Podcasts about tumors

Circulating tumor DNA (ctDNA), a minimally invasive blood-based biomarker, has emerged as one of the most promising advances in cancer surveillance. Today, we will explore how ctDNA is transforming the management of colorectal cancer and anal squamous cell cancer across the disease continuum—from risk stratification and adjuvant therapy decision-making to surveillance and early detection of recurrence. Through landmark clinical trials, real-world applications, and emerging research, we will examine how ctDNA is helping move cancer care closer to the goal of truly personalized medicine.Hosts: ·       Dr. Janet Alvarez - General Surgery Resident at New York Medical College/Metropolitan Hospital Center·       Dr. Wini Zambare – General Surgery Resident at Weill Cornell Medical Center/New York Presbyterian·       Dr. Philip Bauer, Assistant Professor of Surgery, Division of Colon and Rectal Surgery, The Ohio State University Wexner Medical Center, Arthur G. James Cancer Hospital·       Dr. J. Joshua Smith MD, PhD, Chair, Department of Colon and Rectal Surgery at MD Anderson Cancer CenterGuests:Dr. Paul Romessor ·      Director of Colorectal and Anal Cancer, Department of Radiation Oncology·      Associate Attending Radiation OncologistMemorial Sloan Kettering Cancer CenterDr. Jeanne Tie ·      Medical Oncologist | Lower GI Unit ·      Lower GI Research Lead ·      Chair | Lower GI Working Party | GI Cancer TrialsPeter MacCallum Cancer Centre Dr. Takayuki Yoshino·      Professor, Global Center of Research Excellence for Advanced Medicine (G-CORE),Keio University School of Medicine·      Executive Advisor to Hospital East Director·      Director, Department of Global Oncology·      Chief, Department of Gastrointestinal OncologyNational Cancer Center Hospital EastLearning Objectives:·      Describe the biological basis and clinical applications of circulating tumor DNA (ctDNA) as a biomarker of minimal residual disease (MRD) in colorectal cancer.·      Interpret the prognostic significance of postoperative and longitudinal ctDNA testing and its role in predicting recurrence risk across stages of colorectal cancer.·      Evaluate evidence from landmark clinical trials, including DYNAMIC and GALAXY, supporting ctDNA-guided treatment de-escalation and escalation strategies in colorectal cancer.·      Discuss emerging applications of ctDNA monitoring in personalized cancer care, including surveillance, treatment response assessment, and future clinical trial directions. References:·      Ando, K. et al. (2026). Molecular Residual Disease and Recurrence in Rectal Cancer Patients Undergoing Upfront Surgery: A Prospective Cohort Study. Annals of Surgery. https://pubmed.ncbi.nlm.nih.gov/39854721/ (Note: If direct access is limited, the article is available via PMC: PMC12695342)·      Romesser, P. B. et al. (2026). Tumor-informed circulating tumor DNA stratifies recurrence risk and survival in anal squamous cell carcinoma. Nature Communications. https://pubmed.ncbi.nlm.nih.gov/38347209/·      Tie, J. et al. (2025). Circulating tumor DNA analysis guiding adjuvant therapy in stage II colon cancer: 5-year outcomes of the randomized DYNAMIC trial. Nature Medicine. https://pubmed.ncbi.nlm.nih.gov/39943485/·      Tie, J. et al. (2025). Circulating tumor DNA-guided adjuvant therapy in locally advanced colon cancer: the randomized phase 2/3 DYNAMIC-III trial. Nature Medicine. https://pubmed.ncbi.nlm.nih.gov/39974258/Please visit https://behindtheknife.org to access other high-yield surgical education podcasts, videos and more.  If you liked this episode, check out our recent episodes here: https://behindtheknife.org/listenBehind the Knife Premium: https://behindtheknife.org/premiumOral Board Review: https://behindtheknife.org/oral-boardOral Board Simulator: https://behindtheknife.org/oral-board/simulatorGeneral Surgery Oral Board Review Course: https://behindtheknife.org/premium/general-surgery-oral-board-reviewTrauma Surgery Video Atlas: https://behindtheknife.org/premium/trauma-surgery-video-atlasDominate Surgery: A High-Yield Guide to Your Surgery Clerkship: https://behindtheknife.org/premium/dominate-surgery-a-high-yield-guide-to-your-surgery-clerkshipDominate Surgery for APPs: A High-Yield Guide to Your Surgery Rotation: https://behindtheknife.org/premium/dominate-surgery-for-apps-a-high-yield-guide-to-your-surgery-rotationVascular Surgery Oral Board Review Course: https://behindtheknife.org/premium/vascular-surgery-oral-board-reviewColorectal Surgery Oral Board Review Course: https://behindtheknife.org/premium/colorectal-surgery-oral-board-reviewSurgical Oncology Oral Board Review Course: https://behindtheknife.org/premium/surgical-oncology-oral-board-reviewCardiothoracic Oral Board Review Course: https://behindtheknife.org/premium/cardiothoracic-surgery-oral-board-reviewDownload our App:Apple App Store: https://apps.apple.com/us/app/behind-the-knife/id1672420049Android/Google Play: https://play.google.com/store/apps/details?id=com.btk.app&hl=en_US

Highlights from the PER® CME activity "Tumor Board: Evolving Immunotherapy Strategies for Stage I-III NSCLC" — this podcast is not certified for credit. To participate in the full accredited activity and earn CME credit, use the link below.In this podcast, experts Tina Cascone, MD, PhD; Puneeth Iyengar, MD, PhD; and Paula A. Ugalde Figueroa, MD; discuss evolving immunotherapy strategies for stage I to III non–small cell lung cancer (NSCLC), spanning surgical work-up and the shifting definition of resectability, perioperative immunotherapy trial data, the way that pathologic response guides treatment decisions, and the integration of radiation with immunotherapy in unresectable disease.Earn CME credit by completing the full accredited activity (available through June 30, 2027): https://www.gotoper.com/courses/tumor-board-evolving-immunotherapy-strategies-for-stage-i-iii-nsclc-1This podcast, including the narration, was developed by PER® (Physicians' Education Resource®, LLC) editorial staff from the full online CME activity developed with these faculty. The narration was voiced by a PER staff member or by an AI tool. The podcast contains no product advertising. The full activity is supported by an educational grant from AstraZeneca Pharmaceuticals.This content is for educational purposes only and is not a substitute for the independent clinical judgment of a health care professional. Faculty may discuss investigational or off-label uses; consult prescribing information for any products discussed.

Bem-vindo à Rádio Minghui. As transmissões incluem assuntos relativos à perseguição ao Falun Gong na China, entendimentos e experiências dos praticantes adquiridas no curso de seus cultivos, interesses e música composta e executada pelos praticantes do Dafa. “Vida e esperança renovadas – o poder curativo do Falun Dafa” é um livro compilado a partir de diversos casos notáveis de cura e recuperação integral da saúde devido à prática e o cultivo do Falun Dafa. Os relatos daqueles que se curaram, revelam a preciosidade e o poder altamente curativo do Falun Dafa, quando seus princípios e métodos são aplicados corretamente. Episódio 8: Tumor no cérebro e doença óssea desapareceram.

Aunque tiene 70 años de carrera y desde hace dos necesita un doble trasplante de pulmón, Jorge Ortiz de Pinedo se mantiene activo en el medio artístico donde debutó a los ocho años, a instancias de sus padres Don Oscar Ortiz de Pinedo y de su madre Lupita Pallás.

Rebecca's story is one of extraordinary resilience. What began as a routine induction quickly turned into a life-threatening postpartum emergency, followed by the discovery of a rare orbital tumor, multiple surgeries, and a long road through PTSD and healing. In this heartfelt Listener Series episode, Rebecca shares how community, therapy, faith, and giving back helped her reclaim her life after birth trauma. If you've ever felt like your trauma became your identity, this conversation offers hope that healing is possible, even if it takes time.In this episode, we discuss:✨ Rebecca's difficult second pregnancy and the unexpected vision changes that led to the discovery of an orbital tumor

Highlights from the PER® CME activity "Tumor Board: Optimizing NSCLC Care—Leveraging the Latest Evidence on Targeted Therapy and Immuno-Oncology" — this podcast is not certified for credit. To participate in the full accredited activity and earn CME credit, use the link below.In this podcast, experts Justin Gainor, MD; Julia Rotow, MD; and Urs Weber, MD; discuss targeted therapies and immunotherapy to treat advanced non-small cell lung cancer (NSCLC).Earn CME credit by completing the full accredited activity (available through June 29, 2027): https://www.gotoper.com/courses/tumor-board-optimizing-nsclc-careleveraging-the-latest-evidence-on-targeted-therapy-and-immuno-oncology-1fgrThis podcast, including the narration, was developed by PER® (Physicians' Education Resource®, LLC) editorial staff from the full online CME activity developed with these faculty. The narration was voiced by a PER staff member or by an AI tool. The podcast contains no product advertising. The full activity is supported by educational grants from BioNTech; Iovance Biotherapeutics, Inc; Lilly; Nuvation Bio; Revolution Medicines, Inc; and Rigel Pharmaceuticals.This content is for educational purposes only and is not a substitute for the independent clinical judgment of a health care professional. Faculty may discuss investigational or off-label uses; consult prescribing information for any products discussed.

