ https://www.medicalnewstoday.com/articles/267834.php https://www.healthline.com/nutrition/23-studies-on-low-carb-and-low-fat-diets http://clinchem.aaccjnls.org/content/50/10/1725

To interpret lab results your typical doctor will use standard reference ranges that are based on averages from a random sample of people.  Your labs are compared to these ranges to evaluate your health status and to guide potential treatment.  If reference ranges have such an important role, wouldn’t it make sense to have them reflect optimal health rather than typical health? We’re looking at some recent and large-scale studies today that suggest your cholesterol numbers don’t mean what mainstream medicine might have you believe.  Dr. Tommy Wood, MD, PhD is with me to discuss optimal reference ranges for cholesterol and triglycerides, as well as other lab tests that are more reliable for predicting cardiovascular disease and all-cause mortality. Need some help interpreting your blood tests? In this interview, we introduce the Blood Chemistry Calculator. Here’s the outline of this interview with Dr. Tommy Wood: [00:03:02] All-cause mortality: Dying from any cause. [00:03:38] Study: Fulks, Michael, Robert L. Stout, and Vera F. Dolan. "Association of cholesterol, LDL, HDL, cholesterol/HDL and triglyceride with all-cause mortality in life insurance applicants." J Insur Med41.4 (2009): 244-253. [00:05:54] Higher is not necessarily better for HDL. [00:07:23] Lower limits for triglycerides. [00:07:50] Study: Iannello, S., et al. "Low fasting serum triglyceride level as a precocious marker of autoimmune disorders." MedGenMed: Medscape general medicine 5.3 (2003): 20-20. Podcast: Risk Assessment in the Genomic Era: Are We Missing the Low-Hanging Fruit? With Dr. Bryan Walsh. [00:11:09] Arbitrary cutoffs are created in order to compare groups statistically. [00:12:25] Study: Zuliani, Giovanni, et al. "Combining LDL-C and HDL-C to predict survival in late life: The InChianti study." PloS one 12.9 (2017): e0185307. [00:13:19] Study: Orozco-Beltran, Domingo, et al. "Lipid profile, cardiovascular disease and mortality in a Mediterranean high-risk population: The ESCARVAL-RISK study." PloS one 12.10 (2017): e0186196. [00:17:27] Total cholesterol. [00:18:44] Optimal reference range for total cholesterol: 120 - 240 mg/dL (under age 60, all-cause mortality). [00:19:55] Optimal range for women 200 - 300 mg/dL (over 60). [00:20:11] Study: Petursson, Halfdan, et al. "Is the use of cholesterol in mortality risk algorithms in clinical guidelines valid? Ten years prospective data from the Norwegian HUNT 2 study." Journal of evaluation in clinical practice 18.1 (2012): 159-168. [00:21:46] Familial hypercholesterolemia. [00:23:01] LDL is part of the immune system. [00:23:32] Insulin resistance as a cause of high cholesterol. [00:24:23] Thyroid problems as a cause of high LDL. [00:26:19] Ivor Cummins (see first graph on page). [00:27:23] Optimal reference range of LDL for men/women under age 60:  80 - 170 mg/dL. [00:29:44] HDL graphs found within study: Fulks, Michael, Robert L. Stout, and Vera F. Dolan. "Association of cholesterol, LDL, HDL, cholesterol/HDL and triglyceride with all-cause mortality in life insurance applicants." J Insur Med41.4 (2009): 244-253. [00:30:42] Alcohol as a potential cause of high HDL. [00:33:01] Optimal reference range for triglycerides: 50 - 90 mg/dL. [00:35:23] Triglyceride : HDL ratio 1 - 2 is optimal if measuring in mg/dL. [00:37:16] Total cholesterol : HDL ratio of 3 - 4 is optimal. [00:39:32] Keto hyper-responders. [00:40:15] APOE4. [00:40:40] Thomas Dayspring. [00:41:01] True Health Diagnostics. [00:41:20] LDL-P: the total number of particles carrying the LDL cholesterol. [00:41:51] LDL particle size: small dense vs large fluffy. [00:42:33] Peter Attia’s blog and his posts pertaining to cholesterol. [00:43:08] Dave Feldman. His website: cholesterolcode.com. [00:45:37] Endurance exercise: effect on cholesterol and triglycerides. [00:46:23] Facebook groups: Lower Insulin and Optimising Nutrition. [00:46:43] Gudmundur Johannsson, CEO of the Icelandic Health Symposium. [00:46:55] Sepsis, endotoxins: worse outcomes with lower LDL. [00:49:39] Statins: Ever a good idea? [00:51:28] Tommy in a kiosk. [00:53:25] Link to the blood calculator.

Noninvasive VT ablation, Riata leads, NOAC/DOAC therapies, HDL-C and infection risk, and fibrosis in triathletes are discussed in this week's podcast.

