Podcasts about Inflammation

Humans spend roughly 70% of their days in a fight or flight response. It is common to be stressed, anxious, and worried. But it's not healthy. These types of emotions resonate at lower frequencies. How can we shift to more positive emotions? And release emotions that may be stored or trapped in our biofield?   Dr. Sina McCullough is the creator of the online program GO WILD: How I Reverse Chronic & Autoimmune Disease and the co-host of the Beyond Labels podcast with Joel Salatin.   Today she explains how stored emotions in our bio-field can dictate the way our genes express themselves, and how emotions like fear, sadness or anger can express genes that create inflammatory conditions. She discusses the ill effects of Adverse Childhood Experiences (known as ACES) and unresolved traumas. She goes over therapies (like tapping and breath work) that help us move emotion through the body to prevent and reverse disease. And she also reminds us of the healing power of self-love and acceptance.   Visit her website: drsinamccullough.com Sign up for our email list on our website: westonaprice.org Order recordings from our 2021 Wise Traditions conference here. Check out our sponsors Optimal Carnivore and BetterHelp

In COVID-19 clinical update #90, Dr. Griffin covers FDA expansion for booster doses, 3 more at home antigen tests approved by FDA, immune correlates analysis of mRNA-1273 vaccine, risk for stillbirth, PROVENT prophylaxis trial results, fluvoxamine recommendations, advice on molnupiravir, automated text messaging service for monitoring illness, and long COVID-19 after vaccination and infection. Hosts: Daniel Griffin and Vincent Racaniello Subscribe (free): iTunes, Google Podcasts, RSS, email Become a patron of TWiV! Links for this episode Expanded eligibility for booster doses (FDA) More rapid antigen tests approved (FDA) Immune correlates for mRNA-1273 (Science) Risk for still birth with and without COVID-19 (MMWR) PROVENT phase III prophylaxis trial (AstraZenica) Fluvoxamine guidelines (IDSA) COVID-OUT trial (Univ Minnesota) Monoclonal antibody treatment in vaccinated infected (J Inf Dis) Steroid use in non-oxygen requiring patients (QJM) Doxycycline trial (Lancet) Efficacy of inhaled ciclesonide (JAMA) Advise on use of molnupiravir (EMA) Text messaging for monitoring disease (Ann Int Med) Long COVID after vaccination and infection (Res Square) Ivermectin for West Nile virus (Medpage Today) Letters read on TWiV 834 Timestamps by Jolene. Thanks! Intro music is by Ronald Jenkees Send your questions for Dr. Griffin to daniel@microbe.tv

Madiha Saeed is on a mission as the Holistic Mom to help children live healthier, happier, more mindful lives. Learn about the inflammation epidemic that is afflicting children today and what we as parents can do to help our children make more rational, healthy decisions by choosing nutrient-rich foods, focusing on gratitude and optimism, and creating a home environment where they can thrive. [0:40] What can we do as parents to raise mindful and resilient children with a combination of functional medicine and parenting? That's the question that Madiha's new book tries to answer. [1:25] Because of widespread chronic inflammation, children are unable to make rational decisions today which are resulting in a number of societal issues. [3:10] Madiha's mission began after seeing her newborn child struggle to simply breathe. She started her journey of self-healing and put those lessons into practice to help her children as well. [5:35] Chronic disease has quadrupled amongst children since the 1960s. Now 1 out of 2 American children has a chronic health condition. By 2025, the projection is that 80% of children will be diagnosed with a chronic health condition. ADHD has increased 167% and by current projections 1 in 4 children will be diagnosed with autism by 2033. [8:35] By understanding the why and the what, we can understand the root cause of suffering, which is that our children are living unbalanced lives. The decisions children make every day are determined by their brain, and studies have shown that inflammation reduces the connection between the prefrontal cortex and amygdala, both of which are needed to make rational decisions. [10:30] During a research study, they found that children with behavioral issues had high levels of key inflammatory markers. Inflammation can impact babies in the womb. Society lives unbalanced lives and the chronic inflammation that comes as a result is passed from mother to child. [12:30] Endocrine disruptors have been found to be closely linked to inflammation, hormone imbalances, and gender confusion that we are seeing now. Medications that were commonly prescribed to pregnant women in the past decades are being found to have multi-generational impacts and increased suffering. [16:10] There are thousands of chemicals that are released on a regular basis and we have no idea what their long-term impacts are. BPA is a common culprit that is found in most plastics, including baby bottles. [18:00] We need to be more mindful of what is going into our children's bodies and what they are wearing. As parents, we need to empower our children to make positive changes to their daily lifestyles and improve the future. [21:00] Our consumer choices matter. Science has proven that gratitude and optimism strengthen the link between the prefrontal cortex and the amygdala and improves overall health and wellbeing. [22:15] When a child has a chronic health condition, it can become hard to focus on anything else, but if you can shift the focus to the lessons they can learn and what is going right in their lives, it can help them optimize their brain, body, and health simply by reducing the overall stress level. [23:20] Devices and social media are addicting for children. We need to incorporate stress management practices like nature and physical play to balance out their daily routine. [24:55] There is a direct connection between our gut and our brain. The microbiome is vital to helping a child's brain develop fully and reduce inflammation. Nutrients regulate every single chemical reaction in a child's body. [26:25] Madiha uses a diet framework that starts with vegetables, proteins, and healthy fats. Make it easy and fun for your children to eat healthy food and teach them at a young age how it helps them keep their hormones in balance. [28:10] During the pandemic, diabetes has doubled in children. [28:55] Unfortunately, children today are deficient in a number of nutrients, and this causes a cascade of health issues. Madiha typically begins supplementing with vitamin D, fish oil, and probiotics. [32:10] The more kids can enjoy the process and participate in creating the healthy food they need, the more they will consume. [33:30] Mindfulness shows us how best to respond at many different levels at once. It allows children to have the perspective they need to live a healthy life. [35:20] The Holistic Rx is meant for anyone taking care of children who wants direction on how to live a mindful and healthy life. It centers around the child's health and diet, and how to help them recover from inflammation, insulin resistance, and more.     Mentioned in this Episode: theholisticrx.com holisticmommd.com @holisticmommd youtube.com/thegirlfrienddoctor dranna.com/show     Always seek the advice of your own physician or qualified health professional before starting any treatment or plans. Information found here and results are provided for informational purposes only and are not intended to replace a one-on-one relationship with a qualified healthcare professional and are not intended as medical advice.

For years, advertising has told us, “Don't let pain hold you back.”We quickly reach for meds and gimmicks to get us through the day. But are we causing more harm than good? On this episode, we discuss pain management. We explore how we deal with discomfort, and ways to find the root of the issue.We cover acute vs. chronic pain, inflammatory foods, behavior modification, and give some ideas on how to get pain cleared up and get you and your clients moving well. So get ready for another episode of the Movement Podcast-- powered by FMS.SHOW NOTES & LINKS:✅   Indian Clubs Online Course - Limited Time 30% off with promo code: CLUBCOURSE at checkout 

A new study finds longer daily fasts were demonstrated to produce more favorable improvements in biomarkers that are associated with metabolic and cardiovascular health as well as inflammation. Let's break it down... Support your fasting lifestyle with Berberine HCl & Alpha Lipoic Acid by by MYOXCIENCE Nutrition: https://bit.ly/berberine-biotin-ala-stack Use code Podcast to save Save 40% off this at-home A1C test by Biocoach: http://bit.ly/BOGO-A1C-test Use code HIH10 Links to notes: https://bit.ly/30WjpeE REF: Moro, T., Tinsley, G., Pacelli, et al. (2021). Twelve Months of Time-restricted Eating and Resistance Training Improves Inflammatory Markers and Cardiometabolic Risk Factors. Medicine and science in sports and exercise, 53(12), 2577–2585. Time Stamps 0:00 Intro 0:18 New Study 0:08 Testing 16 Hour VS 12 Hour Feeding Windows 0:27 Markers of Inflammation decreased 1:17 Only four hour difference in feeding window 2:22 Study Title: 3:43 Testing your metabolic health 4:42 Berberine & metabolic health 5:50 Feeding Window comparisons 6:43 How Calories were distributed 7:36 Whey protein post workout 7:50 TRF group ate less calories by accident 8:33 Strength and muscle loss between two groups 11:08 Testosterone did decrease 11:53 Insulin, Leptin and Adiponectin 12:44 HDL, Triglycerides and glucose 13:52 Chronic Inflammation 15:11 Trade offs to consider

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Inflammation is a big part of both osteoarthritis and rheumatoid arthritis, so it's important that we are taking the correct steps to protect our body. This is where important anti-inflammatory nutrients such as green tea, curcumin and Vitamin D come into play. Take advantage of an exclusive podcast offer today by visiting http://www.invitehealth.com/podcast. For more information on the products or studies mentioned in this episode, click here. 

Today, I am blessed to have here with me Nina Teicholz. She is an investigative science journalist and leader in nutrition reporting who is challenging the conventional wisdom on dietary fat–particularly, whether saturated fat causes heart disease and whether fat really makes you fat.  The New York Times bestselling author of The Big Fat Surprise. Teicholz also serves as Executive Director of The Nutrition Coalition, an independent non-profit group that promotes evidence-based nutrition policy. She is one of a new generation of researchers arguing that diets lower in carbohydrates are a scientifically sound approach for reversing nutrition-related diseases.   For more than half a century, we've been told to eat a diet high in grains, low in fat, saturated fat (and cholesterol), but the last two decades of research have led a growing number of scientists  to conclude that this diet, despite being rigorously tested, could never be shown to prevent any kind of disease. Teicholz's work also explains why this diet has remained official policy for so long: the roles played by crusading scientists, the food industry, and more. In this episode, Nina opens the show by explaining her obsession with studying fat. Nina realized that people were afraid to talk about fat because the food industry was pushing their agenda. Nina explains what was wrong in the 1950s, leading most people to believe that saturated fats and dietary cholesterol cause heart disease. Later, we talk about why the American Heart Association gets so many health facts wrong. Tune in as Nina busts common myths around red meat and who is really pushing vegan and vegetarian diets. Order Keto Flex: http://www.ketoflexbook.com -------------------------------------------------------- / / E P I S O D E   S P ON S O R S  PureForm Omega Plant Based Oils (Best Alternative to Fish Oil): http://www.purelifescience.com Use ben4 for $4.00 off. Upgraded Formulas Hair Mineral Deficiency Analysis & Supplements: http://www.upgradedformulas.com Use BEN10 at checkout for 10% off your order.  Paleo Valley beef sticks, apple cider vinegar complex, organ meat complex & more. Use the coupon code KETOKAMP15 over at https://paleovalley.com/ to receive 15% off your entire order. Text me the words "Podcast" +1 (786) 364-5002 to be added to my contacts list.  [03:00] Why Nina Became Obsessed With Studying Fats Nina was assigned to write a story on trans-fat. During her research, Nina came across studies pointing out the flaws in a low-fat diet. However, so many scientists at universities were terrified to talk to Nina about fat. Why? Because people in the food industry were paid to give scientists a hard time. Nina realized there was something really wrong going on here that had such enormous implications. Nutrition science from the very beginning has been heavily influenced by the food industry. For instance, the vegetable oil industry wanted to go after people for attacking vegetable oils in any way. You see the same tactics happening today on social media.    [08:55] Polyunsaturated Fats vs. Saturated Fats vs. Monounsaturated Fats Fatty acids are long carbon chains.  Poly means many. Polyunsaturated fats have many double bonds. Each time there's a double bond in the chain, it kinks the chain. Some examples of polyunsaturated fats: Corn oil Safflower oil Sunflower oil Canola oil     Monounsaturated fats are the same carbon chain but with one double bond. If you want to use oil, it's better to use olive oil because it only has one double bond. Saturated means that the carbon chain is statured with hydrogen, and there is no double bond. It is a flat chain, and it makes a solid like butter. Saturated fats are actually the best for cooking, and they're the healthiest for eating because they do not oxidize or cause inflammation.   [17:55] What Went Wrong In The 1950s With Ancel Keys and President Eisenhower The idea that fat, cholesterol, and animal foods are bad for health began in the 1950s.  The US was really in a panic over the rising tide of heart disease, which had been virtually nonexistent in the early 1900s. In the 1930s, heart disease became the number one killer.  A panic started when President Eisenhower himself had a heart attack in 1955. Eisenhower's doctor was convinced by Ancel Keys that saturated fats and dietary cholesterol cause heart disease.  Plus, Ancel Keys got his ideas adopted by the American Heart Association.  Ancel came out with a statement saying to avoid saturated fat and cholesterol in order to prevent heart attacks. We are still dealing with this in 2021.    [23:00] Why Are Seed Oils Approved by the American Heart Association?  How is it possible for the American Heart Association to continue to ignore so much scientific literature? More than 20 papers published in the field have concluded that we got it wrong on saturated fats.  There is no data to justify the authorities' limits on these seed oils. It's challenging to trust the government with our health when they recommend seed oils.   [31:00] Sorry Vegans, Meat-Eating Is Healthy For Humans  Nina did not know how controversial red meat was until she put a picture of it on the cover of her book.  Sadly, many people think that if you eat meat, you're a bad person, you don't believe in climate change, and you're not doing your part to protect the climate. There's this moral revulsion that has been created against meat. Influencers in the spheres of science and public health have vilified one of the healthiest foods on the planet.  Meat was developed by humans in order to have a convenient and cheap source of protein.   [33:15] Myth: Meat Causes Diabetes   Diabetes is caused by elevated blood sugars. Sugar causes elevated blood sugars, so do carbs.  Where's the sugar in meat? It's just nonexistent.  It's impossible that meat would cause diabetes. Red meat consumption has gone down around 28% since 1970. Whereas, diabetes has skyrocketed out of control.    [34:15] Myth: Red Meat Causes Colorectal Cancer The WHO decided that red meat and processed meats cause colorectal cancer. This decision was based on these kinds of weak science called epidemiological or observational studies that show associations instead of causation. The data they used was self-reported dietary data, and we all lie about what we eat. There needs to be a more significant discussion about the bias against red meat.   [38:30] Why People Are Pushing Vegetarian and Vegan Diets The animal rights movement does not want people eating animals. The Seventh Day Adventist Church has a religious belief that people should eat a vegan diet.Plus, the food industry has an enormous investment in plant-based foods. Also, many companies want to hop on the climate change bandwagon.  Many vegan burgers have vegetable oils that are not healthy.    [41:30] Myth: There's a Correlation Between Red Meat Consumption and Heart Disease The original reason that red meat was thought to cause heart disease was based the fact that it contains saturated fat and cholesterol. However, research shows that saturated fat and cholesterol do not cause heart disease.  Therefore, foods containing saturated fat and cholesterol don't cause heart disease. The correlation between saturated fat, cholesterol, and heart disease has been more rigorously and extensively studied than almost any other scientific question in the history of nutrition science.    [47:15] Which To Cut First: Smoking Cigarettes, Processed Sugars, or Vegetable Oils  People smoked historically for hundreds of years tobacco, but they did not get cancer or heart disease until the introduction of sugar. Nina says that smoking is probably safer than processed sugars or vegetable oils.  Between sugar and vegetable oils, Nina says that vegetable oils are safer.  People who go low-carb will see massive improvements even if they continue to use vegetable oils.    AND MUCH MORE!   Resources from this episode:  Check out Nina's Website: https://ninateicholz.com Follow Nina Teicholz Twitter: https://twitter.com/bigfatsurprise Facebook: https://www.facebook.com/NinaTeicholz/ LinkedIn: https://www.linkedin.com/in/ninateicholz/ Get The Big Fat Surprise: Why Butter, Meat and Cheese Belong in a Healthy Diet: https://www.amazon.com/Big-Fat-Surprise-Butter-Healthy/dp/1451624433/benazadi-20 Join the Keto Kamp Academy: https://ketokampacademy.com/7-day-trial-a Watch Keto Kamp on YouTube: https://www.youtube.com/channel/UCUh_MOM621MvpW_HLtfkLyQ Order Keto Flex: http://www.ketoflexbook.com -------------------------------------------------------- / / E P I S O D E   S P ON S O R S  PureForm Omega Plant Based Oils (Best Alternative to Fish Oil): http://www.purelifescience.com Use ben4 for $4.00 off. Upgraded Formulas Hair Mineral Deficiency Analysis & Supplements: http://www.upgradedformulas.com Use BEN10 at checkout for 10% off your order.  Paleo Valley beef sticks, apple cider vinegar complex, organ meat complex & more. Use the coupon code KETOKAMP15 over at https://paleovalley.com/ to receive 15% off your entire order. Text me the words "Podcast" +1 (786) 364-5002 to be added to my contacts list.  *Some Links Are Affiliates* // F O L L O W ▸ instagram | @thebenazadi | http://bit.ly/2B1NXKW ▸ facebook | /thebenazadi | http://bit.ly/2BVvvW6 ▸ twitter | @thebenazadi http://bit.ly/2USE0so ▸clubhouse | @thebenazadi Disclaimer: This podcast is for information purposes only. Statements and views expressed on this podcast are not medical advice. This podcast including Ben Azadi disclaim responsibility from any possible adverse effects from the use of information contained herein. Opinions of guests are their own, and this podcast does not accept responsibility of statements made by guests. This podcast does not make any representations or warranties about guests qualifications or credibility. Individuals on this podcast may have a direct or non-direct interest in products or services referred to herein. If you think you have a medical problem, consult a licensed physician.

