POPULARITY
2 episodes with arteriosclerosis
2 episodes with arteriosclerosis
2 episodes with arteriosclerosis
2 episodes with arteriosclerosis
4 episodes with arteriosclerosis
A Rebelião Saudável nasceu da união de diversos profissionais de saúde que pensam diferente e cujo foco é promover saúde e bem estar, com comida de verdade e sem medicamentos.Semanalmente a Rebelião se reune no app Telegram para discussão de tópicos importantes relacionados a Nutrição Humana e Qualidade de vida. Nessa semana, conversamos conversamos sobre Transcitose: O Elo Perdido entre LDL e Aterosclerose!Estudos comentados no Podcast:BOLANLE, I. O.; DE LIEDEKERKE BEAUFORT, G. C.; WEINBERG, P. D. Transcytosis of LDL Across Arterial Endothelium: Mechanisms and Therapeutic Targets. Arteriosclerosis, Thrombosis, and Vascular Biology, v. 45, p. 468–480, abr. 2025. DOI: 10.1161/ATVBAHA.124.321549.Subbotin VM. Excessive intimal hyperplasia in human coronary arteries before intimal lipid depositions is the initiation of coronary atherosclerosis and constitutes a therapeutic target. Drug Discov Today. 2016 Oct;21(10):1578-1595. doi: 10.1016/j.drudis.2016.05.017. Epub 2016 Jun 2. PMID: 27265770.Vídeo sobre transcitose no YouTube: https://youtu.be/j3p85NFtoa8
❤️ Bonjour,Bienvenue dans ce nouvel épisode consacré au cholestérol !
A Japanese team has found that social loneliness decreases the levels of oxytocin, known as the "happy" or "love" hormone, in mice, resulting in lipid metabolism disorders in the liver and worsening arteriosclerosis.
“Antioksidan ing panganan lan tanduran sing asifat neuroprotektif bisa nyingkiri arteriosclerosis lan njaga arteri resik” - “Kita gesang lan mobah mosik wonten ing Panjenenganipun; kita nunggil kaliyan Panjenenganipun lan kaliyan Sang Rama”
Want to add a healthy habit to your daily routine that is absolutely free and incredibly effective? Looking to reduce insulin resistance and lose visceral fat? Want to boost mental health and improve cognitive function? Look no further than walking! Tune in to hear us unpack the myriad of research-supported benefits. In this episode, we discuss the incredible benefits of walking, from lowering blood pressure to improving heart rate variability to reducing stress and so much more. Learn about the magic number when it comes to step count, our thoughts on walking in nature vs. on a treadmill, and get practical tips for getting those steps! Also in this episode: Naturally Nourished Teas are buy 3 get 1 FREE, use code FREETEA Gift cards at Naturally Nourished Detox Masterclass 1/8 Keto Masterclass 1/15 Walking Pad C2 use code ALIMILLERRD for savings Health Benefits of Walking Lowers Blood Pressure Hypertension: Brisk walking for 30 minutes, five days a week reduces blood pressure (Hypertension, 2020). Improves Cholesterol Levels Cholesterol: Effects on LDL and HDL cholesterol (Journal of the American Heart Association, 2021). Lipid Profiles: Walking improves triglycerides and HDL (Atherosclerosis, 2021). Reduces the Risk of Coronary Artery Disease Coronary Artery Disease Risk: 150 minutes of walking weekly (Circulation, 2022). Enhances Cardiorespiratory Fitness Reduces Systemic Inflammation Systemic Inflammation: Walking lowers CRP and IL-6 (Arteriosclerosis, Thrombosis, and Vascular Biology, 2020). Systemic Inflammation: Walking reduces inflammatory cytokines (The Journal of Endocrinology, 2022). Helps Maintain Healthy Weight and Prevent Obesity Improves Heart Rate Variability Heart Rate Variability: HRV improvement with regular walking (Heart, 2022). Prevents Peripheral Artery Disease Peripheral Artery Disease: Walking improves circulation and function in PAD patients (Journal of Vascular Surgery, 2021). Reduces Resting Heart Rate Enhances Endothelial Function Supports Recovery After Cardiac Events Improves Insulin Sensitivity Insulin Sensitivity: Improvements with post-meal walks (Diabetes Care, 2021). Enhances Glucose Regulation Boosts Fat Oxidation Fat Oxidation: Brisk walking boosts fat metabolism (Journal of Applied Physiology, 2022). Reduces Visceral Fat Reduction of visceral fat after 10,000 steps/day (Obesity, 2021). Promotes Energy Balance Energy Balance: 12,000 steps/day for maintaining weight (Medicine & Science in Sports & Exercise, 2020). Regulates Hormones Related to Metabolism Increases Mitochondrial Efficiency Improves Metabolic Flexibility Prevents Metabolic Syndrome Helps Manage Type 2 Diabetes Mental health Stress Reduction: Nature walks lower cortisol more than treadmill (Environmental Research, 2022). Stimulates Neurogenesis and Brain Plasticity Brain Connectivity: Walking improves default mode network activity (Journal of Aging Research, 2021). Enhances Neurotransmitter Balance Supports Autonomic Nervous System Regulation Improves Sensory Integration Vestibular Function: Enhancing balance and stability with walking (Frontiers in Neuroscience, 2021). Strengthens Cognitive Function Neurogenesis and Cognitive Function: Exercise-induced brain growth (Nature Neuroscience, 2021). Promotes Myelination and Nerve Health Enhances Emotional Regulation via the Vagus Nerve Reduces Neurological Disease Risk Synchronizes the Nervous System Through Rhythmic Movement Improves Sleep and Circadian Rhythm Bone and Joint Health Immune System Support Longevity and Reduced Mortality Gut Health Gut Health: Positive effects on microbiota diversity (Gut Microbes, 2020). The Science of Step Counts Thoughts on Nature vs. Treadmill Walking Cognitive Benefits: Nature walking improves attention restoration (Nature Neuroscience, 2021). Proprioception: Benefits of uneven terrain in natural settings (Journal of Sports Medicine, 2023). Motivation: Outdoor walkers maintain habits better than treadmill users (Behavioral Medicine, 2022). Immune Boosting: Increased NK cell activity in forest walkers (International Journal of Environmental Health Research, 2021). Sponsors for this episode: According to extensive research by the Environmental Working Group, virtually every home in America has harmful contaminants in its tap water. That's why you've got to check out AquaTru. AquaTru purifiers use a 4-stage reverse osmosis purification process, and their countertop purifiers work with NO installation or plumbing. It removes 15x more contaminants than ordinary pitcher filters and are specifically designed to combat chemicals like PFAS in your water supply. Naturally Nourished Podcast listeners can use code ALIMILLERRD at AquaTru.com to save 20% off.
“Antioksidan ing panganan lan tanduran sing asifat neuroprotektif bisa nyingkiri arteriosclerosis lan njaga arteri resik” “Kita gesang lan mobah mosik wonten ing Panjenenganipun; kita nunggil kaliyan Panjenenganipun lan kaliyan Sang Rama”
Cómo funciona la colaboración con Fanté https://hijosdelaresistencia.com/fante/ Elige lo que prefieras: 10% descuento con el código PODCASTHDLR Acceso a regalos y formación exclusiva con el código REGALOHDLR ____________________________________________________________ Apúntate a nuestra Newsletter aquí: https://hijosdelaresistencia.com/un-email-semanal Entrena con nosotros: https://hijosdelaresistencia.com/formulario/ Accede a La Academia https://academia.hijosdelaresistencia.com/ ____________________________________________________________ Las enfermedades vasculares son la principal causa de muerte a nivel mundial y deja cerca del 30% de las muertes en España liderando el top junto con las enfermedades oncológicas. En este episodio hablamos con el Dr José María Mostaza, Jefe de Sección de Medicina Interna del Hospital La Paz, Codirector de la Unidad de Riesgo Vascular del Hospital La Paz y Profesor de la Facultad de Medicina de la Universidad Autónoma de Madrid, Presidente de la Sociedad Española de Arteriosclerosis y Ex Presidente del grupo de Riesgo Vascular de la Sociedad Española de Medicina Interna, para ahondar en una problemática que parece crecer año tras año a pesar de las investigaciones y los avances científicos ____________________________________________________________ También pueden seguirnos en nuestras redes sociales: https://www.instagram.com/hijosdelaresistencia_oficial/ https://www.instagram.com/ruben.espinosa_/
Professor Erica Spatz MD talks to Dr Funmi Okunola MD about the effects of Long COVID on the heart. Professor Spatz is a cardiologist and clinical investigator at the Centre for Outcomes Research and Evaluation. She is the Associate Professor of Cardiology and Associate Professor of Epidemiology at Yale School of Medicine in the USA and is the Director of the Preventative Cardiovascular Health Program. REFERENCES1.Shah SM, Odanovic N, Kunnirickal S, Feher A, Pfau SE, Spatz ES. Chest pain and coronary endothelial dysfunction after recovery from COVID‐19: A case series. Clinical Case Reports. 2022 Apr;10(4):e05612.2.HilserJR, Spencer NJ, Afshari K, Gilliland FD, Hu H, Deb A, Lusis AJ, Wilson Tang WH, Hartiala JA, Hazen SL, Allayee H. COVID-19 Is a Coronary Artery Disease Risk Equivalent and Exhibits a Genetic Interaction With ABO Blood Type. Arteriosclerosis, Thrombosis, and Vascular Biology. 2024 Nov;44(11):2321-33.
Get ahead with VETAHEAD and join Dr. Proença on 15 minutes of ZooMed (exotic animal medicine) content. Today's episode is packed with insights on adipocytic (fat) tumors and xanthomas in our feathered friends! Join Dr. Proença as she breaks down a massive study covering 20 years of data on parrot adipocytic tumors, revealing key risk factors, common sites, and surprising associations with other health issues like arteriosclerosis and hepatic lipidosis. Ever wondered if age or species puts your patients at higher risk? Or which types of tumors are more likely to pop up in those Amazons and cockatiels? Tune in to get the lowdown on everything you need to know about these sneaky tumors, and how to better inform your clients about prognosis and care. Get ready to take your avian practice to the next level! Click here to get your VETAHEAD E-Magazine! Click here to receive a VETAHEAD Gift! Do you want to access more ZooMed (exotics) knowledge directly from specialists? Come with us and #jointhemovement #nospeciesleftbehind Head to VETAHEAD Website Join our VETAHEAD Community Follow @the_vetahead on Instagram Subscribe to @vetahead channel on YouTube Follow @vetahead on Facebook Follow @vetahead on TikTok
❤️ Bonjour,Bienvenue dans cet épisode consacré au renforcement musculaire
Because cardiovascular disease is the world's leading cause of death, researchers have been looking for ways to diagnose it early. Low-frequency sounds have been used to assess the elasticity of blood vessels, but until now, the elastic waves being studied were too fast to get precise measurements. Sibylle Gregoire (INSERM) discusses how here team has been able to image a different type of elastic wave, opening up the possibility to more precise assessments and diagnosis of cardiovascular disease in the future. Associated paper: Sibylle Gregoire, Gabrielle Laloy-Borgna, Johannes Aichele, Fabrice Lemoult, and Stefan Catheline. "Flexural pulse wave velocity in blood vessels." J. Acoust. Soc. Am. 155, 2948–2958 (2024). https://doi.org/10.1121/10.0025855.Read more from The Journal of the Acoustical Society of America (JASA).Learn more about Acoustical Society of America Publications.Music Credit: Min 2019 by minwbu from Pixabay.
N-acetyl cysteine (NAC) shows promise for heart attack preventionHeart attacks and strokes are a leading cause of death in developed countries - accounting for ~20% of all deaths in the U.S. Frequently, heart attacks and strokes are caused by blood clots (blood platelets that form when they are not needed, causing a narrowing/blockage of blood vessels) formed through arterial thrombosis. Current antiplatelet agents (e.g., aspirin) are effective but can increase major bleeding risk. As such, there is a growing need to prevent arterial thrombosis different from antiplatelet agents.A recent study published in Arteriosclerosis, Thrombosis, and Vascular Biology investigated the potential of NAC as an agent to prevent arterial thrombosis. Utilizing both [cell-based] human blood models and mouse (in vitro) models, the research demonstrated that NAC significantly delayed and even prevented thrombus formation dose-dependently without increasing bleeding risks.Findings:*NAC treatment extended clot formation times by up to 3.7 times compared to controls in the human blood [cell] model.*NAC entirely inhibited platelet aggregation and occlusive clot formation at higher doses than the above point in the cell model.*A 400 mg/kg (via injection in rodents) dose of NAC in mice effectively prevented arterial occlusion post-injury.*Lower doses (200 mg/kg - via injection in rodents) of NAC reduced clot stability, suggesting working as both an acute and preventative clotting therapy.The study showed that NAC interferes with von Willebrand factor (a large protein crucial for blood clotting) activity. NAC acts against VWF rather than platelets to prevent clot formation. Thus, providing a safer alternative to traditional antiplatelet drugs that carry higher bleeding risks. Support the Show.
“Antioksidan ing panganan lan tanduran sing asifat neuroprotektif bisa nyingkiri arteriosclerosis lan njaga arteri resik” “kita mbutuhake pengalaman pribadi Karo Gusti Allah sakdurunge kita andum bab iku marang wong liya”-
Do it now!At the end is the memory exercise that brought a Russian Guinness record to memorize. We see people using their smartphones extendedly and that affects the neck, and the brain negatively. What affects our memory?First the blood supply to our brain.Two arteries: vertebral arteries are completely in the spinal Chanel and the internal carotid arteries, they split into the Anterior and posterior arteriesIf you turn your head to the extreme left or right side, it will influence even your healthy vertebral blood flow. If the vertebral arteries get blocked or pinched, that will cause headaches. If you have the carotid arteries blocked, then Arteriosclerosis will develop there… and Stroke…We can use special massages to loosen our muscles and vertebrae.Intrinsic massage for the neckYou massage the back of your neck where your head starts, and try to go inside this gap between the neck and the head. I recommend the Decathlon Aptonia Vibration Electronic Massage Device and use the smallest of the 3 tip balls massager.Where the pain is, massage that strongly.Then get a neck roll lie on your back and press with your neck until your shoulder blade lifts up you can also help with elbows to press against the ground do this 10 to 15 times.Then lay on the stomach in an elevated place so that the head can swing up up and down freely. Do this 10 to 15 times.And lay on the side so that the head can wing up and down freely. Do this for the left and right sides 10 to 15 times. Finally the exercise of your memory! You will increase your memory.You will gain more awareness of what you do.Let you fall asleep easily.Go to remember your entire day vividly when lying in bed… What you did what you not did…How you brushed your teeth... Try to remember your day in every detail until you go to bed and fall asleep…And so you remember all your events better and better…This was the exercise of one of the best brains, the world record in the Guinness book to remember the last 1000 digits after the decimal point. My Video: How to improve memory by 116-117 times? https://youtu.be/UH06217DUocMy Audio: https://divinesuccess.net/wp-content/uploads/2021/Podcast4/How-to-improve-memory-by-116-117-times.mp3
Looking 4 Healing Radio with Dr. Bryan Ardis – What are the most common cardiovascular disease states and symptoms that the majority of people worldwide are struggling with today? Heart disease is still one of the number one causes of death and all of America and around the world each year. If you or a loved one has ever been diagnosed with high blood pressure or hardening of their arteries, ever had a heart attack, or have...
Looking 4 Healing Radio with Dr. Bryan Ardis – What are the most common cardiovascular disease states and symptoms that the majority of people worldwide are struggling with today? Heart disease is still one of the number one causes of death and all of America and around the world each year. If you or a loved one has ever been diagnosed with high blood pressure or hardening of their arteries, ever had a heart attack, or have...
Looking 4 Healing Radio with Dr. Bryan Ardis – While taking a drug like statin drugs to lower your risk of heart attacks and strokes, I do not believe it is a good choice, knowing that the drug causes men and women throughout the world to develop type 2 diabetes. Did you also know that aspirin which is the second most prescribed drug to people with this condition? Do you know it's published to cause hallucinations and vomiting of blood?
Looking 4 Healing Radio with Dr. Bryan Ardis – While taking a drug like statin drugs to lower your risk of heart attacks and strokes, I do not believe it is a good choice, knowing that the drug causes men and women throughout the world to develop type 2 diabetes. Did you also know that aspirin which is the second most prescribed drug to people with this condition? Do you know it's published to cause hallucinations and vomiting of blood?
