Podcasts about proinflammatory

In this episode of Accelerated Health with Sara Banta, I explore the fascinating world of cytokines, the molecules that serve as your body's communication network. Discover how cytokines regulate inflammation, immunity, and overall health while playing a critical role in maintaining balance within your body. I break down what cytokines are, the difference between pro-inflammatory and anti-inflammatory cytokines, and how factors like diet, stress, and sleep influence their activity. Plus, learn practical tips to support a balanced immune response and optimize your overall well-being. Supplements Featured In This Episode:• Accelerated Scalar Copper® https://www.acceleratedhealthproducts.com/products/accelerated-scalar-copper • Accelerated Liver Care™ https://www.acceleratedhealthproducts.com/products/accelerated-liver-care • Acceleradine® Iodine https://www.acceleratedhealthproducts.com/products/acceleradine-iodine-supplement • Accelerated C60™ https://www.acceleratedhealthproducts.com/products/accelerated-c60 Not sure what food to eat and avoid? This guide is for you.⬇️

In this episode we explore the intricate connection between inflammation and diabetes. We break down the difference between acute and chronic inflammation and how the latter, at the cellular level, intertwines with insulin resistance, further complicating health issues like high blood glucose, high blood pressure, high cholesterol, and weight gain. We also dive into practical, nutrition-based strategies that can help you regain control. With a focus on nutrition, we cover foods that increase inflammation. And we explore the benefits of an anti-inflammatory diet rich in whole, nutrient-dense foods. And we highlight specific nutrients such as magnesium and nutraceuticals like turmeric that can be a powerful ally in the fight against inflammation. This episode is packed with valuable information to help you make informed nutrition choices to reduce inflammation and achieve better health.CHAPTERS3:06 What is inflammation?7:14 How inflammation influences diabetes health9:31 Proinflammatory foods16:10 The Dietary Inflammatory Index18:22 Anti-inflammatory foods and diet24:21 Eat to beat inflammation; eat to treat diabetesFor show notes and resources, please visit: https://Type2DiabetesTalk.comTo share your questions and suggestions, leave us a voice message or email at: https://Type2DiabetesTalk.com/messageExplore our proven programs and services, visit: https://Type2DiabetesTalk.com/programsSubscribe to our free weekly newsletter for podcast updates, valuable nutrition tips and more: https://Type2DiabetesTalk.com/subscribe

References Guerra, DJ. 2024. Uncollected writings. The Journal of Nutritional Biochemistry 2023. Volume 112, February. 109217 Walker, Cindy.1950 Blue Canadian Rockies. Cover "the Byrds"(1969). https://youtu.be/nzOHtU8Sb3c?si=5GAj7VPzIr7o0OO_t Heinichen J. D. 1711 (?)Concerto in A minor for violin https://youtu.be/V-E25Q-wjwc?si=bbWdZTNEUPGitY-S --- Send in a voice message: https://podcasters.spotify.com/pod/show/dr-daniel-j-guerra/message Support this podcast: https://podcasters.spotify.com/pod/show/dr-daniel-j-guerra/support

Is Keto A Proinflammatory Diet? Sunil Pai, MD • https://sanjevani.net/ • Book - An Inflammation Nation: The Definitive 10-Step Guide to Preventing and Treating All Diseases through Diet, Lifestyle, and the Use of Natural Anti-Inflammatories #SunilPai #Inflammation #WholeFood  #PlantBased Sunil Pai, MD is an internationally recognized expert in Integrative Medicine, author, radio host, health activist/influencer and thought leader in the wellness industry. His book An Inflammation Nation: The Definitive 10-Step Guide to Preventing and Treating All Diseases through Diet, Lifestyle, and the Use of Natural Anti-Inflammatories Is about Changing your daily routine and eating habits to restore and maintain your health can be challenging. But compared to surgery or extensive drug regimens with debilitating side effects, the effort is decidedly worth it. Here to make things a bit easier, Dr. Sunil Pai presents a ten-step guide to help you prevent and treat disease through diet and lifestyle changes, as well as through the use of natural anti-inflammatories. With extensive information on the production of food, pharmaceuticals, and dietary supplements, this remarkable resource pulls back the veil on what's really in the foods and products you consume daily—and how they're affecting your health. All too often, conventional health care simply manages diseases rather than actually resolving them. By understanding that inflammation is the underlying trigger mechanism to all ailments, you can learn to prevent, reverse, and treat most chronic illnesses—including cancer—by applying integrative medicine's natural, evidence-based solutions. Informative, educational, and enlightening, this book will help you understand the truth and motivate you to start taking back your health! Dr. Pai also became one of the first Board Certified doctors in Holistic Integrative Medicine in the United States and he specializes in the health benefits of plant-based diets and the use of natural anti-inflammatories for the prevention and treatment of chronic diseases. Dr. Pai is also a Clinical Assistant Professor at the Department of Family and Community Medicine at the University of New Mexico School of Medicine and conducts seminars and workshops on a variety of health conditions. Dr. Pai lectures at national conferences and is actively publishing in the field of Integrative Medicine. Due to his success with cancer supportive therapies, Dr. Pai has been featured in many internet documentary series including and a variety of online health summits. Dr. Pai is known for being a health activist/influencer. He is sought out lecturer for speaking about the hidden truths within the food, pharmaceutical and dietary supplement industries. Dr. Pai consults with clinics in U.S., Curacao, Dubai, Thailand, India, Costa Rica and China on teaching his integrative medicine chronic disease and cancer supportive protocols. Dr. Pai's Integrative Medicine approach, evaluation, products and services are highly used by celebrities, actors, and musicians in the entertainment and music industries as well as professional athletes to improve and maintain their performance and longevity of their careers. Dr. Pai's hobbies include playing drums, guitar and music trivia and he thus he is known as the “RocDoc”. Dr. Pai lives in Albuquerque, New Mexico and his other interests include hiking and walking his dog, plant based cooking and yoga. To Contact Dr Sunil Pai M.D.go to sanjevani.net Disclaimer:Medical and Health information changes constantly. Therefore, the information provided in this podcast should not be considered current, complete, or exhaustive. Reliance on any information provided in this podcast is solely at your own risk. The Real Truth About Health does not recommend or endorse any specific tests, products, procedures, or opinions referenced in the following podcasts, nor does it exercise any authority or editorial control over that material. The Real Truth About Health provides a forum for discussion of public health issues. The views and opinions of our panelists do not necessarily reflect those of The Real Truth About Health and are provided by those panelists in their individual capacities. The Real Truth About Health has not reviewed or evaluated those statements or claims. 

Endotoxins Create A Cascade Of Proinflammatory Triggers That Increase Your Risk Of Obesity And Diabetes Sunil Pai, MD • https://sanjevani.net/ • Book - An Inflammation Nation: The Definitive 10-Step Guide to Preventing and Treating All Diseases through Diet, Lifestyle, and the Use of Natural Anti-Inflammatories #SunilPai #Inflammation #WholeFood  #PlantBased Sunil Pai, MD is an internationally recognized expert in Integrative Medicine, author, radio host, health activist/influencer and thought leader in the wellness industry. His book An Inflammation Nation: The Definitive 10-Step Guide to Preventing and Treating All Diseases through Diet, Lifestyle, and the Use of Natural Anti-Inflammatories Is about Changing your daily routine and eating habits to restore and maintain your health can be challenging. But compared to surgery or extensive drug regimens with debilitating side effects, the effort is decidedly worth it. Here to make things a bit easier, Dr. Sunil Pai presents a ten-step guide to help you prevent and treat disease through diet and lifestyle changes, as well as through the use of natural anti-inflammatories. With extensive information on the production of food, pharmaceuticals, and dietary supplements, this remarkable resource pulls back the veil on what's really in the foods and products you consume daily—and how they're affecting your health. All too often, conventional health care simply manages diseases rather than actually resolving them. By understanding that inflammation is the underlying trigger mechanism to all ailments, you can learn to prevent, reverse, and treat most chronic illnesses—including cancer—by applying integrative medicine's natural, evidence-based solutions. Informative, educational, and enlightening, this book will help you understand the truth and motivate you to start taking back your health! Dr. Pai also became one of the first Board Certified doctors in Holistic Integrative Medicine in the United States and he specializes in the health benefits of plant-based diets and the use of natural anti-inflammatories for the prevention and treatment of chronic diseases. Dr. Pai is also a Clinical Assistant Professor at the Department of Family and Community Medicine at the University of New Mexico School of Medicine and conducts seminars and workshops on a variety of health conditions. Dr. Pai lectures at national conferences and is actively publishing in the field of Integrative Medicine. Due to his success with cancer supportive therapies, Dr. Pai has been featured in many internet documentary series including and a variety of online health summits. Dr. Pai is known for being a health activist/influencer. He is sought out lecturer for speaking about the hidden truths within the food, pharmaceutical and dietary supplement industries. Dr. Pai consults with clinics in U.S., Curacao, Dubai, Thailand, India, Costa Rica and China on teaching his integrative medicine chronic disease and cancer supportive protocols. Dr. Pai's Integrative Medicine approach, evaluation, products and services are highly used by celebrities, actors, and musicians in the entertainment and music industries as well as professional athletes to improve and maintain their performance and longevity of their careers. Dr. Pai's hobbies include playing drums, guitar and music trivia and he thus he is known as the “RocDoc”. Dr. Pai lives in Albuquerque, New Mexico and his other interests include hiking and walking his dog, plant based cooking and yoga. To Contact Dr Sunil Pai M.D.go to sanjevani.net Disclaimer:Medical and Health information changes constantly. Therefore, the information provided in this podcast should not be considered current, complete, or exhaustive. Reliance on any information provided in this podcast is solely at your own risk. The Real Truth About Health does not recommend or endorse any specific tests, products, procedures, or opinions referenced in the following podcasts, nor does it exercise any authority or editorial control over that material. The Real Truth About Health provides a forum for discussion of public health issues. The views and opinions of our panelists do not necessarily reflect those of The Real Truth About Health and are provided by those panelists in their individual capacities. The Real Truth About Health has not reviewed or evaluated those statements or claims. 