In COVID-19 clinical update #89, Dr. Griffin reviews upcoming meeting on FDA emergency use authorization for molnupiravir, 25% of US cases in children, reinfection associates with presence of antibodies, national surveillance for acute flaccid myelitis in the US, and monoclonal antibody treatment of infection in vaccinated, high-risk individuals. Hosts: Daniel Griffin and Vincent Racaniello Subscribe (free): iTunes, Google Podcasts, RSS, email Become a patron of TWiV! Links for this episode Scott Hammer on TWiV 52 Meeting for molnupiravir EUA (FDA) SARS-CoV-2 reinfection associates with antibodies (Clinical Inf Dis) AFM surveillance in US (CDC) Monoclonal antibody treatment in high-risk patients (J Inf Dis) Letters read on TWiV 831 Timestamps by Jolene. Thanks! Intro music is by Ronald Jenkees Send your questions for Dr. Griffin to daniel@microbe.tv

This month on Episode 30 of Discover CircRes, host Cynthia St. Hilaire highlights four original research articles featured in the October 29 and November 12 issues of Circulation Research. This episode also features a conversation with Dr Elisa Klein from the University of Maryland about her study, Laminar Flow on Endothelial Cells Suppresses eNOS O-GlcNAcylation to Promote eNOS Activity.   Article highlights:   Subramani, et al. CMA of eNOS in Ischemia-Reperfusion Liu, et al. Macrophage MST1 Regulates Cardiac Repair Van Beusecum, et al. GAS6/Axl Signaling in Hypertension Pati, et al. Exosomes Promote Efferocytosis and Cardiac Repair   Cindy St. Hilaire:        Hi and 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 articles presented in our October 29th and November 12th issues of Circulation Research. I also will speak with Dr Elisa Klein from the University of Maryland about her study, Laminar Flow on Endothelial Cells Suppresses eNOS O-GlcNAcylation to Promote eNOS Activity.   Cindy St. Hilaire:        The first article I want to share is titled, Chaperone-Mediated Autophagy of eNOS in Myocardial Ischemia Reperfusion Injury. The first author is Jaganathan Subramani and the corresponding author is Kumuda Das from Texas Tech University Health Sciences Center. Reestablishing blood flow to ischemic heart muscle after myocardial infarction is critical for restoring muscle function but the return of flow itself can cause damage, a so-called reperfusion injury. The generation of reactive oxygen species or ROS and loss of nitric oxide or NO both contribute to reperfusion injury.                                       Reperfusion injury is exacerbated when the NO producing enzyme, endothelial nitric oxide synthase or eNOS, produces damaging super oxide anions instead of NO. This switch in eNOS function is caused by glutathionylation of the enzyme, termed SG-eNOS. But how long this modification lasts and how it is fixed is unclear. This group used an in vitro model of ischemia reperfusion where human endothelial cells are exposed to several hours of hypoxia followed by reoxygenation. In this model, they found the level of SG-eNOS steadily increases for 16 hours and then sharply decreases. By blocking several different cellular degradation pathways, they discovered that this decrease in S-G eNOS was due to chaperone mediated autophagy with the chaperone protein, HSC70, being responsible for SG-eNOS destruction. Importantly, this team went on to show that pharmacological D-glutathionylation of eNOS in mice promoted NO production and reduced reperfusion injury, suggesting this approach may be of clinical benefit after myocardial infarction.   Cindy St. Hilaire:        The second article I want to share is titled Macrophage MST1/2 Disruption Impairs Post-Infarction Cardiac Repair via LTB4. The first author is Mingming Liu and the corresponding author is Ding Ai and they're from Tianjin Medical University. Myocardial infarction injures the heart muscle. These cells are unable to regenerate and instead a non-contractile scar forms and that fibrotic scar can lead to heart failure.                                     Cardiomyocytes specific inhibition of the kinase MST1 can prevent infarction induced death of the cells and preserve the heart function, suggesting that it may have clinical utility. However, MST1 also has anti-inflammatory properties in macrophages. So inhibition of MST1 in macrophages may delay inflammation resolution after MI and impair proper healing. Thus, targeting this enzyme for therapy is not a straightforward process. This study examined mice lacking MST1 in macrophages and found that after myocardial infarction, the inflammatory mediator leukotriene B4 was upregulated in macrophages and the animal's heart function was reduced compared to that of wild type controls. Blocking the action of leukotriene B4 in mice reduced infarction injuries in the hearts of MST1-lacking animals and enhanced repair in the injured hearts of wild type animals given an MST1 inhibitor. The results suggest that if MST1 inhibition is used as a future post infarction regenerative therapy, then leukotriene B4 blockade may prevent its inflammatory side effects.   Cindy St. Hilaire:        The next article I want to share is titled Growth Arrest Specific-6 and Axl Coordinate Inflammation and Hypertension. The first author is Justin Beusecum and the corresponding author is David Harrison and they're from Vanderbilt University. Inflammation contributes to hypertension pathology but the links of this relationship are unclear. It's thought one trigger of inflammation may be the hypertension-induced mechanical stretch of vascular endothelial cells. Mechanical stretch causes endothelial cells to release factors that convert circulating monocytes into inflammatory cells. And one such factor is the recently identified Axl and Siglec-6 positive dendritic cells, also called AS DCs.                                       AS DCs produce a large amount of inflammatory cytokines but little is known about the role of AS DCs or their cytokines in hypertension. This group found elevated levels of AS DCs in hypertensive people compared to normal tensive individuals. Mechanical stretch of human endothelial cells promoted the release of GAS6, which is an activator of the AS DC cell surface kinase, Axl. This stretch induced GAS6 release also promoted conversion of co-cultured monocytes to AS DCs. Inhibition of GAS6 or Axl in the co-cultured system prevented conversion of monocytes to AS DCs. This team went on to show that hypertensive humans and mice have elevated levels of plasma GAS6 and that blocking Axl activity in mice attenuated experimentally induced hypertension and the associated inflammation. This work highlights a new signaling pathway, driving hypertension associated inflammation and identifies possible targets to treat it.   Cindy St. Hilaire:        The last article I want to share is titled Novel Mechanisms of Exosome- Mediated Phagocytosis of Dead Cells in Injured Heart. The first author is Mallikarjun Patil and Sherin Saheera and the corresponding author is Prasanna Krishnamurthy from the University of Alabama, Birmingham. After myocardial infarction inflammation must quickly be attenuated to avoid excessive scarring and loss of muscle function. Macrophage mediated efferocytosis of dead cells is a critical part of this so-called inflammation resolution process. And resolution depends in part on the protein. MFGE8. MFGE8 helps macrophages engage with eat me signals on the dead cells and loss of macrophage MFGE8 delays inflammation resolution in mice. Because stem cell-derived exosomes promote cardiac repair after infarction and are anti-inflammatory and express MFGE8, this group hypothesized that perhaps part of a stem-cell derived exosomes proresolven activity may be due to boosting macrophage efferocytosis.                                     They showed that stem cell derived exosomes did indeed boost efferocytosis of apoptotic cardiomyocytes in vitro and in vivo. An in vitro experiments showed that if exosomes lacked MFGE8 then efferocytosis by macrophages was reduced. Furthermore, after myocardial infarction in mice, treatment with MFGE8 deficient exosomes did not reduce infarct size and did not improve heart function compared to control exosomes. These results suggest MFGE8 is important for the cardioprotective effects of stem cell-derived exosomes. And that this protein may be of interest for boosting efferocytosis after myocardial infarction and in other pathologies where inflammation is not readily resolved.   Cindy St. Hilaire         So today, Dr Elisa Klein from the Department of Biomedical Engineering at the University of Maryland is with me to discuss her study Laminar Flow on Endothelial Cells Suppresses eNOS O-GlcNAcylation to Promote eNOS Activity and this article is in our November 12th issue of Circulation Research. So Dr Klein, thank you so much for joining me today.   Elisa Klein:                 Thank you for having me.   Cindy St. Hilaire:        Yeah. So broadly your study is investigating how blood flow patterns specifically, kind of, laminar and oscillatory flow, how those blood flow patterns impact protein modifications and activity. So before we, kind of, get to the details of the paper, I was wondering if you could just introduce for us the concept of blood flow patterns, how they change in the body naturally but then how they might influence or contribute to disease pathogenesis in the vessels?   Elisa Klein:                 Sure. So obviously we have blood flow through all of our vessels and since we are complex human beings, we have complex vascular beds that turn and that split or bifurcate. And so every place we get one of these bifurcations or a turn in a vessel, the blood flow can't quite make that turn or split perfectly. So you get a little area where the flow is a oscillatory or what we call disturbed. There's lots of different kinds of disturbed flow. And the reason why that's important is because you tend to develop atherosclerotic plaques at locations where the blood flow is disturbed. So in my lab, we look a lot at what it is about that disturbed flow that makes the endothelial cells there dysfunctional and that leads to the atherosclerotic plaque development.   Cindy St. Hilaire:        That is so interesting. So I can picture how this is happening in a mouse at the bifurcation of different arteries but how are you able to model this in vitro? Can you describe the setup and then also how that setup can mirror the physiological parameters?   Elisa Klein:                 Sure. So we have a couple of different systems we can use to model this and they all have their advantages and disadvantages, right? So a few years ago we made a system that's a parallel plate flow chamber. So you basically have your cells that you see that on a microscope slide and you use a gasket that's a given shape and that either drives the flow… Usually it drives the flow straight across the cells. So that's a nice laminar steady flow. And we see that the cells align and they produce nitric oxide in that type of flow which are measures that they are responding to the flow in vitro. So, a few years ago we made a device that actually makes the flow zigzag as it goes across the endothelial cells. And that creates these little pockets of disturbed flow and we did that in our parallel plate flow chamber.                                       And that parallel plate flow chamber is really good for visualizing the cells. So you can stick it on a microscope. You can see what's happening, we can label for specific markers but it's not good for doing the things that we did in this Circ Research paper, where we want it to measure metabolism, because you need a lot more cells to measure metabolism and we needed a better media to cell ratio, so less media and more cells. So for this one, we designed and built a cone-and-plate device. So what it is, it's a cone and you spin that cone on top of a dish of endothelial cells and that cone produces flow. So it's going around in a circle. And if we just make it go around in a circle, it'll produce a steady laminar flow but if we oscillated it, so basically we kind of turn it back and forth, it'll make this oscillating disturbed flow. And then we have our dish of cells.                                     We do this in a 60-millimeter dish and then we have a small amount of media in there and a lot of cells. And we can culture the cells in there for a while.                                     Cindy St. Hilaire:        That is so neat. And so I'm assuming that then your cone system is very tuneable. You could either speed it up, slow it down or change that oscillatory rate with different, I guess, shifts of it? Elisa Klein:                 Yeah, that's exactly right. So we can do all those things. It's programmable with a motor and so we can run whatever type of flow we want. Cindy St. Hilaire:        That's great. So before your study, what was known regarding this link between hemodynamics and endothelial cell dysfunction and also endothelial cell metabolism? Because I feel like that's a really interesting space that a lot of people look at, kind of, metabolism and EC dysfunction or they just look at shear stress and EC dysfunction and you're, kind of, combining the three. So what was kind of the knowledge gap that you were hoping to investigate? Elisa Klein:                 Yeah, so we're really interested in macrovascular endothelial cell dysfunction. So this pro atherosclerotic phenotype that you can get in endothelial cells. And most of the work on endothelial cell metabolism had actually been done in the context of angiogenesis. So how much energy and how do cells get their energy to make new blood vessels? And that's more of a microvascular thing. So there was a study that came out before ours, actually, before we started this study, that was looking at how steady laminar flow could decrease endothelial cell glycolysis. And so that was after 72 hours of flow and they showed some gene expression changes at that time. Our study is shorter than that and we were still able to see a decrease in glycolysis in our cells in laminar flow. Before we started this study, no one had really looked at disturbed flow. So in the meantime, there are a few other papers that came out showing that the cells don't decrease glycolysis when they're in disturbed flow but not so much connecting them back to this function of making nitric oxide. Cindy St. Hilaire:        So we were kind of dancing to the topic of O linked N acetylglucosamine or how do you say it? Elisa Klein:                 GlcNAC. Cindy St. Hilaire:        GlcNAC? O- GlcNAC. So, O- GlcNAC is a sugar drive modification and I think it's added to Syrian and three Indian residues and proteins. Elisa Klein:                 Yup, that's right. Cindy St. Hilaire:        Okay, good. And that modification, it does help dictate a protein's function. And you were investigating the role of this moiety on endothelial nitric oxide synthase or eNOS and so what exactly does this GlcNAC do for eNOS' function and under what conditions or disease states is this modification operative? Elisa Klein:                 Yeah. So there's some really important studies from a little bit ago that showed that eNOS gets GlcNAcylated in animals with diabetes, right? So if you have constantly high sugar levels, you get this modification of eNOS. The thought was that eNOS gets GlcNAcylated at the same site where it gets phosphorylated. But a more recent study came out and said, well, maybe that's not the case but it definitely gets GlcNAcylated somewhere where it affects this phosphorylation site. So it may be near it and prevent the folding or prevent the phosphorylation site availability. So if the eNOS gets GlcNAcylated, the thought is that it can't get phosphorylated and therefore it can't make nitric oxide. Cindy St. Hilaire:        And so an interesting thing about this GlcNAcylation, which is probably the hardest thing I've ever said on this podcast, is that it's integrated with lots of different things. Obviously you need glycolysis and the substrates from the breakdown of sugars to make that substrate but also the enzymes that make that substrate are required. And so what's known about that balance in endothelial cells? Is there much known regarding the metabolic rate of the cells and this N-Glcynation? Elisa Klein:                 Yeah. So endothelial cells are thought to be highly glycolytic in terms of how they use glucose but they definitely take up glutamine to fuel the tricarboxylic acid or TCA cycle. And another paper came out a few years ago showing that quiescent and endothelial cells metabolize a lot of fatty acids. So they're fueling their energy needs that way. So there wasn't a lot known about GlcNAcylation in endothelial cells.                                     A lot of this work has been done in cancer cells, which are also highly glycolytic but their metabolism actually seems like it's maybe more diverse than people have thought for a long time. So the weird thing about GlcNAcylation, which if you're used to working with phosphorylation there's a thousand different enzymes that can phosphorolate right. But with GlcNAcylation there's one enzyme that's known to put the GlcNAC on and one enzyme that's known to take it off. And so they're global, right? So in our studies, if we say, okay, we're going to knock down that enzyme, you're effecting every single protein in the cell that's GlcNAcylated. And obviously ourselves in particular, we're not a big fan of that. Especially once you put them in flow, they were, like, nope, we're not going to make it. Cindy St. Hilaire:        Well, and that's a perfect segue to my next question because your results show that this flow really did not alter the expression of these enzymes that either add or subtract to the moiety. And rather it was the Hexosamine Biosynthetic Pathway that was decreased itself. So can you maybe give us a quick primer on what that is exactly and how that pathway feeds into the glycosylation... I think you wrote in the paper of over 4,000 proteins? So how would that fit in and why eNOS then? Elisa Klein:                 Yeah, so the Hexosamine Biosynthetic Pathway is one of these branch pathways that comes off glycolysis and there are these numbers sometimes there are these pathways out there and people say for the HBP in particular, 2% to 5% of the glucose that's going down through glycolysis gets shunted off into the HBP. We've done a lot of looking to try and figure out exactly where that 2% to 5%- Cindy St. Hilaire:        Yeah, what exact percentage? Elisa Klein:                 Yeah, but some percentage of it comes down and we really thought there were going to be changes in these enzymes that do the GlcNacylation, we thought there might be changes in the localization of the proteins and it's possible that those things do occur. We just couldn't detect them in our cells. And in the end, what we showed was the main thing was that when you have cells and steady laminar flow, you just decreased glycolysis. And therefore, that 2% to 5% goes down. So you seem to make less of this UDP- GlcNAC, which is the substrate that gets put on to eNOS in this case. The really strange thing that we could not explain despite a lot of work and obviously we don't get to put all of our experiments that didn't work in the paper- Cindy St. Hilaire:        The blood, sweat and tears gets left out. So- Elisa Klein:                 Exactly. So we tried really hard to figure out why it was eNOS specifically, right? Because in steady laminar flow, you see a lot of these like GlcNAcylated  proteins and a lot of them didn't change but eNOS changed hugely, essentially this GlcNAcylation just went away for the cells and steady laminar flow. So we couldn't quite answer that. We're still working on that part of the question and looking at some of the other proteins that maybe get GlcNAcylated more in this case and trying to figure out what they are. Cindy St. Hilaire:        I thought one of the cool results in your paper was one of the last ones. It was the one in healthy mice. In that you looked at healthy mice, just normal C57 black 6 mice that were 10 weeks old. So they just, kind of, reached maturity but you looked at their kind of these bifurcations and you looked at the inner aortic arch where there is more disturbed flow and you saw, similar to your in vitro studies, that there was this higher level of O-GlcNAcylation compared to the outer arch in the descending order. So my question is, these are healthy mice that are relatively young, they're not even full adults yet. That takes a couple more months. And so what are your thoughts about the role of this O-GlcNAcylation specifically on eNOS in driving atherogenesis. Where do you think this is happening in the disease process? It appears if it's in these wild type mice, it's already happening early. So where do you think this is most operative in the disease pathogenesis? Elisa Klein:                 I mean, I think it's very early, the effects of disturbed flow on endothelial cells. I can't imagine that there's a time when it's not having an effect on the cells. So I teach college students and I tell them all the time you think you're invincible now but these choices you're making today are going to affect your cardiovascular future in 50 years, which is very hard to accept. So I think it's very early in the process and I think it's only made worse by the things that we eat, in particular, that changed our blood sugar and our blood fatty acids and things like that. And our lab is looking into this more to try and see how when you change your blood metabolites then how does that then also affect this GlcNAcylation and the endothelial cell metabolism and then how does that affect endothelial cell function? Cindy St. Hilaire:        Yeah. And it's funny, it's really making me think of those, kinds of, extreme diets like keto diets and things like that where you're just like depleting sugar. And obviously there's lots of controversy in that field, but if you just think about the sugar aspect what is that doing to those EC cells? Why do you think endothelial cells have this response? Meaning why do you think it is that they've adapted to induce a metabolic shift in response to disturbed flow? Because, obviously it's not going to be perfect laminar flow everywhere. So what do you think it is that provides some sort of advantage in the shift? Elisa Klein:                 That's a really good question. I haven't thought about the advantage that it might provide. There are a lot of things that are going on in this area of disturbed flow. So there is the shear stress, the differential shear stress that the cells are experiencing. There's also transport issues, right? So if you have this area of disturbed flow, you have blood and the contents of the blood, including the white blood cells and the red blood cells, everything else that's, kind of, sitting around in that area and not getting washed downstream as quickly. So it is possible that maintaining glycolysis provides energy for repair or for protecting the endothelial cell from some sort of inflammatory insult or something like that, that's happening in the area of disturbed flow. And I feel like I just read something recently, it was in a different genre but... if they stopped the increased glycolysis or stop the metabolic shifts, it actually was worse.                                     Right? So I also believe that we treat humans for a single metabolic change, right? So if you have diabetes, I'm going to give you this drug and if you have high triglycerides, I'm going to give you this drug. But it's possible that if you have this metabolic abnormality, your body shifts the rest of your metabolism to protect the cells because of that metabolic abnormality. And so part of what we do as engineers is try and build computational models or we can take into account some of this complexity. So that's a really interesting question and my guess is that there are some protective aspects of this maintenance of high glycolysis and disturbed flow. Cindy St. Hilaire:        Yeah, maybe it would be perfectly fine until we get athero and then it all goes awry. So in terms of... obviously it's early days and I know you're a bioengineer but in terms of translational potential, what do you think your findings suggest about future potential therapies or future targets for which we can use to develop therapies? Is modulating this O-GlcNAcylation itself, a viable option? Elisa Klein:                 I don't think that modulating it is a super viable option, right? Because as I said, when we tried to change those enzymes ourselves did not enjoy going through flow or anything else. So it's very hard to change it overall. What I think is these things that are coming out about how metabolism may shift for endothelial cells when they're activated versus when they're quiescent, right? So when laminar flow or cells are quiescent, they decrease glycolysis, they increase fatty acid oxidation. Those things are important to take into consideration when you are treating a person who has a metabolic disorder. So that's the biggest translational piece that I think is, how do we give therapies that modify the metabolism of a cell holistically instead of trying to hit one pathway in particular.                                     We have done some studies where we tried to give endothelial cells something to inhibit a specific metabolic pathway and you see the cell shifts its entire metabolism to account for that. So we're starting to look at some of these other drugs like statins or metformin that do change endothelial cell metabolism, possibly even the SGLT2 inhibitors and trying to see not just how they change glycolysis but how they change metabolism as a whole and how that then affects endothelial cell function. Cindy St. Hilaire:        So what are you going to do next on this project? Elisa Klein:                 So on this project, so we have some stuff in the works like I said on statins and how statins work together. And one of our big goals is to sort of build a comprehensive metabolic model of the endothelial cell. So this study really focused on glucose but there are other things that endothelial cells metabolize, glutamine, and fatty acids, and trying to look at some of those and then seeing how changes in the glycolytic pathway may affect some of those other pathways. We also have some really nice mass spec data part of which is in this paper but part of which is going to go into our next work, which is looking at how laminar flow impacts some of the other side branch pathways that are in metabolism and coming off of glycolysis as well as the TCA cycle, right? So we don't think of endothelial cells as being big mitochondrial energy producers but they do use their mitochondria. And so we think it's really interesting and part of our goal of building an endothelial cell model and then hopefully a model of the complexity of the whole vascular wall. Cindy St. Hilaire:        Wow. That would be amazing. Well, Dr Elisa Klein from the University of Maryland, thank you so much for joining me today. This is an amazing study and I'm looking forward to seeing hopefully more of your future work. Elisa Klein:                 Thank you so much. It was a pleasure. Cindy St. Hilaire:        That's it for the highlights the from October 29th and November 12th issues of Circulation Research. Thank you for listening. Please check out the CircRes Facebook page and follow us on Twitter and Instagram with the handle @CircRes or #DiscoverCircRes. Thank you to our guest, Dr Elisa Klein. This podcast is produced by Asahara Ratnayaka, edited by Melissa Stoner and supported by the editorial team of Circulation Research. Some of the copy texts for 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 exciting discoveries and basic cardiovascular research. This program is copyright of the American Heart Association, 2021. The opinions expressed by speakers on this podcast are their own and not necessarily those of the editors or of the American Heart Association. For more information, visit AHAjournals.org.