Continuing the discussion of digital technologies in Ham Radio, George and Jeremy invite Kenneth Finnegan W6KWF back to do a very deep dive on Packet Radio, AX.25, and KISS modes.  We talk TNCs, equipment, and practical applications of Packet Radio this week on The Workbench. Kenneth Finnegan - https://twitter.com/KWF http://blog.thelifeofkenneth.com MMDVM Zumboard - http://mmdvm.blogspot.com/ DStar Registration - http://www.dstargateway.org/D-Star_Registration.html DMR Registration - https://www.dmr-marc.net/cgi-bin/trbo-database/register.cgi New Elecraft AX1 Antenna - https://va2ss.com/2017/10/19/elecraft-ax1-ultraportable-1720-meter-antenna-system/ Pacificon - http://www.pacificon.org/ Microwave Update 2017 - http://www.microwaveupdate.org/ Sierra Radio Systems - http://www.sierraradio.net/ Motrolla CDM1250 - https://www.motorolasolutions.com/en_us/products/two-way-radios/analog-business-radios/discontinued/cdm1250.html#tabproductinfo Motrola CDM1550 - https://www.motorolasolutions.com/en_us/products/two-way-radios/analog-business-radios/discontinued/cdm1550.html#tabproductinfo eMMC to SD Card adapter - https://ameridroid.com/products/emmc-adapter Raspberry Pi Compute Module - https://www.raspberrypi.org/products/compute-module-3/ http://blog.thelifeofkenneth.com/2017/08/building-stand-alone-raspberry-pi.html TAPR - https://www.tapr.org/packetradio.html Bell 202 Modem - https://en.wikipedia.org/wiki/Bell_202_modem TNC - https://en.wikipedia.org/wiki/Terminal_node_controller Nationwide Packet Network of BBS - https://en.wikipedia.org/wiki/Bulletin_board_system AMPRNet - https://en.wikipedia.org/wiki/AMPRNet AX.25 - https://www.tapr.org/pub_ax25.html https://en.wikipedia.org/wiki/AX.25 TNC-X Raspberry Pi - https://tnc-x.com/TNCPi.htm Kantronics TNCs - http://www.kantronics.com/ Soundcard Packet - https://www.soundcardpacket.org/ Direwolf - http://info.aprs.net/index.php?title=Dire_Wolf AGWPE - https://www.sv2agw.com/downloads/ UZ7HO Soundcard Modems - http://uz7.ho.ua/packetradio.htm OSI Model - https://en.wikipedia.org/wiki/OSI_model AFSK - https://en.wikipedia.org/wiki/Frequency-shift_keying HDLC - https://en.wikipedia.org/wiki/High-Level_Data_Link_Control KISS - https://en.wikipedia.org/wiki/KISS_(TNC) Outpost Software - http://www.outpostpm.org/index.php Alinco - http://alinco.com/Products/ham/mbl/DR-135/ http://www.scc-ares-races.org/freqs/packet-freqs.html HR360 APRS Shows - http://hamradio360.com/index.php/2017/01/24/ham-radio-360-all-about-aprs-with-w6kwf/ http://hamradio360.com/index.php/2017/03/07/ham-radio-360-aprs-follow-up-listener-qa/  

If you are interested in the low-carb, moderate protein, high-fat, ketogenic diet, then this is the podcast for you. We zero in exclusively on all the questions people have about how being in a state of nutritional ketosis and the effects it has on your health. There are a lot of myths about keto floating around out there and our two amazing cohosts are shooting them down one at a time. Keto Talk is cohosted by 10-year veteran health podcaster and international bestselling author Jimmy Moore from “Livin’ La Vida Low-Carb” and Pittsburgh, PA functional medicine practitioner Dr. Will Cole from DrWillCole.com who thoroughly share from their wealth of experience on the ketogenic lifestyle each and every Thursday. We love hearing from our fabulous Ketonian listeners with new questions–send an email to Jimmy at livinlowcarbman@charter.net. And if you’re not already subscribed to the podcast on iTunes and listened to the past episodes, then you can do that and leave a review HERE. Listen in today as Jimmy and Will peel back the layers of your low-carb, high-fat, ketogenic questions in Episode 85. BECOME A NUTRITIONAL THERAPY PRACTITIONER Sign up by February 2018 for the 9-month program NOTICE OF DISCLOSURE: Paid sponsorship *****SPECIAL THANKS to Jordan******   Go to PayPal.me/KetoTalk to make a donation.  You can set up automatic monthly payments there THE PERFECT KETO SUPPLEMENT USE COUPON CODE LLVLC FOR 15% OFF NOTICE OF DISCLOSURE: Paid sponsorship   KEY QUOTE: “Food comes first. I don't think you can supplement your way into an optimum, healthy, ketogenic diet.” — Dr. Will Cole MAKE KETO EASIER WITH FBOMB JIMMYLOVESFBOMB FOR 10% OFF YOUR FIRST FOOD ORDER NOTICE OF DISCLOSURE: Paid sponsorship Here’s what Jimmy and Will talked about in Episode 85: RESPONSE FROM A LISTENER: Hey, Jimmy and Dr. Cole, I listened to your discussion in Episode 81 of Keto Talk about the difficulty in getting life insurance and I wanted to let you know that there are actually carriers that will issue up to $1 million policies up to the best rating class without having to go through any blood/urine profile or physical exam. If they are healthy and between the ages of 18-54 and have not been declined or rated from a life insurance carrier before, this option is available. It could be a good fit for someone that thinks their blood levels may be "abnormal" from the insurance company perspective and want to avoid doing labs. Just an FYI for people to talk to their insurance broker about this. Thanks, Justin HOT TOPICS: Zero carb diets Exogenous ketones To Test or Not To Test For Ketones Join The Keto Clarity Club For $1 Blood Ketone Test Strips!   – That keto diet you think is working wonders could kill you – Furore over ketogenic diet – The Silicon Valley execs who don't eat for days: 'It's not dieting, it's biohacking' – Mick Jagger gets satisfaction from diet that could add 10 years to his life KEY QUOTE “If you're eating zero-carb, make sure you're eating nose to tail to ensure you are getting all the micronutrients you need.”  – Jimmy Moore – Why am I having painful leg cramps while on keto outside of electrolyte imbalance? How do you resolve them without supplementation? Hi, Jimmy and Dr. Cole, I love this podcast, been listening since Day 1. I’ve been eating low-carb for several years and about a year and a half ago I went full-on keto. I love this way of eating and have seen a lot of benefits from it. I regularly see average ketones of 1.7 mmol/L. However, there is one drawback I experience at least once a week and upwards of four times a week. It’s the dreaded leg cramps. They are more common at night, often when I’m sleeping, but I’ve experienced them pretty much anytime throughout the day. I believe the ketogenic lifestyle truly is the ideal way to eat, but I shouldn’t be having this major and often quite painful side effect, right? I’ve heard you discuss the issue of muscle cramps in the past and how they’re typically due to dehydration and/or electrolyte depletion or imbalance. The quandary I now have is how can I really consider this ketogenic diet to be “ideal” if it leaves me with this leg cramp issue that I seemingly have to solve with supplementation. Obviously, if this way of eating was being implemented by our ancestors and it was causing them this problem, they wouldn’t have been able to solve it with supplements. I don’t have any major health issues and am not metabolically broken. But this nagging problem with my ketogenic diet makes me wonder how it can truly be the perfect way to eat? Any ideas why my electrolytes may be out-of-whack and leading to leg cramps? Or could the cramps possibly be due to something else I’m not aware of? I appreciate your help. Keep up the good work! Brian   – STUDY: Red meat halves risk of depression 1. Why am I experiencing a sudden dip in my energy levels while eating ketogenic when energy has been great? Dear Jimmy and Will, I’ve been following the ketogenic diet for nearly a year at the age of 75 and have experienced great energy eating grass-fed meats, fresh farm eggs, and organic vegetables. But over the past month I’ve noticed my energy has taken a dive and I thought it might be the heat of the summer. But my blood pressure also dropped so low (70/42) that I had a tough time just standing up. My doctor had me wear a heart halter and discovered I have tachycardia. Of course, now I have to see a cardiologist and I’m sure he’s gonna flip out about my numbers eating keto: Total cholesterol 294, LDL-C 198, HDL-C 85, triglycerides 55, LDL-P 2100, small LDL-P 386, VLDL 11, fasting blood glucose 90, Vitamin D 97.0, C-Reactive Protein 1.1 Do you have any suggestions for me? Brenda   2. Is there concern about a low Vitamin C intake while eating a restricted ketogenic diet like the one outlined in The Plant Paradox? Hi, Jimmy and Dr. Cole, A friend of mine read the book The Plant Paradox by Dr. Steven Gundry and is following his dietary advice. After reviewing their recommendations (essentially no legumes, no grains, low/no fruit, no vegetables that contain seeds on the inside like cucumbers, squash, etc) it seems that she would easily fall into the ketogenic diet recommendations. She recently met with her naturopath who was leery of keto because of a supposedly low vitamin C intake. Do you have any insight into this and how a ketogenic dieter would get Vitamin C? I usually follow a Paleo/keto diet but have never considered micronutrient deficiencies as a concern because I am eating so much plant matter. Thank you in advance! Alexandria 3. How do I avoid the onslaught of sugar and crappy carbage while I am in the hospital? Will they honor my request to keep the sugar and carbs out of my diet? Hey guys, What is a patient who eats keto supposed to do when they are in the hospital? I need to have aortic heart valve and stem replacement surgery someday and I worry about what this hospital stay will do to me. I’m a severely insulin resistant Type 2 diabetic who had an A1c of 10.4 prior to going on a ketogenic diet. Three months after going keto, that number dropped to 5.6. I’m keto for life now, but this hospital stay will be a challenge to avoid the crappy carbage they like to serve as well as the sugar-filled goop they put in the feeding tubes. I already know my healing won’t happen properly with high blood sugar and insulin levels and the hospital will simply medicate and inject me with insulin to deal with it. If I asked my hospital to avoid doing this, will they follow my wishes? I suppose I could just fast the entire time I am in the hospital, but do you have any suggestions about this? Thanks so much for helping me with this. Ethan KETO TALK MAILBOX – Does a ketogenic diet help or hurt with anxiety issues? Hey Jimmy and Will, I just found and subscribed to Keto Talk—thank you for the great information! I’m thinking seriously about getting into the keto thing for myself, but I am doing my homework first. I am a 61-year-old carb addicted female who needs to lose at least 50 pounds. I was recently diagnosed as pre-diabetic and I want to get myself back to feeling happy and well again. My question for you guys revolves around how keto helps with anxiety issues. Is there any medical, scientific, or other data with ketogenic diets and anxiety? Or does it make anxiety worse (ugh…I hope not)? Thank you again! Kim iTunes reviews:   LINKS MENTIONED IN EPISODE 85 – SUPPORT OUR SPONSOR: Join Jimmy Moore’s Keto Support Group: KetoClarityAcademy.com – SUPPORT OUR SPONSOR: Join The Keto Clarity Club For $1 Blood Ketone Test Strips! BestKetoneTest.com – SUPPORT OUR SPONSOR: The world’s freshest and most flavorful artisanal olive oils. Get your $39 bottle for just $1. – SUPPORT OUR SPONSOR: Become A Nutritional Therapy Practitioner – SUPPORT OUR SPONSOR: Jump start your ketogenic diet with PerfectKeto.com/Jimmy (USE PROMO CODE LLVLC FOR 15% OFF) – SUPPORT OUR SPONSOR: Drop an FBOMB for the freshest, high-quality fats from JimmyLovesFBomb.com (Get 10% off your first food order with coupon code “JIMMYLOVESFBOMB”) – That keto diet you think is working wonders could kill you – Furore over ketogenic diet – The Silicon Valley execs who don't eat for days: 'It's not dieting, it's biohacking' – Mick Jagger gets satisfaction from diet that could add 10 years to his life – STUDY: Red meat halves risk of depression – Jimmy Moore from “Livin’ La Vida Low-Carb” – DR. Will Cole D.C. from DrWillCole.com – HELP KEEP KETO TALK ON THE AIR: MAKE A DONATION HERE