“Antioksidan jroning panganan lan tanduran sing duwe kasiat neuroprotektif bisa nyingkrihake arteriosclerosis lan njaga arteri resik” - “Misi kuwi saka ing asale lan tujuane ya mung Gusti Allah piyambak.“
“Antioksidan ing panganan lan tanduran sing asifat neuroprotektif bisa nyingkiri arteriosclerosis lan njaga arteri resik” - “Kita gesang lan mobah mosik wonten ing Panjenenganipun; kita nunggil kaliyan Panjenenganipun lan kaliyan Sang Rama”
In this episode, we review the high-yield topic of Arteriosclerosis from the Cardiovascular section. Follow Medbullets on social media: Facebook: www.facebook.com/medbullets Instagram: www.instagram.com/medbulletsofficial Twitter: www.twitter.com/medbullets --- Send in a voice message: https://podcasters.spotify.com/pod/show/medbulletsstep1/message
Thanks for listening or watching. Please hit subscribe where you're watching or listening so you don't miss out on future episodes. Please leave a review, it takes 30 seconds and really helps get these exciting messages out there. And if you or anyone you know could benefit from a mental health tune-up, head over to metpsy.com where myself and psychiatrist Dr. Rachel Brown coach you to better mental health. Discussion 7:40 Autoimmunity in Africa (Trowell & Burkitt, 1981) 18:20 Daughter's allergies (Goodrich, 2011) 20:46 Intestinal permeability & wheat (Visser et al., 2009) 22:28 Celiacs who are allergic to mitochondria (Cervio et al., 2007; Volta et al., 2002) 23:20 Increasing prevalence of Celiac (Catassi et al., 2010; Rubio–Tapia et al., 2009) 35:35 Wheat, goat grass, 33-mer (Brouns et al., 2022) 38:45 Wheat in Egypt (Abu-Zekry et al., 2008) 43:00 Wheat and T1DM (Ciacci & Zingone, 2016) 47:25 Wheat is a carcinogen (O'Farrelly et al., 1986) 50:50 Wheat and schizophrenia (Dohan, 1966) 52:38 Poison ivy and PUFA (Xia et al., 2004) 56:34 PUFA up to 20% of American diet (National Cancer Institute, 2019) 57:42 Brown & Goldstein and LDL (Goldstein et al., 1979) 58:54 Steinberg & Witztum and modified LDL (Steinberg et al., 1989) 1:00:00 OxLDL and auto-antibodies (Hörkkö et al., 1996) 1:00:02 Antiphospholipid syndrome and cardiolipin (Hörkkö et al., 1996; Tuominen et al., 2006) 1:09:16 400-1000x as oxidized as normal LDL (AOCS American Oil Chemists' Society, 2021) 1:11:56 All autoimmune diseases involve oxidative stress—seed oil toxicity (Pagano et al., 2014) 1:12:20 Oxidized linoleic acid induces beta-amyloid (Arimon et al., 2015) 1:14:00 Insulin resistance and oxLDL (Li et al., 2013) 1:19:06 Homicide and linoleic acid consumption (Drewitt-Smith & Rheinberger, 2019; Hibbeln, 2007; Hibbeln et al., 2004) 1:21:20 Smoking and CVD-free populations (Lindeberg et al., 1994; Sinnett & Whyte, 1973) 1:25:28 OxLDL and beta cells (Abderrahmani et al., 2007) Other References Hibbeln, J. R. (2007). From Homicide to Happiness – A Commentary on Omega-3 Fatty Acids in Human Society. Nutrition and Health, 19(1–2), 9–19. https://doi.org/10.1177/026010600701900204 Hibbeln, J. R., Nieminen, L. R. G., & Lands, W. E. M. (2004). Increasing homicide rates and linoleic acid consumption among five western countries, 1961–2000. Lipids, 39(12), 1207–1213. https://doi.org/10.1007/s11745-004-1349-5 Sinnett, P. F., & Whyte, H. M. (1973). Epidemiological studies in a total highland population, Tukisenta, New Guinea: Cardiovascular disease and relevant clinical, electrocardiographic, radiological and biochemical findings. Journal of Chronic Diseases, 26(5), 265–290. https://doi.org/10.1016/0021-9681(73)90031-3 Tuominen, A., Miller, Y. I., Hansen, L. F., Kesäniemi, Y. A., Witztum, J. L., & Hörkkö, S. (2006). A Natural Antibody to Oxidized Cardiolipin Binds to Oxidized Low-Density Lipoprotein, Apoptotic Cells, and Atherosclerotic Lesions. Arteriosclerosis, Thrombosis, and Vascular Biology, 26(9), 2096–2102. https://doi.org/10.1161/01.ATV.0000233333.07991.4a Volta, U., Rodrigo, L., Granito, A., Petrolini, N., Muratori, P., Muratori, L., Linares, A., Veronesi, L., Fuentes, D., Zauli, D., & Bianchi, F. B. (2002). Celiac disease in autoimmune cholestatic liver disorders. The American Journal of Gastroenterology, 97(10), 2609–2613. https://doi.org/10.1016/S0002-9270(02)04389-7
Dr. Berg talks about the effects of high blood sugar on the arteries. Take the Dr. Berg 30-Day Fasting Challenge: https://bit.ly/drberg30daychallenge Dr. Berg's Keto and IF Lab: https://www.facebook.com/groups/drbergslab/ ADD YOUR SUCCESS STORY HERE: https://bit.ly/3zZgZKm Find Your Body Type: https://www.drberg.com/body-type-quiz Talk to a Product Advisor to find the best product for you! Call 1-540-299-1557 with your questions about Dr. Berg's products. Product Advisors are available Monday through Friday 8 am - 6 pm and Saturday 9 am - 5 pm EST. At this time, we no longer offer Keto Consulting and our Product Advisors will only be advising on which product is best for you and advise on how to take them. Dr. Eric Berg DC Bio: Dr. Berg is a chiropractor who specializes in weight loss through nutritional & natural methods. His private practice is located in Alexandria, Virginia. His clients include senior officials in the U.S. government & the Justice Department, ambassadors, medical doctors, high-level executives of prominent corporations, scientists, engineers, professors, and other clients from all walks of life. He is the author of The 7 Principles of Fat Burning. Dr. Berg's Website: http://bit.ly/37AV0fk Dr. Berg's Recipe Ideas: http://bit.ly/37FF6QR Dr. Berg's Reviews: http://bit.ly/3hkIvbb Dr. Berg's Shop: http://bit.ly/3mJcLxg Dr. Berg's Bio: http://bit.ly/3as2cfE Dr. Berg's Health Coach Training: http://bit.ly/3as2p2q Facebook: https://www.facebook.com/drericberg Messenger: https://www.messenger.com/t/drericberg Instagram: https://www.instagram.com/drericberg/ YouTube: http://bit.ly/37DXt8C
In this episode, a panel of experts discuss identifying appropriate risk assessment strategies to accurately determine the level of VTE risk for patients. Claim CE and MOC Credit at bit.ly/EvalPatVTE
Regularly eating foods high in flavonoids, like fruits, cruciferous vegetables, and tea, might lower your risk of future heart disease. In a new study published in the journal Arteriosclerosis, Thrombosis, and Vascular Biology, Australian researchers determined that older women who consumed high levels of flavonoids were less likely to develop extensive abdominal aortic calcification. This […] The post 340. A diet high in flavonoids might lower your risk of heart disease appeared first on Dr. David Geier - Feel and Perform Better Than Ever.
Join the Sanders Sisters as they welcome the holidays and the last episode of their first season of Floss & FlipFlops! In this episode, the sisters discuss the 12 medical conditions on Santa's list that can indicate a bigger systemic complication, and how you can integrate your knowledge of these conditions in helping your patients achieve lifelong health! Floss and Flip-Flops with the Sanders sisters features hosts dental hygienist and speaker Katrina M. Sanders, RDH, and podiatrist Dr Elizabeth Sanders, DPM. Together, the sisters discuss the oral-systemic link and its impact—from your teeth down to your toes. The podcast is produced monthly by Dental Products Report® and Modern Hygienist®, in partnership with The Sanders sisters. For additional content for dental professionals visit DPR and MH at dentalproductsreport.com. Katrina Sanders, RDH, can be reached at: Website: katrinasanders.com Facebook Instagram LinkedIn EPISODE 12 REFERENCES: Tattersall, M. C., et. al. (2015). Asthma Predicts Cardiovascular Disease Events: The Multi-Ethnic Study of Atherosclerosis. Arteriosclerosis, Thrombosis, and Vascular Biology, 35(6), 1520-1525. Yeh, E. T. H., & Bickford, C. L. (2009). Cardiovascular Complications of Cancer Therapy: Incidence, Pathogenesis, Diagnosis, and Management. J Am Coll Cardiol, 53(24), 2231-2247. Chaikriangkrai, K., et. a l. (2015). Additive prognostic value of coronary artery calcium score and renal function in patients with acute chest pain without known coronary artery disease: up to 5-year follow-up. Int J Cardiovasc Imaging. 31(8), 1619-1626. Liu, Y., et. al. (2014). Kidney Stones and Cardiovascular Risk: A Metaanalysis of Cohort Studies. Am J Kidney Dis, 64(3), 402-410. Uddin, S. M. I., et. al. (2018). Erectile Dysfunction as an Independent Predictor of Future Cardiovascular Events: The Multi-Ethnic Study of Atherosclerosis. Circulation. doi:10.1161/circulationaha.118.033990 Clarson, L. E., et. al. (2015). Increased risk of vascular disease associated with gout: a retrospective, matched cohort study in the UK Clinical Practice Research Datalink. Annals of the Rheumatic Diseases, 74(4), 642-647 Beckman, J., Duncan, M., et al. HIV and PAD. March 12, 2018. Circulation; 10.1161.117.032647 van Nimwegen, F. A., et. al. (2015). Cardiovascular disease after Hodgkin lymphoma treatment: 40-year disease risk. JAMA Intern Med. doi: 10.1001/jamainternmed.2015.1180 Rodondi, N., et al. (2010). Subclinical hypothyroidism and the risk of coronary heart disease and mortality. JAMA, 304(12), 1365-1374. Larsson Susanna, C., et. al. (2019) Thyroid Function and Dysfunction in Relation to 16 Cardiovascular Diseases: A Mendelian Randomization Study. Circulation: Genomic and Precision Medicine, 0(0). doi:10.1161/CIRCGEN.118.002468 Adelborg, K., et. al. (2018). Migraine and risk of cardiovascular diseases: Danish population based matched cohort study. Bmj, 360. doi:10.1136/bmj.k 96 Chapple ILC, Potential mechanisms underpinning the nutritional modulation of periodontal inflammation. J Am Dent Assoc. 2009; 140 (2): 178-184. Hujoel P. Dietary carbohydrates and dental-systemic diseases. J Dental Res. 2009; 88 (6): 490-502. Lee M, et al "Current Helicobacter pylori infection is significantly associated with subclinical coronary atherosclerosis in healthy subjects: A cross-sectional study" PloS One 2018; 13(3): e0193646. Shah NH, LePendu P., Bauer-Mehren A., et al. (June 10, 2015). Proton Pump Inhibitor Usage and the risk of MI in the general population. LLoS ONE 10(6). Mercado FB, Marshall RI, Bartold PM. Inter-relationships between rheumatoid arthritis and periodontal disease. A Review. J Clin Periodontol 2003; 30: 761-772.
Videos: Ontario College of Physicians and Surgeons state unvaccinated are meantally ill (0:48) Pandemic Amnesty': Do you Forgive and Forget? (8:19) Experts try to calm the angry AI, w Elon Musk Part 2 – (8:00) MEP Clare Daly – Speech from Nov 23 (1:12) How Long Would Society Last During a Total Grid Collapse? (14:56) The ultimate stress buster: L-theanine Columbia University Medical Center, November 16, 2022 Honestly, who would have thought that stress can cause heart damage equivalent to smoking five cigarettes? This is according to a study conducted by Columbia University Medical Center and published in the American Journal of Cardiology. The study reveals how an amino acid known as L-theanine reduces both stress levels and heart rate. As a way to increase stress levels, scientists asked 12 participants to solve a mentally stressful task in four double blind trials. L-theanine was given to participants in one of the four trials before dealing with the stressful task. In the second group, study subjects took L-theanine midway through the work. In the third and fourth variations, subjects were respectively given a placebo and nothing at all before attempting the task. In comparison to the placebo group, there was a reduced amount of immunoglobulin (a stress marker in saliva released by the immune system after exposure to viruses, bacteria, and other foreign entities) and a lower heart rate in participants who took L-theanine. The researchers explained that L-theanine works by suppressing the sympathetic nervous system responsible for the ‘fight or flight' response during emergency situations. This is achieved by blocking a chemical known as glutamate (L-glutamic acid) that carries electric signals transmitted from nerve cells to the rest of the body cells. The conclusion was that L-theanine plays a major role in terms of influencing psychology (mind) and physiology (body) function during stressful situation. Greater flavonoid intake associated with less arterial calcification Edith Cowen University (Australia), November 23 2022. The December 2022 issue of Arteriosclerosis, Thrombosis, and Vascular Biology reported a study that uncovered a relationship between greater consumption of plant compounds known as flavonoids and decreased calcification in the abdominal aorta, which supplies blood to the abdominal organs and lower limbs. Greater abdominal aortic calcification has been associated with an increased risk of stroke, heart attack and dementia. The study included 881 participants in the Perth Longitudinal Study of Ageing Women. Dietary questionnaire responses were analyzed to determine total and individual flavonoid intake. Women whose total flavonoid intake was among the top 25% of participants had a 36% lower risk of extensive abdominal aortic calcification than women whose intake was among the lowest 25%. Among women whose intake of individual flavonoids known as flavan-3-ols and flavonols was among the top 25%, respective risks were 39% and 38% lower. Those who consumed 2–6 cups per day of black tea (the main source of total flavonoid intake in this study), had a 16%–42% lower risk of extensive abdominal aortic calcification than women who were not tea drinkers. “In most populations, a small group of foods and beverages—uniquely high in flavonoids—contribute the bulk of total dietary flavonoid intake,” first author Ben Parmenter noted. “The main contributors are usually black or green tea, blueberries, strawberries, oranges, red wine, apples, raisins/grapes and dark chocolate.” “Out of the women who don't drink black tea, higher total non-tea flavonoid intake also appears to protect against extensive calcification of the arteries,” he continued. “This implies flavonoids from sources other than black tea may be protective against abdominal aortic calcification when tea is not consumed.” “Abdominal aortic calcification is a major predictor of vascular disease events, and this study shows intake of flavonoids, that could protect against abdominal aortic calcification, are easily achievable in most people's diets,” he concluded. Researchers discover that vitamin C improves health for children of pregnant smokers Oregon Health & Science University, November 22, 2022 Researchers at Oregon Health & Science University have found that vitamin C supplementation to pregnant women unable to quit smoking significantly improves airway function and respiratory health in their offspring at 5 years of age. While previous studies have shown that vitamin C improves airway function in infants, this is the first study to demonstrate that the improvement in airway function can be maintained through preschool age. The study published this week in JAMA Pediatrics. Despite anti-smoking efforts and a steady decrease of smoking among the adult population over the past decade, the addictive properties of tobacco products can make quitting smoking incredibly challenging for many individuals. Roughly 10% of American women continue to smoke in pregnancy, each year resulting in about 400,000 infants being exposed to smoke in-utero, or in the uterus. In-utero smoke exposure from maternal smoking during pregnancy can be dangerous for a developing baby and is linked to poor health outcomes, including impaired fetal lung development, decreased airway function and an increased risk for wheezing and asthma. Additionally, decreased airway growth early in life causes increased risk for serious lifelong conditions, such as chronic obstructive pulmonary disease, which is now the third leading cause of death worldwide. For this study, participating women were enrolled in a double-blind, randomized controlled trial to receive either vitamin C (500 mg/day) or a placebo. Statistical analyses showed that the effect of vitamin C supplementation to pregnant smokers prior to 23 weeks of gestation consistently resulted in significantly better airway function in their offspring at 5 years old. While the findings may improve the health of the many children who face in-utero smoke exposure, these findings may have even broader implications: The results may potentially lead to better understanding of—and treatments for—the health impacts of other smoke exposures, including indoor and outdoor air pollution, vaping and wildfires. Decades of air pollution undermine the immune system, lymph nodes study finds Columbia University Irving Medical Center, November 23, 2022 The diminished power of the immune system in older adults is usually blamed on the aging process. But a new study by Columbia immunologists shows that decades of particulate air pollution also take a toll. The study found that inhaled particles from environmental pollutants accumulate over decades inside immune cells in lymph nodes associated with the lung, eventually weakening the cells' ability to fight respiratory infections. The findings—published Nov. 21 in Nature Medicine—offer a new reason why individuals become more susceptible to respiratory diseases with age. The Columbia researchers weren't initially looking at air pollution's influence on the immune system. More than ten years ago, they began to collect tissues from deceased organ donors to study immune cells in multiple mucosal and lymphoid tissues. Such cells have been largely inaccessible to researchers studying the immune system where sampling is limited to peripheral blood. “When we looked at people's lymph nodes, we were struck by how many of the nodes in the lung appeared black in color, while those in the GI tract and other areas of the body were the typical beige color,” says Donna Farber, Ph.D., the George H. Humphreys II Professor of Surgical Sciences at Columbia University , who led the study. And as the researchers collected more tissue from younger donors, they also noticed an age difference in the appearance of the lung's lymph nodes: Those from children and teenagers were largely beige while those from donors over age 30 looked were tinged with black and got darker with increasing age. “When we imaged the lung's blackened lymph nodes and found they were clogged with particles from airborne pollutants, we started to think about their impact on the lung's ability to fight infection as people age,” Farber says. In the new study, she and her colleagues examined tissues from 84 deceased human organ donors ranging in age from 11 to 93, all nonsmokers. They found that the pollutant particles in the lung's lymph nodes were located inside macrophages, immune cells that engulf and destroy bacteria, viruses, cellular debris, and other potentially dangerous substances. The macrophages containing particulates were significantly impaired: they were much less capable of ingesting other particles and producing cytokines—chemical “help” signals—that activate other parts of the immune system. Macrophages in those same lymph nodes that did not contain particulates were unimpaired. “We do not know yet the full impact pollution has on the immune system in the lung,” Farber adds, “but pollution undoubtedly plays a role in creating more dangerous respiratory infections in elderly individuals and is another reason to continue the work in improving air quality.” Biologist explains how cannabinoids cause tumor cells to commit suicide Compultense University (Spain): November 17, 2018 A molecular biologist from Compultense University in Madrid, Christina Sanchez, has been studying the molecular activity of cannabinoids for over a decade. Through her studies, she and colleagues found that tetrahydrocannabinol , (THC) which is the main psychoactive part of cannabis, kills tumerous cells while allowing healthy cells to be. It was an unexpected discovery when Sanchez and crew were studying brain cancer cells to grasp a better understanding of how they function. They observed that when cells were exposed to THC, the tumeral cells stopped growing then destroyed themselves. This occurred both in lab tests and animal trials. Sanchez first reported her miraculous findings back in 1998. According to Sanchez ,”After the discovery of this compound that is called THC, it was pretty obvious that this compound had to be acting on the cells, on our organism, through a molecular mechanism.” Research finds that the human body is designed