You've heard of prebiotics and probiotics, but do you know about postbiotics? You do now. This week, Dr. Heather Zwickey talks about the advantages of the lesser known biotic and how postbiotics can help decrease inflammation in your patients. Each Thursday, join Dr. Raja and Dr. Hadar, board certified dermatologists, as they share the latest evidence based research in integrative dermatology. For access to CE/CME courses, become a member at LearnSkin.com.   Heather Zwickey, PhD serves as the Director of Innovation and Communication for Thaena, Inc, a company focused on postbiotics. Dr. Zwickey is also a Professor of Immunology at the National University of Natural Medicine and the University of Western States, and currently co-leads an NIH funded clinical research training program focused on training the next generation of integrative medicine researchers.

On Episode 10 of the Stroke Alert Podcast, host Dr. Negar Asdaghi highlights two articles from the November 2021 issue of Stroke: “Biomarkers of Coagulation and Inflammation in COVID-19–Associated Ischemic Stroke” and “Treatment-Associated Stroke in Patients Undergoing Endovascular Therapy in the ARUBA Trial.” She also interviews Dr. S. Claiborne Johnston about “Ischemic Benefit and Hemorrhage Risk of Ticagrelor-Aspirin Versus Aspirin in Patients With Acute Ischemic Stroke or Transient Ischemic Attack.” Dr. Negar Asdaghi: 1) What is the net ischemic benefit derived from combination of ticagrelor and aspirin treatment in patients with mild ischemic stroke or transient ischemic attack? 2) Is the ischemic stroke in patients hospitalized with COVID-19 associated with the rise in biomarkers of inflammation and coagulopathy? 3) What are the characteristics associated with periprocedural stroke in patients treated endovascularly for an unruptured AVM? We'll discuss these topics and much more at today's podcast. Stay with us. Dr. Negar Asdaghi:                        Welcome back to the Stroke Alert Podcast. My name is Negar Asdaghi. I'm an Associate Professor of Neurology at the University of Miami Miller School of Medicine and your host for the monthly Stroke Alert Podcast. For the November 2021 issue of Stroke, we have a large selection of topics, from peanut consumption reducing the risk of ischemic stroke, and the decline in the rate of progression of coronary atherosclerosis in patients on a Mediterranean diet, to how the efficacy of endovascular thrombectomy diminishes in patients with more pervious thrombus composition, which I encourage you to review in addition to our podcast today. Dr. Negar Asdaghi:                        Later in the podcast, I have the distinct honor of interviewing Dr. Claiborne Johnston from Dell Medical School at UT Austin on his latest work with data from the THALES trial to clarify the net ischemic benefits derived from a combination of ticagrelor and aspirin therapy in comparison with the risks of hemorrhage associated with this treatment in patients with mild and moderate stroke and TIA. But first with these two articles. Dr. Negar Asdaghi:                        COVID-19–associated ischemic stroke, or CAIS, is a new term that, unfortunately, stroke physicians need to be familiar with. While acute ischemic stroke can occur in parallel from, say, traditional causes of stroke in patients infected with coronavirus, ischemic stroke and other thrombotic events, such as myocardial infarction, pulmonary embolism, deep vein thrombosis, and acute limb thrombosis, can occur in the setting of overt hyperinflammation and subsequent coagulopathy that is observed in patients hospitalized with severe COVID-19 illness. Dr. Negar Asdaghi:                        Elevated D-dimer, although quite non-specific, has emerged as a marker of COVID-19–associated coagulopathy, but whether an elevated D-dimer in isolation or in combination with various other inflammatory and coagulation markers is associated with development of acute in-hospital ischemic stroke in those hospitalized with COVID is not known. Dr. Negar Asdaghi:                        So, in the current issue of the journal, in the article titled "Biomarkers of Coagulation and Inflammation in COVID-19–Associated Ischemic Stroke,” Dr. Charles Esenwa from the Department of Neurology at Montefiore Medical Center and colleagues did an interesting analysis of over 5,000 patients with COVID-19 who were admitted to one of the Montefiore Health System hospitals between March 1, 2020 and May 8, 2020. This was a retrospective analysis, so they had to work with the available biomarkers for each patient and use a machine learning cluster analysis of these biomarkers to divide the patients basically based on five biomarkers to four clusters. Dr. Negar Asdaghi:                        The following five biomarkers were chosen by this machine learning cluster analysis. These included CRP, D-dimer, LDH, white BC, and PTT. So, they had to come up with some arbitrary rules to exclude biomarkers that were either missing in over 30% of their population, and they also excluded those patients that were hospitalized for a long period of time, and they chose a 30-day hospitalization and over. And they also only used the first reading for each biomarker. Again, these were arbitrary rules that were set forth by the authors, and they found some alarming findings. When they clustered patients based on similarities in these biomarkers, they came up with predicted models for combined thrombotic events and acute ischemic stroke. Dr. Negar Asdaghi:                        For example, in the cluster where the patients had the highest mean values for CRP, D-dimer, LDH, and white BC, and a relatively low PTT, these patients had the highest prevalence of acute ischemic stroke. They had the highest prevalence of in-hospital strokes and severe strokes and highest percentage of total thrombotic events. In contrast, the cluster with the lowest mean of all of these five biomarkers had no cases of in-hospital acute ischemic strokes; they had the lowest prevalence of composite, all thrombotic events, and patients had the least severe complications. Dr. Negar Asdaghi:                        So, they also tested the effects of biomarkers individually for prediction of acute ischemic stroke. And it turns out that when they used a lone marker, only D-dimer again was associated with acute ischemic stroke. Very interestingly, D-dimer was specifically elevated in those COVID-19 patients in whom the stroke was ultimately classified as cryptogenic. Dr. Negar Asdaghi:                        So, what does that mean? That means that it's more likely that a stroke had occurred in the setting of severe COVID-19 hyperinflammatory response, and less likely associated with other classical causes of stroke. Dr. Negar Asdaghi:                        So, what did we learn overall from this study? Well, hospitalized COVID-19 patients with a combination of high CRP, D-dimer, LDH, and white BC, and slight reduction in their PTT, had a 4.5-fold increase in the risk of in-hospital mortality and a fivefold increase in the risk of in-hospital stroke as compared to the COVID-19 patients with the lowest mean values for all the five biomarkers mentioned above. So, important information to keep in mind as we treat hospitalized COVID-19 patients, and we await more prospective data on this topic. Dr. Negar Asdaghi:                        Arteriovenous malformations, or AVMs, are congenital vascular lesions that are associated with long-term excess mortality and morbidity, essentially almost all related to their risk of intracerebral hemorrhage. Roughly half the patients with brain AVMs present with intracerebral hemorrhage, resulting in a first-ever hemorrhage rate of about 0.5 per 100,000 person years. Dr. Negar Asdaghi:                        Annual risk of hemorrhage is estimated at 1 to 4% for all comers with AVMs, but varies significantly, and can be as low as 0.9% in patients with unruptured, superficially located brain AVMs with superficial drainage, but may be as high as over 34% in patients with ruptured, deeply seated brain AVMs with deep venous drainage. So, treatment would entirely be dependent on the type of presentations and characteristics of each patient with an AVM. Dr. Negar Asdaghi:                        Whether unruptured AVMs should be managed clinically or treated either endovascularly or surgically is the subject of the ARUBA trial that is a randomized trial of unruptured brain AVMs. The enrollment of ARUBA was halted by the study's DSMB board, but medical management was found to be superior to treatment arm for the primary outcome of symptomatic stroke and death. Dr. Negar Asdaghi:                        Since then, there's been a lot of focus in the literature and comparison of outcomes between treated and untreated patients with unruptured AVMs, but less has been published on characteristics of patients who suffered from periprocedural stroke, an important part of the primary outcome of ARUBA. So, in the current issue of the journal, we have the study titled “Treatment-Associated Stroke in Patients Undergoing Endovascular Therapy in the ARUBA Trial.” Dr. Negar Asdaghi:                        Dr. Joshua Burks and colleagues from the Department of Neurosurgery at the University of Miami and colleagues evaluated 64 patients with unruptured AVMs enrolled in the ARUBA trial who underwent endovascular treatment as part of the trial and looked at the characteristics of those who suffered a perioperative stroke, defined as a stroke recorded at or within 48 hours of intervention, as this would represent a direct procedure-related complication rather than sequelae of, say, treated or partially treated AVM itself. Dr. Negar Asdaghi:                        All patients who initiated endovascular intervention, including attempted interventions in cases where therapy was aborted secondary to technical or anatomical limitations, were included regardless of randomization or subsequent withdrawal from the study beyond 48 hours following the intervention. So, what they found was that 16% of interventions resulted in stroke, 11% hemorrhagic, and 5% ischemic strokes. And they had no perioperative mortality, which is good news. Dr. Negar Asdaghi:                        In univariate analysis, they found many factors that were more commonly seen in patients that suffered from perioperative stroke as compared to those who did not have a stroke perioperatively. Those factors included, for instance, female sex. Over half of these patients were female. Close to half were enrolled in France. And over 40% of those who suffered a stroke in the perioperative timeframe had Spetzler-Martin grade two AVMs. Dr. Negar Asdaghi:                        When they accounted for all confounding variables, they found that endovascularly treated unruptured AVMs that are supplied by the posterior cerebral artery cortical feeders and those with Spetzler-Martin grade two and three had a higher perioperative stroke risk as compared to their counterparts without these characteristics. Interestingly, there are also significant geographical disparities in the risk of stroke in that patients treated in the United States or Germany had a significantly lower stroke risk than patients treated in other countries. Dr. Negar Asdaghi:                        So, what did we learn from this study? There are patients and lesion characteristics that increase the risk of stroke associated with endovascular treatment of unruptured AVMs. The current study suggests that AVMs with cortical arterial feeders from posterior cerebral artery and those with grade two and three Spetzler-Martin were associated with a higher risk of procedural and periprocedural stroke. Dr. Negar Asdaghi:                        And very importantly, as with every surgical intervention, the risk of a procedure is operator-dependent, as well as center-dependent. And these are important factors to keep in mind as technology evolves and more treatments become available to decide whether to keep or to refer patients with unruptured AVMs to a more experienced center. Dr. Negar Asdaghi:                        Patients with mild ischemic stroke and transient ischemic attack are at high risk of having recurrent ischemic events, especially in the immediate aftermath of their symptom onset. Early diagnosis and initiation of secondary preventive measures, such as antiplatelet or anticoagulation therapies, in the appropriate setting considerably reduce this recurrent risk. Dr. Negar Asdaghi:                        Multiple randomized trials have shown that as compared to treatment with a single antiplatelet agent, dual antiplatelet treatment is more effective in reducing the risk of stroke and other major vascular events in the TIA mild stroke population, a benefit that comes with an expected increase in the risk of hemorrhage. Dr. Negar Asdaghi:                        THALES trial is one of the latest trials to determine the efficacy of dual, which is combination of ticagrelor and aspirin, versus mono-antiplatelet therapy, that is aspirin alone, in eligible patients with non-cardioembolic acute ischemic stroke and TIA. Now, it's important to keep in mind that the primary outcome of THALES is a composite of stroke or death, which included both ischemic and hemorrhagic events. Dr. Negar Asdaghi:                        Now, it's important to understand that while in the setting of a clinical trial, combining the risks associated with dual antiplatelet therapy, which is hemorrhage, and the potential treatment benefit, that is reduction of recurrent ischemic events, is appropriate as part of the outcome selection. In routine practice, this type of primary outcome can obscure the actual trade-offs between the benefits of dual antiplatelet treatment and its inherent hemorrhagic risk. Dr. Negar Asdaghi:                        So, in this issue of the journal, in the study titled "Ischemic Benefit and Hemorrhage Risk of Ticagrelor-Aspirin Versus Aspirin in Patients With Acute Ischemic Stroke or Transient Ischemic Attack," the THALES investigators led by Dr. Claiborne Johnston sought to separate the ischemic benefits of combination of ticagrelor and aspirin therapy from its hemorrhagic risks in patients enrolled in the trial. Dr. Negar Asdaghi:                        I'm joined today by Professor Johnston to discuss the findings of this paper. Dr. Johnston absolutely needs no introduction to the stroke community and our readership. He's a Professor of Neurology at Dell Medical School at the University of Texas at Austin. He's a leader in the field of cerebrovascular disorders, has served as the primary investigator of multiple randomized trials and large prospective studies to evaluate the preventive treatment outcomes in TIA and mild stroke, and has pioneered the development and validation of predictive models for recurrent stroke in this population. He's authored over 700 peer-reviewed manuscripts, has won several awards for research and teaching, and is recognized for his leadership in the field of medicine and healthcare. Dr. Negar Asdaghi:                        Good morning, Clay. We're delighted that you could join us on the podcast. Dr. S. Claiborne Johnston:           Well, thank you. It's wonderful to be here. Thank you for having me. Dr. Negar Asdaghi:                        Thank you. So, THALES is an exciting new addition to the most recent trials of dual antiplatelet therapy that studied mostly the role of clopidogrel and aspirin combination therapy. Can you please start us off by telling us why did we need a new trial in a very similar patient population? Dr. S. Claiborne Johnston:           Well, the primary reason was, yes, clopidogrel works in combination with aspirin in the setting, but clopidogrel is actually a prodrug. It requires conversion in the liver to its active form. And polymorphisms in CYP2C19 and Cyt P450 pathways are really common and associated with an inability or limited ability to convert that prodrug into its active form. So, there are a number of people who may not benefit much, if at all, from clopidogrel. So, it's kind of surprising that it works as well as it does. Dr. S. Claiborne Johnston:           Ticagrelor doesn't have that problem. It's not a prodrug. It acts directly on the P2Y12 inhibitor. And so, the hope was that we would have a more consistent and pronounced effect on risk reduction in patients after TIA and mild to moderate strokes. Dr. Negar Asdaghi:                        Primary efficacy outcome in THALES was different from the primary efficacy outcome chosen for the POINT trial, that was major ischemic events and death from ischemic vascular events, and that of the CHANCE trial, that was a combination of ischemic and hemorrhagic strokes in 90 days. Can you please tell us about the thought process behind choosing this particular primary efficacy outcome in THALES? Dr. S. Claiborne Johnston:           Yeah, so this was encouraged by the regulatory authorities. And so the primary efficacy outcome in THALES is all stroke, hemorrhagic and ischemic, and all death, hemorrhagic and ischemic. And we teased apart just the ischemic etiologies in POINT. Dr. S. Claiborne Johnston:           The rationale was that we were including all the major outcomes that the drug could impact. The problem is that people forget that it includes hemorrhagic events, and then they weigh that efficacy outcome against the safety outcome. And so there's confusion. There's sort of double-counting of safety elements in doing that comparison. Dr. Negar Asdaghi:                        Okay, great. And now, before we hear about how you disentangled the two safety and efficacy outcomes, can you please remind our listeners about the primary results of THALES, which was published obviously a few months ago? Dr. S. Claiborne Johnston:           Yeah, sure. So, it showed that the combination of ticagrelor and aspirin works. It reduced the stroke and death by about 17% over the 30-day period of treatment. So robust effect. There were some increased hemorrhages, and looking at severe hemorrhage as defined by the GUSTO definition, there was almost a fourfold increase, but it was tiny in absolute terms of 0.4% increase. Dr. Negar Asdaghi:                        Okay. So, now it's very important, as you mentioned, this disentangling of recurrent ischemic, again, safety from efficacy outcomes. Your current study that is published in the November issue of Stroke clarified these results. And we're excited to hear about those results. Dr. S. Claiborne Johnston:           That's right. So, there were two problems with the way people have interpreted the results of the THALES trial. One is this entanglement of safety events and both efficacy outcome and the safety outcome. The other was the use of relative risks as opposed to absolute risks, because a high relative risk for a rare event is less important than a small relative risk for a more difference between more common events. And so we wanted to deal with both of those issues. Dr. S. Claiborne Johnston:           So, we defined new outcomes that were not entangled. So, we defined major ischemic events, similar to what we had done in POINT, and then we defined major hemorrhage as being basically irreversible hemorrhage, and compared outcomes in the two groups. And what we found was that when we did it that way, for every 1,000 patients treated, we avoided 12 major ischemic events and produced three major hemorrhages. So, about a four-to-one ratio of ischemic benefit to hemorrhage risk. And that was true at various cutpoints for disability. Dr. S. Claiborne Johnston:           So, if we said, "Okay, yes, you had an event, and are you disabled at last follow-up at 30 days?" Then if we said that, there was also a four-to-one difference in disabling events, ischemic versus hemorrhagic. And if we said a two or greater, so moderate disability or worse, it was the same ratio, four-to-one. Dr. Negar Asdaghi:                        Okay, so four-to-one ratio of benefit. That's an important number to keep in mind. Also reassuring to see that this net clinical benefit or net clinical impact of the combination of therapy was practically the same across all the pre-specified subgroups in the trial. Were you at all surprised by the subgroup analysis? Dr. S. Claiborne Johnston:           Well you know if you do enough subgroup analyses, you're going to find differences, right? And thankfully, we have the looking at interaction terms to keep us honest, but even so, you look at 20 and you're going to have some significant interaction terms, as well. But yeah, it was reassuring that the effects were so consistent across groups. Dr. S. Claiborne Johnston:           I think there's been a tendency to over-interpret results from subgroup analyses. We don't have any evidence to suggest that we should be doing that here. I'm sure we can pick out groups that do better, and we've done that actually. The group with atherosclerosis does particularly well, but is that a chance event or is that real? I think we just have to be super-cautious about subgroup analyses. Dr. Negar Asdaghi:                        So, absolutely. One of the subgroups that I'm personally very interested in is just the time subgroup. So, all of the patients in THALES were enrolled within the first 24 hours, and the subgroup analysis did not show that there were any differences in terms of the net benefit between those that were enrolled earlier, within the first 12 hours, and those that were enrolled later, between 12 and 24 hours. But in routine clinical practice, we often see patients with TIA and mild stroke actually presented to us later than that timeframe entirely. Should we be giving them dual antiplatelet treatment? Dr. S. Claiborne Johnston:           That's a great question. So, we did an analysis in POINT where we modeled out, would we still have an important significant net benefit if we had started the trial later? And we didn't start the trial later, right? So, this was just pretending like anybody who had an event early on was not in the study in starting at a later timepoint and modeling that out. And basically what we found was that for out to three days, there was still a benefit. And, in fact, if you look at that data and look at those tables, you could even say, even out to five days. Dr. S. Claiborne Johnston:           I would say it's not unreasonable to do that given that the risks are so small and they're going to be even later with later treatment. But I would say, too, that even though we're not seeing greater impact within that first 24 hours versus 12 to 24, it just makes sense with event rates being as great as they are early on that if you don't treat with a preventive medication before an event occurs, it doesn't work. So, it just makes sense that as much as possible we ought to treat people as early as possible after their events. Dr. Negar Asdaghi:                        Very important findings and things to keep in mind. I want to ask you about the top two takeaway messages from the study. Dr. S. Claiborne Johnston:           One is that there's a favorable benefit-to-risk ratio for ticagrelor/aspirin in mild to moderate actually ischemic stroke and high-risk TIA from THALES. So that would be number one. Dr. S. Claiborne Johnston:           And then number two is watch your endpoints carefully. Think carefully, too, about whether balancing safety to efficacy events really makes sense and also whether focusing on relative risks really makes sense. I would encourage us, even though our journals tend to push us towards relative risks and we're more familiar with those, I'd encourage us to get more comfortable with using absolute risks in the way we look at data, but also in the way we talk to patients about their impact. Dr. Negar Asdaghi:                        Fair enough. I remember a few years ago, you visited us here at the University of Miami to deliver the annual Cerebrovascular Scheinberg Lecture. And you had mentioned that the idea of dual antiplatelet therapy treatment of patients with TIA mild stroke had come to you many years back when you were still in training, but it took many years for that idea to turn into reality, into randomized trials, and now translated into clinical practice. Dr. Negar Asdaghi:                        At the time, if you recall, this was right before you went to Europe to present the primary results of POINT at the European conference. And the trial results were not publicly available, so you were sworn to secrecy. You couldn't tell us about the results. It's been a few years since then. You've already completed yet another trial on this topic. Can I ask what's next for you and your team as it pertains to acute treatment of patients with TIA and mild stroke? Dr. S. Claiborne Johnston:           Well, there are a few things. So, CHANCE-2 is a really interesting trial. My role in that was peripheral, just really advisory, but it's an exciting trial. So, basically it's looking at people with those CYP2C19 polymorphisms that I mentioned before, people who don't rapidly and readily convert clopidogrel to its active form, and randomizing them to clopidogrel versus ticagrelor. Dr. S. Claiborne Johnston:           So, it's going to give us some head-to-head data on the two drugs and the people who may benefit the most from ticagrelor. And that is complete, and that will be published in the next few months. So, I that's going to be an important trial in people's thinking about how best to approach these patients. Dr. S. Claiborne Johnston:           The second is, you know, we're not done. We still have a 5% risk of events, even in those three dual antiplatelet therapy. And so we need more agents. And we need to think about secondary prevention extending to other groups as well, just as you said, longer periods of time, more severe strokes, people after thrombolysis/thrombectomy. Those are big groups of patients at extreme risk for secondary events, and we have no agents and no data right now. Dr. S. Claiborne Johnston:           I would be concerned about dual antiplatelet therapy in those patients, just given what we've seen about the risks of hemorrhage in the existing groups, which are again manageable and shouldn't change people's decision about treatment. But for the groups I just mentioned, risks of hemorrhage start to get greater. And so one worries about whether dual antiplatelet therapy's the right thing or whether other agents make more sense. So, yeah, we're interested in looking at other agents, some novel, for those other indications as well. Dr. Negar Asdaghi:                        Professor Johnston, thank you for your time, and we look forward to covering more of your research in the future. Dr. S. Claiborne Johnston:           Well, thank you. It's been a pleasure. Dr. Negar Asdaghi:                        Thank you. Dr. Negar Asdaghi:                        And this concludes our podcast for the November 2021 issue of Stroke. Please be sure to check out the November table of contents for a full list of publications, including two important topical review articles, one on thrombus composition after thrombectomy, and one on pearls and pitfalls of perfusion imaging in acute ischemic stroke, as advanced neuroimaging continues to play a critical role in decision-making for acute stroke therapies. Dr. Negar Asdaghi:                        Now, speaking of advanced neuroimaging and the immense role that neuroimaging plays in our day-to-day practice, let's take a moment as we end our November podcast to remember how the concept of medical imaging first began over 120 years ago with the discovery of X-ray by German professor of physics Wilhelm Röntgen. Dr. Negar Asdaghi:                        On Friday, November 8, 1895, while experimenting with electricity, Röntgen accidentally discovered a new kind of rays that he referred to as X-rays. He soon realized that X-rays were capable of passing through most substances, including the soft tissues of the body, but left bones and metals visible. Dr. Negar Asdaghi:                        One of his earliest photographic plates of his experiments was a film of his wife Bertha's hand with her wedding ring clearly visible. This was the first time that the inside of human body was seen without performing surgery. Dr. Negar Asdaghi:                        From Röntgen's first X-ray image to the advanced neuroimaging that we review today on our portable devices, I can't help but wonder, what will your accidental discovery on a Friday fall afternoon in November do to advance the field of science and stroke 100 years from now, as we continue to stay alert with Stroke Alert. Dr. Negar Asdaghi:                        This program is copyright of the American Heart Association, 2021. The opinions expressed by speakers in this podcast are their own and not necessarily those of the editors or of the American Heart Association. For more, visit AHAjournals.org.