In this episode Sal, Adam & Justin speak with Dr. Cabral about inflammation, it's benefits and the detrimental effects of excess levels. What is inflammation? Why do people have it? (2:57) What causes people to get stuck in the ‘breakdown recovery trap'? (6:52) Proinflammatory foods and the common signs. (9:21) His call to action when it comes to arachidonic acids. (16:46) Natural supplements that can lower cholesterol. (22:59) Anti-inflammatory foods you can eat to reduce your inflammatory load. (26:51) Grain-fed vs grass-fed debate. (32:01) What kind of testing can we do to test our inflammation levels? (34:36) Revealing the guy's inflammation scores and how to improve them. (38:11) Justin. (41:04) Doug. (48:02) Sal. (50:34) Adam. (52:38) Related Links/Products Mentioned For Mind Pump listeners only Equi.life is offering a FREE At-Home Inflammation Score Test Shipped Right to Your Door. (Customer pays shipping and handling and First-time test-buying customers only). Visit Seed for an exclusive offer for Mind Pump listeners! **Promo code MINDPUMP at checkout for 20% off your first month's supply of Seed's DS-01™ Daily Synbiotic** Special Promotion: MAPS Anabolic Advanced Launch only for $97! **Coupon code AA60 at checkout** (Ends February 26th, 2023) New research may explain unexpected effects of common painkillers The Breakdown Recovery Trap, Why You Aren't Progressing – Mind Pump Blog The Top 5 Most Inflammatory Foods to Avoid | Dr. Stephen Cabral Metabolism pathways of arachidonic acids: mechanisms and potential therapeutic targets Kyolic® Aged Garlic Extract   Red yeast rice - Mayo Clinic Psyllium fiber: Regularity and healthier lipid levels? The 7 Most ANTI-INFLAMMATORY Foods (Anti Inflammatory Diet) | Dr. Stephen Cabral Mind Pump #1777: Cooking Oils That Can Make You Sick With Max Lugavere Big 5 Labs - EquiLife Dairy Farmer Reveals Surprising Reason Cows Eat Skittles - Newsweek Mind Pump Free Resources     Mind Pump Podcast – YouTube Featured Guest/People Mentioned Dr. Stephen Cabral (@stephencabral) Instagram Website Podcast Max Lugavere (@maxlugavere) Instagram

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2022.12.27.522037v1?rss=1 Authors: Dos Santos, R. S., Guzman-Llorens, D., Perez-Serna, A. A., Nadal, A., Marroqui, L. Abstract: Aims/hypothesis: Type 1 diabetes is characterised by pancreatic islet inflammation and autoimmune-driven pancreatic beta cell destruction. Type I interferons, such as IFNalpha, are key players in early human type 1 diabetes pathogenesis, as the activation of the tyrosine kinase 2 (TYK2)-signal transducer and activator of transcription (STAT) pathway induces inflammation, a long-lasting MHC class I overexpression, endoplasmic reticulum (ER) stress, and beta cell apoptosis (in synergy with IL-beta). As TYK2 inhibition has been suggested as a potential therapeutic target for the prevention or treatment of type 1 diabetes, we investigated whether the selective TYK2 inhibitor deucravacitinib could protect beta cells against the damaging effects of IFNalpha and other proinflammatory cytokines (i.e. IFNgamma and IL-1beta). Methods: Inflammation, ER stress, and apoptosis were evaluated by real-time PCR, immunoblot, immunofluorescence, and nuclear dyes. The promoter activity was assessed by luciferase assay and insulin secretion and content by ELISA. All experiments were performed in the human EndoC-betaH1 cell line. Results: Pre-treatment with deucravacitinib prevented IFNalpha effects, such as STAT1 and STAT2 phosphorylation and protein expression as well as MHC class I hyperexpression, in a dose-dependent manner without affecting beta cell survival and function. Comparison between deucravacitinib and two Janus kinase inhibitors, ruxolitinib and baricitinib, showed that deucravacitinib blocked IFNalpha- but not IFNgamma-induced signalling pathway. Pre-treatment with deucravacitinib protected beta cells from the pro-apoptotic and proinflammatory effects of two different combinations of cytokines: IFNalpha + IL-beta and IFNgamma + IL-1beta. Moreover, this TYK2 inhibitor could partially revert apoptosis and inflammation in cells previously treated with IFNalpha + IL-1beta or IFNgamma + IL-beta. Conclusions/interpretation: Our findings suggest that, by protecting beta cells against the deleterious effects of proinflammatory cytokines without affecting beta cell function and survival, deucravacitinib could be repurposed for the prevention or treatment of early type 1 diabetes. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2022.11.24.517638v1?rss=1 Authors: Nemade, H. N., Mehrkens, D., Lottermoser, H. S., Yilmaz, Z. E., Schelemei, P., Picard, F. R., Geissen, S., Schwab, G. F., Hoyer, F. F., Guthoff, H., Hof, A., Nettersheim, F. S., Sachinidis, A., Winkels, H., Baldus, S., Pasparakis, M., Adam, M., Mollenhauer, M. Abstract: Background: Receptor-interacting serine/threonine-protein kinase 1 and 3 (RIPK1 and RIPK3) dependent cell death has been identified as a crucial mediator of abdominal aortic aneurysm (AAA) development. RIPK3 mediates phosphorylation of Mixed lineage kinase domain like pseudokinase (MLKL) thereby inducing its oligomerization and translocation to the cell membrane. Given the dual role of RIPKs being involved in necroptosis as well as in apoptosis induction, the specific role of MLKL-induced necroptotic cell death in AAA remains unclear. Methods: We monitored elastase-perfusion (PPE) induced progression of AAA in C57BL/6N (WT), RIPK1 kinase deficient (Ripk1D138N/D138N), MLKL knockout (Mlkl-/-) and MLKL phosphodeficient (MlklAA) mice by ultrasound measurements, histological analyses and bulk mRNAseq techniques to assess structural and molecular aortic changes. Bone marrow transplantation studies in WT and MlklAA mice were utilized to dissect the role of MLKL in smooth muscle cells (SMCs) and myeloid cells in AAA development. MLKL expressing human SMCs were generated to investigate necroptosis-induced proinflammatory cytokine secretion and subsequent polymorphonuclear neutrophil (PMN) migration and activation in vitro. Results: Ultrasound analysis showed that ~70% of the WT animals developed PPE induced-AAA with significant aortic structural alterations and enhanced myeloid cell infiltration. In contrast, Ripk1D138N/D138N, MlklAA, and Mlkl-/- mice were protected from AAA. This protection was associated with reduced adverse extracellular matrix (ECM) remodeling and leukocyte infiltration. MLKL deficiency was associated with a significant downregulation of genes involved in fibrinolysis, anti-inflammatory response, immune response and complement activation in aortic tissue in AAA. Bone marrow transplantation studies showed the lack of MLKL in SMCs to be the main driver of AAA protection. Proinflammatory cytokine secretion was elevated in necroptosis induced SMCs and resulted in a significant accumulation and activation of PMN. Conclusions: Overall, these findings indicate that MLKL-induced necroptotic SMC death and subsequent proinflammatory leukocyte activation plays a causative role in AAA development and suggests that pharmacological inhibition of MLKL may represent a promising treatment strategy for AAA disease. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

Dr. Mary-Louise Rogers is an Associate Professor at the College of Medicine and Public Health at Flinders University and Dr. Michael Benatar is a Professor of Neurology and Chief of the Neuromuscular Division and Executive Director of the ALS Center at the University of Miami. They will be discussing their recent publication titled “Urinary neopterin: A novel biomarker of disease progression in amyotrophic lateral sclerosis,” which discusses the importance of biomarkers in ALS.