When we talk about EMF and cancer, the conversation usually focuses on risk. But what if electromagnetic fields could actually help treat cancer? In this episode, I break down a fascinating new study showing how pulsed electromagnetic field therapy altered the genetic profile of bladder cancer cells in the lab -- and what this tells us about the complex relationship between EMF and human biology. This isn't about fear. It's about understanding how the same technology that requires caution in one context might offer therapeutic benefits in another. In This Episode How pulsed electromagnetic fields changed gene expression in bladder cancer cells Why the same technology that poses risks can also treat disease What FDA-approved cancer treatments already use electromagnetic fields The key difference between therapeutic EMF and everyday exposure Featured Study Read the full study: Pulsed Electromagnetic Field Therapy Alters the Genomic Profile of Bladder Cancer Cell Line HT-1197 See all studies at shieldyourbody.com/research

Reciben a 656 mexicanos deportados de EE. UU.  Protestas en Maine tras operativo del ICE  Francia le dio al mundo el sistema métrico   Más información en nuestro podcast#grc

Gastrointestinal stromal tumors (GISTs) are the most common mesenchymal tumors of the digestive tract. Although many GISTs can be effectively treated with targeted therapies, their response to treatment depends largely on the specific genetic alterations driving tumor growth. Advances in molecular testing have transformed the management of these tumors, allowing clinicians to tailor treatment based on each patient's genetic profile. A case report published in Volume 17 of Oncotarget, titled “Small bowel GIST harboring concurrent KIT exon 9 duplication and SDHC mutation: A case report,” describes an exceptionally rare case involving a patient whose tumor carried two genetic alterations that are traditionally considered mutually exclusive. Full blog post - https://www.oncotarget.org/2026/07/13/rare-genetic-combination-in-gastrointestinal-tumor-offers-new-insights-into-precision-cancer-care/ DOI - https://doi.org/10.18632/oncotarget.28863 Correspondence to - Joseph G. Crompton - jcrompton@mednet.ucla.edu Abstract video - https://www.youtube.com/watch?v=eB_QG2vBNCE Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28863 Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/ Keywords - cancer, GIST, KIT duplication, SDHC mutation, genetic testing, case report To learn more about Oncotarget, please visit https://www.oncotarget.com and connect with us: Facebook - https://www.facebook.com/Oncotarget/ X - https://twitter.com/oncotarget Instagram - https://www.instagram.com/oncotargetjrnl/ YouTube - https://www.youtube.com/@OncotargetJournal LinkedIn - https://www.linkedin.com/company/oncotarget Pinterest - https://www.pinterest.com/oncotarget/ Reddit - https://www.reddit.com/user/Oncotarget/ Spotify - https://open.spotify.com/show/0gRwT6BqYWJzxzmjPJwtVh MEDIA@IMPACTJOURNALS.COM

Krebs zählt zu den größten medizinischen Herausforderungen unserer Zeit. Doch noch nie waren die Möglichkeiten, eine Krebserkrankung zu erkennen, gezielt zu behandeln und langfristig zu kontrollieren, so vielfältig wie heute. Die moderne Krebsmedizin verbindet hochpräzise Diagnostik mit innovativen Therapien, die individuell auf die biologischen Eigenschaften eines Tumors und die Bedürfnisse jedes einzelnen Patienten abgestimmt werden. In unserer heutigen Folge gewähren wir einen Einblick in die wichtigsten Entwicklungen der modernen Krebsmedizin.

This episode is sponosored by Hulu. Stream PRISON BREAK on Hulu in the U.S. and Disney+ Internationally. Sarah Wayne Callies and Paul Adelstein discuss Prison Break episode 407, “Five the Hard Way,” opening with an explanation of the craps term “hard way” before reflecting on the production's Las Vegas shoot at the newly opened Planet Hollywood, including staying and filming on-site, the surreal “bubble” of casino life, and practical details like overheated door handles and early-morning casino atmosphere. They highlight comedic beats (including the Carrot Top gag), wardrobe and continuity decisions around Sara's outfits and scars, and debate story choices such as Sara's repeated honeypot attempts and the episode's “gay panic” pivot to Sucre, criticizing its logic and gender imbalance while noting how such writing would differ today. Callies shares a vivid on-set memory tied to postpartum depression, describing how it affected her behavior, went unrecognized for years, and later improved after seeking acupuncture and herbal support. They also touch on T-Bag and Gretchen's dynamic and briefly discuss TV scoring trends and how music guides audience engagement. For the full experience of enjoying Prison Breaking With Sarah & Paul, subscribe to our Patreon channel where you can watch Sarah & Paul's running commentary on Ep 306 while re-watching the episode on Hulu or your home DVD collection. You can also watch in a group with other fans on our fan-led Discord server. Subscribe here: ⁠⁠⁠⁠https://patreon.com/user?u=116411884⁠⁠⁠⁠ -or- Click Link in Bio Patreon Subscribers get access to all of our Watch Parties and FanFiction (all captioned in six languages - English, French, Spanish, German, Portuguese, and Turkish), exclusive Ask Me Anything's with Sarah & Paul, and unannounced Discord drop-ins on our always rollicking server with fans and friends who come together from around the world. All for less than a cup of coffee. Leave us your comments, shoot us an email, or leave us a voicemail - we love hearing from all of you! prisonbreaking@caliber-studio.com (401) 3-PBREAK Watch the episode on YouTube - / @prisonbreakpodcast Follow us on Instagram - / prisonbreakpodcast Follow us on TikTok - / prisonbreakpodcast Merch!!! - https://pbmerch.printify.me/products #fyp #michaelscofield #saratancredi #michealscofield #prisonbreakedits #prisonbreak #wentworthmilleredits #wentworthmiller #editor #fyy #fyppp #saratancrediedit #prisonbreakseason1 #sarahwaynecallies #prisonbreakseason2 #scofield #fy #sarascofield #saratancrediedits #scofield Logo design by John Nunziatto @ Little Big Brands. If you want one yourself, reach out at https://www.littlebigbrands.com/ and tell him we sent you. PRISON BREAKING WITH SARAH & PAUL is a Caliber Studio production. Learn more about your ad choices. Visit megaphone.fm/adchoices

Host: Darryl S. Chutka, M.D.  Guests: Jake Eide, M.D. & Rijul Kshirsager, M.D.  Skull base tumors are not commonly seen in a primary care practice, yet it's important for us to recognize them when they do present. These tumors can be either benign or malignant, however because of their proximity to important structures in the brain, even benign tumors can cause serious complications. Their presentation can be subtle, and they are frequently mistaken for other more commonly seen health problems. Which presenting symptoms should give us concern? What are some common physical exam findings associated with these tumors, and what's the best initial imaging study to order? These are some of the questions I'll be asking my guests, Dr. Jake Eide and Dr. Rijul Kshirsagar, both surgeons in the Department of Otorhinolaryngology at the Mayo Clinic as we tackle “Skull Base Tumors.”  Connect with us! Mayo Clinic Talks Podcast Season 6 | Mayo Clinic School of Continuous Professional Development 