Inflammation. We've all heard we should avoid, prevent, and/or reduce it. But, where does inflammation really come from, and which diet is the right one for heading it off at the pass? Is it possible that mitigating this chronic health-threatening condition can be as simple (nobody said EASY...) as managing stress, getting enough sleep, and sustaining an eating and movement lifestyle that feels good? In this episode, Certified Nutritional Coach Rachel Hughes of The Meno Memos does a deep dive into what chronic inflammation really is and how it can affect our health, and offers some simple strategies for heading it off at the pass. We also talk about the hormonal changes happening in a woman's 40s and 50s, menopause symptoms like the dreaded "brain fog", and the disparities in access to quality healthcare that negatively impacts women of color. Our Sponsor Elevate your shoe game with cute styles + amazing comfort. Check out the Brinkley Bootie for walking the dog or running errands on wet, chilly days! Try it on yourself with Vionic's 30 Day Wear Test - return any purchase within 30 days for a full refund, even if it's been worn outside. Get free shipping through Dec. 31, 2021 when you use code MOR at vionicshoes.com. About Rachel Hughes is a mid-life mother, wife, CNC and perimenopausal blogger. She wants to create safe spaces where peri- and menopausal women can help each other navigate these particular years together with honesty, thoughtfulness and a lot of laughter.  Rachel has worked with chronic pain patients for over 10 years; and believes that food, nutrients and movement can be used as powerful tools to help people rebalance and heal themselves from all sorts of physical and physiological challenges, including those driven by fluctuating hormones. With her platform, she hopes to encourage women to inspire each other to dispense stories and insights about everything from food to fashion, career to beauty! Episode Links Be sure to follow along and read Rachel's BlogYou can also follow her on Instagram @themenomemosShare your favorite episode with your friendsFor more from Meagan, you can also follow @meaganfrancis

We're back with another case study from our Integrative Health practice working with real people in the real world…   Our goal is to help people that have struggled for years to discover their underlying root cause imbalances through at-home Functional Medicine lab testing…   And today, we're going to be going through an inflammation case study with a client struggling with hormone imbalances, pain, and mood issues - Enjoy the show and let me know what you thought! - - -   Show Notes & Resources: http://StephenCabral.com/2113 - - - Dr. Cabral's New Book, The Rain Barrel Effect https://amzn.to/2H0W7Ge - - - Join the Community & Get Your Questions Answered: http://CabralSupportGroup.com - - - Dr. Cabral's Most Popular At-Home Lab Tests: > Complete Minerals & Metals Test (Test for mineral imbalances & heavy metal toxicity) - - - > Complete Candida, Metabolic & Vitamins Test (Test for 75 biomarkers including yeast & bacterial gut overgrowth, as well as vitamin levels) - - - > Complete Stress, Mood & Metabolism Test (Discover your complete thyroid, adrenal, hormone, vitamin D & insulin levels) - - - > Complete Stress, Sleep & Hormones Test (Run your adrenal & hormone levels) - - - > Complete Food Sensitivity Test (Find out your hidden food sensitivities) - - - > Complete Omega-3 & Inflammation Test (Discover your levels of inflammation related to your omega-6 to omega-3 levels)

Coach Mike digs into part  on autoimmune health and introduces the next topic of Disordered Eating vs Eating Disorders.  Recapping the autoimmune series actionable steps, important takeaways and opening up the dialogue for the next topic.Timestamp - Podcast Topic Starts at 00:59Resources discussed in this episode:What Is Disordered Eating? (eatright.org)Https://www.eatright.org/health/diseases-and-conditions/eating-disorders/what-is-disordered-eating(Ad) Amazon.com: Everlywell Food Sensitivity Test - Learn How Your Body Responds to 96 Different Foods - at-Home Collection Kit - CLIA-Certified Labs - Ages 18+ (Not Available in NY, NJ, RI) : Health & Household -https:// www.amazon.com/dp/B076QFSJM1?ref=exp_lifeofafighter_dp_vv_d(Ad) Probiotic - Amazon.com: Microbiome Labs MegaSporeBiotic : Health & Household - https://www.amazon.com/dp/B07TJ4TH8Q?ref=exp_lifeofafighter_dp_vv_dGut HealthGut Bacteria (pcrm.org) - https://www.pcrm.org/health-topics/gut-bacteriaGood bacteria for your gut - Mayo Clinic Health System - https://www.mayoclinichealthsystem.org/hometown-health/speaking-of-health/good-bacteria-for-your-gutFermented FoodsFermented foods for better gut health - Harvard HealthThe benefits of probiotics bacteria - Harvard HealthSleep HygieneDoctor's Corner with Dr. Eric Fete: The Importance of Sleep - LOF Podcast 240 (buzzsprout.com) - https://www.buzzsprout.com/50782/5564062-doctor-s-corner-with-dr-eric-fete-the-importance-of-sleep-lof-podcast-240Let's take the guesswork out of health and fitness. For more resource mentioned from our FREE LOF Newsletter, access to the Fitness Vault or 28 Day Nutrition reset or our additional programs, courses, and coaching, as well as our social media and amazon streams/shop Click Here - https://linktr.ee/lifestyle_of_fitnessSupport the show (https://paypal.me/lifeofafighter)Support the show (https://paypal.me/lifeofafighter)

In this episode of the Brawn Body Podcast, Dan is joined by Jimmy St Louis, author, entrepreneur, former NFL Player, Crossfit athlete, and member of the US National Rowing Team! It's safe to say that Jimmy has done it all! Jimmy is the founder of the Cognitive Health Institute, a virtual and onsite, membership-based institute, focused on improving the cognitive health of a wide demographic. The Cognitive Health Institute was created to improve the health and wellness of a wide audience. The treatment protocol focused on gut health to reduce systemic inflammation, thus lowering the likelihood, as well as the symptoms of autoimmune diseases, and neurodegenerative diseases. Jimmy is a strong advocate of a life dedicated to wellness. He is the founder of the lung health institute, as well as the first and only online marketplace to buy and sell franchises, franchise123.com. In addition to his business endeavors, Jimmy played football professionally for the NFL's Tennessee Titans as a tight end and most recently was a member of the 2016 United States Rowing Team. His accomplishments include four national medals as well as a third-place finish in the 2016 Olympic trials. For more on Jimmy and the Cognitive Health Institute, you can visit their website at https://cognitivehealthandwellness.com/ or purchase Jimmy's book on Amazon here: https://www.amazon.com/Cognitive-Health-Wellness-Institute-Anti-Inflammatory/dp/B09CRTR7GR/ref=tmm_pap_swatch_0?_encoding=UTF8&qid=&sr=  To keep up to date with everything we are currently doing on the podcast, be sure to subscribe and follow @brawnbody on social media!  This episode is brought to you by CTM band recovery products - the EXACT soft tissue recovery technology used by Dan. CTM Band was founded by Dr. Kyle Bowling, a sports medicine practitioner who treats professional athletes (and was a guest on the Brawn Body Podcast!).  You can check out their website here: https://ctm.band/collections/ctm-band ... while you're there, be sure to use the coupon code "BRAWN10" for 10% off! --- This episode is sponsored by · Anchor: The easiest way to make a podcast. https://anchor.fm/app --- Send in a voice message: https://anchor.fm/daniel-braun/message Support this podcast: https://anchor.fm/daniel-braun/support

Vitamin D is essential for a healthy gut microbiome—find out why! Vitamin D3 and K2 Vitamin D and Inflammation: https://youtu.be/Q2P6Q76rfEA https://youtu.be/EvGH3kG5u4c FREE COURSE ➜ ➜ https://courses.drberg.com/product/how-to-bulletproof-your-immune-system/ FREE MINI-COURSE ➜ ➜ Take Dr. Berg's Free Keto Mini-Course! ADD YOUR SUCCESS STORY HERE: https://bit.ly/3z9TviS Talk to a Dr. Berg Keto Consultant today and get the help you need on your journey (free consultation). Call 1-540-299-1557 with your questions about Keto, Intermittent Fasting, or the use of Dr. Berg products. Consultants are available Monday through Friday from 8 AM to 10 PM EST. Saturday & Sunday from 9 AM to 6 PM EST. USA Only. Dr. Eric Berg DC Bio: Dr. Berg, 51 years of age 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

Dr Austin Perlmutter, MD is back on the podcast to give us a a complete overhaul of the immune system, inflammation and what we can do to optimise for both.Some types of inflammation are damaging to the body, while others, usually more transient and playing a signaling role, can be beneficial. Chronic inflammation creates reactive oxygen species that damage DNA, cellular proteins, and lipids. This type of inflammation plays a key role in the development of many diseases, including cancer, cardiovascular disease, and diabetes.The immune system is the body's natural defense system. It does not reside in one single part of the body—rather, it is made up of a network of cells, molecules, tissues, and organs working together to protect the body.The most crucial part of this entire podcast?When Austin and I break down the what and the why behind increased inflammation and decreased immunity. We go into strategies and interventions you can use to have a better performing brain and live a healthier life.   Find Austin here on Instagram: @austinperlmutter Thank you to our Sponsors:Eight Sleep- get $150 off using code NEUROMUSE - get 10% off using code NEUROYou can follow me or contact me here ---Newsletter: https://bit.ly/3ewI5P0Instagram: thediamondboss_Twitter : louisanicola_Please leave a review on Apple iTunes!The information provided in this show is not medical advice, nor should it be taken or applied as a replacement for medical advice. The Neuro Experience podcast, its employees, guests and affiliates assume no liability for the application of the information discussed. 