to use cannabis compounds. In the eighties, research first showed the human body contains two targets for THC. One is the endocannabinoid system which processes THC through an endogenous framework. Then the various cannabinoid receptors throughout the body that use them. In conjunction, the body benefits from cannabinoids via these two natural systems. Cannabis is the only place in nature where some certain cannabinoids are found. Sanchez continues, “The endocannabinoids, together with the receptors and the enzymes that synthesize, that produce, the endocannabinoids and that degrade the endocannabinoids, are what we call the endocannabinoid system. We now know that the endocannabinoid system regulates a lot of biological functions: appetite, food intake, motor behavior, reproduction, and many, many other functions. And that's why the plant has such a wide therapeutic potential.” Cannabis cannabinoids, when consumed, work with the body's natural endocannabinoid system and bind to the receptors in the same manner as endogenous cannabinoids. The effects cancer-wise as demonstrated in animal models of breast and brain cancers is that the cancerous cells self destruct. A big advantage of cannabinoids is their unique ability to specifically target tumor cells with no effect on normal cells. This gives cannabinoids the advantage over chemotherapy which targets way more then the actual target Spending Time in the Forest or the Field: Investigations on Stress Perception and Psychological Well-Being University of Freiburg (Germany), November 16, 2022 Research suggests that stays in a forest promote relaxation and reduce stress compared to spending time in a city. The aim of this study was to compare stays in a forest with another natural environment, a cultivated field. Healthy, highly sensitive persons aged between 18 and 70 years spent one hour in the forest and in the field at intervals of one week. The primary outcome was measured using the Change in Subjective Self-Perception (CSP-14) questionnaire. Secondary outcomes were measured using the Profile Of Mood States (POMS) questionnaire and by analyzing salivary cortisol. The medicinal use of forests is of increasing interest worldwide. Forest air is refreshing because trees clean the air of pollutants such as nitrogen oxides and sulfur oxides, produce oxygen, and release volatile bioactive terpenes into the air . Research from Japan, South Korea], China, Taiwan, Australia, the United States, Italy, Norway, Iceland, Finland, and Austria suggests that spending time in the forest promotes relaxation, lowers stress hormones and blood pressure and strengthens the immune system. Most studies compared stays in the forest to stays in the city. Accordingly, forests potentially contribute to the prevention of stress-related diseases. Controlled studies have shown positive effects in high blood pressure, chronic heart failure, COPD and chronic neck pain. In addition, spending time in the forest seems to improve psychological well-being. Spending time in forests reduced adrenaline and noradrenaline in urine, cortisol in saliva and self-rated stress perception; it also induced relaxation in controlled trials. This indicates that forest stays can reduce stress. The available data also indicate that “forest bathing”, i.e., walking, standing or sitting in a forest with the purpose of relaxation, perceiving the environment and inhaling phytoncides stabilizes the autonomic nervous system by reducing the sympathetic and activating the parasympathetic tones. With regard to the immune system, which is linked to stress response and vegetative nerve system, an increase in the activity of natural killer cells and the expression of anti-cancer proteins such as perforin, granzyme A/B, granulysin could be demonstrated. In view of these findings, forests could make an important contribution to the prevention of stress-related diseases. As shown in previous studies, the stressful environment of a city was most often compared to a forest; it remains unclear whether forests have specific effects or are just acting as natural environments. Therefore, we wanted to compare two natural but polar-opposite environments. In cultivated fields, sensory impressions are different from the forest. In order to maximize profitability, fields are mostly structured into rectangular shapes and usually mainly one type of plant is found, while in a natural forest, different types of plants grow side by side. Accordingly, visual, auditory and olfactory impressions are less diverse in fields than in forestsThe play of light and shadow that characterizes the forest atmosphere is not found in fields. The plants are usually not tall enough to provide shade, whereas the height of the trees in the forest can provide a sense of shelter. Field paths are more often sealed than forest paths, which changes haptic perception when walking on them. Thus, there are significant differences in the types of sensory impressions between forests and fields. Highly sensitive persons (HSP), due to their subtle perception, intensely perceive stimuli that others might not even consciously notice. These stimuli may consist of the behavior or moods of other people, the media, medications, pain, and hunger [32]. They perceive stimuli, positively or negatively, to a higher degree, which may, on the one hand, lead to a prolonged reaction time, and on the other hand to more intense feelings and emotional excitability. Our main outcome results show that, as soon as one hour after entering the forest, participants felt a sense of security, relaxation and inner connectedness. In summer, forest interventions had a better effect on vitality. Our study was the first to use the CSP-14 questionnaire, and the comparisons between field and forest interventions were also novel. Forest interventions significantly lowered perceptions of depression, anxiety, hostility, fatigue, confusion and total mood disturbance, and greatly increased vigor. This study shows that forests are not the only kind of natural environment that can promote psychological well-being. The characteristics and qualities of natural environments might influence people's mood and well-being differently. There might also be differences dependent on the preferences of the respective individuals. We regard it as meaningful to study these different effects of nature on the human soul and body in more detail. In addition, future studies examining the effects of different natural environments on human health should respect seasonal aspects and weather conditions.
Spondylolisthesis - defined by a slipped vertebra spondylos "a vertebra," and in plural "the backbone," From the gk: “olisthánein" = to slip Spondylosis - involves the separation of the pars interarticularis “Osis” - breakdown of ATHERO + SCLER + OSIS Athero = groats Scler = hardening Osis = diseased condition of atherosclerosis is a medical disorder that damages the lumen of the arteries by plaque deposits. Atherosclerosis is mostly a failure of controlled cholesterol and fat levels in the body. ARTHR- (“joint”) and going through SCLER- (“hard”) ARTHR- (“joint”) and going through POD- (“feet”) Arthropods are invertebrate animals having an exoskeleton, a segmented body, and paired jointed appendages ARTERIO + SCLER + OSIS Arterio = windpipe Scler = hardening Osis = diseased condition of/ breakdown of Arteriosclerosis is a disease that blocks the wall of arteries due to aging. Osteo = bone Arthro = joint Itis = inflammation Osteoarthritis is a degenerative joint disease, in which the tissues in the joint break down over time Osteopenia is decreased bone mass osteo=bone penia=poverty Osteoporosis osteo=bone poro=porous/pores Osis = breakdown Osteomalacia Bone Malakos = soft (mal=bad) Osteo + myl +itis = An infection of the bone Bone + muscle/marrow + inflammation Osteomalacia is more common in women and often happens during pregnancy. It's not the same as osteoporosis. Both can cause bones to break. --- Support this podcast: https://anchor.fm/liam-connerly/support
References Dr. Guerra lecture notes Prog Neurobiol. 2018 Apr-May; 163-164: 27–58. Arteriosclerosis, Thrombosis, and Vascular Biology. 2006;26:28–40 --- Send in a voice message: https://anchor.fm/dr-daniel-j-guerra/message Support this podcast: https://anchor.fm/dr-daniel-j-guerra/support
In this episode of the Heart podcast, Digital Media Intern, Dr. Andrew Perry, is joined by Dr. Alan Daugherty, from the University of Kentucky, and Editor-in-Chief of the Arteriosclerosis, Thrombosis, and Vascular Biology journal. They discuss the latest developments in transcriptomics and how they might be used to understand the causes of vascular disease. If you enjoy the show, please subscribe to the podcast to get episodes automatically downloaded to your phone and computer. Also, please consider leaving us a review at https://itunes.apple.com/gb/podcast/heart-podcast/id445358212?mt=2
Your doctor told you high blood pressure is dangerous. You're going to get a heart attack or stroke. You listen to your doctor and take a pill every day for years. Now you have cancer. Why do you have cancer if you did everything you were supposed to do?
Episode 67: Covid, Food, and HIV. Medical students discuss the relationship between high cholesterol and COVID-19, the effect of food order in postprandial glucose and insulin, and HIV history. Moderated by Hector Arreaza, MD. During this episode you will listen to three medical students discussing some topics that they found interesting during their family medicine rotation. All the credit goes to them because they read these topics and provided a very good summary. I hope you enjoy it.____________________High Cholesterol and COVID-19By Milan Hinesman, MS3, Ross University School of MedicineGiven the current state of the world, there's been a lot more attention to COVID-19 presentation, risks, and treatment. One study conducted by Dr. Kun Zhang and collaborators shows that there may be a relationship between higher total cholesterol levels and ApoB levels to increased risk of COVID-19 infection[1]. Dr. Zhang used a mendelian randomization from the UK Biobank data to test for lipid effects on COVID susceptibility and severity. The study performed analysis of data from the host genetics initiative consisting of more than 14,000 cases and more than one million controls showing a potential positive causal effect between high total cholesterol and ApoB and COVID susceptibility. A mendelian randomization is a process of taking genes which functions are already known and measuring their response to exposure to a disease in observational studies[2]. In short, high cholesterol and high ApoB are linked to COVID-19 infection.This is Rio Bravo qWeek, your weekly dose of knowledge brought to you by the Rio Bravo Family Medicine Residency Program from Bakersfield, California. Our program is affiliated with UCLA, and it's sponsored by Clinica Sierra Vista, Let Us Be Your Healthcare Home. __________________________Impact of food order on glucose after meals. By Yvette Singh, MS3, American University of the CaribbeanIn the management of diabetes, health care providers usually assess glycemic control with fasting plasma glucose and pre-prandial glucose measurements, as well as by measuring Hemoglobin A1c. Therapeutic goals for Hemoglobin A1c and pre-prandial glucose levels have been established based on the results of controlled clinical trials. Unfortunately, many patients with diabetes fail to achieve their glycemic goals. Elevated glucose after eating may be the cause of poor glycemic control leading to vascular complications. Postprandial hyperglycemia is one of the earliest abnormalities of glucose homeostasis associated with type 2 diabetes. This is one of the important therapeutic targets for glycemic control. Current studies show that the amount and timing of carbs in the diet primarily influence blood glucose levels. Other studies also show that eating whey protein before meals, as well as changing the macronutrients in meals, reduces postprandial glucose levels; however, these studies did not have patients with type 2 diabetes. The main author of this study was Alpana P. Shukla and many other collaborators. The title is Food Order Has a Significant Impact on Postprandial Glucose and Insulin Levels, published by the American Diabetes Association on Diabetes Care in July 2015.This study was performed to analyze the order of food consumption with vegetables, protein and carbohydrates and its effects on postprandial glucose in overweight/obese patients with type 2 diabetes being treated with metformin. Subjects were studied for 1 week. They were given a meal with the same number of calories, after fasting for 12 hours: 55g protein, 68g carbs, and 16g fat. They were asked to eat carbs first, then to eat vegetables and protein fifteen minutes later. This order was reversed during the second week. Their postprandial glucose and insulin levels were measured at 30/60/120 mins after meals. The statistical studies showed an average post prandial glucose decrease by more than 25% when protein was consumed first. As well as the average post prandial insulin levels decreased by more than 40%. These results demonstrated that the timing of carbs during a meal has a significant impact on glucose and insulin levels comparable to some pharmacological agents. Reduced insulin excretion with this meal pattern may also improve insulin sensitivity. This may help patients with type 2 diabetes control their HbA1c, and possibly help reverse early diabetes. Educating patients about this approach is not controlling how much they are eating or restricting their diet so patients will likely comply with this recommendation. Eat your protein first!The potential problems of this study are that it was a small sample size (11 patients), limited food types, and insulin was measured only up to 120 minutes after meals. Further studies are needed to demonstrate the full effectiveness of this recommendation.___________________HIV Series Part I: HIV HistoryBy Robert Dunn, MS3, Ross University School of Medicine This is an HIV series for the Rio Bravo qWeek Podcast. The following episodes will include some of the history of HIV, transmissibility, the PARTNER-1 and PARTNER-2 studies, and will finalize with a full episode on HIV prevention. Today we are starting with HIV history.Prejudice against those with HIV stems from the history surrounding the virus. Between 1981-1983, cases of rare infections like Pneumocystis carinii pneumonia (PCP) and aggressive cancers like Kaposi Sarcoma were appearing predominantly amongst gay men and injection drug users. Even children were presenting with AIDS creating misconceptions of how the disease was transmitted by touch. By 1982, this syndrome was referred to as the Gay-Related Immunodeficiency (GRID), which we now know as AIDS. Some History of HIVThe start of the Human Immunodeficiency Virus (HIV) was thought to have started in the Democratic Republic of Congo in 1920 when the virus crossed species to humans and gave its ability to infect humans[4]. In 1981, five young gay men in Los Angeles, California, presented with a rare lung infection called Pneumocystis carinii pneumonia (PCP). Two other groups of men also presented with a rare and aggressive cancer called Kaposi Sarcoma, in New York and California. By December of the same year, the first case of PCP was found in an injection drug user. And by the end of the year, there were 270 reported cases of this severe immunodeficiency and about 121 of them had already died from it, almost 50%. In 1982, due to the prevalence of these rare diseases being present among gay men, the syndrome was called the Gay-Related Immune Deficiency (GRID). The CDC later officially called the disease the Acquired Immune Deficiency Syndrome (AIDS). The term “gay cancer” was used in Venezuela before AIDS was known.In 1983, the disease was found in both women and children. In May 1983, in a joint conference between the Pasteur Institute in France and the National Cancer Institute, they announced that LAV and HTLV-III were the same virus and the cause of AIDS.In 1985, Ryan White, a teenager with hemophilia was banned from school when he was diagnosed with HIV after he received contaminated blood products. Ryan later died at 18 years old due to AIDS-related illnesses. At the same time, the FDA licensed the first commercial blood test to detect HIV. A foundation was later created to provide primary care and medications for low-income HIV patients.In 1987, the first antiretroviral drug, Zidovudine (AZT) was approved by the FDA to treat for HIV. In 1991, the famous basketball player Magic Johnson announced he tested positive for HIV and retired immediately. After his retirement he planned to educate young people about the virus which helped dispel stereotypes. Also in 1991, the famous singer of Queen announced he had AIDS and died the next day.In 1993, the movie Philadelphia with Tom Hanks promoted further discussion about HIV and AIDS. In June 1995, the first protease inhibitor was approved by the Food and Drug Administration (FDA), which started the era for Highly Active Antiretroviral Therapy (HAART). This brought down the rate of AIDS-related deaths and hospitalizations by 60-80%. Of special note, in 1986, the FDA passed the policy to ban all men who had sex with men (MSM) from 1977 onward, from donating blood or plasma to avoid the risk of transmitting HIV or Hepatitis A. This policy was amended in December 2015, when the revised policy said any MSM within the last 12 months, would need to wait at least 1 year before donating blood. In light of the COVID-19 pandemic, the FDA amended it its policy once more to decrease the wait time to 3 months form the last time the man had sex with another man.____________________________Conclusion: Now we conclude our episode number 67 “Covid, Food, and HIV.” Kudos to Milan, Yvette and Robert, they presented relevant information for our practice of medicine. They taught us that high cholesterol is a risk for COVID-19 infection; Also, when you eat proteins first, your glucose and insulin after meals are lower than when you eat carbs first; and you will be hearing from Robert for a couple episodes regarding HIV. Today he gave us a little piece of HIV history. Even without trying, every night you go to bed being a little wiser.Thanks for listening to Rio Bravo qWeek. If you have any feedback about this podcast, contact us by email RBresidency@clinicasierravista.org, or visit our website riobravofmrp.org/qweek. This podcast was created with educational purposes only. Visit your primary care physician for additional medical advice. This week we thank Hector Arreaza, Milan Hinesman, Yvette Singh, and Robert Dunn. Audio edition: Suraj Amrutia. See you next week! _____________________References:Zhang, K. Dong, S. Guo, et. al., Causal Associations Between Blood Lipids and COVID-19 Risk: A Two-Sample Mendelian Randomization Study. Arteriosclerosis, Thrombosis, and Vascular Biology, originally published on September 9, 2021. https://doi.org/10.1161/ATVBAHA.121.316324. What is Mendelian Randomization and How Can it be Used as a Tool for Medicine and Public Health? Opportunities and Challenges, Webinar announcement given by Professor George Davey Smith on November 27, 2018. Centers for Disease Control and Prevention, https://www.cdc.gov/genomics/events/precision_med_pop.htm Alpana P. Shukla, Radu G. Iliescu, Catherine E. Thomas and Louis J. Aronne, Food Order Has a Significant Impact on Postprandial Glucose and Insulin Levels, Diabetes Care 2015 Jul; 38(7): e98-e99. https://doi.org/10.2337/dc15-0429. History of HIV and AIDS Overview. Avert, October 10, 2019. https://www.avert.org/professionals/history-hiv-aids/overview. Accessed on September 21, 2021. Shaw, Maggie. FDA's Revised Blood Donation Guidance for Gay Men Still Courts Controversy. AJMC, April 3, 2020. https://ajmc.com/view/fdas-revised-blood-donation-guidance-for-gay-men-still-courts-controvery. Accessed on September 21, 2021. BAYER, R. (2015), Science, Politics, and the End of the Lifelong Gay Blood Donor Ban. Milbank Quarterly, 93: 230-233. https://doi.org/10.1111/1468-0009.12114. Ways HIV can be Transmitted. Centers for Disease Control and Prevention, April 21, 2021. https://www.cdc.gov/hiv/basics/hiv-transmission/ways-people-get-hiv.html. Accessed on September 21, 2021.