BUFFALO, NY – July 6, 2026 – A new #casereport was #published in Volume 17 of Oncotarget on July 2, 2026, titled “Renal oncocytoma: Α case report and literature review.” The study was led by first and corresponding author Areti Kalfoutzou from the Second Propaedeutic Department of Internal Medicine, Attikon General Hospital, National and Kapodistrian University of Athens, Greece. Renal oncocytoma is a rare benign tumor of the kidney that accounts for approximately 5–9% of renal epithelial tumors. Although it is considered benign, it often resembles kidney cancer on imaging studies, making accurate diagnosis challenging. Because treatment strategies differ substantially between benign oncocytoma and malignant renal tumors, establishing the correct diagnosis is essential to avoid unnecessary surgery while ensuring appropriate patient care. In this report, the researchers describe the case of an 82-year-old woman who presented with two months of gross hematuria. Contrast-enhanced computed tomography (CT) identified a 55 × 34 mm exophytic lesion arising from the upper pole of the left kidney. Based on its imaging characteristics, the mass was initially classified as a Bosniak category IV renal lesion, raising strong suspicion for renal malignancy. Full press release - https://www.oncotarget.net/2026/07/06/rare-benign-kidney-tumor-case-highlights-value-of-biopsy-and-minimally-invasive-treatment/ DOI - https://doi.org/10.18632/oncotarget.28893 Correspondence to - Areti Kalfoutzou - areti.kalfoutzou@haf.gr Abstract video - https://www.youtube.com/watch?v=C7TBLT3tbfA Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28893 Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/ Keywords - cancer, cryoablation, image-guided biopsy, kidney neoplasms, minimally invasive surgery, renal oncocytoma To learn more about Oncotarget, please visit https://www.oncotarget.com and connect with us: Facebook - https://www.facebook.com/Oncotarget/ X - https://twitter.com/oncotarget Instagram - https://www.instagram.com/oncotargetjrnl/ YouTube - https://www.youtube.com/@OncotargetJournal LinkedIn - https://www.linkedin.com/company/oncotarget Pinterest - https://www.pinterest.com/oncotarget/ Reddit - https://www.reddit.com/user/Oncotarget/ Spotify - https://open.spotify.com/show/0gRwT6BqYWJzxzmjPJwtVh MEDIA@IMPACTJOURNALS.COM

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In this episode of It Takes Balls, Tony Florio shares one of the most unusual testicular cancer stories featured on the podcast. An attorney, husband, and father of two young kids, Tony was on paternity leave when he developed a persistent ache in his lower abdomen. There was no lump, no testicular pain, and no obvious signs of testicular cancer, just a nagging discomfort that refused to go away.After a CT scan revealed a large abdominal mass, doctors initially suspected a sarcoma or paraganglioma, two diagnoses with far different prognoses than testicular cancer. Even after a scrotal ultrasound came back normal, Tony continued searching for answers. Using AI tools to better understand his medical reports and advocating for additional testing, he pushed for tumor markers that ultimately helped point his medical team in a different direction.Tony underwent major surgery to remove a retroperitoneal mass, entering the operating room knowing he could potentially lose part of his colon or even a kidney. Fortunately, the surgery was successful, and pathology revealed what nobody initially expected: a germ cell tumor consisting primarily of teratoma, embryonal carcinoma, and yolk sac tumor components. Even more unusual, doctors never found a tumor in either testicle, leaving questions about whether his cancer represented a burned-out testicular cancer or a rare extragonadal germ cell tumor.The episode also explores the emotional side of facing cancer while raising two young children. Tony reflects on the fear of not being there for his family, the support he received from his wife, friends, and neighbors, and the faith that helped carry him through the most uncertain moments. He also discusses postoperative complications, including a painful pneumothorax that landed him back in the hospital, as well as the surprising recommendation from his tumor board.This conversation is a powerful reminder that testicular cancer symptoms don't always start in the testicle, that self-advocacy matters, and that sometimes the most important part of the journey is simply getting the right diagnosis. Whether you're navigating a recent diagnosis, interested in rare presentations of germ cell tumors, or looking for hope during surveillance, Tony's story offers insight, perspective, and encouragement.Provide your feedback on the podcast:https://www.testicularcancerawarenessfoundation.org/itbsurveyJoin The Ball Room:https://www.testicularcancerawarenessfoundation.org/theballroomWant to be a guest? Apply here:https://www.testicularcancerawarenessfoundation.org/it-takes-balls-submissionsFollow Testicular Cancer Awareness Foundation:⁠https://www.testescancer.orghttps://www.x.com/testescancer⁠⁠https://www.instagram.com/testescancerhttps://www.facebook.com/tca.orgFollow Steven Crocker:https://www.instagram.com/stevencrockerhttps://www.facebook.com/steven.crocker2Theme song: No Time Like Now - Tom Willner www.tomwillner.com

Glioblastoma is considered one of the most aggressive brain cancers, with survival often limited to about a year, largely because tumors adapt by rewiring how they use nutrients and energy Tumors divert vitamin B3 (niacinamide) away from normal energy production into a pathway that supports their survival, suggesting a metabolic weakness that could potentially be targeted This altered pathway may drain key cellular resources, meaning cancer cells appear to burn through materials they need to grow, which may create an opportunity to disrupt their fuel supply In a Science Advances study, high-dose vitamin B3 therapy was associated with improved short-term outcomes in patients, with over 80% showing no disease progression at six months in early findings, along with stronger immune activity against tumors Supporting your body's energy production and immune response through diet, lifestyle, and structured nutrient intake may help influence the same metabolic systems cancer depends on

Immune discusses a snippet on how EBV infection alters the immunopeptidome and promotes multiple sclerosis, and a paper on head and neck cancers harboring bacteria that create an immunosuppressive environment and promote immunotherapy resistance. Hosts: Vincent Racaniello, Cindy Leifer, Stephanie Langel, and Brianne Barker Subscribe (free): Apple Podcasts, RSS, email Become a patron of Immune! Links for this episode MicrobeTV Discord Server EBV, Golli-MBP presentation and multiple sclerosis (Cell, 2026) Intratumoral bacteria promote resistance to cancer immunotherapy (Nat Cancer, 2026) Time stamps by Jolene Ramsey. Thanks! Music by Tatami. Immune logo image by Blausen Medical Send your immunology questions and comments to immune@microbe.tv Information on this podcast should not be construed as medical advice.

 My guest provides advanced, patient-centered care for stroke, brain aneurysms, and a wide range of neurovascular conditions. Dr. Liff is recognized for his expertise in both medical and catheter-based treatments, including procedures such as cerebral angiography, mechanical thrombectomy, aneurysm coiling and stenting, carotid stenting, and embolization for arteriovenous malformations and tumors.Dr. Liff completed his undergraduate studies in Cognitive Science at Johns Hopkins University, earned his medical degree from SUNY Upstate Medical University, and trained in Neurology at Albert Einstein College of Medicine, where he served as Chief Resident. He specialized in fellowships in Vascular Neurology at Mt. Sinai Hospital and Endovascular Neurosurgery at NYU Langone Medical Center.He has presented original research at major conferences and published it in respected journals. Dr. Liff is a senior member of the Society of Neurointerventional Surgery and is dedicated to serving patients throughout the Tri-State Area, performing procedures at leading hospitals such as St. Francis Hospital, NYU Langone Hospital Long Island, and Lenox Hill Hospital. https://jeremyliffmd.com/#homehttp://www.yourlotandparcel.orgSupport the show

In this episode, Saranne invites you to join her for a lighthearted and informative discussion on the importance of having our affairs in order, even before a cancer diagnosis. With her signature humor and personal anecdotes, Saranne emphasizes the importance of wills, healthcare proxies, and durable power of attorney, while also sharing a humorous joke and offering practical tips on finding legal assistance. Tune in to discover how laughter can be found even in serious topics and how taking care of our legal affairs can bring peace of mind during challenging times.2025 People's Choice Podcast Awards Best Health Series FinalistRanked the Top 5 Best Cancer Podcasts by CancerCare News in 2024 & 2025,and #1 Rated Cancer Survivor Podcast by FeedSpot in 2024 to 2025. Beating Cancer Daily is listened to in 148 countries across 7 continents and features over 420+ original daily episodes hosted by Stage IV survivor Saranne Rothberg. To learn more about Host Saranne Rothberg and The ComedyCures Foundation:https://www.comedycures.org/ To write to Saranne or a guest:https://www.comedycures.org/contact-8 To record a message to Saranne or a guest:https://www.speakpipe.com/BCD_Comments_Suggestions To sign up for the free Health Builder Series live on Zoom with Saranne and Jacqui, go to The ComedyCures Foundation's homepage:https://www.comedycures.org/ Please support the creation of more original episodes of Beating Cancer Daily and other free ComedyCures Foundation programs with a tax-deductible contribution:http://bit.ly/ComedyCuresDonate THANK YOU! Please tell a friend whom we may help, and please support us with a beautiful review. Have a blessed day! Saranne

Featuring perspectives from Dr Mrinal Gounder and Dr Richard F Riedel, including the following topics: Introduction (0:00) Desmoid Tumors — Dr Gounder (2:58) Soft Tissue Sarcoma — Dr Riedel (28:29) CME information and select publications

Highlights from the PER® CME activity "Live Tumor Board: Translating Biomarker Insights and Therapeutic Advances Into Endometrial Cancer Practice" — this podcast is not certified for credit. To participate in the full accredited activity and earn CME credit, use the link below.In this podcast, experts Kathleen N. Moore, MD, MS, FASCO; Ritu Salani, MD, MBA; Casey Cosgrove, MD; and Ebony R. Hoskins, MD, FACOG, discuss several cases of endometrial cancer using biomarkers to drive treatment decisions.Earn CME credit by completing the full accredited activity (available through June 26, 2027):https://www.gotoper.com/iog26endometrial-activityThis podcast, including the narration, was developed by PER® (Physicians' Education Resource®, LLC) editorial staff from the full online CME activity developed with these faculty. The narration was voiced by a PER staff member or by an AI tool. The podcast contains no product advertising. The full activity is supported by educational grants from BioNTech; Eisai, Inc.This content is for educational purposes only and is not a substitute for the independent clinical judgment of a health care professional. Faculty may discuss investigational or off-label uses; consult prescribing information for any products discussed.