In today's episode, I talk about what happens your immune system kicks in. It can do it for a number of reasons. Pathogens, irritants, or even trauma can all cause your immune system to go on alert. Today we'll find out what happens when it does. --- Support this podcast: https://anchor.fm/generalfitnesscompany/support

00:00 - Skip setup music, catch-up, life in 2021, inflation, do you need a vaccine to live in Mexico? 23:09 - Low testosterone (T) and/or high estrogen/T ratio predict COVID-19 mortality 27:53 - Vitamin D3 anabolic, calcitriol catabolic for muscle/thymus 33:19 - Idealabs update: 10-Methoxy-Harmalan, vitamin K2 in olive oil 58:33 - Endotoxin (LPS) may directly cause cancerization of normal cells 39:53 - Placebo effect plays role in antidepressant impact on anxiety 49:11 - Omega-3 increase risk of atrial fibrillation (afib) 51:53 - PUFA are remarkably estrogenic, toxic to the ovaries 58:08 - Serotonin, SSRI drugs may be the cause of IBD, Parkinson's, diabetes, etc. 01:09:34 - Restoring oxidative metabolism has curative effects on cancer (leukemia) 01:15:18 - Vitamin K3, more idealabs updates, outro

Please join authors Babken Asatryan and Anwar Chahal, and Associate Editor Ntobeko Ntusi as they discuss the Primer article "Inflammation and Immune Response in Arrhythmogenic Cardiomyopathy: State-of-the-Art Review." Dr. Carolyn Lam: Welcome to Circulation on the Run, your weekly podcast summary and backstage pass to the journal and its editors. We're your co-hosts, I'm Dr. Carolyn Lam, associate editor from the National Heart Center and Duke National University of Singapore. Dr. Greg Hundley: And I'm Dr. Greg Hundley, associate editor, director of the Pauley Heart Center at VCU Health at Richmond, Virginia. Well, Carolyn this week, our feature discussion, we're not going to go with one of our original articles, but we are going to feature a primer and a primer is a state of the art review article. The topic is going to be on arrhythmogenic cardiomyopathy and we'll be looking at the role of inflammation and the immune response in arrhythmogenic cardiomyopathy. But before we get to that feature, how about we grab a cup of coffee and talk about some of the other articles in the issue? Would you like to go first? Dr. Carolyn Lam: I would, because guess what? I'm going to be talking about prescription opioids. We know these are a major contributor to the ongoing epidemic of persistent opioid use. What do you think is the incidence after cardiac implantable electronic device procedures? Greg, let's start with a Greg Hundley quiz. I'll give you multiple choice, how about that? Do you think it is 1%, 10%, 25%. 50%? Dr. Greg Hundley: All right, Carolyn, I'm going to guess here. I'm going to go 10%. Dr. Carolyn Lam: Smart. Well, guess what? Today's paper actually gives us insight into that question, it's from Dr. Frankel from the hospital of the university of Pennsylvania and his colleagues, and these authors performed a retrospective cohort study using data from a national Administrative Claims Database from 2004 to 2018 of patients undergoing cardiac implantable electronic device procedures. Adult patients were included if they were opioid naive during the 180 day period before the procedure and did not undergo another procedure with anesthesia in the following 180 days. Dr. Carolyn Lam: Persistent opioid use, which is what we're interested in, was defined by filling an additional opioid prescription more than 30 days following the procedure. So, here's your answer. Of the more than 143,000 patients meeting these inclusion criteria, 11%, so you were right Greg, 11% filled an opioid prescription within 14 days of surgery. Among these patients, persistent opioid use occurred in 12.4% of patients, 30 to 180 days after surgery. The likelihood for developing persistent opioid use was increased for patients who had a history of drug abuse, pre-operative muscle relaxant or benzodiazepine use or opioid use in the prior five years. Also, patients who have prescribed more than 135 milligrams of oral morphine equivalence had a significantly increased risk of persistent opioid use. Dr. Carolyn Lam: Now, this is important because all physicians who perform cardiac implantable electronic device procedures and care for these patients should be aware of the risk of persistent opioid use. This is discussing in editorial by Dr. Kandil from UT Southwestern. Dr. Greg Hundley: Very interesting Carolyn, so connecting sometimes the prescription use of opioids after cardiac implantable electronic devices. Great presentation. Well, my first paper comes to us from the world of preclinical science and it's from our prior editor in chief Dr. Joseph Loscalzo from Brigham and Women's Hospital and the Harvard Medical School. So Carolyn, interferon gamma, producing CD4 positive and CD8 positive T-lymphocytes, have been identified as the predominant pathological cell subsets in human atherosclerotic plaques. Dr. Greg Hundley: While the immunological consequences of these cells have been extensively evaluated, their interferon gamma mediated metabolic effects on endothelial cells remains unknown. So Carolyn, the purpose of this study was to determine the metabolic consequences of the T-lymphocyte cytokine interferon gamma on human coronary artery endothelial cells. Dr. Carolyn Lam: Interesting. So what did Dr. Loscalzo and colleagues find? Dr. Greg Hundley: Right, Carolyn. So, the authors found that interferon gamma impairs endothelial glucose metabolism via altered tryptophan metabolism while depleting NAD plus, which results in a metabolic shift toward increased fatty acid oxidation, and therefore, Carolyn, this work suggests a novel mechanistic basis for pathologic T-lymphocyte endothelial interactions in atherosclerosis, mediated by interferon gamma, linking endothelial glucose, tryptophan, and fatty acid metabolism with NADH and ATP generation and their adverse endothelial functional consequences. Dr. Carolyn Lam: Oh, very nice, Greg. Thank you. The next paper describes a comprehensive characterization of cardiomyopathy caused by filament C truncating variance. Dr. Greg Hundley: Whoa. Okay, Carolyn. Now what is filamin-C? Dr. Carolyn Lam: I thought you may ask and I wasn't going to quiz you, see Greg? The filamin-C gene can cause a striated muscle protein that crosslinks actin and anchors cell membrane proteins to the cytoskeleton, sarcolemmal and sarcomere Z-disc. So, the co-corresponding authors of today's paper Drs. Mestroni and Taylor from University of Colorado, Denver Anschutz Medical Campus, analyzed longitudinal clinical data from an international multicenter cohort of 85 carriers of this filamin-C truncating variants. And this is what they found. Dr. Carolyn Lam: First, the cardiomyopathy associated with filimin-C truncating variants appeared to be a disease with heterogeneous phenotypic presentation, ranging from typical dilated cardiomyopathy to arrhythmogenic, right ventricular cardiomyopathy, and with frequently overlapping forms. Dr. Carolyn Lam: Number two, left ventricular ejection fraction was associated with the risk of death, either all cause or non-arrhythmic, heart transplantation, or LVAD, but not with the risk of sudden cardiac death or major ventricular arrhythmias, highlighting the need for alternative strategies of stratification of the arrhythmic risk in these patients with the filimin-C truncating variant cardiomyopathy. Dr. Carolyn Lam: And number three, this cardiomyopathy was associated with a high risk of ventricular arrhythmias with frequencies of life-threatening ventricular arrhythmias, not significantly different from things like Lamin and desmoplakin cardiomyopathy. Dr. Greg Hundley: Well, Carolyn, just fantastic. My next paper comes to us from Professor Lena Claesson-Welsh from Uppsala University and Carolyn, palmdelphin belongs to the family of paralemmin proteins implicated in cytoskeletal regulation and single nuclide polymorphisms in the palmdelphin locus that result in reduced expression are strong risk factors for development of calcific aortic valve stenosis, and predict the severity of the disease. Dr. Carolyn Lam: Wow, interesting. Palmdelphin, great. So tell us, what did they find and what are the clinical implications please? Dr. Greg Hundley: Right, Carolyn, great question. So first, calcific aortic valves stenosis patients with the single nucleotide polymorphism RS754 3130 express reduce palmdelphin levels in valve endothelial cells, which shows hallmarks of palmdelphin deficiency, such as loss of cytoplasmic RanGAP1, altered nuclear morphology and nuclear rest of P53 of P21. Carolyn, second, gene-regulatory changes affecting actin reorganization, are detected in seemingly healthy regions of calcifying bowels, in agreement with disturbed actin-dependent processes, being an early event, instigating the calcific process. And so Carolyn, the take home message is that palmdelphin is prominently expressed in endothelial cells and the presence of the palmdelphin single nucleotide polymorphism correlated both with a Barrett endothelium and calcific aortic valve stenosis suggesting that endothelial cell dysfunction is essential in development of calcific aortic valve disease. Dr. Carolyn Lam: Oh, wow, wow. Thank you for translating that into the clinical implication. Thanks Greg. Let's maybe discuss what else is in today's issue. There's a prospective piece by Dr. Kirchof entitled “In Patients With Recently Diagnosed Atrial Fibrillation, Think Anticoagulation And Rhythm Control.” There's an exchange of letters between Drs. Liao and Hakala regarding the article Cardiovascular Risk Factor Trajectory Since Childhood And Cognitive Performance In Midlife, The Cardiovascular Risk In Young Finns, study. Dr. Greg Hundley: And Carolyn, I've got a research letter from Professor Ramin entitled “Association Between Sarcomeric Variants In Hypertrophic Cardiomyopathy In Myocardial Oxygenation, Insights From A Novel Oxygen-Sensitive CMR Approach.” Well, how about now we get onto that primer feature discussion relating to arrhythmogenic cardiomyopathy? Dr. Carolyn Lam: Yay. All right, let's go, Greg. Dr. Greg Hundley: Well, listeners, we are now onto our feature discussion and this week we've got a different aspect to the feature discussions. We're going to work through a review article and what we call as a primer. It's one of our state-of-the-art family of publications, where we take a topic and perform a review on a new evolutionary concept that might be occurring in a particular field. This week, we are going to discuss arrhythmogenic cardiomyopathy and we have with us two of the authors of this primer, Dr. Babken Asatryan from Bern, Switzerland and also Dr. Anwar Chahal from Lancaster, Pennsylvania. And of course, as always, we invite one of our associate editors and we have with us this week Ntobeko Ntusi from South Africa. Welcome gentlemen and Babken, let's start with you. Can you give us just a little bit of review regarding arrhythmogenic cardiomyopathy? We hear that term as opposed to arrhythmogenic right ventricular cardiomyopathy, and then maybe also, what are the underlying fundamental histopathologic and pathophysiologic findings associated with this disease? Dr. Babken Asatryan: Thank you, Greg. It's really an absolute pressure being here and thank you for your invitation again. So arrhythmogenic cardiomyopathic is genetically-determined heart disease and the common cause of sudden cardiac death in individuals younger than 40 years of age, it's characterized pathologically by fibrosis and/or fibro fatty infiltration of the myocardium. This infiltration provides a substrate for electrical and stability and leads to ventricular arrhythmias ranging from isolated premature ventricular contractions to sustain ventricular tachycardia and ventricular fibrillation. Live ventricular arrhythmias are cardio manifestations of the orthogenic cardiomyopathy, and they typically occur at early stages of the disease, preceding pathological and functional abnormalities. We call that a concealed stage of the disease. Dr. Babken Asatryan: The typical form for arrhythmogenic cardiomyopathy, which has been previously termed as arrhythmogenic right ventricular cardiomyopathy, primarily affects the right ventricle and has been recognized for decades. Following implementation of postmortem autopsy, increased use of contrast, enhanced cardiac MRI, and improved understanding of the genotype phenotype correlations, more recently cases with more pronounced left ventricular involvement have been discovered as well as cases with biventricular involvement of the disease. Dr. Babken Asatryan: Nowadays, we believe that around 60% of cases have also left ventricular involvement, even if they're diagnosed based on the 2010 task force criteria for arrhythmogenic cardiomyopathy. Causative variants in desmosomal genes are identified in about 60% of patients with typical arrhythmogenic right ventricular cardiomyopathy. Dr. Babken Asatryan: Recently, there have been studies reporting non-desmosomal gene variants in patients with arrhythmogenic right ventricular cardiomyopathy, as well as in those left ventricular and biventricular forms of the disease. But the left ventricular form is quite new to us, so we are learning a lot every day about this disease. Dr. Babken Asatryan: The pathogenesis of this condition appears to be quite complex. We know that these pathogenic variant in desmosomal genes can initiate several pathways and these could be gene dependent. What we do know, that these eventually lead to fibrosis and fibro fatty infiltration of the myocardium, which is the hallmark feature of arrhythmogenic cardiomyopathy. Dr. Greg Hundley: And patients present generally when, in terms of lifespan? Dr. Babken Asatryan: So, patients present in between 30 to 40 years of age, there's a typical presentation for arrhythmogenic cardiomyopathies but young presentations are also common nowadays, particularly. So, programs in families, they usually present 30 to 40 years of age. But in families, we do discover patients who have typical arrhythmogenic right ventricular cardiomyopathy or left and right ventricular involvement were younger at age, but they still need the criteria. Dr. Greg Hundley: And then when we diagnose this condition, do we also need to think about, at least clinically, looking for other affected individuals within a family? Dr. Babken Asatryan: Absolutely. So most of the arrhythmogenic biventricular cardiomyopathy, arrhythmogenic left ventricular cardiomyopathy cases are autosomal dominant diseases. So, this means if an individual carries a pathogenic variant in one of the genes responsible for the condition, the likelihood that the first degree family members will carry the same variant is about 50%. The disease however, presents with reduced penetrance and variable expressivity. Some of the family members may have just arrhythmias and others may develop arrhythmias and structural heart disease. And some of the individuals who carry pathogen occurrence in desmosomal are the genes responsible for the condition may not show phenotype at all. So, that makes the decision-making in families quite challenging. Dr. Greg Hundley: Very nice. Well, thank you so much Babken and now, we're going to turn to one of your co-authors, Anwar and Anwar, in this primer, you start to present a new sort of theme, that inflammation actually may play a role in this disease, at least in terms of adverse events. Can you describe a little bit what your team was thinking here and what took you in this direction and what are some of the research that you've revered here that supports this new line of thinking?   Dr. Anwar Chahal: Thanks, Greg and Ntobeko, for first, the kind invitation to come on this podcast. I must add that I normally listen to the podcast and very much enjoy it, so it's a great honor and privilege for us. Dr. Anwar Chahal: Let me contextualize it, I think it's important to think about what are problems are when we evaluate cases, whether that's the program or the family members, and try to determine what's actually going on. There's been a number of changes over the last 15 years that really evolve around a better understanding and the availability of multimodality imaging, which has altered the way we evaluate these cases. If you look at the 2010 taskforce criteria, for example, they talk about volumetric changes and injection fractions by echo or MRI, and even ventriculogram synapse on fluoroscopy, which I don't think many people do anymore, but they don't mention gadolinium enhancement, and there is an updated version that will come out and talk about that, and the advantages of MRI and even contrast-enhanced CT, and now 18F-FDG, CT PET imaging. Dr. Anwar Chahal: So, the patient journey and the problem that we face is that actually some people present with very unusual features, chest pain, troponin rise, undergo coronary angiography, normal coronary arteries, or unobstructed coronary arteries. We put them through MRI scanners and we see a little bit of gadolinium enhancement. We follow them over the next five years or so, and it develops into taskforce criteria, positive ARVC. So, that's the sort of clinical angle where we've started to see this. Dr. Anwar Chahal: As we put people through scanners, we see the hearts lights up on PET scanners, pretty reproducibly and reliably, that tells us that there's some inflammation there. We look back into the literature and actually very, very early work that was done, autopsy-based, some of it endomyocardial biopsy-based describing lymphocytic infiltrates. Usually that's dry, as you say, or sterile, but there have been reports of even viral pathogens. Dr. Anwar Chahal: That's where it stirred this debate up for us about whether there's this signal that we're seeing there, what is it? What's actually going on? It raises a question, we recognize the other mechanisms, the fiber fatty replacement, the apoptotic pathways, that contribute to that. But there's such variable expressivity with this disease. It's a difficult disease to pin down and it raises a question. What are these other effect modifiers? Is there something else that we do not recognize? And that's really what's driven this. Dr. Anwar Chahal: Our group of co-authors are leaders in the field. Some of them are colleagues in veterinary medicine, Dr. Anna Geltser, and we work together on boxer dog patients. So, she is a practicing vet and a scientist, and has lots of boxer dogs with arrhythmogenic cardiomyopathy. We've been looking at how we could utilize that as a model to test some of the findings that we have in humans and pioneering work really by Bob Hamilton in Toronto, in this paper where they described anti-DSG2 antibodies, which were found not only in humans, whatever the underlying genotype, but also in boxer dogs with arrhythmogenic cardiomyopathy. And that's been followed up with work from Europe, describing anti-heart antibodies, anti-intercalated disk antibodies. Dr. Anwar Chahal: It doesn't really matter what the genotype is, but we're seeing these antibodies there and we're seeing these positive scans indicating inflammation. So the big question is, is this inflammation of primary insult or is it secondary? Is it that the heart in somebody with a genetic cardiomyopathy is predisposed, maybe the remodeling is affected. Bob Hamilton thinks this is probably the best explanation to explain why, whatever the genotype, that these antibodies were positive, that actually that myocardium becomes exposed. The epitope of DSG is now exposed to the immune system, which mounts an antibody response, and hence you see the rise in these antibodies, but it's possible it could it be primary as well. With COVID, and this is a bit of a stretch, so just bear with me there, with COVID we've been recognizing that there's myocardial injury. Dr. Anwar Chahal: There's not as much myocarditis as we expected, but there's been, with virus SARS-CoV-2, we know regular human coronavirus is a recognized cause of viral myocarditis. So, the question really arose are we going to see a lot more of this myocarditis? In our lab discussion, it was, "Well, do you think we're going to see something similar in that we've seen with arrhythmogenic cardiomyopathy, these genetically predisposed individuals are more likely to get invaded? Now, we haven't really seen that with COVID and I won't delve too much into it, but going back to the classical viral infections that we see with myocarditis, here's a really, really interesting biological link. Most of them invade through the desmosome, so with SARS-CoV-2, we see the ACE2 receptors as the way the virus really invades. But with these regular coxsackie virus, for example, parvovirus, a lot of them invade through the desmosome, and that's where we thought, here's a link. Dr. Greg Hundley: Very nice. Ntobeko, you see a lot of papers come across your desk. What attracted you to this group of investigators and this particular review article? Dr. Ntobeko Ntusi: Thank you very much, Greg. I want to start by congratulating Babken, and Anwar for a really fantastic submission, which as an associate editor, was an absolute pleasure to handle. There really are six things that stood out for me about this article. The first one really relates to the question that you ask Babken, which relates to the nomenclature and people have traditionally thought of this is a disease of the right ventricle. I think it's now timely to consider a clear change in nomenclature, that recognizes not only right ventricular involvement, but also left ventricular involvement. And the common finding of biventricular disease in patients with ACM. Dr. Ntobeko Ntusi: The second really important contribution for me from this primer was that we've always thought of arrhythmogenic cardiomyopathies as a genetic disorder with abnormalities in the genes, encoding components of the desmosome. Many groups recently, including our own group that described novel mutations for arrhythmogenic cardiomyopathy in adhering to poultry and other genes outside of the desmosome are showing that the genetic underpinnings are much wider. But the key contribution here is really the consideration of the centrality of inflammation to the pathogenesis of this disease. Anwar has spoken to some length about that, so I won't rehash those comments, but for me, what is key for future work in this area is really to clarify whether the inflammation, as in with many other forms of cardiovascular disease, is merely an epiphenomenon, or whether it plays a critical role in the causal pathway for the phenotypes that we see. Dr. Ntobeko Ntusi: The next important feature for me was the review of the literature and evidence in the association with myocarditis. So, we've seen lots of case reports and small case series showing young people presenting with myocarditis and meeting either the Dallas criteria histologically, or the Lake Louise criteria on imaging, and then subsequent genetic testing confirming the diagnosis of an arrhythmogenic cardiomyopathy. I thought for the first time with quite a compelling review of the link between these two. Dr. Ntobeko Ntusi: The fourth important contribution relates really to the contribution of imaging modalities, both in diagnostics, but critically in risk stratification for this clinical entity. And for me, the importance of cardiovascular magnetic resonance, either with planimetric mapping or late gadolinium enhancement to really add to our ability to predict future events. Dr. Ntobeko Ntusi: Then there's been quite a number of publications in the last five years that have clarified our understanding of the at risk patient with arrhythmogenic cardiomyopathy who's likely to suffer a sudden cardiac death event. This tends to be somebody who was young, who was male, who has a history of documented non-sustained ventricular tachycardia or a history of syncope and on ECG, quite extensive T wave inversion. So again, this is nicely reviewed, and we think about those as candidates who'll benefit from implantation of an ICD. Dr. Ntobeko Ntusi: Then I thought for me, the last really nice contribution from this piece was the review of advancing our understanding of the hot phase. So in all forms of heart muscle disease, we speak of the presentation of patients with the chest pain syndrome, with a troponin leak, but unobstructed coronaries. On further investigation, we don't really find any other evidence of an inflammatory event. We call this a hot phase. And in some case reports in small case series, endomyocardial biopsy has revealed the association of these, whether in TCM, HCM, or arrhythmogenic cardiomyopathy with lymphocytic infiltration. I thought this was all very nicely reviewed. Dr. Ntobeko Ntusi: So, the question that really left me with having read this review, was whether in the future, we may actually need to consider targeting inflammatory pathways as a therapeutic target in this heart muscle disorder. Thanks Greg. Dr. Greg Hundley: Yes. Thanks so much in Ntobeko. You've really led us to the next question that I'm going to ask both Babken and Anwar, you've discussed where do you feel this field is moving and what is the next study or series of studies we need to perform. Babken, first you, and then Anwar. Babken, what do you think is the next study to be performed in this space? Dr. Babken Asatryan: I so much agree with Ntobeko, that perhaps understanding better what can be targeted in these patients, in order to prevent development of phenotype or least to prevent cardiac events, is perhaps the most important next step. In our first figure, we have summarized this potential mechanisms, involving inflammation leading to with arrhythmogenic cardiomyopathy in these patients. We have also highlighted the potential mechanisms that perhaps in the future can be targeted. This could include both targeting the inflammatory cytokines, as well as the primary agents that cause the myocardial inflammation in patients, depending on the results that we will receive over the next years and perhaps animal models should be the next step to better understand how similar arrhythmogenic cardiomyopathy phenotype, where inflammatory contributors to the phenotype are important. And then we can understand whether this can be the same in humans as well. Dr. Greg Hundley: Very nice. And Anwar, do you have anything to add? Dr. Anwar Chahal: Yes. So, agree with that. I guess I would add what are we doing to try to help decipher this? So some of the work that we're doing, I mentioned earlier with the boxer dog patients, who have arrhythmogenic cardiomyopathy. So some of the aspects that we're actually looking at is taking swab cells to see if we can phenotype as a alternative tender myocardial biopsy. And one of the co-authors, Angeliki Asimaki, really pioneered that as a alternative tool because the desmosis are ubiquitous and this may help us phenotype patients better. But also, we want to look at using that as a tool in the pheno copies of arrhythmogenic cardiomyopathy. So we would advocate, re-phenotyping people as well as possible and trying to use some of these techniques. Dr. Anwar Chahal: The next thing we're really looking at is antibody based tools, either working with collaborators, who've already described these antibodies such as anti-DSG2, anti-heart antibody, and anti-skeletal disc to see if we can develop those and perhaps identify others in both human and ox models. And that will then hopefully open the way for us to develop therapeutics that may be able to target those and address that, and maybe use these antibodies as markers to see disease progression, or halting of disease. Dr. Greg Hundley: Very nice. Well listeners, we want to thank Dr. Babken Asatran from Bern, Switzerland, Anwar Chalal from Lancaster, Pennsylvania, and our own associate editor, Ntobeko Ntusi from South Africa, really helping us see this new scientific consideration regarding the potential role of inflammation in causal pathways of adverse manifestations of arrhythmogenic cardiomyopathy. Well, on behalf of Carolyn and myself, we want to wish you a great week and we will catch you next week on the run. This program is copyright of the American Heart Association, 2021. The opinions expressed by speakers in this podcast are their own and not necessarily those of the editors or of the American Heart Association. For more visit ahajournals.org.