LEXINGTON, Ky. (September 23, 2021) – UK's Saha Cardiovascular Research Center recently held its annual Cardiovascular Research Day, an event that showcases innovative research in cardiovascular health. The event features prominent speakers in the field of cardiovascular health, and was the first in-person scientific conference in the field of lipid and lipoprotein metabolism and cardiovascular disease in nearly two years. With 250 attendees from UK and nearly 40 other universities, the event featured a wide variety of research activity from scientists and researchers, from trainees to prominent senior scientists. This week's episode of ‘Behind the Blue' features the director of the Saha Cardiovascular Research Center and chair of the UK Department of Physiology, Dr. Alan Daugherty. Dr. Daugherty is also the Gill Heart Foundation Chair of Preventive Cardiology. He serves as editor-in-chief of the American Heart Association's Arteriosclerosis, Thrombosis and Vascular Biology (ATVB) journal, and his research focuses on molecular mechanisms of vascular diseases, including atherosclerosis and aortic aneurysms. "Behind the Blue" is available on iTunes, Google Play, Stitcher and Spotify. Become a subscriber to receive new episodes of “Behind the Blue” each week. UK's latest medical breakthroughs, research, artists and writers will be featured, along with the most important news impacting the university. For questions or comments about this or any other episode of "Behind the Blue," email BehindTheBlue@uky.edu or tweet your question with #BehindTheBlue. Transcripts for this or other episodes of Behind the Blue can be downloaded from the show's blog page. To discover what's wildly possible at the University of Kentucky, click here.
Colesterol y Arteriosclerosis
Credits: 0.25 AMA PRA Category 1 Credit™ CME/CE Information and Claim Credit: https://www.pri-med.com/online-education/podcast/frankly-speaking-cme-237 Overview: Solid evidence shows that adverse pregnancy outcomes (APOs) correlate with an increased risk of cardiovascular disease (CVD) in women. Evidence is also becoming clearer that lactation and breastfeeding may have CV protective benefits as well. Social determinants of health play a significant role in these diseases; facts support that Black, Hispanic and Asian American women suffer from worse pregnancy outcomes than White American women. Join us while we discuss the recent American Heart Association (AHA) guideline update regarding the association of increased risk of CVD and metabolic disease with APOs and what can be done to reduce these risks. Episode resource links: Adverse Pregnancy Outcomes and Cardiovascular Disease Risk: Unique Opportunities for Cardiovascular Disease Prevention in Women. Nisha I. Parikh, MD, MPH, Chair, Juan M. Gonzalez, MD, Cheryl A.M. Anderson, PhD, Suzanne E. Judd, PhD, Kathryn M. Rexrode, MD, Mark A. Hlatky, MD, Erica P. Gunderson, PhD, Jennifer J. Stuart, ScD, Dhananjay Vaidya, PhD, Vice Chair, On behalf of the American Heart Association Council on Epidemiology and Prevention; Council on Arteriosclerosis, Thrombosis and Vascular Biology; Council on Cardiovascular and Stroke Nursing; and the Stroke Council. https://www.ahajournals.org/doi/abs/10.1161/CIR.000000000000096 Schwartz, EB. (reviewing Parikh NI et al. Circulation 2021 Mar 29). Preventing Heart Disease in Women: New Guidance from the American Heart Association. NEJM: Journal Watch, April 12, 2021. https://www.jwatch.org/na53433/2021/04/12/preventing-heart-disease-women-new-guidance-american-heart?ijkey=3l3eCvQLl Clinical Statements and Guidelines. AHA/ACOG Presidential Advisory. Volume 137, Issue 24, 12 June 2018, Pages e843-e852. https://doi.org/10.1161/CIR.0000000000000582 https://www.jwatch.org/na53433/2021/04/12/preventing-heart-disease-women-new-guidance-american-heart Guest: Susan Feeney, DNP, FNP-BC, NP-C Music Credit: Richard Onorato
Credits: 0.25 AMA PRA Category 1 Credit™ CME/CE Information and Claim Credit: https://www.pri-med.com/online-education/podcast/frankly-speaking-cme-237 Overview: Solid evidence shows that adverse pregnancy outcomes (APOs) correlate with an increased risk of cardiovascular disease (CVD) in women. Evidence is also becoming clearer that lactation and breastfeeding may have CV protective benefits as well. Social determinants of health play a significant role in these diseases; facts support that Black, Hispanic and Asian American women suffer from worse pregnancy outcomes than White American women. Join us while we discuss the recent American Heart Association (AHA) guideline update regarding the association of increased risk of CVD and metabolic disease with APOs and what can be done to reduce these risks. Episode resource links: Adverse Pregnancy Outcomes and Cardiovascular Disease Risk: Unique Opportunities for Cardiovascular Disease Prevention in Women. Nisha I. Parikh, MD, MPH, Chair, Juan M. Gonzalez, MD, Cheryl A.M. Anderson, PhD, Suzanne E. Judd, PhD, Kathryn M. Rexrode, MD, Mark A. Hlatky, MD, Erica P. Gunderson, PhD, Jennifer J. Stuart, ScD, Dhananjay Vaidya, PhD, Vice Chair, On behalf of the American Heart Association Council on Epidemiology and Prevention; Council on Arteriosclerosis, Thrombosis and Vascular Biology; Council on Cardiovascular and Stroke Nursing; and the Stroke Council. https://www.ahajournals.org/doi/abs/10.1161/CIR.000000000000096 Schwartz, EB. (reviewing Parikh NI et al. Circulation 2021 Mar 29). Preventing Heart Disease in Women: New Guidance from the American Heart Association. NEJM: Journal Watch, April 12, 2021. https://www.jwatch.org/na53433/2021/04/12/preventing-heart-disease-women-new-guidance-american-heart?ijkey=3l3eCvQLl Clinical Statements and Guidelines. AHA/ACOG Presidential Advisory. Volume 137, Issue 24, 12 June 2018, Pages e843-e852. https://doi.org/10.1161/CIR.0000000000000582 https://www.jwatch.org/na53433/2021/04/12/preventing-heart-disease-women-new-guidance-american-heart Guest: Susan Feeney, DNP, FNP-BC, NP-C Music Credit: Richard Onorato
Today on Like it Matters Radio Mr Black goes into the hardening of our hearts and minds. Sclerosis is a medical term that deals with the hardening of some organ or thing. Arteriosclerosis, is the hardening of our arteries. When this happens those arteries become increasingly ineffective, unable to do what they were created to do. When the arteries harden it restricts blood flow to your organs and tissues. Organs and tissues that don't get fed and nurtured, cease to exist, to function. Might I suggest as a people, as a country and as human beings our hearts seem to be hardening and we are growing cold toward each other? Tune into Like It Matters Radio, for an hour of power as Mr. Black, plays doctor and prescribes a solution to what's ailing America as he discusses: Callus to Callous! See omnystudio.com/listener for privacy information.
La thrombocytopénie thrombotique immunitaire induite par certains vaccins contre la COVID, dont ceux produits par AstraZeneca et Johnson et Johnson, a fait couler beaucoup d'encre dans l'actualité. Quels sont les risques réels, les symptômes à surveiller et la conduite à adopter pour le pharmacien ? Pierre Lemieux, pharmacien au CIUSSS de la Mauricie et du Centre du Québec, a bien voulu nous éclairer sur le sujet. Références : 1. Thrombocytopénie immunitaire prothrombotique induite par le vaccin – TIPIV (ou TTIV) en contexte de vaccination contre la COVID-19. INSPQ. Version du 19 avril 2021 https://publications.msss.gouv.qc.ca/msss/fichiers/directives-covid/dgaumip-030-rev1_thrombocytopenie-tipiv-%20vaccin-covid-19.pdf 2. Comité consultatif national de l'immunisation (CCNI). Recommandations sur l'utilisation des vaccins contre la COVID-19. Mise à jour du 23 avril 2021. https://www.canada.ca/content/dam/phac-aspc/documents/services/immunization/national-advisory-committee-on-immunization-naci/recommendations-use-covid-19-vaccines/recommandations-utilisation-vaccins-covid-19-fr.pdf 3. Mahase E. AstraZeneca vaccine: Blood clots are “extremely rare” and benefits outweigh risks, regulators conclude BMJ 2021; 373 :n931 doi:10.1136/bmj.n931 https://www.bmj.com/content/373/bmj.n931 4. Les thromboses (caillots sanguins) et les vaccins contre la COVID-19. Thrombose canada Foire aux questions. Avril 2021. https://thrombosiscanada.ca/wp-uploads/uploads/2021/04/COVID-19-vaccine-and-Thrombosis-FAQs-April-2-2021_FR.pdf 5. Tacquet et al. Cerebral venous thrombosis: a retrospective cohort study of 513,284 confirmed COVID-19 cases and a comparison with 489,871 people receiving a COVID-19 mRNA vaccine, preprint https://osf.io/a9jdq/ 6. Katsanos et al. The Impact of SARS‐CoV‐2 on Stroke Epidemiology and Care: A Meta‐Analysis Ann Neurol. 2020 Dec 9 : 10.1002/ana.25967 (2020) https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7753413/ ; 7. Andreas Greinacher et coll. Anti-SARS-CoV-2 Spike Protein and Anti-Platelet Factor 4 Antibody Responses Induced by COVID-19 Disease and ChAdOx1 nCov-19 vaccination, 09 April 2021, PREPRINT (Version 1) available at Research Square https://www.researchsquare.com/article/rs-404769/v1 8. Scully et coll. Pathologic Antibodies to Platelet Factor 4 after ChAdOx1 nCoV-19 Vaccination. NEJM April 16, 2021. DOI: 10.1056/NEJMoa2105385 https://www.nejm.org/doi/full/10.1056/NEJMoa2105385 9. Gowthami M et coll. Heparin-Induced Thrombocytopenia A Focus on Thrombosis. Arteriosclerosis, Thrombosis, and Vascular Biology. 2021;41:141–152 https://www.ahajournals.org/doi/pdf/10.1161/ATVBAHA.120.315445 10. CDC. Coronavirus Disease 2019 (COVID-19) Vaccines https://www.cdc.gov/vaccines/acip/meetings/slides-2021-04-23.html 11. The Gamalaya Center Statement https://sputnikvaccine.com/newsroom/pressreleases/the-gamaleya-center-statement/ 12. Greinacher A. et coll. Towards Understanding ChAdOx1 nCov-19 Vaccine-induced Immune Thrombotic Thrombocytopenia (VITT). 2021. Preprint. https://assets.researchsquare.com/files/rs-440461/v1/8eabf306-6fd4-4a89-a7a3-8f4d06c89a55.pdf
Today on Like it Matters Radio Mr Black goes into the hardening of our hearts and minds. Sclerosis is a medical term that deals with the hardening of some organ or thing. Arteriosclerosis, is the hardening of our arteries. When this happens those arteries become increasingly ineffective, unable to do what they were created to do. When the arteries harden it restricts blood flow to your organs and tissues. Organs and tissues that don't get fed and nurtured, cease to exist, to function. Might I suggest as a people, as a country and as human beings our hearts seem to be hardening and we are growing cold toward each other? Tune into Like It Matters Radio, for an hour of power as Mr. Black, plays doctor and prescribes a solution to what's ailing America as he discusses: Callus to Callous! www.likeitmattersradio.com www.likeitmatters.net See omnystudio.com/listener for privacy information.
On today’s episode of JIMMY RANTS on The LLVLC Show, we take a look at a new “study” that makes a dubious connection between Keto and coronary calcium. “How can they say with a straight face that this is a low-carbohydrate diet? It’s not even close!” - JIMMY MOORE One of the major benefits of eating a low-carb diet are the incredible cardiovascular health improvements that happen as a result of restricting carbohydrate and increasing fat and protein. Lower triglycerides, lower blood sugar, lower blood insulin, lower inflammation, higher HDL cholesterol, reduced blood pressure, and more are the signs that you’re eating less carbs in your diet. But a new study from Chinese researchers is now claiming a low-carb diet, especially one consisting of animal-based fat and protein, Will lead to progression of coronary artery calcium (CAC). In this episode of JIMMY RANTS on The LLVLC Show, I read from the October 16, 2020 study published by Chinese researchers in the journal Arteriosclerosis, Thrombosis, and Vascular Biology entitled “Low-Carbohydrate Diet Score and Coronary Artery Calcium Progression.” They claim that the participants in the “low-carb“ cohort saw the greatest progression of CAC as compared to the moderate and higher carb cohorts. What do they consider low-carb—45-49% of total energy intake! Oh, I have so much to say about this very bad scientific study and you can hear all about it in today’s episode!
This episode covers arteriosclerosis!
Vast numbers of people in the world live with high blood pressure, but there are others who do not suffer from this disease of affluence. High blood pressure is the forerunner of other deadly diseases, such as diabetes, strokes, aneurysms, congestive heart failure, kidney failure, etc. The good news is that this does not have to be you! Diet and lifestyle have much to do with the outcome. Even though the subject is involved, the solutions to each condition overlap greatly, so that solving one problem will bring relief to other associated conditions as well. Listen in, or send an email to prompt us to answer related questions. We enjoy having you with us.