BUFFALO, NY – June 24, 2026 – A new research paper was published in Volume 17 of Oncotarget on June 9, 2026, titled “TRAIL-R2 in the shadows: Epigenetic silencing and clinical implications in breast cancer.” The study was led by first author Nuzhat Khursheed from the University of Kashmir and corresponding authors Asia Asiaf from the Central University of Kashmir and Showkat Ahmad Ganie from the University of Kashmir. Breast cancer remains one of the most common cancers affecting women worldwide. While advances in diagnosis and treatment have improved outcomes for many patients, researchers continue to investigate the molecular changes that enable tumor cells to survive, grow, and spread. One process receiving increasing attention is epigenetic regulation, in which genes are switched on or off without altering the underlying DNA sequence. In this study, researchers examined TRAIL-R2, also known as death receptor 5 (DR5), a protein that plays an important role in triggering apoptosis, the programmed cell death process that helps eliminate damaged or abnormal cells. Loss of apoptotic signaling is a hallmark of cancer, but the clinical significance and epigenetic regulation of TRAIL-R2 in breast cancer have remained incompletely understood. The investigators analyzed matched tumor and adjacent normal breast tissue samples from 67 patients. Using methylation-specific PCR, quantitative real-time PCR, and western blotting, they evaluated TRAIL-R2 promoter methylation as well as its gene and protein expression levels. The analysis revealed that TRAIL-R2 was frequently silenced in breast tumors. More than half of tumor samples showed promoter hypermethylation, a chemical modification that can suppress gene activity. At the same time, both TRAIL-R2 mRNA and protein expression levels were significantly lower in tumor tissues than in adjacent normal breast tissue. Further analysis demonstrated that TRAIL-R2 hypermethylation was more common in invasive ductal carcinoma, the most common subtype of breast cancer, and in patients with a history of oral contraceptive use. Reduced TRAIL-R2 expression was also associated with advanced tumor stage and several clinicopathological features linked to more aggressive disease. The researchers observed a strong inverse relationship between promoter methylation and TRAIL-R2 expression, suggesting that epigenetic silencing may contribute directly to loss of this important apoptotic receptor. Tumors with reduced TRAIL-R2 activity may become less susceptible to programmed cell death, potentially allowing cancer cells to survive and progress. Full press release - https://www.oncotarget.net/2026/06/24/trail-r2-silencing-linked-to-more-aggressive-breast-cancer/ DOI - https://doi.org/10.18632/oncotarget.28891 Correspondence to - Asia Asiaf - asiaf29@cukashmir.ac.in, and Showkat Ahmad Ganie - showkatganie@kashmiruniversity.ac.in Abstract video - https://www.youtube.com/watch?v=BvhkOYLTJUY Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28891 Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/ Keywords - cancer, TRAIL-R2/DR5, promoter methylation, breast cancer biomarkers, tumor suppressor gene, apoptotic signalling pathways To learn more about Oncotarget, please visit https://www.oncotarget.com and connect with us: Facebook - https://www.facebook.com/Oncotarget/ X - https://twitter.com/oncotarget Instagram - https://www.instagram.com/oncotargetjrnl/ YouTube - https://www.youtube.com/@OncotargetJournal LinkedIn - https://www.linkedin.com/company/oncotarget Pinterest - https://www.pinterest.com/oncotarget/ Reddit - https://www.reddit.com/user/Oncotarget/ Spotify - https://open.spotify.com/show/0gRwT6BqYWJzxzmjPJwtVh MEDIA@IMPACTJOURNALS.COM

Learn about the Healing Power of Prolonged Fasting: HEREWhat if the secret to deep healing isn't doing more, but going further?Most people assume that repeating short fasts is just as powerful as completing one long fast. Stack enough three-day fasts together and you'll eventually get the same result, right?It's a reasonable assumption, but it may be costing you the deeper healing you're working so hard to reach.Dr. Katie breaks down something many people have never been taught: short fasts and prolonged fasts are not the same healing tool. Short fasts are genuinely valuable. They can support ketosis, lower insulin, improve metabolic flexibility, and put pressure on cancer cells. Dr. Katie does a three-day fast herself every month.But she says they stop short of the second tier.That second tier begins after the early detox window, when the body moves into a much deeper fasting state. Around day eight is the threshold where the fast stops being just a metabolic tool and begins to reveal a much deeper layer of healing. Dr. Katie believes most people never reach because they keep restarting the clock.Chapters:00:04:22 - Why Short Fasts Reset the Clock00:05:21 - Detox Starts After Day Four00:06:21 - Why Long Fasts Need Supervision00:07:23 - The Danger of Refeeding Wrong00:08:21 - The Magic of Day Eight00:09:31 - The Body Targets Damaged Tissue00:10:22 - When Tumor Shrinkage Becomes Possible00:12:17 - The Mind Finally Quiets00:13:20 - Healing Crises Begin00:16:49 - Why You Can't Stack Short Fasts00:17:32 - Cancer Deserves the Full Distance00:18:52 - The Brain Tumor That Disappeared00:19:45 - Why Refeeding Matters Most00:21:00 - Fasting Opens Emotional Healing00:23:19 - What Cancer Experts Would Do00:24:45 - Physical and Emotional Healing Arrive TogetherEvery time you break a fast, your body doesn't just pause. It resets. Dr. Katie uses one simple analogy that makes this clear, and once you hear it, the difference between stacking short fasts and completing a prolonged fast becomes hard to unsee.Press play to learn why Dr. Katie believes anyone fasting for cancer needs to understand the difference between stopping early and going the full distance.Join Dr. Katie's 3-Day Guided Fast, for expert support, daily live calls, and a community to fast alongside: Sign-Up Follow Dr. Katie Deming on InstagramWatch on YoutubeDISCLAIMER: The Born to Heal Podcast  is intended for informational purposes only and is not a substitute for seeking professional medical advice, diagnosis, or treatment. Individual medical histories are unique; therefore, this episode should not be used to diagnose, treat, cure, or prevent any disease without consulting your healthcare provider.A thought-provoking podcast explores cancer through the lens of holistic medicine and functional medicine, discussing causes of cancer, metabolic health, and unconventional approaches like water fasting, fasting and autophagy, and detox, while weighing fasting benefits against chemo side effects and radiation side effects, sharing stories of a cancer survivor navigating chemotherapy, natural medicine, holistic healing, and even spiritual healing on the path toward cancer remission and holistic health. 

Send comments and feedback In this episode of Sharp Waves, host Nancy welcomes renowned neurologist and neuro-oncologist Dr. Katie Peters from the Preston Robert Tisch Brain Tumor Center to discuss the important connection between brain tumors and epilepsy. Dr. Peters shares her expertise on how brain tumors can contribute to seizure disorders, the challenges patients face, and the latest approaches to diagnosis, treatment, and care. Whether you're a healthcare professional, patient, caregiver, or simply interested in neuroscience, this insightful conversation offers valuable perspectives on navigating these complex neurological conditions. Tune in for an engaging discussion with one of the field's leading experts.  Sharp Waves episodes are meant for informational purposes only, and not as clinical or medical advice.Let us know how we're doing:  info@ilae.orgThe International League Against Epilepsy is the world's preeminent association of health professionals and scientists, working toward a world where no person's life is limited by epilepsy. Visit us on Facebook, Instagram, and LinkedIn.

Northwell Health's Norwalk Hospital is the first in Connecticut to perform histotripsy for liver tumors, introducing a new noninvasive cancer treatment for patients with primary or metastatic disease. We got more details about the game changer treatment from Dr. Dan Labow, chair of surgical services and a surgical oncologist in the Conn. and Hudson Valley markets of Northwell.

After experiencing a number of illness when he was 2 years old going into the spring of 2025, Caitlyn and CJ Jennings thought that their beloved son Brooks was experiencing normal illnesses that many toddlers may experience. Unfortunately that was not the case. Brooks was diagnosed with a Fusion Mesenchymal Tumor that was located in his lung and then spread to his Pelvic Bone. Brooks continued to feel well until August of last year when his health went downhill, leading to his passing on October 25th of 2025.