Matt Parks, Founder and CEO of One Less CBD discusses CBD and how it can help reduce inflammation that causes pain. MATT PARKS FOUNDER & CEO During his decade as Vice President at Williams Medical Supply, Matt's efforts grew the company from a regional to national supplier while maintaining a steadfast promise to ensure new patients can be serviced. Understanding that his success was a direct result of building long-term relationships, he was imbued with a great appreciation for small business. Also during his time in medical supplying, he observed the rise of the opiate epidemic, a problem he knew stemmed in part from a lack of quality options in chronic pain and inflammation treatment. These experiences united seamlessly guiding his decision to create One Less CBD.  Resources: http://onelesscbd.com/backpain onelesscbd.com The Cox 8 Table by Haven Medical  

Oftentimes low back pain is treated with inappropriate medications, surgery, and other risky interventions. However, medical guidelines say that conservative care should be the first option tried. Join Dr. Rountree and Kristi as they discuss low back pain studies, laser therapy for low back pain, and why surgery should be avoided for some patients.We have begun live-streaming this podcast. Watch this episode on Facebook right here, and see the next episode LIVE in two weeks right here! Studies mentioned in this episode:Photo biomodulation therapy for chronic low back pain: time to move on.Photo biomodulation therapy is not better than placebo in patients with chronic nonspecific low back pain: a randomized placebo-controlled trial.YouTube ChannelLaser Therapy Institute - for PatientsVisit the LTI website for more information and to find a laser therapy provider near you.  Are you a healthcare provider?Laser Therapy Institute Podcast

Today's episode will be the first in a series on the seven stages of Alzheimer's. For the first episode, we are going to be discussing what Alzheimer's is and what the common signs and symptoms are, and how it is being treated today. Then, we'll move on to a brief overview of the seven stages before taking an in-depth look at stages one and two. Now let's move on to the rest of the show.   According to the Alzheimer's Association, Alzheimer's is a type of dementia that affects memory, thinking, and behavior. Symptoms eventually grow severe enough to interfere with daily tasks. Alzheimer's is the most common cause of dementia, a general term for memory loss and other cognitive abilities serious enough to interfere with daily life. Alzheimer's disease accounts for somewhere between 60 and 80 percent of dementia cases.   Alzheimer's is a progressive disease. In most cases, symptoms worsen gradually over several years. After being diagnosed with Alzheimer's disease, a person usually lives anywhere from four to eight years, but in some cases, individuals have lived for over 20 years with Alzheimer's.   Everyone experiences Alzheimer's differently. There are many different signs and symptoms of Alzheimer's that you should be aware of, especially if you are concerned that you or a loved one may be experiencing any of the symptoms.   The Alzheimer's Association lists 10 early signs and symptoms of Alzheimer's that you should be on the lookout for. The first sign they suggest is memory loss that disrupts daily life. As we age, we may begin to forget things and not be able to easily recall information, like names or specific memories, but we may be able to recall the information later. Not being able to recall the information at all is an early sign of Alzheimer's. One example of this is your loved one asking the same question repeatedly because they don't remember asking it or hearing your answer.   The second sign to look for is challenges in planning or problem solving. Trouble keeping track of finances or making a recipe they have made numerous times can both be examples of trouble planning or problem solving. Making the occasional mistake paying bills, however, is not an example of this. Mistakes happen but having an issue figuring out how to pay their bills or adding numbers may be a sign your loved one has Alzheimer's.   Having difficulty completing familiar tasks is the third sign you should be looking for. Not remembering how to drive to a place your loved one has been to many times or not remembering how to write or organize their grocery list how they normally do can be an early sign of Alzheimer's.   Another sign is being confused with times or places. Not knowing what day of the week it is can be an indicator that your loved one is confusing times or places, but it can also just be a normal sign of aging. Not knowing what season it is or not knowing where they are is mainly what we are referring to with this sign.   Trouble understanding visual images and spatial relationships is the fifth sign that the Alzheimer's Association lists. Vision problems unrelated to cataracts can be a sign of Alzheimer's. Having trouble judging distance or being unable to differentiate colors are both examples of this sign. These things can also make driving difficult and possibly unsafe for your loved one as well.   Another early sign to look for is new problems with words in speaking or writing. Someone with Alzheimer's may have trouble following or continuing a conversation. They may forget words or the entire rest of their train of thought. Forgetting a word on its own may not be an early sign of Alzheimer's, but constantly forgetting words or using the wrong word may be a sign your loved one has Alzheimer's.   The seventh sign is misplacing things and losing the ability to retrace steps. For this sign, your loved one will lose things and not be able to figure out how to work backwards to find them. Many people with Alzheimer's also tend to put items in unusual places, such as putting their keys in the freezer. As the disease progresses, they may even accuse others of stealing their things.   Decreased or poor judgement is another early sign of Alzheimer's. Your loved one may begin to make poor decisions frequently, like not bathing regularly or taking care of themselves as well as they should and normally would do. Making one bad decision occasionally, like skipping a shower occasionally, or not filling up their car with gas when they should may not be an early sign of Alzheimer's, but repeated decisions like these can be.   Another early sign of Alzheimer's is withdrawal from work or social activities. This sign goes along with forgetting words and having trouble with conversations. Having difficulties following a conversation may lead to having difficulties in social settings and your loved one may withdrawal from activities they once loved. Occasionally being disinterested in hobbies or visiting with friends or family is not a sign that you loved one is withdrawing from their social life. There are times when you yourself don't feel like being social and your loved one experiences times like those, as well. Continuously withdrawing from social situations is the sign you should be looking for in your loved one.   The tenth and last sign that the Alzheimer's Association mentions is changes in mood and personality. Your loved one may experience moods more strongly than they once did. They may become easily upset when they are uncomfortable and lash out at their friends and loved ones.   If you notice any of these signs or symptoms in your loved one, schedule an appointment with their doctor. They may be experiencing normal age-related symptoms and not symptoms of Alzheimer's or another dementia, but their doctor will be able to determine whether they are showing signs of Alzheimer's. Early detection and diagnosis of Alzheimer's can help their doctor develop a treatment plan that will allow your loved one to maintain their independence longer and help control some of the symptoms right away, making their day-to-day life easier.   Some symptoms of Alzheimer's disease may seem like they are just signs of the normal aging process, but they are not. Increasing age is a risk factor of Alzheimer's, but age itself is not a cause of Alzheimer's. Most cases of Alzheimer's happen after age 65, but some happen before that age. Alzheimer's that happens before age 65 is called younger-onset or early-onset Alzheimer's. Individuals diagnosed with early-onset Alzheimer's can be in any of the seven stages of Alzheimer's at the time of their diagnosis.   As we said previously, early detection of Alzheimer's is crucial. The earlier someone is diagnosed, the faster they can start treatment and get back to enjoying their lives and time with their loved ones. Currently, there is no cure for Alzheimer's, but there are a few ways that doctors can treat the symptoms.   A new drug called aducanumab has recently been approved by the FDA to be used to address the underlying biology of Alzheimer's disease. This drug is a treatment and not a cure. According to the Alzheimer's Association, it is the first therapy to demonstrate that removing amyloid, one of the hallmarks of Alzheimer's disease, from the brain is reasonably likely to reduce cognitive and functional decline in people living with early Alzheimer's.   Approval of this therapy underscores the importance of early detection and accurate diagnosis. Treatment with aducanumab should be initiated in patients with mild cognitive impairment or mild dementia stage of disease, the population in which treatment was initiated in clinical trials.    Aducanumab was studied in people living with early Alzheimer's disease and mild cognitive impairment due to Alzheimer's who showed evidence of a buildup of amyloid plaques in the brain. Because of this, this treatment has not yet been recommended for individuals with middle or end stage Alzheimer's.   Other medications treat the symptoms of Alzheimer's, but not the underlying biology, like aducanumab does. There are medications that help treat cognitive issues, like memory problems, and there are medications that help with behavioral and psychological problems. There are also several clinical trials going on to help improve both memory problems and behavioral and psychological problems due to Alzheimer's.   There are also alternative treatment plans that don't require medication. Some supplements and foods may help improve the symptoms of Alzheimer's. A fairly new idea that we recently talked about in a Quick Tips episode is a Dementia Friendly Community. These communities make it safer for those living with dementia to maintain their independence and help them be a part of society after they have been diagnosed with Alzheimer's. To learn more about treatments for Alzheimer's, talk to your doctor today. They can go over treatment options and recommend a best course of action.   You can also call the Alzheimer's Association 24/7 helpline for any questions you may have regarding Alzheimer's disease. They can be reached at 1-800-272-3900.   Now that we've discussed what Alzheimer's is, what some of the signs and symptoms to look for are, and how it is currently being treated, let's move on to a brief overview of the seven stages of Alzheimer's.   You may be familiar with the three most commonly referred to stages of Alzheimer's, the beginning, middle, and end stages, but today we are going to be expanding upon those and talking about all seven stages of Alzheimer's.   The Global Deterioration Scale for Assessment of Primary Degenerative Dementia, which is what we are referring to as the seven-stage model of Alzheimer's disease progression, was created by Dr. Barry Reisberg to provide caregivers an overview of the stages of cognitive function for those suffering from a primary degenerative dementia such as Alzheimer's disease.   The first stage is referred to as no impairment or before symptoms appear. Changes in the brain are happening during this stage, but no noticeable signs or symptoms will be seen. Because there are no signs or symptoms during this stage, people are not normally diagnosed during stage one.   Dr. Wolk, co-director of the Penn Memory Center states that “this time period — often called ‘pre-clinical Alzheimer's disease' — likely begins 10 or 15 years before people have symptoms. Currently, there is no treatment for this pre-clinical stage, but we hope in the future that we will have medicines that can halt the progress before people have symptoms and prevent the disease.”   The second stage of Alzheimer's tends to show up as a very mild decline in cognitive health. According to Senior Link, in this stage, a person with Alzheimer's disease begins to experience the typical forgetfulness associated with aging. They may forget where they left their car keys or their purse. These symptoms are typically not yet noticed by the individual's family members or physician.   The third stage of dementia shows noticeable memory difficulties and is sometimes referred to as a mild decline. Dr. Wolk explains that “for many, this stage brings noticeable changes, and it will become harder to blame age. It's common to be diagnosed in this stage, because this is when a person's daily routine becomes more disrupted.” These first three stages usually occur prior to a diagnosis. An early diagnosis is usually made in stage three, with early-stage dementia being stage four.   Stage four is known as moderate cognitive decline and, as we just said, is what is usually referred to as early-stage dementia. According to Dr. Wolk, in this stage, damage to the brain often involves other aspects of cognition outside of memory, including some difficulty with language, organization, and calculations. These problems can make it more challenging for your loved one to perform daily tasks. Because of the damage to the brain cells, your loved one may also experience other personality changes, such as feeling suspicious of others, having less interest in things, or feeling depressed. These kinds of symptoms can often be improved with medications.   Stages five and six make up mid-stage dementia. Stage five is known as moderately severe cognitive decline or decreased independence. According to the Premiere Neurology Center, from stages one through four, most people will continue to maintain their independence with only minor challenges. However, during stage 5, independence becomes harder since they begin to forget close friends and family, struggle to learn new skills, and may forget to perform basic tasks, like getting dressed. Additionally, emotional changes are also frequently seen during this stage. This can cause hallucinations, delusions, and/or paranoia.   With stage six comes severe symptoms or severe cognitive decline. Dr. Wolk says that living on your own requires you to be able to respond to your environment, like knowing what to do if the fire alarm goes off or the phone rings. During stage six, this becomes difficult for people with Alzheimer's. Your loved one will be experiencing more significant symptoms at this time, which will impact their ability to manage their own care and they will be more dependent on others.   Late or end stage dementia is also known as stage seven - very severe cognitive decline or a lack of physical control. The Premiere Neurology Center says that the final stage of Alzheimer's disease is when the brain has sustained so much damage that it fails to communicate with other parts of the body, causing mental and physical impairment. During this final stage, people require around the clock care and assistance for even the most basic parts of their daily routine.   Now that you know what the seven stages of Alzheimer's are, let's take a closer look at stages one and two.   Stage one is the preclinical Alzheimer's stage or the no impairment stage. Most people are not diagnosed during this stage, but it isn't impossible to be diagnosed during stage one. According to Healthline, you may only know about your risk for Alzheimer's disease due to family history or your doctor may identify biomarkers that indicate your risk.   Your doctor will interview you about memory problems if you're at risk for Alzheimer's, but there will be no noticeable symptoms during the first stage, which can last for years or decades. Changes in the brain can happen up to fifteen years before any signs or symptoms of Alzheimer's even develop.   While Alzheimer's may be undetectable in stage one, knowing the risk factors of Alzheimer's can help you spot signs and symptoms as soon as they appear, and as we have said a few times today, the earlier you can diagnosis Alzheimer's, the better.   Age, gender, genetics, family history, head trauma, brain abnormalities, smoking, high blood pressure, obesity, limited physical activity, lack of mental activity, and a poor diet are all risk factors for Alzheimer's disease.   According to Healthline, Alzheimer's is not a normal part of growing older. However, age is a risk factor for developing this condition. One in nine people over age 65 and one in three people over 85 have Alzheimer's.   Women are one and half to three times more likely to develop Alzheimer's than men. Healthline also states that Researchers have found two classes of genes related to Alzheimer's. Deterministic genes guarantee that people will develop the disease if they live long enough. Usually, people with deterministic genes will develop Alzheimer's in their 30s, 40s, or 50s. The Mayo Clinic estimates that these genes caused the condition in about five percent of people with Alzheimer's.   People with risk genes may or may not develop the disease. However, they are more likely to develop Alzheimer's than people without risk genes.   If your family has a history of Alzheimer's, you are also at a higher risk. The more family members you have had that had Alzheimer's disease, the higher your risk will be, as well.   Researchers have found that if you have had serious head injuries you are also at a higher risk for Alzheimer's disease. Healthline states that the risk increases if the injury involves losing consciousness or happens repeatedly, such as in contact sports. Along with head trauma, scientists have identified brain abnormalities in people who are likely to later develop Alzheimer's. One is the presence of tiny clumps of protein, also known as plaques. The other is twisted protein strands, or tangles. Inflammation, tissue shrinkage, and loss of connection between brain cells are other clues that Alzheimer's may develop.   Smoking can also increase your risk of developing Alzheimer's, as well as numerous other health problems. High blood pressure is another risk factor tied to Alzheimer's. Researchers have found an especially strong correlation between high blood pressure at middle age and the chances of later developing the disease.   Both obesity and limited physical activity increase your risk of Alzheimer's. Being overweight can double your risk. An article published in Maturitas, an international journal of midlife health and beyond found that exercising twice a week during midlife may lower your risk of developing Alzheimer's.   Lack of mental activity is another risk factor for Alzheimer's. When we challenge our mental capabilities by trying new things and learning new things, playing an instrument, or doing other activities that use our minds, we create internal connections that can help protect against dementia.   Lastly, a poor diet can be a risk factor of Alzheimer's. Eating plenty of fruits and vegetables and other healthy foods can help lower your risk of developing Alzheimer's later in life. Developing healthy habits early on can help you live a longer and healthier life overall.   Now that we've taken a closer look at stage one and some things to look out for while you're younger, let's move on to stage two.   With stage two comes some signs and symptoms that were not visible during stage one. According to Alzheimer's dot net, the senior may notice minor memory problems or lose things around the house, although not to the point where the memory loss can easily be distinguished from normal age-related memory loss. The person will still do well on memory tests and the disease is unlikely to be detected by loved ones or physicians.   Healthline says that Alzheimer's disease affects mainly older adults, over the age of 65 years. At this age, it's common to have slight functional difficulties like forgetfulness. But for stage 2 Alzheimer's, the decline will happen at a greater rate than similarly aged people without Alzheimer's. For example, they may forget familiar words, a family member's name, or where they placed something. During this stage, a loved one may notice symptoms, but not usually the person with Alzheimer's. If you recognize any cognitive decline in your loved one, talk to them about scheduling an appointment with their doctor.   In the next episode in our series we will dive into the next stage of Alzheimer's, which is stage three, noticeable memory difficulties. If you are interested in learning more about Alzheimer's before the next episode airs, visit our YouTube channel where you can find an entire playlist dedicated Alzheimer's and dementia. You can also check out the show notes for this episode for resources we used during this episode.   We want to say thank you for joining us here at All Home Care Matters, All Home Care Matters is here for you and to help families as they navigate these long-term care issues. Please visit us at allhomecarematters.com there is a private secure fillable form there where you can give us feedback, show ideas, or if you have questions. Every form is read and responded to. If you know someone who could benefit from this episode, please make sure to share it with them.   Remember, you can listen to the show on any of your favorite podcast streaming platforms and watch the show on our YouTube channel and make sure to hit that subscribe button, so you'll never miss an episode. We look forward to seeing you next time on All Home Care Matters, thank you.   Sources:   https://www.alz.org/alzheimers-dementia/stages   https://www.alz.org/alzheimers-dementia/10_signs   https://www.alz.org/alzheimers-dementia/what-is-alzheimers   https://www.nia.nih.gov/health/what-are-signs-alzheimers-disease   https://www.pennmedicine.org/updates/blogs/neuroscience-blog/2019/november/stages-of-alzheimers   https://www.alzheimers.net/stages-of-alzheimers-disease   https://www.seniorlink.com/blog/the-7-stages-of-alzheimers   https://premierneurologycenter.com/blog/the-7-stages-of-alzheimers-disease/   https://www.alz.org/alzheimers-dementia/treatments/aducanumab   https://www.alz.org/alzheimers-dementia/treatments   https://www.alz.org/alzheimers-dementia/treatments/medications-for-memory   https://www.fhca.org/members/qi/clinadmin/global.pdf   https://www.healthline.com/health/stages-progression-alzheimers#stage1   https://www.healthline.com/health/alzheimers-disease-risk-factors   https://www.maturitas.org/article/S0378-5122(09)00469-1/fulltext