Las opiniones expresadas en este video por el Dr. EDUARDO SCHOLCOFF no pretenden representar consejos médicos ni servir como recomendaciones para el tratamiento, mitigación o prevención de ningún proceso de enfermedad. El video puede compartirse, pero su contenido no puede modificarse, resumirse ni complementarse. La alteración del video o mensaje con logotipos personales, comerciales o números de contacto violaría los derechos de autor. --- This episode is sponsored by · Anchor: The easiest way to make a podcast. https://anchor.fm/app
This month on Episode 17 of the Discover CircRes podcast, host Cindy St. Hilaire highlights four featured articles from the September 25 and October 9 issues of Circulation Research. This episode features an in-depth conversation with Drs David Dichek, Sina Gharib and Tomáš Vaisar regarding their study titled Parallel Murine and Human Plaque Proteomics Reveals Pathways of Plaque Rupture. Article highlights: Cai, et al. Single Cell RNA-Seq in Arteriosclerosis Schuhmann, et al. CD84 in Ischemic Stroke VanOudenhove, et al. Gene Regulatory Dynamics of Developing Human Heart Nie, et al. Periostin is a Target to Treat PH Dr Cindy St. Hilaire: Hi, welcome to Discover CircRes, the podcast of the American Heart Association's journal Circulation Research. I'm your host, Dr Cindy St. Hilaire, from the Vascular Medicine Institute at the University of Pittsburgh, and today I'll be highlighting four articles selected from the late September and early October issues of CircRes. I'll also be interviewing Drs David Dichek, Sina Gharib, and Tomáš Vaisar regarding their study titled Parallel Murine and Human Plaque Proteomics Reveals Pathways of Plaque Rupture. The first article I want to share is titled Single Cell RNA Sequencing of Allograft Cells in Transplant Arteriosclerosis. The first author is Jingjing Cai and the corresponding author is Qingbo Xu from Zhejiang university in Hangzhou, China. Arteriosclerosis is a major contributor to organ transplant failure. The thickening and stiffening of arteries within the grafts results in diminished blood flow supplies and diminished organ function. While it is well understood that atherosclerosis is an inflammatory disease, the details of the cellular and molecular players on this transplant-specific pathology are lacking. Now, Cai and colleagues used single cell RNA sequencing to identify a consensus of cells and cytokines in sclerotic transplanted aortas in mice. Two weeks after transplant, the grafted vessels exhibited signs of arteriosclerosis and by four weeks, this remodeling had worsened significantly. Analyzing the RNA transcripts of over 12,000 individual cells isolated at both two and four weeks, the team discovered that the number of T-cells was greatly increased throughout the process. An early abundance of macrophages gave way to a later wave of B cells and there was also evidence of the development of tertiary lymphoid tissue. They further found that chemokine CCL121 was up regulated after transplant, both the mRNA in the tissues, as well as the protein levels in the animal's blood. The authors then went on to show that blocking CCL121 or its attracting partner, CXC3, significantly delayed arteriosclerosis in the grafted vessel. Hence, this work not only defines the cellular and molecular drivers of arteriosclerosis in grafted vessels, but highlights potential molecular targets for future therapeutic interventions. The second article I want to share is titled CD84 Links T-cell and Platelet Activity in Cerebral Thrombo-inflammation in Acute Stroke. The first author is Michael Schuhmann and the corresponding author is David Stegner, and the work was completed at University of Würzburg in Germany. Ischemic stroke is caused by the occlusion of cerebral blood vessels and it is a leading cause of death and disability worldwide. Despite treatments to degrade or remove clots such as mechanical thrombectomy, infarct size itself can continue to grow even when blood perfusion is re-established. Thrombo-inflammatory processes are thought to mediate this worsening injury, with both T-cells and activated platelets playing a role. Because both T-cells and activated platelets express CD84, which is a self-binding adhesion molecule involved in lymphocyte activation, this team tested the hypothesis that CD84 might mediate stroke inflammatory processes. They went on to show that mice lacking CD84 have smaller infarct sizes with reduced T-cell inflammation after stroke than wild-type animals. Furthermore, mice that specifically lack CD84 in either T-cells or platelets also experienced smaller infarcts. The team went on to show that CD84 promotes T cell migration in vitro. And then in patients with stroke, high expression of CD84 in platelets was associated with poor outcomes. Together, these results suggest that activated CD84-secreting platelets encourage inflammatory T cell migration to the infarct site. And that blocking CD84 activity could be a novel therapeutic strategy for minimizing inflammatory injury after stroke. The third article I want to share is titled Epigenomic and Transcriptomic Dynamics During Human Heart Organogenesis. The first author is Jennifer VanOudenhove and the corresponding author is Justin Cotney. And they're from the University of Connecticut. Congenital heart defects, or CHDs, are common birth abnormalities and while some genes have been linked to congenital heart defects, the majority, close to 60%, have unknown etiologies. It's thought that multiple genetic and environmental factors contribute to congenital heart defects. One of which could be variations in both cis and trans regulatory regions of the genome. To find such heart specific regulatory regions, this team examined heart tissue from human embryos obtained four to eight weeks after conception. They performed chromatin immunoprecipitation experiments to scour the heart genomes for histone modifications associated with increased or decreased gene transcription. They also performed transcriptome analysis to see whether the genomic regions identified by chip corresponded with the activity status of nearby genes. In total, the team found more than 12,000 previously unknown enhancers that were enriched for binding sites for heart specific transcription factors, some of which included GATA, MEF2 and Nkx. These binding sites tended to be close to genes activated in the heart. Many of the regions also contain sequence variations that have been associated with atrial fibrillation. These newly identified sites are potential congenital heart defect candidate loci and the authors have now made their data readily available so that other investigators may study it. The last article I want to share with you before we switch to our interview is titled Periostin: a Potential Therapeutic Target for Pulmonary Hypertension? The first author is Xiaowei Nie from the Shenzhen Third People's Hospital and the corresponding authors are Jingyu Chen and Jin-Song Bian from the Wuxi People's Hospital and the National University of Singapore, respectively. Pulmonary hypertension, or PH for short, is a life-threatening disease where an excess in the proliferation of vascular smooth muscle cells and the deposition of extracellular matrix thickens the walls of the lung vasculature, which leads to an increase in pulmonary blood pressure and ultimately contributes to right heart failure. Vasodilatory medications can be used to treat the symptoms of the disease. However, these medications do not prevent or reverse the underlying pathogenic remodeling. This study now suggests that drugs targeting the secreted extracellular matrix protein, periostin, might be a potential therapeutic strategy for the treatment of pulmonary hypertension. Periostin is an abundant protein in the lung arteries of pulmonary hypertension patients. And it is thought to be involved in cell adhesion and wound healing mechanisms, such as the proliferation and the migration of smooth muscle cells. The team confirmed increased production of periostin in patient lungs, and also found the same to be true for mice with an induced model of pulmonary hypertension. They also showed that genetic deletion of periostin attenuated pulmonary hypertension in mice, while suppression of periostin via RNA inhibition could even reverse pathological vessel thickening and the subsequent right ventricle hypertrophy. The team went on to identify factors HIF-1a and TrkB as factors that mediate periostin's effects in cultured arterial cells. And they suggest that blocking either of these factors or by blocking periostin itself could be a novel strategy for the treatment of pulmonary hypertension patients. Drs Tomáš Vaisar, Sina Gharib, and David Dichek from the University of Washington in Seattle, Washington are here with me today and we're going to discuss their recent study titled Parallel Murine and Human Plaque Proteomics Reveals Pathways of Plaque Rupture. Thank you all so much for joining me today and congratulations on this beautiful and interesting study. So this is an atherosclerotic study, but unlike many in the field, it's really looking at the end stage event called plaque rupture. So for those listeners who are unfamiliar with the term, plaque rupture is when an atherosclerotic plaque degrades and its contents are exposed to the circulation, which can then induce a clotting event and lead to all sorts of adverse pathologies, myocardial infarction, transient ischemic events, stroke. So I'm wondering if we if maybe you can give us a little bit of background about what's known and what really is unknown at least before your study regarding plaque rupture. Dr David Dichek: So the pathogenesis of acute myocardial infarction and stroke was really unknown for many years. And the idea that it was due to acute thrombosis was really confirmed by a study probably 30 years ago, that did angioscopy in the coronary arteries, proximal to a myocardial infarction, and visualized actual clot so that the clot was confirmed to be associated with the acute event. At that point, the question became why would a coronary artery form a clot? And that led to identification of, or histologic studies that identified ruptured caps of atherosclerotic plaques, exposure of the blood to the thrombogenic contents of the lesion, and a thrombus. However, it was not known what the initiating event was in rupture of the plaque cap. And there were a lot of hypotheses and a lot of nice work, but it does still remain an unknown. A significant amount of focus has been devoted to the possibility that proteolysis is the initiating event. And that was sort of the takeoff point from our study because we had developed a mouse model where proteolysis clearly was associated with rupture of plaque caps. And we decided we wanted to get more into the biochemistry of what was going on and go beyond the histology. So that was really what led up to our study. Dr Cindy St. Hilaire: It's really interesting. So, mice are really good and obviously really useful, very well-known model systems to study atherosclerosis and particularly the initial drivers and maybe the mechanisms of the disease pathogenesis, but like many models systems, they're not perfect. So I'm wondering if you could discuss the limitations of murine model systems and specifically for this study, how you were able to overcome some of those limitations. Dr David Dichek: So the limitations of mouse models of plaque rupture are that essentially none of them duplicate the histology of human plaque rupture, particularly the thrombus that occurs on top of the plaque rupture. So there are various mouse models where caps are disrupted, but there's not acute thrombosis. It has been argued in the vascular community as to whether these models are authentic models of plaque rupture, because they don't have the superimposed thrombosis. And the counter argument is well, mice aren't people, they have different hemostatic and coagulation factors that may be differentially regulated. The hemodynamics of small mouse arteries is different from human mouse arteries. And the fact that you don't get a thrombus doesn't necessarily mean that you're not modeling the process that would cause it. So we really accepted that argument as being valid and felt that the occurrence of frank plaque rupture, and that was in our Circulation paper in 2010, in these lesions in the mice, really validated it as an authentic model of cap disruption. And so I agree it's arguable, whether this is an authentic model. But we actually took that issue head on by saying, well, is the biochemistry of the ruptured plaque similar to the biochemistry of a ruptured human plaque? And that if there were similarities that we would gain more confidence in our model being an authentic model of plaque rupture and that it matched not only the histology, but also the biochemistry. Dr Cindy St. Hilaire: One of the main tools you used, you used shotgun proteomics, which I think is just a great name for it. And also a algorithmic learning tool or analysis tool called proteomaps. I was wondering if you could give us a little bit of background about the proteomic aanalysis involved, what does that entail? Especially, when you're comparing a teeny tiny mouse plaque to a larger human plaque and then how that analysis was done? Dr Tomáš Vaisar: So the shotgun proteomics term was coined by John Yates, but way back in the early 1990s. And it's essentially the way how you enumerate the proteins and in more recent forms, you even quantify the abundance of the proteins in a very complex mixture. So shotgun proteomics essentially takes a protein sample. And in this case it was an extract of the tissue and uses protease, trypsin typically, to cut the proteins down to peptides, which are relatively small and relatively well behaved compared to intact proteins. And then using tandem mass spectrometry combined with liquid chromatography separation, basically aims to sequence every single of those peptides or majority of the peptides. And then based from the identification of the sequence of individual peptides piece back together like a jigsaw puzzle, what was the protein present in the original mixture? Dr Cindy St. Hilaire: That's so interesting. I know it's been around for a while. I'm always impressed by it. Dr Tomáš Vaisar: And then the other approach we use it's called Proteomap developed by Ben Cravatt, collaborator on this paper at La Jolla. And that approach uses basically the shotgun approach but as a first step uses gel electrophoresis, SDS PAGE electrophoresis to fractionate the very complex mixture to size segments. Dr Tomáš Vaisar: So you run your complex mixture on a gel, you slice it by size and then run shotgun proteomics experiment on each of those slices after gel digestion. And then Ben developed a set of tools where you identify the proteins and their abundance in each of the bands based on the size and the way it's applied to formation or mapping of proteolytic events is based on the idea of that intact protein will show up at the molecular weight of the intact protein but if it was cleaved by a protease, it will also show up at the molecular weight, which is smaller corresponding to the fragments formed by proteolysis. Then you use set of bioinformatics tools to piece this all together and generate the Proteomaps. Dr Cindy St. Hilaire: You pick it apart, throw it in the machine and then put it back together. That's so cool. It's so amazing. So what were the main findings that you were able to pull out of your comparisons? And I think you had three main groups, if I understood it right? There's the transgenic mouse that has the plaques that don't rupture, and then there's the atherosclerotic mouse that had the transgenic bone marrow, and then you had the human. Can you tell us a little bit about the different groups you compared and then what ultimately you found? Dr David Dichek: Sure. Yes. You are absolutely right. We had what we refer to as the straight transgenic mice that are either transgenic for macrophage overexpressed uPA or not. We also had older mice who had advanced atherosclerosis and receive bone marrow transplants from mice that either had uPA overexpression in bone marrow or not and then we had the human plaque. So those were the three groups. So what we found was that looking at the proteome of those three groups, we were able to find some common biological processes, and this was really Sina's work, but taking the proteomics data and analyzing it with sophisticated bioinformatics tools. We looked not only at the overlap in specific proteins among the models, but the overlap in biological processes, because it may be in different species that there are different proteins, different actors carrying out the same roles. And that's been described in other systems as well. So we were able to identify not only common biological processes, but surprisingly, we were able to identify decreases in specific category of proteins, basement membrane proteins that were common to two of the models, the straight transgenic and the human model and loss of these proteins certainly has a plausible role in precipitating plaque rupture. So I think one aspect of the analysis that's worthy of note is that we initially thought we would observe more profound changes in the bone marrow transplant mice because they had more advanced atherosclerosis. And in fact, we found fewer changes than in the straight transgenic mice, but thinking about it after letting the data talk to us, rather than trying to impose our own on the data- Dr Cindy St. Hilaire: Always a good idea. Dr David Dichek: ... was that the straight transgenic mice were telling us we've been overexpressing urokinase for 20 weeks since we were conceived, and the bone marrow transplant mice had it for only eight weeks. And indeed they had far less loss of basement membrane proteins and far fewer changes in their plaques than the mice that had expressed it for a longer time. And so when one placed the three groups in a chronology of exposure to protease activity with the bone marrow transplant mice, being the shortest exposure than the straight transgenic mice, and then the humans who've had decades of exposure, it really tells you a nice chronological story about the biological processes leading to plaque rupture. And I think that's a generally applicable lesson and can be applied to other problems in cardiovascular biology. And that is when you have a biological process for which you can't get human tissue until after it's occurred because you can't go in and biopsy. Dr Cindy St. Hilaire: I have that problem with valve calcifications that you can't take your valve out early. Dr David Dichek: If you can get a mouse model that duplicates the pathology, then you have access to the steps leading up to the event. And that's what we tried to construct in this study. And really it was really Sina’s analyses that allowed us to make those connections. Dr Sina Gharib: Yeah. Of course, David was kind of the mastermind behind the design of the experiments on the developing of genetic models and Tomáš is a renowned expert in proteomics analysis. And I kind of joined more on the bioinformatics component of this study, tried to put some of the large data that was being generated together. And as David and Tomáš mentioned, of course atherosclerosis is a very complex disease with many, many components. And then of course the mouse model doesn't quite capture all the different pathophysiological events that happen. So one of the aims of this study was to try to integrate and merge the findings from these model without coming a priori with a bias or a pathway or a candidate gene, we decided to do a relatively unbiased shotgun proteomics approach, we actually do for everything. So the challenge then was how to put it all together. And as Tomáš mentioned, there are statistical tools to try to identify a relative abundance of proteins. But, a few things that pure biologists often don't have to encounter is, you're not one or two different proteins, you're looking at thousands of proteins. So there are issues, statistical issues, such as multiple comparisons. If you looked for changes, you're going to find changes just by random chance. So a lot of statistical adjustments had to be made to ensure that those were adjusted for. This are also pathways and processes that were coming out of these results. There's many different pathways that were interrogated. And again, statistically, you want to adjust for the fact that many of those could have been there by random chance. So there's a fair amount of statistical methods that need to be applied for this data. We also did somewhat more sophisticated pathway analysis where we develop networks based on the differential expressed proteins between the ruptured and unruptured plaques to identify connection among these proteins and identify hubs which are highly connected nodes that could potentially drive the biology of a network. So other types of kind of deeper statistical analysis was done, which are maybe more hypothesis-generating because we actually did not follow up on some of these candidates, but I think they really do provide a map or framework to then pursue more mechanistic experiments to see what happens if we knocked out this highly connected node at the plaque rupture site to see if we can either stabilize or manipulate the biology as plaque rupture. Dr Cindy St. Hilaire: Yeah. I mean, that's really the