In this episode, I weigh in on the American Heart Association's new Presidential Advisory and Dietary Fats and Cardiovascular Disease, and all the headlines that have been spinning on the supposed risks of coconut oil. This episode is brought to you by US Wellness Meats. I use their liverwurst as a convenient way to make a sustainable habit of eating a diversity of organ meats. They also have a milder braunschweiger and an even milder head cheese that gives you similar benefits, as well as a wide array of other meat products, all from animals raised on pasture. Head to grasslandbeef.com and enter promo code “Chris” at checkout to get a 15% discount on any order that is at least 7 pounds and is at least $75 after applying the discount but under 40 pounds (it can be 39.99 lbs, but not 40). You can use this discount code not once, but twice! The show notes for this episode can be found at chrismasterjohnphd.com/41. In this episode, you will find all of the following and more: 03:55 The recent headlines on coconut oil 04:52 The American Heart Association’s new Presidential Advisory, “Dietary Fats and Cardiovascular Disease” is not centrally about coconut oil, but it laments its the popularity of coconut oil. 07:10 This is a position paper reinforcing the conventional view about saturated fat as the stance against it within the scientific community has begun to soften around the edges. The 2015 dietary guidelines and the 2016 Ramsden paper reflect that softening. 14:39 The inclusion and exclusion criteria of the “4 core trials” of the AHA meta-analysis 16:38 The 4 core trials 17:00 The Finnish Mental Hospitals Study makes the largest contribution to the AHA conclusion but was not a randomized controlled trial and doesn’t belong in this list. 23:44 The Oslo Diet-Heart Study was included and made a contribution, yet other trials were excluded on the basis of confounding that were far less confounded than Oslo. 27:38 The LA Veterans Administration Hospital Study showed that a vitamin E-deficient diet makes you vulnerable to the heart disease-promoting effects of smoking, and that vegetable oils cause more cancer than cigarettes. 36:41 The Medical Research Council study showed a trend toward a benefit of soybean oil that was not statistically significant. Lack of heat damage to the fats in the diet, coenzyme Q10, and omega-6/omega-3 balance could have played a role in the trend. 41:12 Exclusion of Rose 1965 and Minnesota Coronary Survey from the “4 core trials” was fair. 42:33 Controversy over the possible contribution of trans fats to the results of the Sydney Diet Heart Study. But this as a basis for exclcusion could have excluded the LA Veterans Administration Hospital Study as well. 47:59 The impact of including or excluding MRC and Sydney shows how the conclusions are driven not by the cumulative data but on the qualitative decisions about which studies to include. 52:02 The observational studies are hopelessly confounded by popular campaigns about the heart-healthiness of replacing saturated fat with polyunsaturated fat. 56:08 The experiments in monkeys using lard, palm oil, and dietary cholesterol to bring their plasma cholesterol to 300-400 mg/dL. 58:33 The oxidation of lipoproteins drives atherosclerosis and polyunsaturated fats drive the oxidation. This is embraced by the leading conventional thinkers. 1:06:00 The AHA position on coconut oil is based on its effect on LDL-C, explicitly arguing in favor of ignoring its effects on HDL-C, and explicitly acknowledging the complete absence of clinical evidence. 1:13:12 Coconut oil has benefits unrelated to heart disease, such as the antimicrobial (antifungal and antibacterial) effects of lauric, capric, and caprylic acids, and the increased energy expenditure and decreased appetite caused by capric and caprylic acids. 1:17:00 Coconut oil could protect against heart disease due to its low polyunsaturated fat content. 1:19:32 Traditional Pacific island diets were far higher in saturated fat than the standard American diet, yet heart disease was absent. 1:22:09 The Tokelau Migrant Study showed that the freedom from heart disease on Tokelau, where coconut consumption pushed saturated fat over 50% of calories, was not due to genetics or age.

If you're concerned about your cholesterol, or confused about what to do, this episode is for you. In this episode, I list the four key factors that control blood cholesterol levels and outline the simplest dietary or lifestyle changes we can make to have the biggest impact. This episode is brought to you by US Wellness Meats. Head to grasslandbeef.com and enter "Chris" at checkout to get 15% off your order as long as the final price is over $75 and you order fewer than 40 pounds of meat. You can use "Chris" to get the same discount twice. In this episode, you will find all of the following and more:  00:33 Cliff notes; 09:22 Targeting the low-hanging fruit; 11:50  The total-to-HDL-C ratio as a fingerprint of low LDL receptor activity; 13:20  Other markers such as particle size, particle count, and ApoB as fingerprints of low LDL receptor activity; 16:30  The four factors that control the LDL receptor; 18:50  Intracellular free cholesterol (effects of dietary fiber, cholestyramine, statins, and polyunsaturated fatty acids or PUFAs); 20:37  Thyroid hormone (effects of micornutrients, body fat, and carbohydrate intake); 23:50  Insulin (via PCSK9, effects of the fasting-feeding cycle and carbohydrate intake); 27:00  Inflammation (via PCSK9, effects of acute infection and chronic inflammation); 29:15  Practical approaches to maximizing LDL receptor activity; 29:22  Nutrient-dense whole food diets; 34:00  Thyroid disorder; 37:15   Adrenal stress, circadian stress, inflammatory stress; 39:05  Insulin resistance, body composition, and fatty liver disease; 42:00  Weight loss will improve insulin sensitivity, and for many a low-carb diet is a tool to achieve that, but in an insulin-sensitive person, carbohydrate stimulation of insulin has a powerful beneficial effect on LDL receptor activity; 46:20  Inflammation and PCSK9; 47:00  C-Reactive Protein levels, body composition, diet quality, and exercise; 49:25  Replacing fat with carbohydrate.  