From Susie and Leanne on The Nutrition Couch this episode: We discuss party tips for the silly season: How to build a delicious, but nutritious, party platter; Our 'Client Case Study' is on inflammation: what it is, how do you know you have it and how do you eat to reduce it? Our 'Product Review of the Week' is on V8 Veggie Juice; And finally, our 'Listener Question of the Week' is about the term ‘lean meat': what does this even mean??   So sit back, relax and enjoy this week's episode!  Don't Miss an Episode   Don't forget to subscribe to the podcast so you never miss an episode and follow us on social media @the_nutrition_couch_podcast to ask us questions & see our food product reviews.  It would mean the world to us if you could leave us a 5 star review in the purple Apple podcast app (scroll to the bottom of the app to find the ratings and reviews) as this really helps push up higher in the charts to expose our podcast to more ears.  Please follow Susie on her Instagram & Facebook and Leanne on her Instagram, TikTok and the Leanne Ward Nutrition Podcast. 

In COVID-19 clinical update #88, Dr. Griffin covers vaccine protection among US veterans, absence of long COVID in vaccinated who are infected, single dose of REGEN-COV monoclonal antibody cocktail provides long term protection, and Pfizer protease inhibitor Paxlovid is 89% effective in preventing hospitalization or death. Hosts: Daniel Griffin and Vincent Racaniello Subscribe (free): iTunes, Google Podcasts, RSS, email Become a patron of TWiV! Links for this episode Vaccine protection of US veterans (Science) Long term protection by REGEN-COV (Regeneron) Pfizer protease inhibitor Paxlovid phase 2/3 results (Pfizer) Letters read on TWiV 828 Timestamps by Jolene. Thanks! Intro music is by Ronald Jenkees Send your questions for Dr. Griffin to daniel@microbe.tv

Chronic, low-grade inflammation has been linked to accelerating the aging process. Ben Van Handel had dedicated the past 10 years of his life learning about this process, also known as "inflammaging," and discovered a molecule that is clinically proven to not only stop inflammaging but protect skin as well. His product, Heraux Molecular Anti-Inflammaging Serum is one of our favorites on the pod, so we brought Ben on to discuss what causes the process, how Heraux works, advancements he's currently working on, and what outside factors contribute to inflammaging overall. Plus, Heraux is offering 25% off their serum to Glamgelenos! Use code GLOSSANGELES on HerauxSkin.com to get your discount 11/12-11/19.Shop all products mentioned in this episodeGlossAngelesPod.comCALL US: 424-341-0426Shop products from our episodesJoin our FB Group: https://www.facebook.com/groups/glossangelespodcastInstagram: @glossangelspod, @kirbiejohnson, @saratanTwitter: @glossangelespod, @kirbiejohnson, @saratanEmail: glossangelespodcast@gmail.com See acast.com/privacy for privacy and opt-out information.

In this fun and insightful episode, leading functional medicine expert, Dr. Will Cole, sits down with his friend, Amanda Chantal Bacon - leader in global wellness, creator and founder of Moon Juice. Her brand-new book The Moon Juice Manual is designed to welcome comfort food into your kitchen, while synergistically working to find balance within your mind-body health. Made from adaptogenic blends of mushrooms and herbs, the Moon Juice recipes embrace a fun, transformative, and refurbishing take on your gut and wellness. Dig in as we break down the science behind adaptogens, and discuss their revolutionary role in crafting a new-age of approachable recipes. Learn more: www.drwillcole.com/podcast Drinklmnt.com/artofbeingwell to claim your free LMNT sample pack Athleticgreens.com/willcole for a free one year supply of vitamin D and to give AG1 a try Choczero.com code WILLCOLE for 20% off you order Publicgoods.com/willcole or use code WILLCOLE at checkout for $15 off your first public goods order Produced by Dear Media.

Coach Mike digs into part 2 on autoimmune health.  Sharing more insight with nutrition, gut health as well as exercise and actionable steps of all the above.Timestamp - Podcast Topic Starts at 3:11Resources discussed in this episode:(Ad) Amazon.com: Everlywell Food Sensitivity Test - Learn How Your Body Responds to 96 Different Foods - at-Home Collection Kit - CLIA-Certified Labs - Ages 18+ (Not Available in NY, NJ, RI) : Health & Household -https:// www.amazon.com/dp/B076QFSJM1?ref=exp_lifeofafighter_dp_vv_d(Ad) Probiotic - Amazon.com: Microbiome Labs MegaSporeBiotic : Health & Household - https://www.amazon.com/dp/B07TJ4TH8Q?ref=exp_lifeofafighter_dp_vv_dGut HealthGut Bacteria (pcrm.org) - https://www.pcrm.org/health-topics/gut-bacteria Good bacteria for your gut - Mayo Clinic Health System - https://www.mayoclinichealthsystem.org/hometown-health/speaking-of-health/good-bacteria-for-your-gutFermented FoodsFermented foods for better gut health - Harvard HealthThe benefits of probiotics bacteria - Harvard HealthSleep HygieneDoctor's Corner with Dr. Eric Fete: The Importance of Sleep - LOF Podcast 240 (buzzsprout.com) - https://www.buzzsprout.com/50782/5564062-doctor-s-corner-with-dr-eric-fete-the-importance-of-sleep-lof-podcast-240Let's take the guesswork out of health and fitness. For more resource mentioned from our FREE LOF Newsletter, access to the Fitness Vault or 28 Day Nutrition reset or our additional programs, courses, and coaching, as well as our social media and amazon streams/shop Click Here - https://linktr.ee/lifestyle_of_fitnessSupport the show (https://paypal.me/lifeofafighter)Here at LOF we don't want finances to be the barrier that holds you back. So we created a variety of resources to help support you from FREE to Paid that can fit your budget and goals. See more here - @Lifestyle_Of_Fitness | Linktree Support the show (https://paypal.me/lifeofafighter)

Madiha Saeed, M.D.: “The things that we put in bodies have a dramatic effect on our behaviors.”  Saeed, a board-certified integrative family physician, joins mbg co-CEO, Jason Wachob to discuss how unchecked inflammation can affect your mental health, plus: - The best foods to support immunity & protect your brain - How to enhance the flavor of your veggies - How gratitude can help reduce inflammation - How your behaviors can actually change other people's brains - How to get more plant-based sources of iron Referenced in the episode: - mbg Podcast episode #292, with Saeed. - Saeed's latest book, The Holistic Rx For Kids. - A study on inflammatory markers and behavioral problems in children. - A study on how junk food affects adolescents' brains. - A study on how fruits and vegetables can support children's mental health. - A study on 400 infants showing how gut bacteria can affect cognition. - A study showing childhood obesity linked to psychosocial & cognitive consequences. - A study showing vitamin D levels during pregnancy associated with higher IQ scores. - Recent research on mirror neurons. Enjoy this episode of the mindbodygreen podcast, sponsored by Emergen-C, the dietary supplement and wellness brand for year-round immune support.* Give it a listen and claim your coupon today!   *This statement has not been evaluated by the Food and Drug Administration. This product is not intended to diagnose, treat, cure, or prevent any disease.

Madiha Saeed, MD is a practicing board certified family physician in Naperville and a traditionally published author of a best-selling book The Holistic Rx: Your Guide to Healing Chronic Inflammation and Disease, the best- selling functional medicine children's book series, Adam's Healing Adventures (one of Dr Mark Hyman's favorite pics), and The Pandemic Prescription: Restoring Hope from Quran, Sunnah and Science. Her upcoming books are The Holistic Rx for Kids: Parenting Healthy Brains and Bodies in a Changing World, Adam's Healing Adventure: The Healing Power of Rainbow Foods and The Quranic Prescription: Living Quran and Sunnah to Optimize Health, Healing and Save Our Future. Today we are going to learn about: What causes inflammation. How inflammation works and why it's at the root of all disease. integrative modalities you can use that include supplementation, homeopathy, and aromatherapy. Future generations: teaching this information to children. We discuss her current books: Holistic Rx & Adam's Healing Adventures and how they are creating an opportunity for health ownership in adults and children alike. You can find Dr. Madiha Saeed: Buy the book: https://holisticmommd.com/book/ Find her on Instagram: https://www.instagram.com/holisticmommd/ Want to see who is coming on next and have the chance to submit questions? Join my private FB community. ION* Gut Support: Get a FREE 3oz bottle with your purchase of a 32oz bottle using the code HOLISTICHOUSE. Make sure to put both items in your cart before checking out! The 3oz bottle isn't automatically added, you have to manually add it to your cart. --- Support this podcast: https://anchor.fm/stephanie-center/support

Join us for another great episode of Mi365 Podcasts. In this podcast, we explore the most medicinal substance on Earth. Back then I didn't know the power of mushrooms, did you? If you want to know how mushrooms can save the world, listen now. Join us as Pete talks about these: Epigenetics, Inflammation, Nutrients, Studies on Ganoderma mushrooms How many people are in the hospital because of lifestyle choices they've made? Every single person should supplement their diet. Why? Because you are malnourished since the food where it comes from is also malnourished "I stand for a lot of things. For greatness. I stand for life. I stand for legacy. But I stand for Ganoderma, I stand for it. I've stood for every single day. I've consumed it every day pretty much for eight and a half years." – Pete Cohen Send us a message and tell us what is your biggest takeaway about this episode. And if you want to get your hands on some Ganoderma let me know. ------------------------------------------------- You can take advantage of our new exclusive free training; "How to get ahead, build long-lasting confidence and stay productive in four simple steps” This reveals; ​Why most people never build true long-lasting confidence and never get to live a happy, healthy life ​The exact strategy productive people use to become a master of their own time ​The tools you NEED to create YOUR BEST YEAR EVER https://coaching.mi365.me/workshop All our podcasts are available at: https://petecohen.com/podcast/ I help everyday people achieve their goals & dreams!  Helping and coaching people in my expertise. It is VERY satisfying to change people's lives so they improve and change their health, finances, relationships, confidence, and mindset.    Connect With Me! Come and join our free Pete Cohen Podcast Facebook Group: https://www.facebook.com/groups/223961357935535/ Follow me on Instagram at https://www.instagram.com/petecohen_/ About Pete Cohen: Pete Cohen is one of the world's leading life coaches and keynote speakers. Hundreds of thousands of people from all over the world have been motivated and inspired by Pete's presentations. He has professionally impacted the lives of thousands of people worldwide, including business executives, professional athletes, and everyday people.  Pete focuses on the importance of closing the gap in our lives between where we are and where we want to be, both personally and professionally.  It's then all about coaching you to remove the obstacles that are in your way and helping you install the habits of success.   Pete is the author of 19 published books, several of which have been best-sellers across the world, including Shut the Duck Up, Habit Busting, Life DIY, and Sort Your Life Out. He has also presented his own show on TV called The Coach and was the resident Life Coach on GMTV for 12 years. His new book Inspirators - Leading The Way In Leadership is available for free here - https://book.petecohen.com/   Check out my brand new 30 Day Kick Start Challenge In just 30 days, I will show you the Exact "Step By Step" Method to redesign your life like the top 1%. Feel extraordinary and take hold of life's boundless opportunities Mi365 30-Day Kick Start Your Life Let me guide, coach, and support you. Just give me 30 days and I'll give you the exact step-by-step method for getting you on your A-game and staying there for 365 days! Every day you'll have access to a new training session, introducing you to a new idea or concept. By investing the time each day, the programme will build over the 30 days to put you in a powerful place in your life.

Over 50% of adults have at least one chronic disease, and often these are fueled by a combination of lifestyle choices and chronic inflammation. Discover the latest research and how you can make an impact on todays episode.Episode Highlights:Understanding acute and chronic inflammationNovoPulse – Where recovery meets performance. Learn more about this new technology that reduces pain and inflammation while improving function to get your patients back to the activities they enjoyUpgrade your EHR today by scheduling a demo at EchiroEHRAutomatically get more leads and conversions from your website with The Smart Chiropractor. Click here to schedule your demo. Our members use research to GROW their practice. Are you interested in increasing your referrals? Discover the best chiropractic marketing you aren't currently using right here!

Can virtual classes help seniors with fall prevention and staying fit? What are the impacts of diet on inflammation and mental health? Jeanne Nichols, PhD and Mark Rapaport, MD detail their respective work in mental and physical well-being. Series: "Stein Institute for Research on Aging" [Health and Medicine] [Show ID: 37593]

Can virtual classes help seniors with fall prevention and staying fit? What are the impacts of diet on inflammation and mental health? Jeanne Nichols, PhD and Mark Rapaport, MD detail their respective work in mental and physical well-being. Series: "Stein Institute for Research on Aging" [Health and Medicine] [Show ID: 37593]

Can virtual classes help seniors with fall prevention and staying fit? What are the impacts of diet on inflammation and mental health? Jeanne Nichols, PhD and Mark Rapaport, MD detail their respective work in mental and physical well-being. Series: "Stein Institute for Research on Aging" [Health and Medicine] [Show ID: 37593]

Can virtual classes help seniors with fall prevention and staying fit? What are the impacts of diet on inflammation and mental health? Jeanne Nichols, PhD and Mark Rapaport, MD detail their respective work in mental and physical well-being. Series: "Stein Institute for Research on Aging" [Health and Medicine] [Show ID: 37593]

In this episode of Vitality Radio Podcast, Jared rants about how the Italian Higher Institute of Health has reduced Italy's total official COVID death toll number by 97%. This is because of a decision to change the definition of a fatality to someone who died from COVID, rather than with COVID. This is all the proof you need about the misrepresentations of deaths for the obvious propagandizing of fear. Jared also Interviews Mike Kramarczyk from HPC Formulas to discuss systemic enzymes, a product called Fibrenza, and how supplementing with systemic enzymes can address fibromyalgia, fibroids, endometriosis, systemic inflammation and more. How you might ask? Systemic enzymes go after proteins that don't belong in our body. They discuss what the differences are between systemic enzymes and digestive enzymes and so much more. This episode is PACKED with information. Call Vitality Nutrition to learn more about how Fibrenza may be a very useful supplement in your daily supplementation.You can follow us at @vitalityradio on Instagram, Facebook and Twitter. Check us out online at vitalitynutrition.com. Let us know your thoughts about this episode by using the hashtag #vitalityradio and please rate and review us on Apple Podcasts. Just a reminder that this podcast is for educational purposes only. The podcast has not been evaluated by the FDA. The information within is not intended to diagnose, treat, cure or prevent any disease. Advice given is not intended to replace the advice of your medical professional.