Today's episode is part of an end of year special series. I am resharing some of my most actionable episodes to help you reduce pain on your period and pain flares in general, and to balance your hormones for better periods, less PMS and healthier cycles. I am sharing these episodes because this time of year is often when some of our endo management strategies can go out of the window (and understandably so!). We might have more sugar, less sleep, more alcohol and more blood sugar dysregulation, and as a result, these can all raise inflammation and give our bodies a hard time when it comes to clearing old and excess hormones. So come January or maybe sooner, we tend to have more PMS, worse periods and more pain. So these episodes are designed to provide you with some tips you can quickly implement if you're worried about your upcoming period, or you're feeling rough and need some tips to improve your symptoms. Now of course, it's natural that we want to indulge a bit over Christmas, and so these episodes are not about telling you to be a saint. Instead, they're about practices you can throw in that can just help lessen some of the impact. I am releasing a couple so you can choose strategies you think will help you most and so you have options, but you certainly don't have to try them all! And whilst I'm here, if you find that you want to learn more about how to eat for endo and for hormone balance, or you get to the end of the festive period and you really just want to improve your systems, I now have my Nutrition for Endo Masterclasses, which are available to buy all year round, unlike my courses. Lucky for you, they're still discounted because I haven't had time to change the prices, so you can still get each masterclass for £29.99 or you can buy the bundle for £50. You could also ask for them as a Christmas present! Finally, thank you for listening to this podcast this year, and for sticking with me even with my sporadic release dates as I navigate all of these new courses and offerings with recording my free content. I am wishing you a wonderful festive break (if you celebrate) and a very happy New Year. So, without further ado, let's get to today's episode. I really hope it helps you manage some of your symptoms over this festive period. Six Tips for Reducing Endometriosis Pain in The Week Before Your Period Most of us with endometriosis have experienced debilitating periods that stop us in our tracks and derail our day or week completely. Perhaps we get through with a mix of pain killers or maybe nothing helps at all - whatever is going on for you, today I want to offer you six simple pain relieving strategies that can help alleviate your endometriosis pain when your period arrives. These methods are best begun seven days before your period so the effects build up and compound and I do totally recommend continuing them into your period too, for extra benefits! As always, these are just options - you don't have to do them all nor do you have to do them exactly as suggested, tweak and tailor to your lifestyle and preferences. Consult your GP before adding in supplements. Here are my six tips for reducing your endometriosis pain for when your period starts: Magnesium rich baths, 2 - 3 times the week before your period, with 500g - 600g Epsom salt baths, soaking for at least 10 minutes each times. Two portions of low mercury, fatty fish (sardines, mackerel, anchovies salmon, herring) in addition to 1000mg - 3000mg good quality omega 3 fatty acid supplementation. Turmeric lattes with 1/2 teaspoon turmeric (1g) and 1/4-1/2 teaspoon ginger root powder (350mg-700mg) in addition to ginger tea (made with ginger root powder), raspberry leaf tea and dandelion tea. Always add some fat into your latte to aid absorption of the turmeric - coconut oil, coconut butter, cacao butter or nut butter all would work well. Daily yoga or stretches for endometriosis and pelvic pain. Reduce or eliminate sugar, utilising stevia, inulin root syrup, berries and 100% dark chocolate as alternatives. Eat the rainbow! Get in 5 to 10 servings of fruit and veg a day, focusing more on vegetables (think 80% vs 20%). I hope this episode helps you prepare for your period! Please do let me know if it changes your experience of your next period - I would love to hear from you! Scroll down to the show notes for links to studies, brand recommendations, recipes, etc. Let's get social! Come say hello on Instagram or sign up to my newsletter. Sign up to the wait list for my course, Live and Thrive with Endo here. My new Nutrition for Endo Masterclasses are out now and are on special offer for Black Friday. Get one masterclass for £29.99 (full price £40) or both for £50. Find out more here. My cookbook This EndoLife, It Starts with Breakfast is out now! Get 28 anti-inflammatory, hormone friendly recipes for living and thriving with endometriosis. Order your copy here. If you feel like you need more support with managing endometriosis, you can join Your EndoLife Coaching Programme. A 1-to-1 three month health and life coaching programme to help you thrive with endometriosis. To find out more about the programme and to discuss whether it could be right for you, email me at hello@thisendolife.com or visit my website. This episode is sponsored by The Pod Farm. Learn all about how to start your own podcast with the complete course from The Pod Farm. Aimed at beginners, this course takes a simple and straightforward approach to planning, equipment buying, setting up, recording, editing and hosting your own podcast. With hours of audio and video materials, and downloadable guides and useful links, this multimedia approach aims to have something for every kind of learner. From now until April 15, newsletter subscribers get 20% off the course price. Visit www.thepodfarm.com to enroll or find out more This episode is sponsored by BeYou. Soothe period cramps the natural way with these 100% natural and discreet menthol and eucalyptus oil stick on patches and CBD range. Click here to find out more and to shop: https://beyouonline.co.uk This episode is sponsored by Semaine. Try their supplement for period pain and daily supplement for hormonal balance and PMS prevention with code ENDOLIFE to get 20% off your first order. Show Notes Magnesium Study Magnesium baths for pain article Magnesium--a new therapeutic alternative in primary dysmenorrhea   Omega 3 Fatty Acids NHS fish guidance Dietary fish oil supplementation inhibits formation of endometriosis-associated adhesions in a chimeric mouse model Omega-3 fatty acids (fish oil) as an anti-inflammatory: an alternative to nonsteroidal anti-inflammatory drugs for discogenic pain Effect of omega-3 fatty acids on intensity of primary dysmenorrhea Anti-inflammatory Effects Of Omega 3 Fatty Acid In Fish Oil Linked To Lowering Of Prostaglandin Outsmart Endometriosis by Dr Jessica Drummond Lion Heart Aqua Biome Fish Oil   Lattes and teas Super Turmeric Latte recipe  Curcumin inhibits endometriosis endometrial cells by reducing estradiol production Nicole Jardim Fix Your Period book Dr. Aviva Romm ginger recommendations The effect of ginger for relieving of primary dysmenorrhoea Comparison of Effects of Ginger, Mefenamic Acid, and Ibuprofen on Pain in Women with Primary Dysmenorrhea   Yoga and stretches for pelvic pain Yoga for endometriosis Stretches for endometriosis Pelvic floor and fascia release exercises by Dr. Nicole Cozean   Sugar Inflammatory cytokine concentrations are acutely increased by hyperglycemia in humans: role of oxidative stress Proinflammatory effects of glucose and anti-inflammatory effect of insulin: relevance to cardiovascular disease 100% black sugar free peanut butter mini eggs Hazelnut truffles Absolute Black (can find the bar in Sainsburys) Hotel Chocolat buttons (these are AMAZING, but I don't love their other 100% chocolate products) So Free sweet dark chocolate Raw cacao (you can find this in Sainsburys, but generally you can get raw cacao everywhere and online) Stevia drops  Troo syrup Stevia powder Perfect World ice cream My brownie recipe Sweet Laurel's Bakery blog Endometriosis and dairy episode Endometriosis and caffeine episode Endometriosis and sugar episode Endometriosis and gluten episode Molly Roberson interview   Eat the rainbow Oxidative Stress and Endometriosis: A Systematic Review of the Literature Women with endometriosis improved their peripheral antioxidant markers after the application of a high antioxidant diet

Aging-US published a Special Collection on Eye Disease which included "Activation of C-reactive protein proinflammatory phenotype in the blood retinal barrier in vitro: implications for age-related macular degeneration" which reported that the retinal pigment epithelium (RPE) is considered one of the main targets of age-related macular degeneration (AMD), the leading cause of irreversible vision loss among the ageing population worldwide. Increased levels of circulating pentameric C-reactive protein (pCRP) are associated with higher risk of AMD. Monomeric form of pCRP has been detected in drusen, the hallmark deposits associated with AMD, and we have found that mCRP induces oBRB disruption Dr. Blanca Molins from The IDIBAPS, Hospital Clínic de Barcelona said, "Age-related macular degeneration (AMD) is the primary cause of irreversible vision loss among the ageing population worldwide." AMD presents RPE cell abnormalities, disruption of the outer blood-retinal-barrier (oBRB), and degeneration of photoreceptors. Altered immune responses are thought to contribute to the dry AMD phenotype. Loss of parainflammation control contributes to AMD by invoking a chronic, heightened immune response that causes tissue destruction. mCRP has been identified in ocular drusen and other subepithelial deposits, as well as in the choroid, and contributes to oBRB disruption in vitro. The "non-risk" Factor H (FH) variant can effectively bind to mCRP to dampen its proinflammatory activity. MCRP levels are elevated in individuals with the high-risk CFH genotype [29, 30] - this is because there is no CRP transcription in retinal tissue. The Molins Research Team concluded in their https://www.aging-us.com/article/103655/">Aging-US Research Output, "our findings further support mCRP direct contribution to progression of AMD, at least at the RPE level. The topological experiments elicit that mCRP is proinflammatory when present on the apical side of the RPE. However, mCRP is likely to only reach the apical side of the RPE in compromised RPE health and where barrier functions are compromised. Thus, a plausible scenario would infer that, in the presence of an already aged/damaged RPE, mCRP reaches the apical side of the RPE to amplify the proinflammatory microenvironment and enhance barrier disruption. With respect to previous findings, this pathologic mechanism will be more prevalent in patients carrying the FH risk polymorphism for AMD, where mCRP proinflammatory effects remain unrestrained." Full Text - https://www.aging-us.com/article/103655/text Correspondence to: Blanca Molins email: bmolins@clinic.cat Keywords: age-related macular degeneration, retinal pigment epithelium, inflammation, C-reactive protein About Aging-US Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research as well as topics beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, cancer, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR among others), and approaches to modulating these signaling pathways. To learn more about Aging-US, please visit http://www.Aging-US.com or connect with @AgingJrnl Aging-US is published by Impact Journals, LLC please visit http://www.ImpactJournals.com or connect with @ImpactJrnls Media Contact 18009220957x105 MEDIA@IMPACTJOURNALS.COM