  Dr. Carolyn Lam:             Welcome to circulation on the run. Your weekly podcast summary and backstage pass to the journal and its editors. I'm Dr. Carolyn Lam associate editor for the National heart center and Duke National University of Singapore. Our podcast is really going around the world, and today's feature interview comes to you live from China. Where we will be discussing the prediction of ten year risks of cardiovascular disease in the Chinese population. So now to all our Chinese colleagues out there: Chinese dialect     First here's your summary of this week's journal. The first study challenges the assumption that all patients with vascular disease are at high risk of recurrent vascular events. First author Dr. Kasenbrud corresponding author Dr. Viceren and colleagues form the University Medical center Utric in the Netherlands, provide new data on the estimation of ten year risk of recurrent vascular events and a secondary prevention population. In other words, in patients with established cardiovascular disease they applied the second manifestations of arterial disease or 'smart' score for the ten year risk prediction of myocardial infarction, stoke or vascular death in more than six thousand-nine hundred Dutch patients with vascular diseases ranging for coronary artery disease, cerebral-vascular disease, peripheral artery disease, abdominal aortic aneurysm and poly-vascular disease. Predictors included in the SMART risk score included age, sex, current smoking, diabetes, systolic blood pressure, total cholesterol, HGL cholesterol, presence of coronary artery disease, cerebral-vascular disease, peripheral artery disease, abdominal aortic aneurysm, estimated glomariaol fruition rate, high sensitivity CRP and years since the first manifestation of vascular disease. They further externally validated the risk score in more than eighteen thousand four hundred patients with various types of vascular disease fro the TNT ideals Sparkle and Capri trials.     The overall findings was that the external performance of the SMART risk score was reasonable apart from over-estimation of risk in patients which a ten year risk of more than forty percent. What was striking was the substantial variation in the estimated ten year risk. The median ten year risk of a reoccurring major vascular event was 17 percent but this varied for less than 10 percent in 18 percent to more than 30 percent in 22 percent of patients.     The authors further estimated residual risk at guideline recommend targets by applying the relative risk reductions form meta-analysis to estimated risks for targets for systolic pressure, LDL, smoking, physical activity and use of anti-thrombotic agents. They found that if all modifiable risk factors were at guideline recommend targets only half of the patients would have ten year risk of less than 10 percent. Even with optimal treatment many patients with vascular disease appear to remain at more than a 20 percent or even more than 30 percent of a ten year risk.     The take home message is that a single secondary prevention strategy for all patients with vascular disease may not be appropriate. Instead novel risk stratification approaches may be helpful to individualize secondary prevention by identifying high risk patient which may derive the greatest benefit from novel interventions.                       The next study provides experimental evidence that an indigenous-gastro transmitter hydrogen sulfide may potentially be a therapeutic target in diabetic patients with cardiovascular diseases. In this paper by first author Dr. Chen, corresponding author Dr.Kisher and Colleagues from the Louis Cat's school of medicine Temple University in Philadelphia. Authors aim to evaluate the role of hydrogen sulfide deficiency in diabetes induced bone marrow cell dysfunction and to examine the therapeutic effects of restoring hydrogen sulfide production in diabetic bone marrow cells on ischemic high limb injury in diabetic DBDB mice. They further specifically investigated the effects of hydrogen sulfide deficiency on the nitric oxide pathways under conditions of high glucose. They found that bone marrow cells for diabetic DBDB mice had decreased hydrogen sulfide production and lower levels cystathonine gamma lyaze which is the primary enzyme that produces hydrogen sulfide in the cardiovascular system. Administration of a stable hydrogen sulfide donor and over expression of cystathonine gamma lyaze in diabetic bone marrow cells restore their functional and restorative properties. Further more they demonstrated that the therapeutic actions of hydrogen sulfide were mediated by nitric oxide pathway involving endothelial nitric oxide synthase PT495.     In summary these results support the hypothesis that hydrogen sulfide deficiency plays critical role in diabetes induced bone marrow cell dysfunction and suggests that modulating hydrogen sulfide production in diabetic bone marrow cells may have transformational value in treating critical limbs ischemia.     The next study reinforces the importance of hypertension as a critical risk factor for inter-cerebral hemorrhage, and suggests that Blacks and Hispanics may be a particularly high risk. In this study by DR. Walsh and colleagues for the University of Cincinnati, authors conducted the largest case controlled study to date on treated and untreated hypertension as a risk factor for inter-cerebral hemorrhage. They also investigated whether there was variation by ethnicity. The ethnic racial variations of inter-cerebral hemorrhage or eriche study is a prospective multi-center case controlled study of inter-cerebral hemorrhage among Whites, Blacks and Hispanics. Cases were enrolled from 42 recruitment cites, controls were matched cases one to one by age, sex, ethnicity and metropolitan area. A total of 958 white, 880 black and 766 Hispanic cases of inter-cerebral hemorrhage were enrolled. Untreated hypertension was more highly prevalent in Blacks at almost 44 percent and Hispanics at almost 47 percent compared to whites at 33 percent. Treated hypertension was a significant independent risk factor and untreated hypertension was substantially greater risk factor for all three ethnic groups and across all locations. There was a striking interaction between ethnicity and risk of inter-cerebral hemorrhage, such that untreated hypertension conferred a greater risk of inter-cerebral hemorrhage in Blacks and Hispanics relative to Whites.                         The nest study provides the first prospective multi-centered data on mortality and morbidity in rheumatic heart disease from low and middle income countries. First author Dr. Zulky, corresponding author Dr. Mayoci and authors from Gertrude hospital and University of Cape Town in South Africa present the results of two year follow up of the global rheumatic heart disease registry or remedy study in 3343 children and adults with rheumatic heart disease from 14 low and middle income countries. They found that although patients were young with a median age of only 28 years the 2 year case fatality rate was high at almost 17 percent. The median age at death was 28.7 years. Mortality was higher in low income and low middle income regions compared to upper middle income countries. Independent predictors of death was severe valve disease, more advanced functional class, atrial fibrillation and older age. Where as post primary education and female sex were associated with a lower risk of death. The authors carefully noted that apart from age and gender the independent risk factors for mortality such as severity of valve disease heart failure, atrial fibrillation and low education were all modifiable and thus they called for programs focused on the early detection and treatment on clinical rheumatic heart disease.     