Send us Fan Mail"Who is your daddy, and what does he do?"Grab your juice boxes and secure your nap mats, because this week on Entertain This!, Mitch and Tom are going undercover. That's right—we're strapping on our holsters and heading into the high-stakes, high-caffeine world of 1990's Kindergarten Cop.Join us as we analyze Arnold Schwarzenegger's pivot from unstoppable cyborg assassin to... a man trying to manage a room full of toddlers. Does Arnie have the range, or are the kids actually the ones pulling the strings? We're breaking down the film's iconic quips, the jarring tonal whiplash between "gritty drug bust" and "finger painting," and why this movie remains an essential artifact of 90s cinema madness.Whether you have fond memories of this childhood staple or you're watching it for the first time with cynical adult eyes, this episode is a mandatory field trip.Tune in, settle down, and try to keep your hands to yourselves while you listen. And remember: You're not a patient boy!New episodes drop every Monday. Don't forget to rate, review, and subscribe—or we'll tell the principal. Support the show

Featuring an interview with Prof Bernd Kasper, including the following topics: Case: A woman in her early 30s develops a progressing desmoid tumor in her abdomen during pregnancy(0:00) Case: A woman in her late 30s with a painful small desmoid tumor in her rectus abdominus undergoes cryoablation (8:04) Case: A woman in her late teens with recurrent desmoid tumors in her right thigh undergoes multiple resections (13:58) Case: A woman in her mid 70s has a desmoid tumor causing erosion in her scapular region (17:19) CME information and select publications

In this episode of Head and Neck Innovations, experts in neurotology and neurosurgery discuss the diagnosis and management of lateral skull base tumors, highlighting multidisciplinary collaboration, personalized treatment strategies, and the latest surgical and imaging innovations improving patient outcomes.

Discover how insulin potentiation therapy and hyperthermia offer low-toxicity cancer treatment by boosting drug delivery and immunity. #Hyperthermia #IPT #GentleCancerCare #HealthTalks

Good morning from Pharma Daily: the podcast that brings you the most important developments in the pharmaceutical and biotech world. The industry continues to evolve, with significant scientific advancements, regulatory updates, and strategic business moves shaping the landscape. Let's delve into these developments, starting with some key insights from oncology. In the realm of oncology, minimal residual disease (MRD) is becoming increasingly pivotal. Tumor-informed MRD is being leveraged to design more intelligent trials and interpret early responses, aiding in navigating developmental risks more effectively. This approach was a focal point of discussions at the American Society of Clinical Oncology's annual meeting, where experts emphasized the need to translate precision oncology discoveries into patient care, aiming to surmount existing challenges. The focus on MRD in oncology could lead to earlier detection of treatment responses and personalized therapeutic approaches. Verastem Oncology recently revisited its strategy concerning its combination treatment of avutometinib plus defactinib for metastatic pancreatic cancer. While clinical trials produced moderate results, the company is now redirecting focus toward other promising candidates in its pipeline. Similarly, Novocure faced setbacks as its tumor-treating electric fields device did not achieve its primary endpoint in a Phase 3 glioblastoma trial. These outcomes highlight the persistent challenges in tackling aggressive brain cancers. On the regulatory front, Spero Therapeutics achieved a significant milestone with FDA approval for Utebzi to treat complicated urinary tract infections. This approval marks a turnaround from a previous rejection four years ago, facilitated through a partnership with GSK. Meanwhile, in Europe, Cinnagen secured approval for Zandoriah, a biosimilar of teriparatide, to treat osteoporosis in adults—a testament to their investment in infrastructure and manufacturing capabilities. The industry also sees growing interest in cell therapy automation, with companies like Cellares and Ori Biotech leading the charge. These advancements reflect an industry-wide push towards more efficient manufacturing processes for cell therapies. In metabolic health, Novo Nordisk's oral GLP-1 drug Wegovy has gained significant traction due to its brand familiarity among healthcare providers, crucial in its competition with Eli Lilly's Foundayo. Market trends reveal competitive dynamics within obesity treatments as Novo Nordisk's oral Wegovy outpaces Eli Lilly's offerings due to strong brand recognition. Biogen's acquisition of Raythera for $1 billion underscores its strategic intent to enhance its portfolio with promising preclinical immunology assets. Such acquisitions highlight broader industry strategies focusing on expanding pipelines through targeted investments. This move aligns with Biogen's focus on autoimmune diseases and enhances its preclinical portfolio. In business development news, LabGenius Therapeutics partnered with LG Chem to utilize AI and machine learning for designing multispecific antibodies targeting tumors. This collaboration highlights the growing importance of artificial intelligence in accelerating drug discovery processes within oncology. Clinical trials continue to yield promising results. F2G and Shionogi's antifungal small molecule olorofim demonstrated efficacy comparable to Ambisome in treating invasive aspergillosis—an advancement crucial for infectious diseases with limited treatment options. D&D Pharmatech's Zabopegdutide showed an impressive improvement rate in fibrosis during Phase 2 trials for metabolic dysfunction-associated steatohepatitis, emphasizing the potential of protein-based therapies in treating metabolic liver disorders. Corporate launches reflect strategic maneuvers aimed at advancing therapeutic developments. Innoviva introduced Nortiva Bio to focus on long-acting oral medicines using acquired platform technology from Lyndra Therapeutics—aiming to revolutionize women's health through sustained-release formulations. The financial landscape also shows active movement, exemplified by Kardigan's $400 million IPO aimed at progressing cardiovascular drugs into advanced trials. Alvotech's public offering signals a commitment to biosimilar medicines—a sector poised for growth due to rising demand for cost-effective biologic therapies. Overall, these developments reflect a robust innovation pipeline within the pharmaceutical and biotech industries as they strategically address complex diseases through novel therapies and technologies. As scientific progress accelerates alongside strategic corporate actions, these changes promise enhanced patient care outcomes through groundbreaking treatments that cater to unmet medical needs worldwide.Support the show

What if 90–95% of cancers weren't written in your genes—but in your environment, lifestyle, and daily choices? My guest today Dr B challenges some of the biggest assumptions in modern medicine, drawing on decades of experience examining cancer cells under the microscope. From the hidden drivers of chronic disease to the controversial role of hormone replacement therapy and the critical importance of gut health, this episode explores what happens when we stop asking what disease a person has and start asking why they developed it in the first place.With an unprecedented five board certifications, Dr. Monisha Bhanote brings a comprehensive, systems-based approach to health that few practitioners can match.As the founder of WELLKULÅ and CEO of Travela Wellness, Dr. Bhanote has created comprehensive platforms that make transformative health accessible to individuals and organizations worldwide. Dr B's work bridges the gap between ancient wisdom traditions and modern molecular science, creating personalized, actionable protocols that deliver measurable results.Her clinical and research focus centers on the microbiome-brain-longevity axis—investigating how gut health, inflammation management, and cellular optimization.Contact:Website - https://www.drbhanote.comJoin us as we explore:Breaking genetic dogma once and for all around disease pathology - from cancer to diabetes. Balancing the pros and cons of any approach whether conventional, Pharma or Ayurvedic.A long ranging conversation on hormonal replacement therapy. Tumor vs healthy cell biology.The crisis of gut health, the gut “clock” you didn't know you had and why many answers lie with the millennia old wisdom of Ayurvedic and Chinese medicine.The stress travel puts on your microbiome due to stress, dehydration, hypoxia, humidity, radiation and poor food choices.MentionsStudy - The Negative Influence of Air Travel on Health and Performance in the National Basketball Association: A Narrative Review, https://pmc.ncbi.nlm.nih.gov/articles/PMC6162549/Support the showFollow Steve's socials: Instagram | LinkedIn | YouTube | Facebook | Twitter | TikTokSupport the show on Patreon:As much as we love doing it, there are costs involved and any contribution will allow us to keep going and keep finding the best guests in the world to share their health expertise with you. I'd be grateful and feel so blessed by your support: https://www.patreon.com/MadeToThriveShowSend me a WhatsApp to +27 64 871 0308. Disclaimer: Please see the link for our disclaimer policy for all of our content: https://madetothrive.co.za/terms-and-conditions-and-privacy-policy/