Aging-US published a Special Collection on Eye Disease which included "Activation of C-reactive protein proinflammatory phenotype in the blood retinal barrier in vitro: implications for age-related macular degeneration" which reported that the retinal pigment epithelium (RPE) is considered one of the main targets of age-related macular degeneration (AMD), the leading cause of irreversible vision loss among the ageing population worldwide. Increased levels of circulating pentameric C-reactive protein (pCRP) are associated with higher risk of AMD. Monomeric form of pCRP has been detected in drusen, the hallmark deposits associated with AMD, and we have found that mCRP induces oBRB disruption Dr. Blanca Molins from The IDIBAPS, Hospital Clínic de Barcelona said, "Age-related macular degeneration (AMD) is the primary cause of irreversible vision loss among the ageing population worldwide." AMD presents RPE cell abnormalities, disruption of the outer blood-retinal-barrier (oBRB), and degeneration of photoreceptors. Altered immune responses are thought to contribute to the dry AMD phenotype. Loss of parainflammation control contributes to AMD by invoking a chronic, heightened immune response that causes tissue destruction. mCRP has been identified in ocular drusen and other subepithelial deposits, as well as in the choroid, and contributes to oBRB disruption in vitro. The "non-risk" Factor H (FH) variant can effectively bind to mCRP to dampen its proinflammatory activity. MCRP levels are elevated in individuals with the high-risk CFH genotype [29, 30] - this is because there is no CRP transcription in retinal tissue. The Molins Research Team concluded in their https://www.aging-us.com/article/103655/ Aging-US Research Output, "our findings further support mCRP direct contribution to progression of AMD, at least at the RPE level. The topological experiments elicit that mCRP is proinflammatory when present on the apical side of the RPE. However, mCRP is likely to only reach the apical side of the RPE in compromised RPE health and where barrier functions are compromised. Thus, a plausible scenario would infer that, in the presence of an already aged/damaged RPE, mCRP reaches the apical side of the RPE to amplify the proinflammatory microenvironment and enhance barrier disruption. With respect to previous findings, this pathologic mechanism will be more prevalent in patients carrying the FH risk polymorphism for AMD, where mCRP proinflammatory effects remain unrestrained." Full Text - https://www.aging-us.com/article/103655/text Correspondence to: Blanca Molins email: bmolins@clinic.cat Keywords: age-related macular degeneration, retinal pigment epithelium, inflammation, C-reactive protein About Aging-US Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research as well as topics beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, cancer, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR among others), and approaches to modulating these signaling pathways. To learn more about Aging-US, please visit http://www.Aging-US.com or connect with @AgingJrnl Aging-US is published by Impact Journals, LLC please visit http://www.ImpactJournals.com or connect with @ImpactJrnls Media Contact 18009220957x105 MEDIA@IMPACTJOURNALS.COM

Proinflammatory state during sleep in covid 19 pandemic ,and importance of sleep after vaccination

Drs Nuelle and Cook discuss Use of a Hyperosmolar Saline Solution to Mitigate Proinflammatory and Degradative Responses of Articular Cartilage and Meniscus for Application to Arthroscopic Surgery

Drs Nuelle and Cook discuss Use of a Hyperosmolar Saline Solution to Mitigate Proinflammatory and Degradative Responses of Articular Cartilage and Meniscus for Application to Arthroscopic Surgery

Inflammation happens to all of us at some point or another. It’s your body’s response to injury or damage. Whether you develop an infection or break an arm, your immune system triggers inflammation to begin the healing process. It’s a self defense mechanism. Contrary to popular belief, inflammation isn’t all bad but if it goes on for too long or you have too much, it can lead to health issues. On this episode Emily and I talk about how to test your level of inflammation, ways to lower inflammation and much more. What is inflammation? [6:02] What causes inflammation [7:03] C-Reactive Protein Test [8:32] Proinflammatory foods [10:00] Metabolically healthy [10:55] Lab review & preventive measures [14:00] Sleep and inflammation [16:13] Nightshades and joint pain [17:07] Omega-3 benefits [18:31] Ways to lower inflammation [21:45] Curcumin/ Turmeric [25:15]  Mitochondria [28:15] Gut issues [29:29] Bone broth - Kettle and Fire, Bolyards [31:55]   Follow us on IG: @wellness.unfiltered Follow Kelley: @kelley_bugger Follow Emily: @emilyzwilling

Most of us with endometriosis have experienced debilitating periods that stop us in our tracks and derail our day or week completely. Perhaps we get through with a mix of pain killers or maybe nothing helps at all - whatever is going on for you, today I want to offer you six simple pain relieving strategies that can help alleviate your endometriosis pain when your period arrives. These methods are best begun seven days before your period so the effects build up and compound and I do totally recommend continuing them into your period too, for extra benefits! As always, these are just options - you don’t have to do them all nor do you have to do them exactly as suggested, tweak and tailor to your lifestyle and preferences. Consult your GP before adding in supplements. Here are my six tips for reducing your endometriosis pain for when your period starts: Magnesium rich baths, 2 - 3 times the week before your period, with 500g - 600g Epsom salt baths, soaking for at least 10 minutes each times. Two portions of low mercury, fatty fish (sardines, mackerel, anchovies salmon, herring) in addition to 1000mg - 3000mg good quality omega 3 fatty acid supplementation. Turmeric lattes with 1/2 teaspoon turmeric (1g) and 1/4-1/2 teaspoon ginger root powder (350mg-700mg) in addition to ginger tea (made with ginger root powder), raspberry leaf tea and dandelion tea. Always add some fat into your latte to aid absorption of the turmeric - coconut oil, coconut butter, cacao butter or nut butter all would work well. Daily yoga or stretches for endometriosis and pelvic pain. Reduce or eliminate sugar, utilising stevia, inulin root syrup, berries and 100% dark chocolate as alternatives. Eat the rainbow! Get in 5 to 10 servings of fruit and veg a day, focusing more on vegetables (think 80% vs 20%). I hope this episode helps you prepare for your period! Please do let me know if it changes your experience of your next period - I would love to hear from you! Scroll down to the show notes for links to studies, brand recommendations, recipes, etc. Let's get social! Come say hello on Instagram, Twitter and Facebook or sign up to my newsletter. If you feel like you need more support with managing endometriosis, you can join Your EndoLife Coaching Programme. A 1-to-1 three month health and life coaching programme to help you thrive with endometriosis. To find out more about the programme and to discuss whether it could be right for you, email me at hello@thisendolife.com or visit my website. I am now offering one-off two hour sessions for those of you who aren’t quite ready for a 12 week coaching programme. This intensive deep dive session will kick start your journey to living and thriving with endometriosis and give you a plan that you can take forward and work on alone. Click here to find out more about the programme. My cookbook This EndoLife, It Starts with Breakfast is out now! Get 28 anti-inflammatory, hormone friendly recipes for living and thriving with endometriosis. Order your copy here. This episode is also sponsored by my free Endometriosis Diet Grocery List. This pdf list includes all the foods I buy on a monthly basis, categorised into easy sections. I share my personal endometriosis diet plan, free recipe resources, recommendations to help you get started with the endometriosis diet and nutrition tips. Download here. This episode is sponsored by The Pod Farm. Learn all about how to start your own podcast with the complete course from The Pod Farm. Aimed at beginners, this course takes a simple and straightforward approach to planning, equipment buying, setting up, recording, editing and hosting your own podcast. With hours of audio and video materials, and downloadable guides and useful links, this multimedia approach aims to have something for every kind of learner. From now until April 15, newsletter subscribers get 20% off the course price. Visit www.thepodfarm.com to enroll or find out more This episode is sponsored by BeYou. Soothe period cramps the natural way with these 100% natural and discreet menthol and eucalyptus oil stick on patches and CBD range. Click here to find out more and to shop: https://beyouonline.co.uk   Show Notes Magnesium Study Magnesium baths for pain article Magnesium--a new therapeutic alternative in primary dysmenorrhea   Omega 3 Fatty Acids NHS fish guidance Dietary fish oil supplementation inhibits formation of endometriosis-associated adhesions in a chimeric mouse model Omega-3 fatty acids (fish oil) as an anti-inflammatory: an alternative to nonsteroidal anti-inflammatory drugs for discogenic pain Effect of omega-3 fatty acids on intensity of primary dysmenorrhea Anti-inflammatory Effects Of Omega 3 Fatty Acid In Fish Oil Linked To Lowering Of Prostaglandin Outsmart Endometriosis by Dr Jessica Drummond Lion Heart Aqua Biome Fish Oil   Lattes and teas Super Turmeric Latte recipe  Curcumin inhibits endometriosis endometrial cells by reducing estradiol production Nicole Jardim Fix Your Period book Dr. Aviva Romm ginger recommendations The effect of ginger for relieving of primary dysmenorrhoea Comparison of Effects of Ginger, Mefenamic Acid, and Ibuprofen on Pain in Women with Primary Dysmenorrhea   Yoga and stretches for pelvic pain Yoga for endometriosis Stretches for endometriosis Pelvic floor and fascia release exercises by Dr. Nicole Cozean   Sugar Inflammatory cytokine concentrations are acutely increased by hyperglycemia in humans: role of oxidative stress Proinflammatory effects of glucose and anti-inflammatory effect of insulin: relevance to cardiovascular disease 100% black sugar free peanut butter mini eggs Hazelnut truffles Absolute Black (can find the bar in Sainsburys) Hotel Chocolat buttons (these are AMAZING, but I don’t love their other 100% chocolate products) So Free sweet dark chocolate Raw cacao (you can find this in Sainsburys, but generally you can get raw cacao everywhere and online) Stevia drops  Troo syrup Stevia powder Perfect World ice cream My brownie recipe Sweet Laurel’s Bakery blog Endometriosis and dairy episode Endometriosis and caffeine episode Endometriosis and sugar episode Endometriosis and gluten episode Molly Roberson interview   Eat the rainbow Oxidative Stress and Endometriosis: A Systematic Review of the Literature Women with endometriosis improved their peripheral antioxidant markers after the application of a high antioxidant diet  