Well that's it for the summaries, now lets go over to China     For our feature interview today we are going all the way to Beijing at the great Wall meeting where we will be meeting authors as well as editors. So here we have first and corresponding author Professor {Dong Fen Gu} and co-author Professor {Sherliang} both from {Fu Y} hospital Chinese academy of medical sciences in Beijing. Welcome   Dr.Gu: Welcome we are so delighted to be interviewed by you   Dr. Carolyn Lam:   Thank you so much we are so excited to be talking about your paper predicting the ten year risks of cardiovascular disease in the Chinese population. And here we have as well editor in chief Dr. Joe Hill as well as Dr. Amid Kira digital strategies editor and associate editor. Gentlemen how is it in Beijing? And I hear that you have a Chinese greeting for everyone as well.   Joe Hill: {Ni how} and {nuchme and senchmen}   Amid Kira: I can't top that but I agree with what Joe said   Dr. Carolyn Lam: Dr. Gu, could you please tell us what is it that is so different about cardiovascular disease in China compared to what we heard about in the western world.   Dr.Gu: Okay cardiovascular disease is both leading cause of death in China and in United States as well in European countries. However the patterns for components of cardiovascular disease including coronary arteries and stroke are still quite different in the Chinese populations compared united states. For example there are coronary arteries mortality rate in the united states is along the 100 thousand per year and this is the first leading cause of death in the united states. And for stroke the annual mortality rate is along 36 per 100 thousand in the united states populations. However in china the stroke mortality rate among Chinese populations is around the 160 per 100 thousand, so that almost 3.5 to 4 as high as in untied states. Obviously for our lifestyle in including battery behavior quite different you can easily identify one kind of difference in the united states and the Europe restaurants from Chinese restaurants and some western style restaurants you can figure it out.             And another example, smoking rate is major component for risk of cardiovascular disease it is very high in Chinese adult men. It over 50 percent right now but in the united states in the past 50 years it declined immensely. And around maybe less than around 20 percent and from the previous experiment from studies by Dr. Liu Chin from and my colleague Dr.WU they used the questions for predictions of coronary arteries compared to equations and also use the similar prediction model compares that its chemical cardiovascular disease from the united states population and the Chinese population. That to over estimation if we use the united states produced this kind of equation. So based on this kind of scenario we based on Chinese long term larger scales cohort to precede and study our own prediction model.   Dr. Carolyn Lam: Wow that is really fascinating Dr. Gu and I really could not agree with you more because I sort of trained in the united states for quite some time and then I moved back to Singapore and saw for myself in Asia the tremendously high rates of stroke. I was also very struck by the relative youth of the patients suffering cardiovascular disease and the differences in risk factors, the smoking but not just that, obesity is almost defined on a different scale in our relatively sized smaller Chinese population compared to that in the western. Congratulations to you and your team for a successful amazing effort. Could you or Dr. Yang now just let us know what are your main findings.   Dr. Yang:           Well I think there are 2 major finding for our work. First we developed a new prediction risk model you know after analysis is for high risk score or equations released by AJ and ACC and is some other risk scores. We included 6 conditional risk factors in combination with our previous knowledge that included age, treated or untreated ISBP, total classical, HDLC current smoking and diabetes. So this traditional risk factors were set up as a base model and then we use the predefined statistical to include new additional variables they were Chinese special elements. Finally in our model there were rates as constraints and geographic region which means northern part versus the southern part in China and also organization is rural or urban area. And finally the forth one is family history as a CVD so this for additional variables in our model suggest that we maybe as a Chinese prediction and equations has something special. For example we feel more attention for central obesity in primary prevention in Chinese populations and also you know the norther part and the southern part there are large differences in the risk profiles. And so maybe according to our risk prediction model we pay more attentions for the residence living in northern part in China.     And then for the second points I think we found that PCE equation which shows for equations was not appropriate to predict ten year risk of in Chinese populations. For example in our revelation cohort we found that our model just slightly over predicts severity risk by 17 percent in Chinese man but when we use the PCE models released form AHA the over-estimation come to 50 percent so maybe equations from western populations are not appropriate to Chinese populations.   Dr. Carolyn Lam: Thank you so much Dr. Yang I mean those are just such important findings applicable to a huge population in china, like you said. And just as important as the second point that the pooled equations derived from western populations may not be the most appropriate for certain other ethnic populations. I think that a very important message and that why we are so proud to be publishing this in Circulation. Could I ask then are you applying these new equations in your personal clinical practice?   Dr.Gu:   Risk assessment is a fundamental components for prevention of ASSVD. In Chinese we question {turn the PA on} provide a valuable to identify high risk individuals in Chinese populations. And not with just complicated [inaudible 00:18:02] for further analysis. And propose three levels of groups of risk stratification could be identified by cut off 5 percent and 10 percent. So lower risk individuals with predicted activity risk of less than 5 percent should be offered lifestyle wise to maintain the lower risk status. While the moderate risk individual is predicted risk of 5 to 10 percentage for intensive therapeutic lifestyle change wit drug therapy if necessary. For the high individual risk high or large 10 percent teheraph of clinical aliment taken account for physicians recommendation should be required with therapy for the lifestyle modification. Then annually clinic up, including an echocardiographic information for carotid artery back and even for outer [inaudible 00:19:09] CT examinations for coronary artery are recommended. Also blood pressure, lipids, glucose measurement if necessary are suggest according to Chinese guideline. While cardiovascular disease prevention as well as for the epidemic of this kind a lines. For ACVD patients those are different kinds of risk assessment we could know whether their risk profile had been improved or be progressed so that appropriate clinical elements should be taken in clinical practice.   