strength of these unbiased approaches is you can come up with so many more novel targets and pathways that might be contributing. So they're just really great. So one thing I found really interesting, you mentioned that you saw a clear distinction in the proteome and I think it was specifically talking about the human samples because they were large enough to see ruptured area versus non ruptured area, but you really saw a distinct difference in the proteomes of the ruptured area of the plaque versus the non ruptured area of the plaque. And obviously the models you were using are overexpressing a protease. So of course there's a role for proteolysis in this process, which you've now firmly established, but I'm wondering if there are other processes that might also erode the basement membrane. And did you pull up anything that might suggest of other things that are happening or even are there other hypothesis out there that we could test with an approach like yours? Dr David Dichek: I think the pathways that came up have probably all been implicated previously. We have processes like inflammation and complement activation, immune response, thrombosis. That's a post-hoc event. I think what was most unexpected was the decrease in the abundance to basement membrane proteins rather than collagens. So collagen has become the sort of signature protein of stable and unstable plaques and used as a surrogate, people do Picrosirius red staining. It's easy to detect with a histochemical stain, you don't even need an antibody. And surprisingly, we found very few differences in collagens and actually no differences in the type 1 or type 3 collagen, which are thought to be the primary stabilizers of the plaque cap. They weren't significantly different in between ruptured and stable areas of the same plaque. So that was certainly a big surprise. Dr Cindy St. Hilaire: Yeah. Because that would indicate that it's not necessary... We always say thinning of the cap, which obviously we know that there's remodeling, it can get thinner. But you kind of found that the contents were the same, but it's the basement really that was eroded. Dr David Dichek: Yeah. The basement membrane proteins were lost. It used to be said in physiology that if you discovered something new, you should just go to the German literature and go back 30 years and it had already been described. And so, looking back in the literature, there are actually the work of Jean-Baptiste Michelle in France and a scientist in Finland, Petri Kovanen, have actually focused on the potential role of basement membrane in unstable atherosclerosis many years ago, but it was kind of buried in the collagen hypothesis. And I think it needs resurrection. Dr Cindy St. Hilaire: Well, I think this paper has done that so well done there. That's great. Dr Tomáš Vaisar: Would be worthwhile to know that of course, the way you prepare the samples may affect what exactly you're seeing. But we've done very careful characterization of the sample preparation of the extraction procedure to focus, to enrich the exosomal matrix proteins because of this collagen hypothesis. And even with that, we basically saw no difference. Dr David Dichek: Yeah. I think that's an excellent point. If we hadn't found collagen in our extracts, we would not be able to conclude a lot about it. And how you do the extraction, how you process the samples here can really influence what you find. We call it unbiased, but there are technical biases that enter, especially in sample preparation, but our extraction process really was able to extract collagens as well as elastin, which is really infamous for being a- Dr Cindy St. Hilaire: Difficult. Dr David Dichek: ... I really think we were getting a good sampling of the matrix here. Dr Cindy St. Hilaire: I don’t know iif there is an answer for this question, but it's something I'm always thinking about. We always talk about athero being so prevalent because there's no kind of evolutionarily the way to tamp it down, it happens later in life. But can you think of any advantage that the vasculature would have in eroding the basement membrane or altering proteases in a response? I was just trying to think, is this just harnessing a wound healing process that's gone awry or could this ever be protective at all in any way? Dr David Dichek: Well, I think you hit the nail on the head, at least according to my bias. It's a healing response gone awry and that you can really draw out the pathways, basement membrane digestion release of chemotactic peptides as part of the inflammatory response, attraction of more inflammatory cells and then a potential healing response that unfortunately results in digestion of the matrix, which has a morbid or fatal consequence rather than physiologic remodeling. And you're right, that's not selected against. It's selected for, in settings in earlier life infections, for example, perhaps neoplasia, but it's not selected against in late life because people are post reproductive. Dr Cindy St. Hilaire: So what's next for these studies? What questions are you going to attack next with either these models or with some of your proteomic findings? Dr David Dichek: Well, we were just talking about that recently, Tomáš and I, and I think we'd like to look at... For one study, we're interested in doing, plaques that are high risk based on MRI imaging, which is really very well developed here at the University of Washington. And many of those patients have endarterectomies and they don't have ruptured plaques. So they are in a high risk group. So they undergo a endarterectomy for that. Not because they've had a plaque rupture and those plaques might be particularly instructive because they're pre event and won't have the healing response to thrombotic response. And it would be really interesting to see if our studies were confirmed. So that's one direction we're going in. Dr Cindy St. Hilaire: That would be amazing. Luckily, you have access to a whole bunch of human tissue for those kinds of really high impact studies. Dr Sina Gharib: I just wanted to point out that one of the advantages of doing proteomics and being part of the scientific community is that we made all this data available in the manuscript for other researchers to access and confirm. So, really probably the best way to procced with this is to have other investigators replicate our findings and expand on it. So I just want to bring that up because all of that data that was generated has been included within the supplements of this manuscripts and it's accessible to any scientist who wants to pursue further. Dr David Dichek: Yeah, I would add one other direction we'd like to go is we still like to know what the substrates are. We think their disappearance based on their abundance is due to proteolysis. But boy, would it be exciting if we could detect fragments. We were unable to do that in the study, probably because they were lost either in vivo or in processing. Technical advancements in that area, and maybe Tomáš can speak to that, might enable us to actually find more direct evidence of proteolysis. Dr Tomáš Vaisar: Yeah, I mean, to start with, it's really hard to determine physiological substrates of proteases. There's a huge amount of literature identifying proteolytic substrates in vitro, but the physiological substrates are really extremely hard to determine, and especially physiologic in vivo confirming that because in vitro, in a tube, you can mix whatever you want and you modify the ratio of proteins to protease substrate, and you can cleave almost everything with anything. It's a little exaggeration, but it's close. While the physiology substrates in the really complex milia of tissues is extremely hard. And so there has been several approaches developed and one of them is the Proteomaps. The other one is an approach called TAILS developed by Chris Overall at UBC that uses the idea of formation of the neo termini and then tagging the neo termini. So that in the actual sample, you can specifically detect these neo termini formed. But even with that approach, it's really hard to determine what are actual physiological substrates. And on top of that, what are the cleavage sites of the proteases? Dr Cindy St. Hilaire: And I guess the third being, if those substrates are cleaved, are they circulating and can we detect them in a blood sample? That would be, I guess, the gold standard. Well, thank you all so much for joining me today. Congratulations on this really very cool study. Being into human and translational work, I always love mouse studies that bring in lots of human samples. So congratulations on that. And I look forward to your future publications on this. Dr Tomáš Vaisar: Thanks a lot. Dr David Dichek: Thanks. Dr Cindy St. Hilaire: That's it for the highlights from the late September and early October issues of Circulation Research. Thank you so much for listening. Please check out the CircRes Facebook page and follow us on Twitter and Instagram with the handle @CircRes and #DiscoverCircRes. Thank you to our guests, Drs David Dichek, Sina Gharib, and Tomáš Vaisar. This podcast is produced by Rebecca McTavish and Ishara Ratnayake, edited by Melissa Stoner and supported by the editorial team of Circulation Research. Some of the copy texts for the highlighted articles is provided by Ruth Williams. I'm your host, Dr Cindy St. Hilaire. And this is Discover CircRes, your on-the-go source for the most up-to-date and exciting discoveries in basic cardiovascular research.
Jane Ferguson: Hi, everyone. Welcome to episode 29 of Getting Personal: Omics of the Heart, the podcast from Circulation: Genomic and Precision Medicine. I'm Jane Ferguson from Vanderbilt University Medical Center and an associate editor at Circ: Genomic and Precision Medicine. Let's dive in and see what's new in the June issue. First up, Validation of Genome-Wide Polygenic Risk Scores for Coronary Artery Disease in French Canadians from Florian Wünnemann, Guillaume Lettre and colleagues from the University of Montreal. Polygenic scores have the potential to be used to predict disease risk, but have not been broadly validated in different populations. This team was interested in whether polygenic risk scores that have been found to predict coronary artery disease in European ancestry subjects in the UK Biobank would also predict disease in French Canadians. They calculated two different polygenic risk scores in over 3600 cases and over 7000 controls and tested their ability to predict prevalent, incident and recurrent CAD. Both scores predicted prevalent CAD, but did not perform as well in predicting incident or recurrent disease. This maybe because the majority of subjects were on statant treatment. Overall, the study confirms that polygenic risk scores for CAD developed in European ancestry can be used in other populations of European ancestry. However, further work is needed to develop and validate polygenic risk scores in other ancestries and to explore whether well performing risk scores can be developed to predict incident or recurrent disease. Our next paper comes from Farnaz Shoja-Taheri, Michael Davis and colleagues from Emory University and is entitled Using Statistical Modeling to Understand and Predict Pediatric Stem Cell Function. Stem cell therapy is emerging as a potential therapeutic option for treating pediatric heart failure, which otherwise can only be cured through heart transplantation. The success of stem cell therapy depends on many variables, including the reparative ability of the infused cells. In this paper, the author set out to test whether they could predict the behavior of c-kit+ progenitor cells or human CPCs using RNA seq and computational modeling. They obtained CPCs from 32 patients, including eight neonates whose cells are thought to have the highest reparative capacity, and they performed RNA sequencing. The team had previously developed regression models that could link gene expression data from sequencing to phenotypes in the cells, and they tested these models in the CPC cell lines. They tested seven neonate cell lines in vitro and found that cellular proliferation and the chemotactic potential of condition media matched what was predicted by the RNA seq-based model. They used pathway analysis to identify potential mechanisms regulating CPC performance and identified several genes related to immune response, including interleukins and chemokines. They further confirmed the presence of cytokines at the protein level that were associated with well performing cells showing that at least one of the outcomes could be functionally predicted using an ELISA ASA. This type of approach may prove useful to inform ongoing clinical trials to stem cell therapy in congenital heart disease. The next paper, Systems Pharmacology Identifies an Arterial Wall Regulatory Gene Network Mediating Coronary Artery Disease Side Effects of Antiretroviral Therapy comes to us from Itziar Frades, Johan Björkegren, Inga Peter and colleagues from the Icahn School of Medicine at Mount Sinai. They were interested in understanding mechanisms whereby antiretroviral therapy for HIV leads to increased risk for coronary artery disease. They analyzed the transcriptional responses to 15 different antiretroviral therapy or ART drugs in human cell lines and cataloged the common transcriptional signatures. They then cross-referenced these against gene networks associated with CAD and CAD related phenotypes. They found that 10 of 15 ART response networks were enriched for differential expression and connectivity in an atherosclerotic arterial wall of regulatory gene network identified as causal for CAD. They used cholesteryl ester loaded foam cells in an in vitro model to validate their findings and found that ART treatment increased cholesteryl ester accumulation in foam cells which was prevented when the key network regulator gene, PQBP1, was silenced. Their study highlights a gene network which is altered in response to ART and which promotes foam cells formation, highlighting a mechanistic link between HIV treatment and CAD. Targeting this network potentially through PQBP1 maybe a way to reduce the risk of CAD in individuals treated with antiretroviral drugs. The next paper comes from Brooke Wolford, Whitney Hornsby, Cristen Willer, Bo Yang and colleagues from the University of Michigan and is entitled Clinical Implications of Identifying Pathogenic Variants in Individuals With Thoracic Aortic Dissection. They were interested in whether exome sequencing in individuals with thoracic aortic dissection could identify disease associated variance. They conducted exome sequencing in 240 patients and 258 controls and screened 11 genes for potentially pathogenic variance. They identified 24 variance in six genes across 26 cases with no potentially pathogenic variance identified in the controls. They found that carriers of pathogenic variance had significantly earlier age of onset of dissection, higher rates of root aneurysm and greater incidents of aortic disease in family members, while patients without identified variance had more hypertension and a higher rate of smoking. Their study suggests that genetic testing should be considered in patients with thoracic artery dissection particularly in individuals with early age of onset before age 50 and no hypertension with the possibility of cascade screening to follow to identify at risk family members before onset of dissection and possible death. Our next paper is a research letter from Seyedeh Zekavat, Pradeep Natarajan and colleagues from Harvard Medical School, Investigating the Genetic Link Between Arterial Stiffness and Atrial Fibrillation. They aimed to investigate whether arterial stiffness is causal for atrial fibrillation using Mendelian randomization to probe genetic causality. They calculated the genetic component of the arterial stiffness index or ASI, a noninvasive measure of arterial stiffness, in over 131,000 individuals in the UK Biobank. They then assessed whether the genetic predictors of ASI defined as the top six independent variance were also associated with atrial fibrillation in over 225,000 participants in the UK Biobank and in over 588,000 individuals from a multi-ethnic GWAS. They found that the ASI genetic risk score was significantly associated with incident atrial fibrillation in both the UK Biobank and the multi-ethnic AF GWAS. The association held true even after adjustment for age, sex, smoking status, prevalent heart failure, prevalent hypertension, prevalent CAD, prevalent hypercholesterolemia, prevalent diabetes, heart rate, alcohol intake and exercise frequency in the UK Biobank participants. Because some people have hypothesized that atrial fibrillation may actually precede and cause arterial stiffness, the team did the reverse Mendelian randomization experiment and tested whether genetic predictors of AF were associated with the arterial stiffness index. They found no association suggesting that AF does not cause arterial stiffness. In summary, this paper provides genetic evidence supporting arterial stiffness as a causal contributor to atrial fibrillation and suggests that future randomized controlled studies would be warrantied to assess whether methods to reduce arterial stiffness could be protective against atrial fibrillation. The next research letter comes from Scott Damrauer, Kara Hardie, Reed Pyeritz and colleagues from the University of Pennsylvania and is entitled FBN1 Coding Variants and Nonsyndromic Aortic Disease. In this study, the authors were interested in characterizing the frequency of variance associated with Marfan syndrome in the general population. They analyzed data from the Penn Medicine BioBank looking at 12 variance in the FBN1 gene all of which have been reported to associate with Marfan syndrome. Of almost 11,000 individuals who underwent exome sequencing, they identified 70 individuals who were carriers of one of the 12 preselected FBN1 variance. These individuals ranged in age from age 28 to 87 years and 56% of them were male. They combed through clinical data from the participant's electronic health records, including office notes, diagnostic tests and imaging studies. Two individuals had a clinical diagnosis of Marfan syndrome while 21 individuals had evidence of cardiovascular phenotypes related to Marfan syndrome including mitral valve disease, dilated sinus of valsalva, dilated ascending aorta, descending thoracic or abdominal aneurysms or dissections or had undergone surgical procedures involving the mitral valve or thoracic aorta. Compared to age and sex matched controls without known or suspected pathogenic FBN1 variance, the FBN1 variant carriers were significantly more likely to have Marfan syndrome related cardiovascular disease. Although the majority of individuals carrying FBN1 variance did not have documented cardiovascular disease in this study, the data were somewhat limited, meaning that some affected individuals could have been missed. Thus, while the penetrance of these variance appears to be variable, the severe consequences of these FBN1 variance observed in some individuals suggests that clinical screening for carries of these variance is important. To round up this month's issue, we have a scientific statement led by Ferhaan Ahmad and Elizabeth McNally on Establishment of Specialized Clinical Cardiovascular Genetics Programs: Recognizing the Need and Meeting Standards. This statement comes from the American Heart Association Council on Genomic and Precision Medicine, the Council on Arteriosclerosis, Thrombosis and Vascular Biology, the Council on Basic Cardiovascular Sciences, the Council on Cardiovascular and Stroke Nursing, the Council on Clinical Cardiology and the Stroke Council. In this statement, the writing group lays out the importance of establishing specialized centers of care for individuals affected by inherited cardiovascular diseases. As cardiovascular genetics as a field continues to grow and as genomic medicine becomes part of practice, it is essential for programs to evolve to include this new knowledge and specialization. There are significant challenges in interpreting genetic test results and in evaluating counseling and managing the care of genetically at risk family members who have inherited pathogenic variance, but not yet shown signs of disease. Establishing specialized programs to combine cardiovascular medicine and genetics expertise is an effective way to allow for the integration of multiple types of clinical and genetic data and to improve diagnosis, prognostication and cascade family testing in affected individuals and their families. Training individuals in genetic cardiology will allow for improved care and management of risk in affected or at risk individuals and potentially pave the way for genotype specific therapy. This important and timely scientific statement outlines current best practices for delivering cardiovascular genetic evaluation and care in both the pediatric and the adult settings with a focus on team member expertise and conditions that most benefit from genetic evaluation. That's all for this month. Thank you as always for listening and come back next month for the next installment of papers in Genomic and Precision Medicine. This podcast was brought to you by Circulation: Genomic and Precision Medicine and the American Heart Association Council on Genomic and Precision Medicine. This program is copyright American Heart Association 2019.