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2020.07.24.218719v1?rss=1 Authors: Sayed, F. A., Kodama, L., Udeochu, J. C., Fan, L., Carling, G. K., Le, D., Li, Q., Zhou, L., Mathys, H., Wang, M., Niu, X., Mazutis, L., Jiang, X., Wang, X., Wong, M. Y., Gao, F., Telpoukhovskaia, M., Tracy, T. E., Frost, G., Zhou, Y., Li, Y., Brendel, M., Qiu, Y., Cheng, Z., Yu, G., Hardy, J., Coppola, G., Gong, S., Wang, F., DeTure, M. A., Zhang, B., Xie, L., Dickson, D. W., Luo, W., Gan, L. Abstract: The hemizygous R47H variant of TREM2, a microglia-specific gene in the brain, increases risk for late-onset Alzheimers disease (AD). In this study, we identified a subpopulation of microglia with disease-enhancing proinflammatory signatures associated with the R47H mutation in human AD brains and tauopathy mouse brains. Using transcriptomic analysis at the single-nuclei level from AD patients with the R47H or the common variant (CV)-TREM2 with matched sex, pathology and APOE status, we found that the R47H mutation was associated with cell type- and sex-specific transcriptional changes in human AD brains, with microglia exhibiting the most robust alterations. Further characterization revealed that R47H-associated microglial subpopulations had enhanced inflammatory signatures including hyperactivation of Akt, one of the signaling pathways downstream of TREM2. In a newly-generated tauopathy knock-in mouse model expressing one allele of human TREM2 (hTREM2) with either the R47H mutation or CV, R47H induced and exacerbated tau-mediated spatial memory deficits in female mice. Single-cell transcriptomic analysis of microglia from these mice also revealed transcriptomic changes induced by R47H that had significant overlaps with R47H microglia in human AD brains, including robust increases in proinflammatory cytokines, activation of Syk-Akt-signaling, and elevation of a subset of disease-associated microglial signatures. Strikingly, pharmacological Akt inhibition largely reversed the enhanced inflammatory signatures induced by R47H in primary microglia treated with tau fibrils. By unraveling the disease-enhancing properties of the R47H mutation in mouse and human, our findings shed light on an immune-linked AD subtype and provide new directions for modulating microglial immune responses to treat AD. Copy rights belong to original authors. Visit the link for more info

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2020.06.29.166637v1?rss=1 Authors: Kyriatzis, G., Bernard, A., Bole, A., Pflieger, G., Chalas, P., Masse, M., Lecorche, P., Jacquot, G., Ferhat, L., Khrestchatisky, M. Abstract: Neurotensin (NT) acts as a primary neurotransmitter and neuromodulator in the CNS and has been involved in a number of CNS pathologies including epilepsy. NT mediates its central and peripheral effects by interacting with the NTSR1, NTSR2 and NTSR3 receptor subtypes. To date, little is known about the precise expression of the NT receptors in brain neural cells and their regulation in pathology. In the present work, we studied expression of the NTSR2 protein in the rat hippocampus using a model of temporal lobe epilepsy induced by pilocarpine and questioned whether NTSR2 was modulated in conditions of neuro-inflammation. This model is characterized by a rapid and intense inflammatory reaction with a pattern of reactive gliosis in the hippocampus. We show that NTSR2 protein is expressed in hippocampal astrocytes and its expression increases together with astrocyte reactivity following induction of status epilepticus. NTSR2 immunoreactivity is also increased in perivascular astrocytes and their end-feet and is apparent in endothelial cells following induction of status epilepticus. Proinflammatory factors such as IL1{beta} and LPS induced NTSR2 in astrocytes, but also in microglia in vitro. Glial NTSR2 expression showed characteristic immediate early gene response under inflammatory conditions. Treating inflamed glial cells with a vectorized NT analogue decreased NTSR2 expression as well as astrocytic and microglial reactivity. Together, these results suggest that NTSR2 is implicated in astroglial and gliovascular inflammation and that targeting the NTSR2 receptor may open new avenues in the regulation of neuroinflammation in CNS diseases. Copy rights belong to original authors. Visit the link for more info