In COVID-19 clinical update #87, Dr. Griffin reviews PCR cycle threshold and RNA copy number, rapid antigen tests, hospitalization rate after infection or vaccination, allergies and vaccination, community transmission and viral RNA load, early treatment with sotrovimab, meta-analysis of tocilizumab treatment, antibiotic overuse, and guidelines on the use of anticoagulation for thromboprophylaxis. Hosts: Daniel Griffin and Vincent Racaniello Subscribe (free): iTunes, Google Podcasts, RSS, email Become a patron of TWiV! Links for this episode CDC vaccine nod to 5-11 year olds (CDC) Sensitivity of rapid antigen tests (Front Micro) COVID-19 among infected or vaccinated (MMWR) Allergy and vaccination symptoms (JAMA) Community transmission and viral RNA load (Lancet) Early treatment with sotrovimab (NEJM) Tocilizumab treatment meta-analysis (Leukemia) Antibiotic overuse in COVID-19 (Am J Trop Med Hyg) Anticoagulants for thromboprophylaxis (Blood Adv) Letters read on TWiV 826 Timestamps by Jolene. Thanks! Intro music is by Ronald Jenkees Send your questions for Dr. Griffin to daniel@microbe.tv

If you've experienced trauma in your past, know that you're not broken, you're a survivor. Our past experiences can lead to chronic debilitating conditions but they don't have to be a life sentence. Dani Williamson suffered from a number of chronic lifestyle diseases related to her adverse childhood experiences, and now she's on a mission to help people understand how your diet can either heal you or kill you, and how you can overcome what you're suffering from with six steps to living wild and well. [1:05] Adverse experiences and the physical issues that come up from them are contributing to an explosion of depression, disorders, and suicide. Phone calls to suicide crisis headlines have gone up 800% since the beginning of the pandemic. Age 10 to 24 is the fastest growing demographic for suicide. [2:45] Dani grew up in a storm of chaos. Her grandfather died by suicide and her mother attempted to kill herself many times. Dani suffered from chronic diarrhea for years from the stress and 15 years later she was in a bad marriage, diagnosed with lupus, and was on the road to committing suicide. [4:15] Dani's kids were her reason for choosing to continue to live. She packed up and moved and decided to become a nurse practitioner. Despite the improvement in her relationships, Dani was still suffering from several conditions and it wasn't until one doctor, in particular, asked her about her diet did things start to change. [6:20] Checking her food sensitivities changed the trajectory of her career completely. Dani had seen four gastroenterologists before the age of 40 and not one of them asked Dani what she was eating. [6:45] Changing her diet turned her world around. She no longer needed to take medication for lupus or IBS, and she healed the inflammation in her body and now she's on a mission to help other people do the same. [7:35] You can reverse whatever it is that you've turned on from years of chronic dysfunction. [8:30] Adverse childhood experiences don't define us, but they do impact us. Those kinds of experiences can affect the very wiring of your brain. Dani's mother's second marriage was to a child molester who preyed on Dani when she was younger. [9:45] Dani's ACE score was 6. If you have a score of 4 or above, your risk of dying from stroke, heart attack, or suicide goes way up. In Dani's practice, she made the realization that almost all of her patients were suffering from some sort of childhood trauma. Dani now uses the ACE evaluation with every patient in her office. [11:40] Dani recently had a patient with an ACE score of 10 and at the age of 60. [12:35] Dr. Vincent Felitti was an internal medicine doctor and in 1985 noticed that 50% of the participants in his weight loss clinic were dropping out. One day he asked a patient how old they were when they first had sex, and this lead him to the realization that many of his patients had incredibly adverse childhood experiences. [15:00] Dr. Felitti started asking more related questions and developed them into the ACE test. He took the test to a number of different academies and was generally rejected until a person from the CDC recognized the importance of the test and they started one of the largest studies ever on childhood trauma. [16:45] What happens to you before the age of 18 can set you up for a lifetime of chronic lifestyle diseases, depression, suicidal thoughts. Every single chronic lifestyle disease risk is increased by a higher ACE score. [18:30] Every school missed the effect of adverse childhood experiences. Adverse childhood experiences are the single largest public health crisis in the United States and every single pediatrician should be offering this questionnaire.. [19:30] Women are 50% more likely to have an ACE score higher than 5. Your ACE score is directly linked to stress and the hormone cortisol. When cortisol is high chronically, we know that you have a much higher risk of developing an autoimmune disease. [22:50] Dani goes over the 10 ACE questions and how many people assume their experiences are the normal childhood experiences that most people have. [26:50] The ACE score is now a fundamental component of how Dani understands a patient's situation and what may contribute to their issues. [29:15] If you feel triggered right now, this could be your opportunity to recognize what has happened to you and turn things around. Your diet, sleep, and movement define the quality of your life and you can take back control. [31:15] Irregular bowel movements are a clue that you are not eating properly. You should be having a bowel movement once or twice a day, and if that's not the case you need to look at your diet. Your diet controls 90% of your health. [33:30] If your diet is mainly coming from a drive-thru window, you are creating systemic inflammation in your body. Inflammation is the root of every chronic lifestyle disease. [34:45] Many of the people with high ACE scores usually don't have a community around them, and that's a big component of being able to heal. Social interactions reduce stress. We heal in community and in communion with others. [36:30] Giving back to a community takes your mind off your problems and increases oxytocin, one of the most powerful positive hormones in your body. During the pandemic, Dani started hosting physically distanced cookouts each weekend to create a sense of community that was being lost. [38:40] As adults, you have to automate, eliminate, and delegate everything that isn't serving you and your family. [39:40] Dani offers a class to patients before they see her called the six steps to healing. In terms of diet, Dani walks the talk. She started with one small step at a time [40:45] You have to put yourself first because you are worthy of that. It takes time to rewire your brain and beliefs, but when you do and you're running at 100% it trickles down to everything in your life. [42:30] It's also important to find a therapist to help you sort through the trauma in your own life. Don't be afraid to ask if they have a sliding scale if you need to and to find the right therapist for you. [43:40] Dani's book is common-sense practical medicine. She wrote the book so that anyone can understand that garbage in equals garbage out, and that the average person who wants to feel better has a path forward. [45:45] Dani tells the story of a patient suffering from a number of chronic lifestyle diseases, including being morbidly obese and having an ACE score of 9. Between addressing her adverse childhood experiences and finding out what her food sensitivities are, she's turning around her entire world. [50:45] There is no age limit on health. It takes time to change and improve, but when you see the improvements in your life and how you feel, you will feel motivated to stay consistent and keep going. [52:15] Dani and Dr. Cabeca discussthe origin story and benefits of Naltrexone. To find a functional medicine doctor in your area, go to ifm.org or speak to your local compounding pharmacist.       Mentioned in this Episode: daniwilliamson.com youtube.com/thegirlfrienddoctor dranna.com/show     Always seek the advice of your own physician or qualified health professional before starting any treatment or plans. Information found here and results are provided for informational purposes only and are not intended to replace a one-on-one relationship with a qualified healthcare professional and are not intended as medical advice.

Only 1 in 8 of Americans are considered metabolically healthy – a measure of your blood sugar, cholesterol, blood pressure, waist circumference and triglycerides – which is alarming considering metabolic dysfunction is the root cause of many chronic illnesses. WHOOP VP of Performance Kristen Holmes sits down with Dr. Casey Means, a Stanford-trained physician and Chief Medical Officer and Co-Founder of the metabolic health company Levels, for an in-depth discussion on metabolic health. They discuss the prevalence of chronic disease (2:37), inflammation (4:14), chronic illness and lifestyle (6:13), glucose spikes (7:56), metabolic health warning signs (12:55), sleep (17:33), exercise and glucose (25:21), a WHOOP-Levels metabolic health study (28:53), the importance of sleep consistency (39:43), walking after meals (46:33), and why we need to change our lifestyles (50:39). Support the show (http://whoop.com)

Inflammation and inflammatory markers are a huge topic in the gut health world.So I brought the incredible Dr. Tyler Jean on A Gutsy Girl podcast to chat all about it.Inflammatory Markers (and your gut)Resources MentionedDr. Tyler Jean's InstagramChronic Illness Root CauseIBS vs IBD: What's the Difference?Butyrate FoodsPrimal KitchenDr. Tyler Jean's websiteDon't Miss These ThoughtsOur gut health is central to our systemic health. Dr. Tyler JeanThe body has an innate ability to self heal when given the chance.Dr. Jean's personal story and how he came to the world of integrative health.What is chronic inflammation? Dr. Tyler Jean is breaking it down.Chronic inflammation is a symptom that is an adaptive response.What does chronic inflammation have to do with IBS and/or IBD?Symptoms of chronic inflammation3 food categories that cause inflammationWhat Dr. Jean eats on any given dayA sign of good health is being able to tolerate a variety of foods.How to eat sardines (without even knowing it)What is something people get wrong about chronic inflammation?Top things Dr. Jean thinks we can do for gut health.Dr. Jean's top 3 convictions around gut health.Cardinal Signs of InflammationDr. Tyler Jean goes through many different causes of inflammation. Here is a list of xxx he mentions:high blood sugar (hyperglycemia)chronic stresssleep deprivationalcoholinflammatory foodsgut dysbiosisobesitygingivitisnutrient deficienciesFried FoodsSomething I say on the show today and have been talking about more lately is the idea that it's not always the best idea to start with eliminating entire food groups (i.e. gluten, dairy, eggs).Instead, consider cutting things like processed/packaged foods and fried foods first. In other words, cut the ingredient(s) vs the ingredients.Typically that's going to get you much further than arbitrarily cuttingMore from A Gutsy Girl1. Welcome to A Gutsy Girl Podcast2. Hang out on Instagram3. BFF's on YouTube4. Free resource: The Master Gutsy Spreadsheet5. Rated-G Email ClubWrap UpTime to wrap this up. As always, a huge goal for this show is to connect with even more people. Feel free to send an email to our team at podcast@agutsygirl.com. We want to hear questions, comments, show ideas, etc.Did you enjoy this episode? Please drop a comment below or leave a review on Apple Podcasts.Xox,SKH

If you are interested in lipids, you've probably heard of Dave Feldman and his work. If not,  you've got some homework to do, and I think you'll be  amazed at what you find. Dave's work can be found at cholesterolcode.com where he details his multiple, meticulous self-experimental projects. Prior to cholesterol adventures Dave was a senior software scientist and an engineer. He brings this “out of the box” thinking to the world of medicine and we are all better off for it.  He began a low-carb, high-fat diet in April 2015 and has since learned everything he could about it with special emphasis on cholesterol. He saw his own lipid numbers spike substantially after going on the diet and spotted a pattern in the lipid system that's very similar to distributed objects in networks.  Time Stamps: 0:09:20 Podcast begins with Dave Feldman 0:09:45 Responding to the common question: "I feel so good on Animal-Based, but my cholesterol is sky high. What's going on?" 0:20:05 The importance of context in regards to cholesterol  0:26:20 Just because cholesterol is involved in asc sclerosis, that does not mean it is the cause of asc sclerosis 0:33:50 Inflammation and it's role with asc sclerosis 0:36:00 Do we have any experiments that shows LDL is directly harmful to humans? 0:47:05 The more saturated fat you eat, the higher your LDL goes, but does this result in more chronic disease? 0:57:35 PUFA's are essential for humans, but if you're eating saturated fat from grass-fed ruminant animals, you will not become deficient  1:02:44 Familial hypercholesterolemia (FH) and healthy individuals 1:07:40 Macrophages of genetically characterized familial hypercholesterolaemia patients show up‐regulation of LDL‐receptor‐related proteins: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5323824/ 1:14:20 A 72-Year-Old Patient with Longstanding, Untreated Familial Hypercholesterolemia but no Coronary Artery Calcification: A Case Report: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5991918/ 1:15:20 Chimpanzee VS Human LDL 1:15:45 Chimpanzee serum lipoproteins. Isolation, characterisation and comparative aspects of the low density lipoprotein and apolipoprotein-BH: https://pubmed.ncbi.nlm.nih.gov/6477668/ 1:25:05 Distribution of glycosaminoglycans in the intima of human aortas: changes in atherosclerosis and diabetes mellitus: https://pubmed.ncbi.nlm.nih.gov/8477876/ 1:29:20 The importance of hemostasis and how it relates to blood clots 1:35:40 Xanthoma in lean-mass hyper responders who do not have FH 1:40:50 Low Triglycerides–High High-Density Lipoprotein Cholesterol and Risk of Ischemic Heart Disease: https://jamanetwork.com/journals/jamainternalmedicine/fullarticle/647239 1:44:00 Hyperlipidaemia does not impair vascular endothelial function in glycogen storage disease type 1a: https://linkinghub.elsevier.com/retrieve/pii/0021915094900728 1:47:35 If a patient has a rising LDL, but is otherwise healthy, what does Dave suggest? 1:53:00 https://citizensciencefoundation.org/ and where to find more of Dave's work 1:54:30 Dave's current diet Sponsors: Heart & Soil: www.heartandsoil.co  White Oak Pastures: www.Whiteoakpastures.com, use code: CarnivoreMD for 10% off your first order Belcampo: www.belcampo.com use code: CarnivoreMD for 20% off your order Lets Get Checked: 20% off your order at www.TRYLGC.com/paul

My guest today is Dr. Peter Kozlowski, author of UNFUNC YOUR GUT. Dr. Koz practices functional medicine and deals with each patient as a complete picture. He helps patients figure out how to manage or heal c Inflammation, IBS, autoimmune disease, and a myriad of common ailments we can experience, especially living in our modern world. We discuss when is a good time to get your heavy metals tested or SIBO (Small Intestine Bacteria Overload) and how you can really approach Chelation effectively. Dr. Kozlowski offers wonderful guidance and so many useful tips to help support better health, and the best way to approach getting to the bottom of some health issues. Enjoy! Website: www.doc-koz.com Book: Unfunc Your Gut Instagram: @doc_koz INSIDETRACKER -- When you do what you love -- like running, like racing, like enjoying the great outdoors -- you want to do it for life. InsideTracker analyzes your body's data to provide you with a clear picture of what's going on inside you and to offer you science-backed recommendations for positive diet and lifestyle changes. Visit insidetracker.com/gabbyreece for 25% off InsideTracker for a limited time. Learn more about your ad choices. Visit megaphone.fm/adchoices

In this special live-streamed episode of TWiV, Dr. Daniel Griffin fields questions on SARS-CoV-2 and COVID-19 from listeners. Hosts: Daniel Griffin and Vincent Racaniello Subscribe (free): iTunes, Google Podcasts, RSS, email Become a patron of TWiV! Intro music is by Ronald Jenkees Send your questions for Dr. Griffin to daniel@microbe.tv

In COVID-19 clinical update #86, Dr. Griffin discusses virologic features of infection in children, antibody tests should not be used to asses level of protection, test-to-stay programs in schools, FDA authorizes Moderna boosters, results of TOGETHER trial for fluvoxamine, statins and 28 day mortality, and cognitive function in patients. Hosts: Daniel Griffin and Vincent Racaniello Subscribe (free): iTunes, Google Podcasts, RSS, email Become a patron of TWiV! Links for this episode 115,000 healthcare worker deaths (Stat News) Virology features of infection in children (J Inf Dis) Antibody tests not for assessing protection (FDA) Infections in vaccinated healthcare workers (NEJM) Flawed science of antibody testing (JAMA) Test-to-stay in school (US News) Vaccination and non-COVID mortality risk (MMWR) EUA for Moderna booster (FDA) Fact sheet for use of casirivimab and imdevimab (FDA) Effect of early treatment with fluvoxamine (Lancet) Statins and 28-day mortality (J Inf Dis) Cognitive function after COVID-19 (JAMA) Routine vaccination coverage worldwide (MMWR) Letters read on TWiV 823 Timestamps by Jolene. Thanks! Intro music is by Ronald Jenkees Send your questions for Dr. Griffin to daniel@microbe.tv

Content: Facebook, Meta and the Metaverse Ryan Peterson made a difference, supply chain Vitamin D levels and COVID COVID comorbidities, all involve inflammation Inflammation crisis mistaken for COVID crisis AT&T goes full racist, should go out of business If you would like to enjoy this same content plus bonus content from Scott Adams, including micro-lessons … The post Episode 1545 Scott Adams: Let's Talk About AT&T Going Full Racist, Facebook Name Change, Lots More appeared first on Scott Adams Says.

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Get a free Cleaning up Your Mental Mess workbook when you subscribe to my weekly email at drleaf.com! EPISODE DESCRIPTION: In this podcast I talk to leading hormone expert and N.Y. Times best-selling author Dr. Sara Gottfried about hormone balancing and education, how our hormones can impact our mental and physical health, and more! Read the show blog here: https://drleaf.com/blogs/news/how-trauma-impacts-hormones-how-to-use-mind-management-to-treat-hormonal-imbalances For more info on Dr. Gottfried visit: SaraGottfriedMD.com Dr. Gottfried's instagram: @saragottfriedmd Free Gift for Dr. Leaf's subscribers/followers Dr. Gottfried's Guide to Tracking Your Blood Sugar Get my new book Cleaning up Your Mental Mess here: https://www.cleaningupyourmentalmess.com Download my new and improved brain detox app here: https://neurocycle.app Sign up to join my free text program and receive mental health care tips. Just text DRLEAF to 1 (833) 285 3747 Get your tickets to my 2021 Mental Health Retreat: https://www.drleafconference.com OFFERS FROM OUR SPONSORS: -Public Goods: Receive $15 off your first Public Goods order with NO MINIMUM purchase. Just go to https://www.publicgoods.com/DRLEAF. -LMNT: For a limited time, you can claim a free LMNT Sample Pack! For more information and to claim your free offer visit: http://drinklmnt.com/Leaf. -BiOptimizer's Magnesium: For an exclusive offer for my listeners go to http://www.magbreakthrough.com/leaf and use DRLEAF10 during checkout to save 10% on your order PODCAST HIGHLIGHTS 1:30 Why Sara chose to specialize in hormones 4:40 How hormones impact our mental & physical wellbeing 7:50 Cortisol as a mental health marker 12:00 Inflammation & mental health 15:00 Hormones & wellbeing 20:50 Female hormones & health 27:40 Bio-identical hormones 32:50 How our environment can impact our hormones 34:00 Testosterone & the female body 35:30 How trauma can impact our hormones 40:00 The importance of mind management for hormonal health 45:10 Social media, diet culture & hormones ADDITIONAL RESOURCES: -Visit my website at https://drleaf.com for more free resources Follow me on social media for daily mental health tips & strategies: -Instagram: @drcarolineleaf: https://www.instagram.com/drcarolineleaf/- -Facebook: Dr. Caroline Leaf: https://www.facebook.com/drleaf -Twitter: @drcarolineleaf: https://twitter.com/DrCarolineLeaf -Youtube: https://www.youtube.com/drcarolineleaf --- This episode is sponsored by · Anchor: The easiest way to make a podcast. https://anchor.fm/app