BUFFALO, NY – June 17, 2026 – A new #research paper was #published in Volume 17 of Oncotarget on June 8, 2026, titled “DHHC3 interferes with antitumor immunity in melanoma cells.” The study was led by first author and corresponding author Chandan Sharma and corresponding author Martin E. Hemler from the Department of Cancer Immunology and Virology at the Dana-Farber Cancer Institute. Melanoma is one of the most aggressive forms of skin cancer and is highly influenced by interactions between tumor cells and the immune system. Although modern immunotherapies have transformed treatment for many patients, researchers continue to search for molecular mechanisms that enable tumors to evade immune attack and continue growing. In this study, researchers investigated DHHC3, a protein acyltransferase that regulates protein palmitoylation and helps maintain cellular redox balance. Previous studies had linked elevated DHHC3 expression to poor outcomes in several cancers, but its role in melanoma and anti-tumor immunity remained unclear. To explore this question, the team used CRISPR gene editing to eliminate DHHC3 expression in B16F10 melanoma cells. Loss of DHHC3 caused a marked increase in oxidative stress and cellular senescence, as demonstrated by elevated TXNIP expression, increased reactive oxygen species levels, and enhanced expression of senescence-associated markers. Full press release - https://www.oncotarget.net/2026/06/17/protein-linked-to-melanoma-growth-may-suppress-the-bodys-natural-anti-tumor-immune-response/ DOI - https://doi.org/10.18632/oncotarget.28880 Correspondence to - Martin E. Hemler - martin_hemler@dfci.harvard.edu, and Chandan Sharma - csharma@mgh.harvard.edu Abstract video - https://www.youtube.com/watch?v=QQhP2VhzKSE Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28880 Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/ Keywords - cancer, oxidative stress, DHHC3, anti-cancer immunity, palmitoylation, melanoma To learn more about Oncotarget, please visit https://www.oncotarget.com and connect with us: Facebook - https://www.facebook.com/Oncotarget/ X - https://twitter.com/oncotarget Instagram - https://www.instagram.com/oncotargetjrnl/ YouTube - https://www.youtube.com/@OncotargetJournal LinkedIn - https://www.linkedin.com/company/oncotarget Pinterest - https://www.pinterest.com/oncotarget/ Reddit - https://www.reddit.com/user/Oncotarget/ Spotify - https://open.spotify.com/show/0gRwT6BqYWJzxzmjPJwtVh MEDIA@IMPACTJOURNALS.COM

Do you know how tumor-agnostic therapies are helping to reshape cancer treatment pathways? Credit available for this activity expires: 6/16/27 Earn Credit / Learning Objectives & Disclosures: https://www.medscape.org/viewarticle/shaping-future-precision-oncology-biomarker-driven-care-2026a1000jpk?ecd=bdc_podcast_libsyn_mscpedu

In this episode, we review the high-yield topic of⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠ ⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠Soft Tissue Tumors⁠⁠ ⁠⁠from the Oncology section.Follow⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠ ⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠Medbullets⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠ on social media:Facebook: www.facebook.com/medbulletsInstagram: www.instagram.com/medbulletsofficialTwitter: www.twitter.com/medbullets