Dr. Carolyn Lam: Thank you very much Dr. Gu so that just show that these findings are immediately clinically applicable and I trust that means you're suing it in your clinics too, and once again were so happy to be publishing this in Circulation so in the rest of the time in going to now direct questions at Joe and Amid.     How's China been? How are your chopstick skills and any word on how Circulation is being received there?   Joe Hill: Well Carolyn its a delight to be here this is a bustling media that get better and better every year. In about 2 hours we have our first ever Circulation session, we brought several editors here to discuss the types of content that we are looking to publish, the type of work across prevention and population and electrophysiology of heart failure. This is an extraordinary media that is now internationally acclaimed and as we've heard here, the face of cardiovascular disease in Asia is changing. And as you pointed out 60percent of the human race lives in Asia and we want to do everything we can to be here on the ground, in Asia trying to address this curve that is already present and is worsening by the day.   Dr. Carolyn Lam: Amid, you know you've seen the latest statistic on our podcasts and you highlighted that we have quite a number of listeners over there as well. Would you like to tell me how this is all blending it to the digital strategies and anything else you might want to highlight?   Amid Kira: Sure its been an incredible meeting and we get to meet great colleagues like our colleagues today on this podcast and learning so much from this meeting. Our podcast as you pointed out quite a sizable and growing cadre of people in Asia and Japan and China who are listening and we truly want to enhance that as Joe mentioned with the large splurge of cardiovascular disease and the great science that is going on here. Want to make sure that we are able to be apart of that conversation and interact with researcher and clinitions here. In addition to podcast, we are exploring some other options involving social media, specifically in China so stayed tuned in how those develop but we certainly appreciate the importance of being her and interacting where so much of cardiovascular disease and cardiovascular science is occurring.   Dr. Carolyn Lam: That's so great. Joe or Amid now there's a specific we would like to highlight to our listeners the doodle, either of you want to pick that up a bit about blipping the doodle?   Amid Kira: So there is as you know Circulation now has this doodle where we change it periodically and its sort of a fun themed thing. Right now I think it Halloween and we've had several other ones that people have designed to sort of keep thing fresh and light and interesting. There's a new app called blippar which you can download from iTunes or android stores and you can essentially scroll that over with your phone with the doodle and that will take you to new content either table of contents of videos, different kinds of content that it can navigate you to. So I hope people will not only enjoy the doodle kind of anticipate what's next in terms of seasons but will take the time t blip the doodle when they get a chance.   Dr. Carolyn Lam: That great and that blippar- B l I P P A R. You really c should check it out, anyone who is listening to this really check it out you'll be floored. Joe could I just turn the mic to you for any last words about the global outreach of Circulation, I mean its just so amazing that you're there in China   Joe Hill: Well heart disease Carolyn knows no boundaries nor does Circulation. There was a day when cardiovascular disease was largely an issue in the developed world that is long since gone and that's why the study that we are talking about today with these authors is so important because the face of cardiovascular disease is different than in the west, the ways in which it is  evolving id different here than in the west and I like many others foresee an increase a significant increase in the types and prevalence of heart disease here in Asia. for all the reasons that we have been talking about, hypertension, obesity, type two diabetes, smoking the environment all of these challenges I fear are going to lead to a substantial increase in the prevalence of heart disease in Asia and that why we're here on the ground with Circulation in Asia that's why we have one of our major leaders Chong Shong Ma who is here in Beijing. Circulation is in China everyday, it's in Beijing everyday to try and address this problem.   Dr. Carolyn Lam: And you heard it from our editor and chief, so thank you everyone for listening to this episode of Circulation on run. Tune in next week.      

Download Episode02.mp3 Our first PD episode consisting of audio that we were, largely, not responsible for. The recording consists of the majority of a panel discussion that was held on Friday, October 12th, 2012. The panel was held after a screening of We Are Wisconsin at the Workers' Arts and Heritage Centre in Hamilton, Ontario. The panel was moderated by Dr. Stephanie Ross of the Work and Labour Studies Program at York University and included the film's director Amie Williams, Wisconsin union activist Rachel Friedman, and local representatives Lisa Hammond, President of HWETL and Anthony Marco (me), Member of the HDLC Executive and OSSTF District 21. All panel members gave permission for this recording to be uploaded for this podcast. We hope you find it interesting, and we'll back next weekend with a more "traditional" episode.

Single nucleotide polymorphisms (SNPs) in genes involved in fatty acid metabolism (FADS1 FADS2 gene cluster) are associated with plasma lipid levels. We aimed to investigate whether these associations are already present early in life and compare the relative contribution of FADS SNPs vs traditional (non-genetic) factors as determinants of plasma lipid levels. Information on infants' plasma total cholesterol levels, genotypes of five FADS SNPs (rs174545, rs174546, rs174556, rs174561, and rs3834458), anthropometric data, maternal characteristics, and breastfeeding history was available for 521 2-year-old children from the KOALA Birth Cohort Study. For 295 of these 521 children, plasma HDLc and non-HDLc levels were also known. Multivariable linear regression analysis was used to study the associations of genetic and non-genetic determinants with cholesterol levels. All FADS SNPs were significantly associated with total cholesterol levels. Heterozygous and homozygous for the minor allele children had about 4% and 8% lower total cholesterol levels than major allele homozygotes. In addition, homozygous for the minor allele children had about 7% lower HDLc levels. This difference reached significance for the SNPs rs174546 and rs3834458. The associations went in the same direction for non-HDLc, but statistical significance was not reached. The percentage of total variance of total cholesterol levels explained by FADS SNPs was relatively low (lower than 3%) but of the same order as that explained by gender and the non-genetic determinants together. FADS SNPs are associated with plasma total cholesterol and HDLc levels in preschool children. This brings a new piece of evidence to explain how blood lipid levels may track from childhood to adulthood. Moreover, the finding that these SNPs explain a similar amount of variance in total cholesterol levels as the non-genetic determinants studied reveals the potential importance of investigating the effects of genetic variations in early life.