In Episode 138 of Keto Talk, Jimmy and Dr. Will Cole answer your questions about Arteriosclerosis Reversal, Acetyl-CoA, Gastro Event Requiring Antibiotics And Pasta, Fasting And Appendicitis, Keto Aggravating Adrenals and more! HOT TOPICS: VEGAN CORY BOOKER SAYS MEAT EATERS’ DAYS ARE NUMBERED Why is cheating on your keto diet everyone once in a while a bad thing? What do you think about the new sweetener allulose being used in keto products? Does using collagen, bone broth, and MCT oil break your fast and turn off autophagy? Could the carrageenan typically found in heavy cream be the cause of my skin issues? Does having chronic pancreatitis requiring prescription pancreatic enzymes preclude someone from eating keto? “Buyer beware when it comes to some of these food substitutes on the market.” – Jimmy Moore “It's not fair that some of us can tolerate certain foods while others can't, but we have to accept where we are on our health journey at this moment.” – Dr. Will Cole HEALTH HEADLINES: We’ll Always Eat Meat. But More of It Will Be ‘Meat' This Mediterranean diet study was hugely impactful. The science has fallen apart. Scientists Accidentally Discover Drug that Prevents Weight Gain Fasting's Health Benefits May Be Broader Than Scientists Previously Realized Are You A Super Pooper? STUDY: Newly isolated human gut bacterium reveals possible connection to depression Jimmy and Will answer your questions: – Is there any research showing reversal of arteriosclerosis with keto and other lifestyle changes? Hi Jimmy and Will, I’m a big fan of the ketogenic diet and you guys consistently provide some of the best information about this way of eating online. I’ve been doing a lot of research lately on how to reverse arteriosclerosis since it seems most people have some varying level of this develop during their lifetime. I've seen people talk about things like taking magnesium and the MK7 variant of Vitamin K2, but these are only theoretical in nature. Is there any scientific evidence that this actually reverses the progression of heart disease? Is there any research that demonstrates keto and other lifestyle approaches help with this reversal of arteriosclerosis? Thanks again for your fantastic podcast. Tom – Is there any concern with an increased production of Acetyl-CoA when a Type 2 diabetic is eating keto? Hey guys, I have someone in my life who has a biochemistry background claiming that going keto is about the worst thing a person with Type 2 diabetes could possibly do because of excessive production of Acetyl-CoA and that it induces a state of ketoacidosis (which I know is flat-out wrong). When I inquired about the mechanism about how the higher Acetyle-CoA issue happens and what the end result would be from this, she responded with something about DNA damage being done on a neurological level. This doesn’t make any sense to me from what I know about healthy nutritional ketosis and I’d love to offer up a counterpoint to her arguments. She seems to be really confused and it would be great to help educate her on this. Thanks for your help! Sue – What is the best way to recover my gut health from three rounds of strong antibiotics? Hello Jimmy and Dr. Cole, I recently had a gastro event that my gastroenterologist put me on two strong antibiotics (Cipro and Flagyl) for. As a keto dieter, I was shocked when he recommended that I eat lots of pasta before having a colonoscopy. When I told him I eat for ketosis, he chided me by staying that diet is merely political and not actually based on any sound science. I’m almost sure I have leaky gut and declined having the colonoscopy since the antibiotics have surely almost entirely wiped out my gut flora. I’m now eating the Specific Carbohydrate Diet (SCD) and am doing well on it so far. I did have to take another antibiotic (Methylpred) for a pulled tooth recently, so I know my gut health is majorly compromised now. Is there anything else I can do to help further improve my gut health so I don’t have to go through these rounds of antibiotics and recommendations of pasta anytime soon? This has been a very hard winter for me. Thank you for responding to my questions. Mary – Does extended fasting lead to appendicitis and gallstone development? Hey Jimmy and Will, I was inspired to start doing some longer fasting because of your podcasts and decided to do a 7-day fast. It was surprisingly easy for me to do and I felt great after it was finished. But one week after I finished that 7-day fast, I developed appendicitis. Was this somehow related to the fast or is this merely a coincidence? Checking Dr. Google didn’t help me answer this question at all which is why I’m writing to you today. They did find I had a developed a a gallstone which Dr. Valter Longo has said can happen on fasting. I’d love to go back to my regular 24-36 hour fasts, but now I’m scared because I don’t want to lose my gallbladder. Can you help reassure me about this issue? Thank you and best regards, Andy in the Philippines KETO TALK MAILBOX: – Is keto making my adrenal issues worse? Hi Jimmy and Will, Thank you for all you do on Keto Talk to get sound information about healthy eating out to the public. I’ve been keto for just over a year and have lost 32 pounds while improving many of the symptoms of insulin resistance. I’ve felt energetic for my active lifestyle of mountain biking, running, cross country skiing, and snowshoeing. However, lately I’ve been having a few episodes of what I suspect may be symptoms of adrenal insufficiency. I have dealt with low thyroid and my naturopath put me on thyroid hormone replacement to deal with this—but it didn’t help or hinder. The focus of my treatment has been on healing the gut microbiome and I’ve been consuming copious amounts of bone broth and fermented food like yogurt to help with that along with periods of intermittent fasting. I recently dealt with a virus that wouldn’t let go leaving me pretty sick and worn out for about two weeks. When I started feeling better, I noticed my lymph nodes in my neck were noticeably swollen and tender to the touch. At night, the back of my legs were achy near the back side of my knees. Waking up in the morning felt like I was hungover with my eyes swollen, a low-grade headache, nausea, and incredibly lethargic. When my chiropractor touch my T12 on my back, I felt a hot stinging sensation and immediately because nauseous. She told me that is directly tied to the adrenals. Is keto making these adrenal issues worse? From what I’ve seen, the recommendation for adrenal problems is to eat more carbs, but I don’t want to do that for a lot of reasons. Thank you for helping me try to figure this out. Kathy ITUNES REVIEWS: Leave us a review on Apple Podcasts
When I had my stroke at 46, it took a little while for the medical team to settle on the cause. I suppose that's a good thing. We don't want them to rush to a conclusion. Ultimately, they concluded the probable cause was a history of high blood pressure. It didn't make sense to me at the time. In 2015 I developed high blood pressure, AKA hypertension, but I didn't know. That's the thing about high blood pressure -- it doesn't hurt. There was no pain. I only found out because during the last week of December, I began have massive 30 minute pouring nosebleeds every other day. I checked my blood pressure on a home blood pressure machine, and it registered more than 200 over 160. That and the random surprise bleeding got me into the doctor's office. They measured my BP at 162/102. So it had dropped from apparently ER levels by that time. Over the course of the next few months, we worked to get my BP under control through medication and some diet tweaks. By March of 2016, my BP was coming in at 105/75. Be February of 2017, it was down to 100/70. And on June 3, 2017, I had my stroke. I had serious high blood pressure for maybe a year to a year and a half. I had it under control for a year before my stroke. So how could previous high blood pressure cause a stroke? This week, Dr. Nirav Shah, a neurologist at Swedish Medical Center in Seattle and the founder and CEO of Sentinel Healthcare, returns to Strokecast to answer that very question as we talk about just how high blood pressure causes stroke. Bio Dr. Nirav H. Shah is a fellowship trained neurologist and sub-specialist in cerebrovascular and stroke medicine with board certifications in: neurology, stroke medicine, carotid neurosonology, transcranial doppler ultrasound, and neuroimaging. He is a practicing neurohospitalist and served as the stroke medical director at Swedish Medical Center in Seattle. Academically, he is interested in emergent and critical care neurology research and is an associate editor for The Neurohospitalist, a peer-reviewed journal. He enjoys mentoring trainees and collaborating on publications and conference presentations. Outside of clinical care Dr Shah is collaborating with experts to develop scalable technologies capable of ameliorating healthcare’s challenges. He consults with startups and investors to develop technologies and devices so that one day they are available to his patients. He has worked with companies to meet FDA regulations for approval as well as to help them understand the provider perspective of product-market fit. Dr. Shah is also the CEO and Founder of Sentinel Healthcare. He is also a passionate traveler and photographer. Hack of the Week After I lost the use of my left arm, eating became a challenge for some dishes. Sushi was easy. Steak was difficult because to cut a steak, you need to hold it still with your fork and slice with the steak with the knife in your other hand. So how do you manage this out at a restaurant? You've got a couple options. One, of course is to just skip cutting it, pick up the slab of meat with the one usable hand and start chowing down. Of course your dining companions may not prefer that choice. The other option is incredibly simple. When you place your order, ask them to have the kitchen cut up the steak for you. That's it. It's a simple request that will take them just seconds and it solves your problem. Links Lipohyalinosis https://en.wikipedia.org/wiki/Lipohyalinosis C. Miller Fisher on Wikipedia https://en.wikipedia.org/wiki/C._Miller_Fisher C. Miller Fisher On AHA Journals https://www.ahajournals.org/doi/10.1161/STROKEAHA.112.661512 Atherosclerosis on WebMD https://www.mayoclinic.org/diseases-conditions/arteriosclerosis-atherosclerosis/symptoms-causes/syc-20350569 Arteriosclerosis / atherosclerosis on Mayo Clinic https://www.mayoclinic.org/diseases-conditions/arteriosclerosis-atherosclerosis/symptoms-causes/syc-20350569 Lacunar Stroke on Wikipedia https://en.wikipedia.org/wiki/Lacunar_stroke Lacunar Infarction and Small Vessel Disease: Pathology and Pathophysiology https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4325635/ Effect of reducing blood pressure with medications immediately following ischemic stroke https://medicalxpress.com/news/2013-11-effect-blood-pressure-medications-immediately.html Blood Pressure-Lowering Treatment After Subacute Stroke to Prevent Recurrent Stroke, Major Vascular Events, and Dementia https://www.ahajournals.org/doi/full/10.1161/STROKEAHA.118.023087?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub%3dpubmed Higher Blood Pressure May Be Linked to Brain Disease, Alzheimer’s https://www.rush.edu/news/press-releases/higher-blood-pressure-may-be-linked-brain-disease-alzheimers Nirav on LinkedIn https://www.linkedin.com/in/nirav-h-shah/ Nirav at Swedish https://www.swedish.org/swedish-physicians/profile.aspx?name=nirav+h+shah&id=271893 Nirav on Twitter http://twitter.com/NeuroNirav The Neurohospitalist http://journals.sagepub.com/home/nho Nirav’s Photography www.thoughtpotential.com Where do we go from here? Control your blood pressure. If you don't know what it is, find out. Talk with your doctor to develop a plan to drive it to safe levels -- under 120/80 Post a link to this episode on your Facebook, LinkedIn, or Twitter account by using the link http://strokecast.com/bloodpressure If you'd like to hear more from Nirav, check out his other appearances by going to http://Strokecast.com/Nirav Don't get best…get better Strokecast is the stroke podcast where a Gen X stroke survivor explores rehab, recovery, the frontiers of neuroscience and one-handed banana peeling by helping stroke survivors, caregivers, medical providers and stroke industry affiliates connect and share their stories.
Ivor Cummins is a Biochemical Engineer who in 2012 was disturbed by a set of his own abnormal blood test results. Consultation with multiple doctors yielded little insight into the cause of his elevated cholesterol, ferritin and GGT so he turned to his analytical roots to study the problem. In the process, he evaluated hundreds of scientific papers, ultimately concluding that that flawed hypotheses and a breach of the scientific method have resulted in the current “diabesity” epidemic. Ivor is here today with Dr. Tommy Wood talking on topics related to his well-referenced new book, Eat Rich, Live Long: Mastering the Low-Carb & Keto Spectrum for Weight Loss and Great Health. They also discuss the trouble with polyunsaturated oils, advice on fat loss for the insulin sensitive, and the best test for cardiovascular disease risk (hint: it’s not LDL). If you enjoy this podcast, Ivor is a regular presenter at low-carb/keto events and maintains an active blog and social media presence. Here’s the outline of this interview with Ivor Cummins: [00:00:17] Keto Summit, Dave Feldman. [00:00:48] Boundless Health Podcast with Dr. Bret Scher. [00:01:57] Podcast: The True Root Causes of Cardiovascular Disease, with Dr. Jeffry Gerber. [00:02:15] Book: Eat Rich, Live Long: Mastering the Low-Carb & Keto Spectrum for Weight Loss and Great Health, by Ivor Cummins and Jeffry Gerber, MD. [00:02:29] Videos: here and here. [00:03:20] Insulin, IGF-1, acellular carbs. [00:03:56] Sunlight exposure, 25-OH-D video. [00:04:37] Minerals, Study: DiNicolantonio, James J., James H. O’Keefe, and William Wilson. "Subclinical magnesium deficiency: a principal driver of cardiovascular disease and a public health crisis." Open Heart 5.1 (2018): e000668. [00:05:28] Gabor Erdosi, Lower Insulin Facebook Group. [00:05:43] Video: Roads to Ruin? from Physicians for Ancestral Health 2017 conference. [00:06:01] Guðmundur Jóhannsson, gut health; Podcast: Foodloose Iceland. [00:07:40] Study: Schwalfenberg, Gerry K., and Stephen J. Genuis. "The importance of magnesium in clinical healthcare." Scientifica 2017 (2017). [00:08:10] Industrial seed oils. [00:09:05] Unilever sells its margarine business. [00:10:17] Studies: Alvheim, Anita Røyneberg, et al. "Dietary Linoleic Acid Elevates the Endocannabinoids 2‐AG and Anandamide and Promotes Weight Gain in Mice Fed a Low Fat Diet." Lipids 49.1 (2014): 59-69. And: Alvheim, Anita R., et al. "Dietary Linoleic Acid Elevates Endogenous 2‐AG and Anandamide and Induces Obesity." Obesity 20.10 (2012): 1984-1994. [00:10:48] Studies: Nanji, Amin A., and Samuel W. French. "Dietary factors and alcoholic cirrhosis." Alcoholism: Clinical and Experimental Research 10.3 (1986): 271-273. And: Kirpich, Irina A., et al. "Alcoholic liver disease: update on the role of dietary fat." Biomolecules 6.1 (2016): 1. [00:12:09] Book: Deep Nutrition: Why Your Genes Need Traditional Food, by Cate Shanahan, M.D. [00:12:45] Studies: 1. Ramsden, Christopher E., et al. "The Sydney Diet Heart Study: a randomised controlled trial of linoleic acid for secondary prevention of coronary heart disease and death." The FASEB Journal 27.1 Supplement (2013): 127-4. 2. Frantz, Ivan D., et al. "Test of effect of lipid lowering by diet on cardiovascular risk. The Minnesota Coronary Survey." Arteriosclerosis, Thrombosis, and Vascular Biology 9.1 (1989): 129-135. 3. Strandberg, Timo E., et al. "Mortality in participants and non-participants of a multifactorial prevention study of cardiovascular diseases: a 28 year follow up of the Helsinki Businessmen Study." Heart 74.4 (1995): 449-454. 4. Rose, G. A., W. B. Thomson, and R. T. Williams. "Corn oil in treatment of ischaemic heart disease." British medical journal 1.5449 (1965): 1531. [00:13:47] Study: Hooper, Lee, et al. "Reduction in saturated fat intake for cardiovascular disease." The Cochrane Library (2015). [00:15:28] Study: Ip, Clement, Christopher A. Carter, and Margot M. Ip. "Requirement of essential fatty acid for mammary tumorigenesis in the rat." Cancer Research 45.5 (1985): 1997-2001. [00:16:28] Study: Pearce, Morton Lee, and Seymour Dayton. "Incidence of cancer in men on a diet high in polyunsaturated fat." The Lancet 297.7697 (1971): 464-467. [00:16:56] Breast milk composition is now almost 50% PUFA. [00:17:50] David Bobbett. [00:19:59] Book structure. [00:20:51] Fat-loss for the insulin sensitive. [00:21:10] Videos: Jeff Gerber interviews Simon Saunders and Marty Kendall. [00:23:03] Ghrelin. [00:24:21] Protein and lean body mass. [00:26:05] Glucagon, mTOR. [00:26:22] Ron Rosedale. [00:26:34] Valter Longo. [00:27:02] IGF-1 U-shaped curve. [00:28:06] Study: Levine, Morgan E., et al. "Low protein intake is associated with a major reduction in IGF-1, cancer, and overall mortality in the 65 and younger but not older population." Cell metabolism 19.3 (2014): 407-417. [00:28:49] Book: Protein Power: The High-Protein/Low Carbohydrate Way to Lose Weight, Feel Fit, and Boost Your Health - in Just Weeks! By Michael Eades and Mary Dan Eades. [00:30:39] Study: Levine, Morgan E., et al. "Low protein intake is associated with a major reduction in IGF-1, cancer, and overall mortality in the 65 and younger but not older population." Cell metabolism 19.3 (2014): 407-417. [00:31:06] NHANES. [00:31:18] Study: Cohen, Evan, et al. "Statistical review of US macronutrient consumption data, 1965–2011: Americans have been following dietary guidelines, coincident with the rise in obesity." Nutrition 31.5 (2015): 727-732. [00:32:20] Kitavans. [00:34:05] Hyperlipid and Denise Minger. [00:36:37] Icelandic diets for longevity [00:39:07] Cardiovascular disease. [00:39:35] Basic lipid panel. [00:39:45] Study: Castelli, William P. "Lipids, risk factors and ischaemic heart disease." Atherosclerosis 124 (1996): S1-S9. [00:40:24] Ratios. [00:41:54] Study: Johnson, Kevin M., David A. Dowe, and James A. Brink. "Traditional clinical risk assessment tools do not accurately predict coronary atherosclerotic plaque burden: a CT angiography study." American Journal of Roentgenology 192.1 (2009): 235-243. Commentary: Ware, William R. "The mainstream hypothesis that LDL cholesterol drives atherosclerosis may have been falsified by non-invasive imaging of coronary artery plaque burden and progression." Medical hypotheses 73.4 (2009): 596-600. [00:42:30] Familial Hypercholesterolemia and CVD. [00:43:27] cholesterolcode.com, remnant cholesterol, Plasma Atherogenic Index. [00:44:36] Podcast: Health Outcome-Based Optimal Reference Ranges for Cholesterol [00:46:06] Coronary calcium scan. [00:46:25] Study: Nasir, Khurram, et al. "Interplay of Coronary Artery Calcification and Traditional Risk Factors for the Prediction of All-Cause Mortality in Asymptomatic Individuals Clinical Perspective." Circulation: Cardiovascular Imaging 5.4 (2012): 467-473. [00:47:54] Longitudinal score. [00:49:41] Plaque density. [00:50:11] Interview with Matt Budoff. [00:52:37] Video: Dr. Eades at Low Carb Breckenridge, Agatston score. [00:54:38] The Fat Emperor. [00:54:53] Low-carb Breckenridge 2018. [00:55:10] Ketofest, Keto Con, Low-carb USA, Refind Health. [00:55:45] Widowmaker movie.