Dr. Pastore discusses the vital role sleep plays in immunity, how lack of sleep and poor quality sleep can lower your immune system, sleep duration guidelines for optimal health and steps you can take to improve your sleep.    What is “poor” sleep [1:00] Quality sleep for adults 7-9 continuous, uninterrupted hours of sleep per night  Likely not possible for parents, like Dr. Pastore  Teenagers require 8-10 continuous, uninterrupted hours of sleep per night  6.5 - 7 hours for teenagers can have same effect as being inebriated  Sleep science still needs much more research  Those staying home & safe during COVID-19 can cause COVID-19 dreams Intense/horror dreams due to inability to normalize stress/anxiety during the day   Lack of quality sleep mentioned above is directly associated with higher likelihood of being sick after being exposed to a virus [3:55] Studies on common cold  Lack of sleep or disrupted sleep increases risk of getting a virus    Lack of sleep impacted how fast you recover if you do get sick [4:40] Dr. Pastore treating patients & working with other doctors treating patients with COVID-19, those recovering slower & have the virus longer have worse sleep  21 & 23 days of having the active COVID-19 infection  Seen faster COVID-19 recovery of 9 days with better, quality sleep    Quality sleep needs to be uninterrupted [7:05] Difficult for parents waking up for children 7-9 for adults, 8-10 hours for teenager straight    Long-term poor quality sleep increase risk of obesity & diseases that further the risk for infections [9:05]   Medical fact: poor sleep causes cardiovascular disease, diabetes & obesity  Cardiovascular disease, diabetes & obesity increase risk for infections such as COVID-19 or regular flu  Inflammasome is byproduct of being overweight & obesity  Proinflammatory response that can lower immune system  Quality sleep drastically improves fat loss progress  Lack of sleep (as little as 2-3 nights in a row) - cells become temporarily insulin resistant which causes elevation in glucose, can lead to weight gain & fat storage  Chronic lack of sleep can make cells permanently insulin resistant  Quality sleep improves cell-signalling communication between insulin receptor cells & GLUT receptors to let glucose into the cells    Poor sleep lowers your immune system, makes it longer to recover from a virus, increases risk of diseases that can further lower the immune system, and can worsen health if pre-existing disease exists [13:00]  We're all biochemically & genetically unique  Knowing genetics, medical history, biological markers, calcium score    Why does decreased sleep lower the immune system? [14:55] Sleep supports & enhances the initiation of an adaptive immune system response  Adaptive immune system response process: Trouble maker / invading antigen / virus invading body Human immune system takes up antigen & appropriates it Breaks apart the antigen & presents fragments of antigen to T Helper Cells T Helper Cells signal cytokines Interleukin 12 Interleukin 12 calls in T-Helper Cell One Response, supports antigen specific T-Cells T-Helper Cell 1 Response starts B-Cell production of antibodies to always be able to recognize the invading antigen / virus  If the invading antigen is presented in the body again, the body will attack it  Produced in the lymph nodes  Vaccines are a great example of adaptive immunity, producing herd immunity  Sleep turns this response on, lack of sleep turns it off Immune cannot identify the invading antigen  Sleep deprived hepatitis A vaccine patients vs quality sleep hepatitis A vaccine patients Poor sleep patients did not have amplified adaptive immune system response to vaccine Parents typically lose hundreds of hours of sleep    Prescription medications to improve sleep quality [21:05] Dr. James Maas, “Father of Sleep” & other sleep doctors confirm prescription sleep medications will not lead to a perfect night's sleep or “sleep saviours” Have seductive-type affects Can affect memory & perception of sleep quality  Our Neurochemistry of Sleep Podcast  LINK Be aware of side effects Rebound insomnia Dizziness Headaches Difficult swallowing or breathing Worsening depression & suciride ideation Study showed those with highest sleep medication prescriptions had highest risk of all-cause mortality  Study showed increased risk of various cancers, increased risk of dementia  Not getting into a deep sleep, interferes with glucose & cell receptor response    Could be underlying issue or health concern causing lack of sleep [24:20] Chronic pain & arthritis  Breathing disorders  Dietary supplements & stimulants (caffeine) close to bed  Gastoresophorefluz disorder Hypothyroidism, Graves Disease Chronic back pain  Sinus disorder or allergies  Medications can disrupt sleep Birth control Cold medicine  Asthma medication High blood pressure medication  Depression  Thyroid medication Talk to your doctor to find the underlying cause  Pharmacogenetics - PGX  Test genetics to determine drug response based on individual genetics  Medications aren't a one-size fits all Could be nutritional deficiency  Magnesium, Vitamin D Request bloodwork from physician  40% population at risk for low magnesium  Undiagnosed sleep apnea  Temporarily stop breathing, adrenaline wakes you up    Lifestyle changes to implement to improve sleep [29:30] Address stress  Get regular physical activity & exercise  Exercise helps lower stress Caffeine consumption Genetic variations to process caffeine faster/slower Avoid caffeine after 3-4PM  Green tea, diet cola, soft drinks with caffeine  Exposure to artificial light Disrupts normal neurological signalling for sleep, turns off melatonin production Can upregulate alert/excitatory neurotransmitters to keep you awake Blue light blocking glasses Night mode on electronics reducing blue light Limit alcohol  Sedative effect - can help you fall asleep initially  Later in night, causes dopamine rush & interferes with adaptive immune response More consistent alcohol consumption will continue to lower immune system nightly Limit or eliminate nicotine  Vaping, chewing tobacco  Nicotine neurotoxin, extremely addictive Makes it difficult to fall asleep  Sleep in a cool bedroom  Lower temperature helps with sleep   Melatonin for sleep [35:30] Melatonin is both a hormone and neurotransmitter Excreted from penial gland  Exposure to natural light during day, as sun sets, darkness cues melatonin production Helps stimulate our sleep - high affinity melatonin receptors in SCN  MTA & MT1A, MT2 & MT2B receptors - absorbs melatonin & slows excitatory function to prepare for sleep  Promotes sleep by stimulating acute inhibition of neurological firing of awake neurotransmitters in SCN Helps initiate sleep process, but won't benefit rest of sleep cycle  Helps regulate circadian rhythm (sleep/wake cycles) Taking a “low” dose of 1mg of melatonin is still incredibly high compared to what the brain produces naturally   Can produce “hangover” in the morning Fatigued, tired, brain fog, delayed responses Suppressing dopamine responses  Receptors of SCN turned off way past sleep period  Up to 18 hours of hangover Walking wounded: feel better at 8-10PM and take another dose High-dose (1mg+) melatonin should not be a nightly supplement for sleep    Effective natural products for sleep do exist [40:50] Dr. Pastore's poor sleep practicing as a doctor, then being a father Developed sleep supplement Power OFF for his own sleep issues as nothing else worked https://poweronpoweroff.com/products/power-off We can provide you with the scientific paper Dr. Pastore wrote  Help turn off excitatory neurotransmitters before bed to fall asleep Help stay asleep without waking up   Studies on theanine + 5 hydroxytryptophan shown to keep you asleep GABA to help you fall asleep  Most GABA can't cross blood-brain barrier Blood-brain barrier: only allows certain nutrients/neurotransmitters into the brain from the bloodstream to protect the brain  Dr. Pastore used his PhD in nanomedicine to make GABA pass the blood brain barrier  Magnolia plant - honokiol   Studies show honokiol primes receptor for GABA uptake Combination of ingredients address mechanism of turning off cellular stress response constantly being fired by ephedrine (excitatory / awake neurotransmitter) at night  Requires sulphur enzyme system - enzyme phenalethol…..help :)  Cysteine & dimer to create cystine Helps fall back asleep after interrupted sleep Won't prevent you from waking up if needed Formula evolves as new studies & research comes out    Antihistamines / Benadryl before bed [52:55] Dangerous for long-term health Harvard in 2005 urged doctors to advise patients to stop using antihistamines for sleep Antihistamines reduce acetylcholine, which over time increases risk of age-related mental decline Disrupts memory, cognitive sharpness, more forgetful    Wrap-Up [55:15] Aim for 7-9 hours per night Work with physician to find underlying cause for lack of sleep  Stay away from prescription sleep aids & over the counter sleep aids as much as possible Be mindful of melatonin  help@poweronpoweroff.com & https://poweronpoweroff.com/products/power-off www.drrobetpastore.com & @drrobetpastore

This audio/video overview by Dr. Ally Perlina of  goes in depth on Ben's latest gut microbiome results from . In this episode, you'll learn how to customize your diet and lifestyle based on the genetics of your gut. Dr. Perlina is the Chief Translational Science Officer at Viome. She leads the Viome team on the development of actionable pathway analytics, functional microbiome profiling, and integration of Viome test results into food and supplement recommendation logic. Ally came to Viome from working with Dr. Craig Venter at Human Longevity, Inc. She brings over 17 years of industry experience, which include Thomson Reuters, Quest Diagnostics, and several startup organizations where she led R&D groups, scientific product development efforts, and translated knowledge and insights from clinical data analyses into actionable results. S he’s a world-class expert in pathway analysis and translational systems biology, which are critical in addressing the complexities of health and disease from different data types in a meaningful holistic way. This cross-functional perspective and passion for making scientifically powered precision medicine insights actionable and scalable has been Ally’s driving force ever since she was investigating gene expression correlates of brain tumors and patient drug response at UCLA while getting her doctorate training in Human Genetics. Ally’s ability to “translate” the signals from genomics, transcriptomics, metabolomics, etc., into something valuable for human health today allows her to lead a diverse team of scientific, clinical, and nutritional experts that together with data science make truly personalized Viome recommendations with molecular-level precision To learn more about Viome and what it is, you can or check out these previous resources I've created on this cutting-edge way to test all the bacteria in your gut, along with the postbiotics they produce: - Article: - Podcast: - Podcast: - Podcast: During this audio/video, you'll discover: -Ben's GI summary...7:23 Most important themes to address are several specific functions dealing with digestive efficiency Active microbes: There are 134 active microbial species detected in the sample, which means that Richness is within the average range but may need improvement. No active Eukaryotes were detected There are 2 active plant viruses: Prunus necrotic ringspot Pepper mild mottle -Overall microbial richness...9:50 Ben's score is 134 out of 400; average score (5-95 percentile) The microbial could use a boost, but nothing too alarming Recommended foods: enriches and diversifies the microbiome increase microbial diversity contains MUFAs, which are a group of fatty acids; weight management, increases bacterial diversity, decreases inflammation Recommended supplements: and cranberry containing supplements -Metabolic fitness score...18:35 Ben's score is GOOD, in the 18th percentile of the Viome population (improved from Sep. 2018) -Inflammatory activity...21:10 Ben's overall score is AVERAGE LPS biosynthesis pathways: average Methane gas production pathways: needs improvement Sulfide gas production pathways: needs improvement Flagella assembly pathways: average Biofilm, chemotaxis, virulence pathways: average Balance is the goal, not optimal scores in every area Although the score is "average" it's on the higher end of the spectrum -Proinflammatory microbial activity, and active pro inflammatory pathways that indicate potential GI inflammation...32:40 -Butyrate production pathways and active butyrate producers...45:45 Ben's overall score is GOOD is good for metabolic fitness Regulates satiety, good for insulin sensitivity Goes hand in hand with inflammation scores Butyrate is a short chain fatty acid (SCFA); associated with beneficial functions for the host Resistant starches and fibers: resist the digestive system of the host -SCFA production pathways and active SCFA producing microbes...51:40 In addition to butyrate: acetate, acetyl phosphate Active probiotic in Ben's sample Many different pathways that lead to butyrate production -Recommendations for Ben's diet...55:23 (mammal) Phytometabolizing microbes and active pathways: -Digestive efficiency...59:20 Ben's overall score is AVERAGE Protein fermentation: needs improvement Gas production: needs improvement Methane gas production pathways: needs improvement Sulfide gas production pathways: needs improvement Putrescine production pathways: needs improvement Butyrate production pathways: good Salt stress pathways: good Protein fermenters and active protein fermentation pathways Omithine Putrescine Cadaverine Ammonia Urea Recommendations related to protein fermentation: Fennel bulb Alfalfa sprouts Grapefruit -Hydrogen sulfide production pathways and hydrogen sulfide producing microbes...1:15:50 Exacerbated by certain foods Disruptive to the gut lining Proinflammatory if produced in excess Sulfate (or sulfite) is deleterious Recommendations specific to microbial gas production, particularly hydrogen sulfide: Broccoli Brussels sprouts -Vitamins produced by the gut microbes and detox of the microbiome... -And much more... Resources mentioned: - Episode sponsors: -: My personal playground for new supplement formulations, Kion blends ancestral wisdom with modern science. Ben Greenfield Fitness listeners receive a 10% discount off your entire order when you use discount code: BGF10. -: I’ve been using Four Sigmatic products for awhile now and I’m impressed by the efficacies of their mushroom products. I use them. I like them. I support the mission! Receive 15% off your Four Sigmatic purchase when you use discount code: BENGREENFIELD -: You can be sure that I researched all the saunas before I bought mine and Clearlight was the one that stood out from all the rest because of their EMF and ELF Shielding and their Lifetime Warranty. Use discount code: BENGREENFIELD to get $500 off your sauna and a free bonus gift! -: As your qualified candidates roll in, we make it easy to screen & rate them, allowing you to make the best hiring decisions for your business. Try it for free when you use ! Do you have questions, thoughts or feedback for Dr. Ally or me? Leave your comments below and one of us will reply!  