Guest: Terry Jacobson, MD Host: Larry Kaskel, MD Dr. Terry A. Jacobson explains to host Dr. Larry Kaskel the importance of non-HDL cholesterol reporting in lipid management. Dr. Jacobson describes additional lipid parameters that are emerging as valuable adjuncts to the standard panel, including measurements of apolipopprtoeins and LDL particle size and concentration. Specifically, Dr. Jacobson outlines the importance of non-HDL-C as a secondary goal of therapy, and the advantages of non-HDL measurements over traditional lipid parameter for the prediction of cardiovascular events. Most importantly, Dr. Jacobson provides the simple calculation for this measurement which is not yet reported on standard lipid panels, but is easily accessible from the information on these routine panels. Brought to you by:

Das DALI- Verfahren zeichnet sich vor allem durch seine einfache Handhabung und seine Kompatibilität zu Vollblut gegenüber anderen LDL- Apherese Verfahren aus. Die bisher in Studien untersuchten und herstellerseitig zugelassenen Blutflussraten von 60 und 80 ml/min führen in der Regel zu einer Behandlungsdauer pro Behandlung von etwa 2 Stunden. Die hier vorgelegte Studie sollte nun klären, inwieweit es möglich ist die Behandlungsdauer durch Erhöhung der Blutflussrate auf 120, 160, 200 und 240 ml/min zu verkürzen. Die Sicherheit, Biokompatibilität, Selektivität und Effektivität der LDL-C und Lp(a) Reduktion stellten in diesem Zusammenhang die zu untersuchenden Faktoren dar. Das Patientengut bestand aus 13 Patienten mit chronischer Hypercholesterinämie und symptomatischer Atherosklerose die in 7 verschieden Zentren deutschlandweit rekrutiert wurden und über einen bestehenden AV-Shunt verfügten und bereits schon mit dem DALI- Verfahren behandelt worden waren. Das mittlere LDL-C vor Beginn der Behandlungen betrug 162 ± 42 mg/dl. Die Behandlung mit DALI erfolgte wöchentlich. Für jede Blutflussrate waren 3 Anwendungen mit derselben Flussrate geplant, welche von 60 auf 80, 120, 160, 200 und 240 ml/min gesteigert wurden. Das Antikoagulationsschema bestand in einer reinen ACD-A Applikation bei 60 ml/min (heparinfrei) und einer Kombination aus einem Heparinbolus und einer kontinuierlichen ACD-A Infusion mit 2.66 ml/min während der übrigen Flussraten. Die klinische Verträglichkeit und Sicherheit des DALI Verfahrens war hoch. Die klinisch-chemischen Routineparameter sowie die zellulären und nichtzellulären Blutkomponenten zeigten keine signifikanten Veränderungen. Lediglich während 26 der 201 Behandlungen kam es zu leichten klinischen Nebenwirkungen die zu keiner ernsthaften Gefährdung der Patienten führten. Die Reduktion des bestimmten LDL-C betrug durchschnittlich 73%, 66%, 57%, 52%, 51%, 47% bei Qb = 60, 80, 120, 160, 200, 240 ml/min. Die mittlere Reduktion des Lp(a) lag bei 68%, 67%, 62%, 60%, 58%, 56% während die Reduktion von Selektivitätsparametern, wie dem HDL-C, Protein, Albumin und den Immunglobulinen G und M, £ 17% betrug. Durch die Erhöhung der Flussrate konnte die Dauer der Behandlung von Initial 142 Minuten bei Qb = 60 ml/min auf 83 bzw. 45 Minuten bei Qb = 120 bzw. 240 ml/min gesenkt werden. Die Daten der hier vorgelegten Studie implizieren, dass eine sichere und effektive Anwendung des DALI- Verfahrens mit Blutflussraten von bis zu 120 ml/min möglich ist. Die signifikante Senkung der Behandlungsdauer von 142 auf 83 Minuten entspricht dabei einer Zeitersparnis von 42%. Außerdem ist es möglich, das DALI- Verfahren bei 60 ml/min heparinfrei durchzuführen.

Während man in den 80ern von der Bundespest für die Benutzung von Modems noch vor Gericht gestellt wurde, ist der Anschluß der kleinen Pfeifer heute schon Standard. Internet-Computer haben zwar manchmal immer noch kein "@" auf der Tastatur aber ohne Modem werden die Maschinen nicht mehr ausgeliefert. Jeder will auf die Datenautobahn und das möglichst schnell. Waren früher Akustikkoppler die Inkarnation des Fortschritts sind heute analoge Modems schon langsam Auslaufware. ISDN muß es schon sein, wenn es rauschen soll, doch ist damit das Ende der Fahnenstange noch lange nicht erreicht. Und mit ADSL steht der nächste Gebührenoverkill schon vor der Tür. Chaosradio erklärt Begriffe wie Modulation/Demodulation, HDLC, SLIP, PPP und andere Protokolle. Außerdem sprechen wir über Standleitungen, die einzig wahre Form der Datenautobahnzubringer.