Heavy Metal Toxicity (such as Lead, Mercury, Arsenic, Cadmium, Aluminum, Beryllium, Cobalt, Copper, Nickel, Iron) can be the root cause of health problems that go undiagnosed by most doctors. In this episode, find out: --That Heavy Metal Toxicity impacts a higher percentage of children (40% of all children) than adults. And the connection of Heavy Metal Toxicity to Autism, Asperger's Syndrome, Learning Disabilities, Immune Compromise, Kidney Damage, and Liver Damage. --How your well water, proximity to a farm or golf course, or employment in a factory can expose you to Heavy Metal Toxicity. --How Arsenic can result in abnormal behavior as it changes how you think and your personality. And how Mary Todd Lincoln and Michael Jackson both had issues resulting from Heavy Metal Toxicity. --That Aluminum Toxicity is common among children with Autism, Asperger's, and Learning Disabilities. And how Dr. Prather sees "a dramatic change" when they get those levels lowered. --Why each individual dosage of a vaccine can contain different amounts of Heavy Metal Toxicity due to how vaccines are stored. --How Aluminum is listed as a "non-toxic preservative" by the government, which has increased the amount of Aluminum we ingest. And how deodorants contain high levels of Aluminum, which has been connected to Dementia, Alzheimer's, Osteoporosis, and Arteriosclerosis. --That high Copper can cause emotional issues, agitation, and hypersensitivity. --Why Nickel Toxicity is usually associated with dental work. And the weakening of the heart muscle associated with Cobalt (which can come from working in automobile manufacturing). --The Hair Analysis test you should have every year to determine if you have Heavy Metal Toxicity, and why you MUST make sure you are using a well-qualified lab that uses the latest technology to evaluate you. Plus, why Dr. Prather says the Chelation Challenge Test is inferior to the Hair Analysis Test. --Why Chelation to remove Heavy Metals from the body is rarely recommended by Dr. Prather. And why Dr. Prather calls Homeopathy "a magic formula" for detoxification of Heavy Metals in a quicker and safer way with no side effects (and a 100% success rate!). --How high levels of Manganese can produce the same symptoms of Parkinson's Disease. www.TheVoiceOfHealthRadio.com
Do we recognize shock early enough? How do we prioritize our interventions? How can we tell whether we’re making our patient better or worse? World wide, shock is a leading cause of morbidity and mortality in children, mostly for failure to recognize or to treat adequately. So, what is shock? Simply put, shock is the inadequate delivery of oxygen to your tissues. That’s it. Our main focus is on improving our patient’s perfusion. Oxygen delivery to the tissues depends on cardiac output, hemoglobin concentration, the oxygen saturation of the hemoglobin you have, and the environmental partial pressure of oxygen. At the bedside, we can measure some of these things, directly or indirectly. But did you notice that blood pressure is not part of the equation? The reason for that is that blood pressure is really an indirect proxy for perfusion – it’s not necessary the ultimate goal. The equation here is a formality: DO2 = (cardiac output) x [(hemoglobin concentration) x SaO2 x 1.39] + (PaO2 x 0.003) Shock CAN be associated with a low blood pressure, but shock is not DEFINED by a low blood pressure. Compensated Shock: tachycardia with poor perfusion. A child compensates for low cardiac output with tachycardia and a increase in systemic vascular resistance. Decompensated Shock: frank hypotension, an ominous, pre-arrest phenomenon. Shock is multifactorial, but we need to identify a primary cause to prioritize interventions. How they "COHDe": Cardiogenic, Obstructive, Hypovolemic, and Distributive. Cardiogenic Shock All will present with tachycardia out of proportion to exam, and sometimes with unexplained belly pain, usually due to hepatic congestion. The typical scenario in myocarditis is a precipitous decline after what seemed like a run-of-the-mill URI. Cardiogenic shock in children can be from congenital heart disease or from acquired etiologies, such as myocarditis. Children, like adults, present in cardiogenic shock in any four of the following combinations: warm, cold, wet, or dry. "Warm and Dry" A child with heart failure is “warm and dry” when he has heart failure signs (weight gain, mild hepatomegaly), but has enough forward flow that he has not developed pulmonary venous congestion. A warm and dry presentation is typically early in the course, and presents with tachycardia only. "Warm and Wet" If he worsens, he becomes “warm and wet” with pulmonary congestion – you’ll hear crackles and see some respiratory distress. Infants with a “warm and wet” cardiac presentation sometimes show sacral edema – it is their dependent region, equivalent to peripheral edema as we see in adults with right-sided failure. “Warm” patients – both warm and dry and warm and wet -- typically have had a slower onset of their symptoms, and time to compensate partially. Cool patients are much sicker. "Cold and Dry” A patient with poor cardiac output; he is doing everything he can to compensate with increased peripheral vascular resistance, which will only worsen forward flow. Children who have a “cold and dry” cardiac presentation may have oliguria, and are often very ill appearing, with altered mental status. "Cold and Wet" The sickest of the group, this patient is so clamped down peripherally that it is now hindering forward flow, causing acute congestion, and pulmonary venous back-up. You will see cool, mottled extremities. Cardiogenic Shock: Act Use point-of-care cardiac ultrasound: Good Squeeze? M-mode to measure fractional shortening of the myocardium or anterior mitral leaflet excursion. Pericardial Effusion? Get ready to aspirate. Ventricle Size? Collapsed, Dilated, Careful with fluids -- patients in cardiogenic shock may need small aliquots, but go quickly to a pressor to support perfusion Pressor of choice: epinephrine, continuous IV infusion: 0.1 to 1 mcg/kg/minute. Usual adult starting range will end up being 1 to 10 mcg/min. Avoid norepinephrine, as it increases systemic vascular resistance, may affect afterload Just say no to dopamine: increased mortality when compared to epinephrine Obstructive Shock Mostly one of two entities: pulmonary embolism or cardiac tamponade. Pulmonary embolism in children is uncommon – when children have PE, there is almost always a reason for it – it just does not happen in normal, healthy children without risk factors. Children with PE will either have a major thrombophilic comorbidity, or they are generously sized teenage girls on estrogen therapy. Tamponade -- can be infectious, rheumotologic, oncologic, or traumatic. It’s seen easily enough on point of care ultrasound. If there is non-traumatic tamponade physiology, get that spinal needle and get to aspirating. Obstructive Shock: Act Pulmonary embolism (PE) with overt shock: thrombolyse; otherwise controversial. PE with symptoms: heparin. Tamponade: if any sign of shock, pericardiocentesis, preferentially ultrasound-guided. Hypovolemic Shock The most common presentation of pediatric shock; look for decreased activity, decreased urine output, absence of tears, dry mucous membranes, sunken fontanelle. May be due to obvious GI losses or simply poor intake. Rapid reversal of hypovolemic shock: may need multiple sequential boluses of isotonic solutions. Use 10 mL/kg in neonates and young infants, and 20 mL/kg thereafter. Hypovolemic Shock: Act Tip: in infants, use pre-filled sterile flushes to push fluids quickly. In older children, use a 3-way stop cock in line with your fluids and a 30 mL syringe to "pull" fluids, turn the stop cock, and "push them into the patient. Titrate to signs of perfusion, such as an improvement in mental status, heart rate, capillary refill, and urine output. When concerned about balancing between osmolality, acid-base status, and volume status, volume always wins. Our kidneys are smarter than we are, but they need to be perfused first. Distributive Shock The most common cause of distributive shock is sepsis, followed by anaphylactic, toxicologic, adrenal, and neurogenic causes. Septic shock is multifactorial, with hypovolemic, cardiogenic, and distributive components. Children with sepsis come in two varieties: warm shock and cold shock. Distributive Shock: Act Warm shock is due to peripheral vascular dilation, and is best treated with norepinephrine. Cold shock is due to a child’s extreme vasoconstriction in an attempt to compensate. Cold shock is the most common presentation in pediatric septic shock, and is treated with epinephrine. Early antibiotics are crucial, and culture everything that seems appropriate. Shock: A Practical Approach "How FAST you FILL the PUMP and SQUEEZE" Sometimes things are not so cut-and-dried. We'll use a practical approach to diagnose and intervene simultaneously. Look at 4 key players in shock: heart rate, volume status, contractility, and systemic vascular resistance. How FAST you FILL the PUMP and SQUEEZE First, we look at heart rate -- how FAST? Look at the heart rate – is it sinus? Could this be a supraventricular tachycardia that does not allow for enough diastolic filling, leading to poor cardiac output? If so, use 1 J/kg to synchronize cardiovert. Conversely, is the heart rate too slow – even if the stroke volume is sufficient, if there is severe bradycardia, then cardiac output -- which is in liters/min – is decreased. Chemically pace with atropine, 0.01 mg/kg up to 0.5 mg, or use transcutaneous pacing. If the heart rate is what is causing the shock, address that first. Next, we look at volume status. How FAST you FILL the PUMP and SQUEEZE Look to FILL the tank if necessary. Does the patient appear volume depleted? Try a standard bolus – if this improves his status, you are on the right track. Now, we look at contractility. How FAST you FILL the PUMP and SQUEEZE Is there a problem with the PUMP? That is, with contractility? Is this in an infarction, an infection, a poisoning? Look for signs of cardiac congestion on physical exam. Put the probe on the patient’s chest, and look for effusion. Look to see if there is mild, moderate, or severe decrease in cardiac contractility. If this is cardiogenic shock – a problem with the pump itself -- begin pressors. And finally, we look to the peripheral vascular resistance. How FAST you FILL the PUMP and SQUEEZE Is there a problem with systemic vascular resistance – the SQUEEZE? Look for signs of changes in temperature – is the patient flushed? Is this an infectious etiology? Are there neurogenic or anaphylactic concerns? After assessing the heart rate, optimizing volume status, evaluating contractility, is the cause of the shock peripheral vasodilation? If so, treat the cause – perhaps this is a distributive problem due to anaphylaxis. Treat with epinephrine. The diagnosis of exclusion in trauma is neurogenic shock. Perhaps this is warm shock, both are supported with norepinephrine. All of these affect systemic vascular resistance – and the shock won’t be reversed until you optimize the peripheral squeeze. Summary The four take-home points in the approach to shock in children To prioritize your innterventions, remember how patients COHDe: Cardiogenic, Obstructive, Hypovolemic, and Distributive. Your patient's shock may be multifactorial, but mentally prioritize what you think is the MAIN case of the shock, and deal with that first. To treat shock, remember: How FAST You FILL The PUMP and SQUEEZE: Look at the heart rate – how FAST. Look at the volume status – the FILL. Assess cardiac contractility – the PUMP, and evaluate the peripheral vascular tone – the SQUEEZE. In pediatric sepsis, the most common type is cold shock – use epinephrine (adrenaline) to get that heart to increase the cardiac output. In adolescents and adults, they more often present in warm shock, use norepinephrine (noradrenaline) for its peripheral squeeze to counteract this distributive type of shock. Rapid-fire word association: Epinephrine for cardiogenic shock Intervention for obstructive shock Fluids for hypovolemic shock Norepinephrine for distributive shock References Agha BS, Sturm JJ, Simon HK, Hirsh DA. Pulmonary embolism in the pediatric emergency department. Pediatrics. 2013 Oct;132(4):663-7. Dellinger RP, Levy MM, Rhodes A, et al. Surviving sepsis campaign: international guidelines for management of severe sepsis and septic shock: 2012. Crit Care Med. 2013; 41:580-637. Jaff MR et al. for the American Heart Association Council on Cardiopulmonary, Critical Care, Perioperative and Resuscitation; American Heart Association Council on Peripheral Vascular Disease; American Heart Association Council on Arteriosclerosis, Thrombosis and Vascular Biology. Management of massive and submassive pulmonary embolism, iliofemoral deep vein thrombosis, and chronic thromboembolic pulmonary hypertension: a scientific statement from the American Heart Association. Circulation. 2011; Apr 26;123(16):1788-830. Levy B et al. Comparison of norepinephrine-dobutamine to epinephrine for hemodynamics, lactate metabolism, and organ function variables in cardiogenic shock. A prospective, randomized pilot study. Crit Care Med. 2011; 39:450. Micek ST, McEvoy C, McKenzie M, Hampton N, Doherty JA, Kollef MH. Fluid balance and cardiac function in septic shock as predictors of hospital mortality. Crit Care. 2013; 17:R246. Osman D, Ridel C, Ray P, et al. Cardiac filling pressures are not appropriate to predict hemodynamic response to volume challenge. Crit Care Med. 2007; 35:64-8. Ventura AM, Shieh HH, Bousso A, Góes PF, de Cássia F O Fernandes I, de Souza DC, Paulo RL, Chagas F, Gilio AE. Double-Blind Prospective Randomized Controlled Trial of Dopamine Versus Epinephrine as First-Line Vasoactive Drugs in Pediatric Septic Shock. Crit Care Med. 2015;43(11):2292-302. This post and podcast are dedicated to Natalie May, MBChB, MPHe, MCEM, FCEM for her collaborative spirit, expertise, and her super-charged support of #FOAMed. You make a difference. Thank you. Undifferentiated Shock Powered by #FOAMed -- Tim Horeczko, MD, MSCR, FACEP, FAAP
End Time Current Events: 5-26-13–Part 5 Table of Contents: Natural Alternatives for High Blood Pressure Medications, Arteriosclerosis & Receding Gums Click Here to Listen to the Part 5 Audio PDF: End Time Current Events 5-26-13
Dr. Peterson discusses the significance of cholesterol numbers and explains how to compensate for those that are unfavorable
Dr. Peterson discusses the significance of cholesterol numbers and explains how to compensate for those that are unfavorable
Medizinische Fakultät - Digitale Hochschulschriften der LMU - Teil 09/19
The coronary display within the multislice computer tomography (MSCT) enables an exact insight into the intra-coronary conditions, based on the three dimensional reconstruction of the singular slices. The existence of calcium plaques indicates Arteriosclerosis, but also the pre-stages of calcium, which cannot definitely be diagnosed in percutaneous coronary angiography, can be detected by MSCT due to the distinction of density given in Hounsfield-Units (HU). If the density is below 90 HU the concretion attached to the endothelium is defined as soft plaques, up to 129 HU it is called fibrous and above 130 HU calcium plaques. The non-calcificated pre-stages, also described by Davies as “vulnerable Plaques”, tend to become disrupted even stronger than the relatively solid calcium plaques and therefore are responsible for a bigger part of myocardial infarcts. This prospective clinical trial examines the validity of a prognostic statement concerning the occurrence of acute coronary syndrome caused by plaques related to intra-coronary concretions within a period of six months after a 4-slice MSCT-scanning of the heart. 416 individuals (259 male and 157 female) suffering from chest pain, were observed from May 2001 to December 2002. End points of the study are the incidence of a myocardial infarct, catheter revascularisation or lethality. The sensitivity for the correct prediction of myocardial incidence within the six successive months is evaluated in this study at 97% for the male population and 89% for the female population. The negative prediction is 0.99 for male and 0.98 for female. Despite the representative occurrence of end points of the study and despite that the method is valid and reliable under statistical aspects, the prognostic significance of MSCT has to be treated carefully, also on account of the short examination period of six months. Based on individual diagnostic findings, benefits and future options of MSCT concerning non-invasive heart diagnostics could be demonstrated. In addition to it’s eligibility to control the degree of stenosis of venous and arterial bypasses including the sections of insertion and it’s ability to detect coronary anomalies the MSCT method should provide a calcium mass score according to Hong, to enable the documentation of the plaques progress or expansion.
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