In this episode, Dr. Vincent DeLeo talks with Dr. George Han about recent advances in topical psoriasis therapies. Despite the growing popularity of systemic injectables, the vast majority of psoriasis patients are still being managed with topical treatments. Dr. Han reviews some newly available and upcoming agents with novel mechanisms of action that may present safer, more efficacious options for topical treatment of psoriasis. We also bring you the latest in dermatology news and research: 1. Dr. Jill Waibel says treatment with gold microparticles plus lasers is a viable option for acne. https://bit.ly/2IbzHEX 2. Dr. Tina Alster talks about how to cope with patients who get under your skin. https://bit.ly/2IaB2Mb 3. A proinflammatory diet may not trigger adult psoriasis, psoriatic arthritis, or atopic dermatitis. https://bit.ly/2G14tyH Contact us: podcasts@mdedge.com Twitter: @MDedgeDerm  

Paul Wang:         Welcome to the monthly podcast, On the Beat, for Circulation: Arrhythmia and Electrophysiology. I'm Dr. Paul Wang, editor-in-chief, with some of the key highlights from this month's issue.                                 In our first study, Filip Plesinger and associates examined whether a computerized analysis of the body surface 12-lead ECG can be used to measure the ventricular electrical activation delay as a predictor of heart failure or death following resynchronization therapy in a MADIT-CRT trial.                                 The authors found that left bundle branch block patients with baseline ventricular electrical activation delay less than 31.2 milliseconds had a 35% risk of MADIT-CRT endpoints, while patients with ventricular electrical activation delay greater than or equal to 31.2 milliseconds had a 14% risk, P value of less than 0.001.                                 The hazard ratio for predicting primary endpoints in patients with low ventricular electrical activation delay was 2.34 with a P value of less than 0.01. However, ventricular electrical activation delay was not predicted in patients with right bundle branch block or IVCD.                                 In our next study, Karl-Heinz Kuck and associates examined the predictors of long-term clinical outcomes after catheter ablation of atrial fibrillation in 750 patients in the FIRE AND ICE Trial. Using propensity score stratification methods to count for differences in baseline characteristics between sexes, the authors found that female sex with a hazard ratio of 1.37, P equals 0.01, and prior direct current cardioversion with a hazard ratio of 1.40, P equals 0.013 were independently associated with atrial fibrillation recurrence.                                 Female sex with hazard ratio of 1.36, P value of 0.035 and hypertension with a hazard ratio of 1.48, P value of 0.013 independently predicted cardiovascular rehospitalization. A longer history of atrial fibrillation with a hazard ratio of 1.03, P value of 0.039 increased the rate of repeat ablation.                                 After propensity score adjustment, women continued to have higher rates of primary efficacy failure with adjusted hazard ratio of 1.51, P less than 0.05 and cardiovascular rehospitalization with a hazard ratio of 1.40, P less than 0.05.                                 In the next study, Laura Bear and associates examined the reliability of inverse electrocardiographic mapping of cardiac electrical activity from recorded body surface potentials. In five anesthetized closed-chest pigs, torso and ventricular epicardial potentials were recorded simultaneously during sinus rhythm, epicardial, and endocardial ventricular pacing. Two approaches, coupled finite/boundary element methods and a meshless approach based on the method of fundamental solutions, were compared.                                 The authors found that inverse mapping underestimated epicardial potentials more than twofold, P less than 0.0001. Mean correlation coefficients for reconstructed epicardial potential distributions ranged from 0.60 to 0.64 across all methods. Epicardial electrograms were recovered with reasonable fidelity at approximately 50% of the sites, but variation was substantial.                                 General activation spread was reproduced with a mean correlation coefficient of 0.72 to 0.78 for activation time maps with spatio-temporal smoothing. Epicardial foci were identified with a mean location error approximately 16 millimeters. Inverse mapping with method of fundamental solutions was better than coupled finite/boundary element methods.                                 The authors concluded that spatio-temporal variability of recovered electrograms may limit the resolution, with implications for accuracy of arrhythmia localization.                                 In the next study, Pejman Raeisi-Giglou and colleagues examined the incidence of pulmonary vein stenosis in 10,368 patients undergoing atrial fibrillation ablation from 2000 to 2015. Computed tomography scans were performed three to six months after the procedures. Severe pulmonary vein stenosis was observed in 52 patients, or 0.5%. The left superior pulmonary vein represented 51% of all severely stenosed veins.                                 Percutaneous interventions were performed in 43 patients, and complications occurred in five, including three pulmonary vein ruptures, one stroke and one phrenic injury. Over a median follow-up of 25 months, 41, or 79%, of patients remained arrhythmia-free.                                  In our next paper, Koichi Nagashima and associates compared hot balloon ablation and cryoballoon ablation in a 165 consecutive patients who underwent initial atrial fibrillation catheter ablation. Of the 165 patients, 74 propensity score-matched patients equally divided between hot balloon ablation and cryoballoon ablation were studied.                                 Patients' characteristics included age, sex, body mass index, atrial fibrillation subtype, CHA2DS2-VASc score, and left atrial dimension were similar between the two groups. 52% of the hot balloon ablation patients required touch-up with radiofrequency ablation for residual/dormant pulmonary vein conduction versus 24% of the cryoballoon ablation patients with a P value of 0.02.                                 The anterior aspect of the left superior pulmonary vein was the site in 41% of the touch-ups after hot balloon versus the inferior aspect of the inferior pulmonary veins in 22% of the touch-ups after cryoballoon ablation. Hot balloon lesions were smaller with an area of 23.8 centimeters squared compared to cryoballoon ablation lesions having an area of 33.5 centimeters squared with a P value of 0.0007. Within 12 months, both methods had an AF recurrence of 16%.                                 In our next paper, Mildred Opondo and associates randomized 61 patients, mean age 52 years, to either 10 months of high intensity exercise or yoga. The authors found that left atrial volume, Vo2 max, and left ventricular end-diastolic volume increased in the exercise group with no change in the control with a P value of less than 0.0001.                                 The authors did not find significant changes in atrial electrical activity and hypothesized that a longer duration training may be required to induce electrical changes.                                 In our next paper, because there's evidence that the distal part of the ligament of Marshall might be a sympathetic conduit between the left stellate ganglion and the ventricles, Shan Liu and associates randomly divided 29 dogs into a sham ablation group, a ligament of Marshall ablation group, and a left stellate ganglion ablation group. Ablation was performed before occlusion of the left anterior coronary artery.                                 Ligament of Marshall ablation attenuated blood pressure elevation induced by left stellate ganglion stimulation. Both ligament of Marshall ablation and left stellate ganglion ablation similarly prolonged ventricular refractory period and reduced the incidence of ventricular arrhythmias compared with sham ablation.                                 In our next study, Smith and Tester and associates examined the heterologous functional validation studies of putative long-QT syndrome subtype 2, LQT2, associated variants. Genetic testing of 292 sudden infant death syndrome cases identified nine KCNH2 variants, while some of the channels associated the variants can lead to accelerated deactivation and activation gating. Other current levels were similar to wild-type.                                 The authors examined the electronic health records of patients who were genotype positive for these particular sudden infant death syndrome–linked KCNH2 variants and found all of them had a median heart rate–corrected QT intervals less than 480 milliseconds and none had been diagnosed with long-QT syndrome or suffered cardiac arrest.                                 Simulating the impact of dysfunctional gating variants using computational models of the human ventricular action potential predicted that they have little impact on action potential duration. The authors concluded that these rare Kv11.1 missense variants are not long-QT2 causative variants and, therefore, do not represent the pathogenic substrate for sudden infant death syndrome in the variant-positive infants.                                 In our next study, Tina Baykaner and associates performed a systematic literature review and meta-analysis to determine outcomes from ablation of atrial fibrillation drivers in addition to pulmonary vein isolation or as a stand-alone procedure. The authors found 17 studies with a cohort size of 3,294 patients.                                 Atrial fibrillation driver ablation, when added to a pulmonary vein ablation or a stand-alone procedure compared the controls, produced an odds ratio of 3.1 with a P value of 0.02 for freedom from atrial fibrillation and an odds ratio of 1.8 with a P value of less 0.01 for freedom of all arrhythmias in four controlled studies.                                 Adding atrial fibrillation driver ablation to pulmonary vein ablation resulted in a freedom from atrial fibrillation of 72.5%, P value of less than 0.01 and a freedom from all arrhythmias of 57.8% with a P value less than 0.01. Atrial fibrillation termination was 40.5% and predicted favorable outcome from ablation with a P value of less than 0.05. Large multicenter randomized trials are needed to precisely define the benefits of adding driver ablation to a pulmonary vein isolation.                                 In our next study, Hidekazu Kondo and associates found that the adverse atrial remodeling, including atrial inflammation, lipidosis and fibrosis, were induced in both wild-type and Interleukin-10 knockout mice by high fat diet, but the effects were exaggerated in the Interleukin-10 knockout mice. Vulnerability to atrial fibrillation was also significantly enhanced by the high fat diet.                                 The total amount of epicardial and pericardial adipose tissue volume was increased with high fat diet. Proinflammatory and profibrotic cytokines of epicardial and pericardial adipose tissue were also upregulated. In contrast, the protein level of adiponectin was downregulated by the high fat diet. Systemic Interleukin-10 administration markedly ameliorated the high fat diet induced obesity-caused left atrial remodeling and vulnerability to atrial fibrillation.                                 The authors concluded that Interleukin-10 treatment may limit the progression of atrial fibrillation occurring in the setting of a high fat diet.                                 In our next paper, Garcia and Campbell and associates demonstrated the ability to deliver amiodarone epicardially over a sustained period of time. The authors demonstrated in a pig model of atrial fibrillation that an amiodarone containing polyethylene glycol-based hydrogel placed directly on the atrial myocardium in a minimally invasive catheter procedure significantly reduced the duration of sustained atrial fibrillation at 21 and 28 days. The authors found that inducibility of atrial fibrillation was also reduced.                                 In our final paper, Htet Khine and associates examined the effect of spaceflight on the changes in atrial structure, supraventricular beats, and atrial electrophysiology, and to determine whether spaceflight could increase the risk of atrial fibrillation.                                 The authors found that, in 13 that in astronauts, the left atrial volume transiently increased after six months in space without changing atrial function. Right atrial size remained unchanged, while one astronaut had a very large increase in supraventricular ectopic beats, none developed atrial fibrillation. The P-wave amplitude duration did not change over time, but RMS 20 decreased on all fight days except landing day.                                 That's it for this month. Thanks for listening to On the Beat. We hope that you'll find the journal to be the go-to place for everyone interested in the field. See you next month.  