Dr. Deb Muth 00:00:09 Hi there, how are you? Bob Miller 00:00:10 Excellent! Pedaling as fast as humanly possible, but doing okay. Dr. Deb Muth 00:00:14 Good, good. Well, I’m looking forward to our conversation today. This should be amazing. Bob Miller 00:00:20 Yeah, it should be a lot of fun. Dr. Deb Muth 00:00:22 Yeah, anything that’s off-limits for you in, our conversation? Bob Miller 00:00:28 No. Dr. Deb Muth 00:00:29 Okay, anything you want me to make sure we cover for you? Bob Miller 00:00:33 Well, I mean, is it okay if we put a little plug-in for our software? Dr. Deb Muth 00:00:35 Absolutely. Bob Miller 00:00:36 Yeah. Dr. Deb Muth 00:00:37 Absolutely. Bob Miller 00:00:36 Yeah. Dr. Deb Muth 00:00:37 Absolutely. Bob Miller 00:00:38 Hey, can we… can we do a screen share? Yes, we can. Yeah, because I want to show you some maps, and… Dr. Deb Muth 00:00:43 Okay. Things like that, yeah, so… Perfect. So just let me know when you want to do screen share. Bob Miller 00:00:48 Okay. Dr. Deb Muth 00:00:49 And yeah, feel free to plug your software wherever you want to. Bob Miller 00:00:53 Okay, well, good. Let me pull up a, a slide for that, and give me one second, I just want to shut the door to my office to get the noise down. Dr. Deb Muth 00:01:01 No worries. Bob Miller 00:01:16 And, how should I refer to you? Dr. Debb? Dr. Muth, what do you like? Dr. Deb Muth 00:01:18 Dr. Deb is great, or Deb, either way, I’m pretty informal, so… Bob Miller 00:01:22 Yeah, and… Bob is fine for me. Okay. Yeah. Yeah, there you go. Why people feel like they need this, son. Special name, it’s like, seriously. Dr. Deb Muth 00:01:33 Right? I agree. Bob Miller 00:01:35 When I work with my clients, it’s like, Dr. Millison, just, just bop, just, just bop. Dr. Deb Muth 00:01:41 Yep, that’s how I am, too. Just call me Deb, it’s good. Dr. Deb Muth 00:01:44 They feel a little awkward with that, you know? They’re not used to that, but… Bob Miller 00:01:48 Alright. And you’re a naturopath, medical doctor. Dr. Deb Muth 00:01:52 A nastropathic doctor and a nurse practitioner. Oh, nice. Yeah, so I got the best of both worlds, right? Bob Miller 00:01:58 Yeah, damn. Okay. Alright, so here we go… There we go. Alright, so I got that ready, and then I will do a, I will do a screen share. I think you’re gonna really, appreciate what we’ve come up with. We’ve come up with the concept of, Cellular CPR. Dr. Deb Muth 00:02:23 Oh, nice! Bob Miller 00:02:24 And that is, construct the cell membrane, Protect the cell membrane. And restore it if it’s damaged. Dr. Deb Muth 00:02:32 Love that. Bob Miller 00:02:34 I love that. Yeah, so that’s what we’re focusing on, and then how, You know, we want to get to the point that, you know, most people think of genetics, they think of, like, 23andMe or Ancestry. Dr. Deb Muth 00:02:44 Yeah. Bob Miller 00:02:45 And then you have the professional geneticists who are looking at, you know, odd things that could create a disease. We’re looking at functional genomics. Dr. Deb Muth 00:02:54 Which is so much better. Bob Miller 00:02:56 Yeah. Are you familiar with what we do here, or… Dr. Deb Muth 00:02:58 A little bit, a little bit. So, it’ll be new to me, too, so I’m excited. Bob Miller 00:03:03 And how much time do we have? Dr. Deb Muth 00:03:04 We have an hour, give or take a little bit on either side. Do you have a hard stop anywhere? Bob Miller 00:03:10 No, no, I put a, I moved my clients around, and I don’t have anybody till, 3.30, so we’re good. Okay. Dr. Deb Muth 00:03:16 Perfect. Alright. Bob Miller 00:03:18 It’s like we’re getting started early as well, so… Dr. Deb Muth 00:03:19 Yeah, we’re getting started a little bit early, so that’s good. Bob Miller 00:03:22 Yeah, I just got my office cleaned up, so… Dr. Deb Muth 00:03:23 Okay, good. All right, are you all set to get started? Bob Miller 00:03:28 I’m good to go, my friend. Dr. Deb Muth 00:03:29 I’m gonna just record a little intro and a little bit of a, hook for people, and then we’ll get started. I’ll ask you to kind of tell us a little bit about yourself, and then we’ll just take this conversation wherever it’s supposed to go. Bob Miller 00:03:39 Okay, you got it. Dr. Deb Muth 00:03:40 Alright, sounds good. So what if the reason you’re not healing isn’t your diet, your supplements, or your labs, but it’s actually your genes? Dr. Bob Miller is uncovering how genetic variants, when combined with modern toxins, explain why some of us stay sick no matter what we try. Today, we’re talking genetic pathways, detox blocks, and the new science every wellness warrior needs to know. Welcome back to Let’s Talk Wellness Now, the show where we uncover the root causes of chronic illness, exploring cutting-edge regenerative medicine, and empower you to heal from the inside out. I’m Dr. Deb, your medical detective, and today, our guest, Dr. Bob Miller, is a true pioneer in functional genomics. He’s a board-certified traditional naturopath and the founder of Neutrogenetic Research Institute. And he’s the leading groundbreaking research on how genetic variants influence chronic illness, inflammation, and detoxification. His work has been recognized on international stages, uncovering links between genetic expression and conditions like Lyme disease, mast cell activation, or MCAS, and mitochondrial dysfunction. I’m so excited to talk to Dr. Bob today. He is gonna reveal some things that even I don’t know about, so I’m excited to learn alongside of you guys. So… Dr. Bob, let’s get started. Tell us a little bit about yourself, and kind of how you got on this journey. Bob Miller 00:05:04 Well, that’s, that’s interesting. I was sort of like a mid-career coming to the natural health field, because in my early 30s, I found myself with a severe case of ulcerative colitis. Bob Miller 00:05:15 And I was in the hospital for 21 days. probably within hours of death, pleading to death. And they told me I’ve got one option, and that is cut out the colon and wear a bag. Didn’t sound like a lot of fun. Dr. Deb Muth 00:05:27 Not an option I would want. Bob Miller 00:05:29 So, you know, the medical folks wasn’t real happy with me, but I said, yeah, I’d like to explore some alternative things.Never thinking that I’d get into this field, and then I just, you know, worked with some herbalists and things that I found absolutely fascinating. So, that’s how I got into this around 30 years ago. And, haven’t looked back since, and just having a… having a blast as we now move into how our genetics impacts things. So, that’s what we’re gonna… that’s what we’re gonna talk about today. Dr. Deb Muth 00:05:58 I’m excited to talk about this genetic thing. When you started over 30 years ago, what kind of patience and problems first inspired you to dig deeper into that root cause healing and kind of get into the genetic piece of it? Bob Miller 00:06:10 Sure. Well, you know, as a… now, I’m in a part of the country called Lancaster County, Pennsylvania, where there’s a lot of Amish and Mennonite, and they gravitate towards these things.So, this is their first thing to do, and that doesn’t work, then they’ll go other routes. So, you know, back then, we just saw typical, you know, a little tired, constipation. You know, a little bit of fatigue, arthritis, those kind of things. But things have changed dramatically over the years, as people are now getting more chronically sick. You know, it’s worse than it’s ever been. And what we’re finding is the, the culprits Primarily is mold exposure and Lyme disease. When people get those two together, they’re just… it’s an inflammatory cascade that nobody can seem to unravel. So that’s where we spend a lot of our time. And we’re also spending a lot of time looking at mental health, like ADD, ADHD. And, we give… this year I’ll be speaking at three autism conferences. And we can dig into that a little bit as to why we think we’re seeing such a dramatic increase. And aside from autism, that used to be 1 out of 1,000, now it’s 1 out of 33, or 23. You know, we’re also seeing dramatic increases in ADD, ADHD. People are stressed out. And today, I think we’ll have the time to actually go through and show how environmental factors combine with genetics to cause that to happen. So we’ll… we should have a fun visit here today. And today, I think we’ll have the time to actually go through and show how environmental factors combine with genetics to cause that to happen. So we’ll… we should have a fun visit here today. Dr. Deb Muth 00:07:37 This should be a fun visit. We can cover lots of topics. I am so excited. So, you founded Nutri Genetic Research Institute in 2015. What did you hope to accomplish, and what kind of surprised you in your findings so far about that? Bob Miller 00:07:51 Well, you know, let’s back up at what, you know, genetics is used for. Everybody’s familiar with 23andMe and Ancestry that, you know, tells you where your ancestors came from. Then you have your professional geneticists. I mean, these are people with a degree in genetics. And they’ll look for, you know, very odd sort of things that are prone to relate to a disease. So there are disease-related genetics. Well, in functional, we don’t look at either of those. We look at For example, how you’re breaking down your fats and utilizing them. How you’re recycling your glutathione. How you might be handling your iron. And none of those are disease-causing on their own.And none of those are disease-causing on their own. But when they pile up on you, and then combine that with environmental factors, that’s when things start to go south on us. So, that’s what we’re doing, we’re looking at patterns. And our first foray into this was, we did studies on Lyme disease. And our first foray into this was, we did studies on Lyme disease. So, we looked at, like, I think 50 people with Lyme disease. We looked at their genome. So, we looked at, like, I think 50 people with Lyme disease. We looked at their genome. And we found patterns that were more evident in those with Lyme. Now, this doesn’t… these genetics don’t mean you get Lyme, it just means if you get Lyme, you react worse to it. And we found patterns that were more evident in those with Lyme. Now, this doesn’t… these genetics don’t mean you get Lyme, it just means if you get Lyme, you react worse to it. So, as you know, some people get Lyme, they go on a round of antibiotics, and they’re done. So, as you know, some people get Lyme, they go on a round of antibiotics, and they’re done. Others have a little more struggle, and then others are struggling terribly for years. So there’s an old adage of genetics loads the gun, environment pulls the trigger. Dr. Deb Muth 00:09:14 Yeah, that is so true, and I think when we’re talking about Lyme and mold and things like that, we forget sometimes that our genetics can predispose us to be more sensitive to those things, and if we have genetic pathways where we don’t clear things properly, it’s harder for us to get them out of the body. And then you add on that whole rain barrel effect that we’ve always used as a functional medicine term, right? If the barrel’s half full, you’re okay. If it’s full, and now it’s spilling over, it’s a bigger problem. Have you guys found, too, that some of these environmental things actually are changing the genetics of people, or how they’re processing their own genetics? Bob Miller 00:09:53 Well, let’s go back to, Genetics 101. But we’ll go back a little bit further. So, what an interesting mechanism, what a miracle the body is. Bob Miller 00:10:03 Fats, carbohydrates, proteins, drink water, breathe air, expose the sunlight, and somehow everything gets made. I mean, when you just step back and think about that, it’s like, It’s pretty darn amazing. Dr. Deb Muth 00:10:15 I always tell women, you know, the fact that we get pregnant and we have healthy pregnancies and births is a miracle, because if we had to try to control that, that wouldn’t work so well. Bob Miller 00:10:25 Right. Well, that’s another miracle. These microscopic sperm and egg, human being, 9 months later, it’s like. But even inside of us. We are making our hair, our skin, our nails, our blood vessels, our ATP, our energy, it’s all being created. Well, that gets created by enzymes. So, enzymes take one substance, combine it with something else, and make something new. Then another enzyme comes along and does the same thing. Your DNA is the instructions on how to make the enzymes. So, when we are conceived. If it’s a, if