Methods based on nanotechnologies play a growing role in biomedical research. Quantum dots (QDs) are a group of engineered fluorescent nanoparticles suited for advanced imaging applications. The substitution of the particle’s surface with defined molecular structures could enable the adoption as targeted contrast agents or therapeutic devices for a variety of clinical approaches. However, important aspects such as the basic surfacedependent behavior of non-targeted QDs in the organism and arising health effects upon systemic administration remain incompletely understood. Acute inflammatory effects for instance are often initiated on the microcirculatory level and are probably relevant for cardiovascular pathologies observed in epidemiologic and experimental studies of certain nanoparticles. Most in vitro studies show that the surface structures of QDs and other nanoparticles seem to be predominantly accountable for different cytotoxic effects and a variable potential to liberate proinflammatory cytokines. Currently, no systematic in vivo studies have addressed surface-dependent interactions of QDs on the level of the microcirculation and assessed the resulting impact on biokinetics as well as on proinflammatory parameters. Thus, this thesis aimed to i) analyze the incidence of QDsurface- dependent acute microvascular interactions and their influence on key biokinetic parameters and ii) investigate acute immunomodulatory effects on the multistep process of leukocyte recruitment in vivo. For this, three types of commercially available QDs with different surface modifications: carboxyl-QDs, amine- and polyethylene glycol-QDs (amine-QDs) and polyethylene glycol-QDs (PEG-QDs) were used. The physicochemical characterization was done by dynamic light scattering (DLS) analysis and microscale thermophoresis. In a first set of experiments, circulating half-lives, tissue distribution in different organs, and hepatic as well as renal clearance were measured. Ex vivo analysis of QD tissue distribution was performed on selected tissue samples via transmission electron microscopy (TEM) and two-photon microscopy. By combining reflected-light oblique transillumination (RLOT) and fluorescence in vivo microscopy of the murine M. cremaster, interactions of QDs with components of the microcirculation as well as leukocyte migration parameters were visualized and quantified. The extreme short circulating half-life of anionic carboxyl-QDs was related to pronounced clearance by the mononuclear phagocyte system. Beyond this, further investigations showed, for the first time, that the continuous capillary endothelium of skeletal and heart muscle tissue has the capacity to directly extract carboxyl-QDs from the circulation by means of caveolaemediated endocytosis. Carboxyl-QDs were also taken up by perivascular macrophages in the surgically exposed but not in the native M. cremaster and led to a significant increase of adherent and (subsequently) transmigrated leukocytes in this model. Further experiments provided evidence for a probable involvement of mast cells in the intercellular adhesion molecule-1 (ICAM-1)- and endothelial (E)-selectinmediated modulation of leukocyte recruitment. This process is most likely initiated by the endocytosis of carboxyl-QDs through activated perivascular macrophages. The primary activation of tissue-resident perivascular macrophages seems to be the consequence of tissue damage related to the surgical preparation of the cremaster muscle. This is supposedly a prerequisite for the endocytosis of carboxyl-QDs whereupon endothelial and mast cells seem to be secondarily activated in a paracrine fashion that then leads to an increase in leukocyte recruitment.

An Access to Health Experts interview with special guest Rebecca Katz author of "One Bite At A Time". In this interview Rebecca discusses how to avoid pro-inflammatory foods. She also talks about the importance of portion control when cooking and her new book The Power of Yum. Now Free! An archive of Liz's work from 2004 to 2008, this site provides relevant, researched, cutting-edge information from top holistic experts. Our community is comprised of thought leaders, health professionals and intelligent people like you, who are cutting through the clutter of confusing information to get the facts they need to make smart, informed and conscious health decisions for themselves and for their families.www.AccessToHealthExperts.com

Background: Hyperoxic exposures are often found in clinical settings of respiratory insufficient patients, although oxygen therapy (>50% O-2) can result in the development of acute hyperoxic lung injury within a few days. Upon hyperoxic exposure, the inducible nitric oxide synthase (iNOS) is activated by a variety of proinflammatory cytokines both in vitro and in vivo. In the present study, we used a murine hyperoxic model to evaluate the effects of iNOS deficiency on the inflammatory response. Methods: Wild-type and iNOS-deficient mice were exposed to normoxia, 60% O-2 or >95% O-2 for 72 h. Results: Exposure to >95% O-2 resulted in an increased iNOS mRNA and protein expression in the lungs from wild-type mice. No significant effects of iNOS deficiency on cell differential in bronchoalveolar lavage fluid were observed. However, hyperoxia induced a significant increase in total cell count, protein concentration, LDH activity, lipid peroxidation, and TNF-alpha concentration in the bronchoalveolar lavage fluid compared to iNOS knockout mice. Moreover, binding activity of NF-kappaB and AP-1 appeared to be higher in wild-type than in iNOS-deficient mice. Conclusion: Taken together, our results provide evidence to suggest that iNOS plays a proinflammatory role in acute hyperoxic lung injury.

Mon, 1 Jan 2001 12:00:00 +0100 https://epub.ub.uni-muenchen.de/16611/1/10_1159_000046029.pdf Lang, Susanne M.; Stratakis, D.; Schiffl, Helmut