it’s a female, of course, it’s the XX, the two chromosomes. You know, we’ve… everybody’s seen those… the genetics that… Listed pair. So, if it’s a female, the father donated the X enzyme. And the mother has no choice but to give the eggs, so that’s female. If the father donates the Y, you have a male that’s in chromosome number 1. Then 2 through 23 is the rest of the instructions on how to make enzymes. So, what can happen? We can get what are called SNPs, single nucleotide polymorphisms. And SNPs just mean that the instructions to make the enzyme’s not quite as good. So, if one parent gives a SNP on the making of an enzyme, The enzyme’s fine. It works. But, general rule of thumb, It may only work at 70-80% of efficiency. Now, a good analogy is think of an 8-cylinder and a 6-cylinder car. If parents give you good information, that’s like having an 8-cylinder car. If one parent gives you that snip, it’s like having a 6-cylinder car. Now, is a 6-cylinder car a fine car? Sure. It’ll get you from point A to point B, but it’s just going to have the power of an 8-cylinder. Then if both parents give you a SNP on the same enzyme, it may be 30-40%, and that’s like having a 4-cylinder car. Sits in the driveway, looks the same, puts gas in it, everything. But if you’ve got a 4-cylinder car. Probably not a good idea to go cross-country pulling a trailer behind you up and down mountains. Dr. Deb Muth 00:12:29 This is true. Bob Miller 00:12:32 So… We can get an 8-cylinder, 6-cylinder, or 4-cylinder enzyme. Now, if it’s not under a lot of stress, if that 4-cylinder car is just taking you to the bank and the grocery store. It’s just as good as an 8-cylinder car. But if you gotta pull that trailer, and there’s a lot of stress on it, being mountains, it’s gonna struggle. Now, there’s one other little caveat to this, and that is some genetic mutations are gain-of-function. They actually work faster. Now, we have enzymes that do all kinds of things. We have enzymes that make and recycle our antioxidants, but we also have enzymes that make inflammation. No, that’s a good thing, because if we get a virus or bacteria, if you didn’t make inflammation to kill it, well, we’d all die of infection. So, you know, we tend to think of free radicals as bad, antioxidants as good. They both play an important role. But interestingly, some of the major enzymes that make inflammation, they can be overactive. They can be turbocharged. And when they’re stimulated by environmental toxins, they overreact. Bob Miller 00:13:40 And therein lies the problem. When they overreact, we have a problem. Bob Miller 00:13:46 So, if we have genes that overreact when stimulated. And then the enzymes that take care of inflammation are underactive. Then you’re gonna be more inflamed. You know, the majority of people that, you know, come for functional medicine Or naturopathic help, or… Inflammation that they can’t seem to get under control. Dr. Deb Muth 00:14:06 Right. Bob Miller 00:14:07 And we will be, you know, during this hour, we’re going to look at some of the pathways that make that happen. So, what we can do then, we can’t change our genetics. When you’re conceived, that’s the hand you’re dealt. When your life would be over, if someone would take some tissue and measure, it’d be exactly the same as conception. Does it change. Bob Miller 00:14:28 The enzyme’s ability to do its job may be compromised. Because remember I said there’s a, the enzyme takes a cofactor. So an enzyme takes substance A, cofactor, make substance B. Well, if that cofactor’s not there, the enzyme’s not going to work either. So, you could have an 8-cylinder car, and if there’s no gas in it, it’s not going anywhere. So… It’s the strength of the enzyme, it’s the cofactor to do the A to B conversion. And that’s what we’re going to get into. So, many people say, well, where did these SNPs come from? Nobody knows for sure. Sometimes they’re what’s just called de novo, when the sperm and egg go together, the instructions get mixed up a little bit. We do believe a lot of it came from a long time ago, when we were almost wiped out by sexually transmitted diseases. And those STDs were altering the genes when the conception, in other words, when the sperm went into the egg, the STDs were interfering. And causing the problem, so… I often joke, if you want to blame somebody. Blame your great-great-great-great-great-great-great-grandparents for, being a bit promiscuous, so… Dr. Deb Muth 00:15:31 Yeah, for being… having a little too much fun, right? Bob Miller 00:15:35 So, we don’t know for sure, but, you know, there are some that, But most of the SNPs that we get inherit from our parents. So, if you look at a child. And you look at the SNPs. 99.9% of the time, it came from one of the parents. Dr. Deb Muth 00:15:50 In identical twins, do they have the exact same identical makeup? Bob Miller 00:15:54 Yep, Dr. Deb Muth 00:15:56 But not in fraternal twins, correct? Bob Miller 00:15:59 No, no, those could be different, Jeff. Dr. Deb Muth 00:16:00 It could be different because they have different sacs, they’re not sharing that same genetic makeup. Bob Miller 00:16:04 Yeah, so keep in mind, both your mother and your father have, you know, the two And so you get one from one parent, one from another. Dr. Deb Muth 00:16:13 So… Bob Miller 00:16:14 Interesting situation. I had, 3, 3 boys. And, we were looking at an enzyme related to breaking down oxalates. Now, the mother and father each had one SNP, and that’s called heterozygous. Three boys, and they all come together, they’re Amish boys, they’re a lot of fun. And I looked at their genomes, and the one boy didn’t have any SNPs at all. And one had won. And the other one had two. Dr. Deb Muth 00:16:41 Interesting. Bob Miller 00:16:42 So, we don’t quite know how these things get handed off, but with the parents each having one, you could have a child with none, one, or two. So, the one, his ability to break down oxalates, which is fine. The other one was slightly impaired, and the other one was dramatically impaired. So, you can have 3 children, and it all depends what the parents have. Now, if a parent has a homozygous, or 2 copies. And the other parent has nothing. Every child will have one. Okay. If both parents are homozygous, that they both have two, Every child will have two. Dr. Deb Muth 00:17:19 too. Bob Miller 00:17:20 Yes, so that’s the way it works, but, you know, but it’s somewhat rare that both parents are homozygous on an enzyme, but it can happen. Dr. Deb Muth 00:17:27 Do we think that infections today, like Lyme disease or mold exposure, things like that, if the parent, the woman, primarily, I’m thinking, is pregnant, and she actively has these infections. Can those infections affect the genetics, kind of like a past sexual transmission did where we thought back in the day? Bob Miller 00:17:47 Yeah, I… I mean, I’m not that much of a geneticist to answer that for sure, but my thought would be no, that at conception, the pattern’s made. Dr. Deb Muth 00:17:55 Okay. And then that’s… that’s the hand you’re dealt. Bob Miller 00:17:58 Yeah. So, I tell people we have good news and bad news. The good news is we can compensate for the weakness. The bad news is we can compensate for the weakness. Dr. Deb Muth 00:18:09 That is so very true. Bob Miller 00:18:11 Yeah, we can’t, because I often get asked, so we’ll do some things now, and we’ll check my genes again, and they’ll be better. It’s like, nope. Dr. Deb Muth 00:18:18 Oh, – – Bob Miller 00:18:19 You gotta play the hands you’re dealt, so… Dr. Deb Muth 00:18:21 That’s right. Bob Miller 00:18:22 You can test your genetics… if you’re looking at the same enzyme, you can test it every year. It’s not gonna change. It’s like the blueprint. Dr. Deb Muth 00:18:30 It’s good and bad, right? It’s the one test you only have to do once in your lifetime. Bob Miller 00:18:34 No, unless, you know, like, our. Dr. Deb Muth 00:18:36 All the time. Bob Miller 00:18:37 Yeah, now our test looks at, called the Functional Genomic Analysis Test of your genomic Resource. We look at 220,000 steps. Dr. Deb Muth 00:18:46 Wow, that’s a lot. Bob Miller 00:18:47 That’s not all of them. Dr. Deb Muth 00:18:49 Right. Bob Miller 00:18:50 So, maybe in the next year, we’re gonna come out with our third version of the chip. And then, if someone wants to get those new things that weren’t on it, they’d have to repeat. But whatever we measured is gonna stay the same. Dr. Deb Muth 00:19:03 That’s a lot of SNPs to look at. Bob Miller 00:19:05 Keeps us busy. Dr. Deb Muth 00:19:06 But there’s still, but there’s still SNPs that we. Bob Miller 00:19:09 That we’d like to have that we don’t have, so… Bob Miller 00:19:11 We started out with version 1 on our genetic test, then we worked with version 2, and we’re already compiling a list of what version 3 would look like. So if somebody has our version 2, And we’re saying, you know what, it’d be nice if we could see these, well, then you’d repeat, but it won’t change what you already know, so… Dr. Deb Muth 00:19:29 Got it, got it. So, when you started out, and you started looking at the research of Lyme disease and chronic infections, which detox pathways are most important for people who struggle with those conditions? Bob Miller 00:19:43 Okay. You know what might make sense as we do a screen share, and I’ll actually show you the pathway. Does that make sense? Bob Miller 00:19:48 Alright, so… let’s see if I… let me just press the share… Dr. Deb Muth 00:19:52 Yep, you should just be able to press share. Bob Miller 00:19:54 And… number 2. Okay. Are we seeing the screen there? Bob Miller 00:20:01 Okay. Dr. Deb Muth 00:20:02 So, this is a map that we made. Bob Miller 00:20:05 And by the way, this is not… All-inclusive of all the things we look at, but we believe this is a core issue. So, where we’re going to start here, there’s something called the microglia. And the microglia are glial cells. They’re in the brain and the central nervous system. And they’re very interesting little creatures, because most of the time, and this is just a drawing of what they sort of look like. Most of the time, they’re in what’s called the M2 anti-inflammatory mood. What that means, these little guys pick up dirt, debris, Recycle them. Turns on an enzyme called interleukin-10 that’s anti-inflammatory. And just kind of does general housekeeping. And just kind of does general housekeeping. However, when a trigger comes along. However, when a trigger comes along. They… it’s the same glial cell, but it moves over to a very pro-inflammatory enzyme. A pro-inflammatory glial cell. And it triggers these 3 enzymes, Actually, these four. That are pro-inflammatory. Tumor necrosis vector alpha, Interleukin-6. NF Kappa B, Inos. Now, these create inflammation. So you might think, well, why is that good? Well, if you have some foreign invader, virus, bacteria coming in, parasite. If you didn’t have these guys coming to the rescue, you would just die of infection. So, these guys are your friend unless they’re your worst enemy. Because TNFA, and we’ll show you when we actually do a demo account, TNFA can be overactive. So, in other words, it over-responds. Interleukin-6 can be overactive. And if Kappa-B can be overactive. The INOS, and I’ll explain each of these as we go through a demo, can be overactive. Now, what that means is, you’re very good at killing virus and bacteria. But this is where autoimmune disease comes in, and just inflammatory conditions. Now, this is just speculation, but we think what happened is, as you know. Thousands of years ago, we didn’t have refrigeration, we didn’t have sewer, we didn’t have pure water, and we didn’t have antibiotics. So, if you made it to 40, you were an old-timer, because everybody was dying of infection. So, what we believe happened is, by what’s called natural selection, Having these overactive. A thousand years ago was to your advantage. Dr. Deb Muth 00:22:31 Hmm. Bob Miller 00:22:32 But now… We have pure water, we have refrigeration, we have sewers, we have antibiotics. But now we have environmental factors that are stimulating them. Now it’s to our disadvantage. And we’ll talk about that a little bit as it relates to the hemochromatosis genes and maybe the G6PD. Dr. Deb Muth 00:22:48 Yep. Bob Miller 00:22:49 Now, why are we becoming so inflamed? Let’s look at the triggers. Now, one of my, favorite expressions is. I was born all the way back in 1954. Dr. Deb Muth 00:23:01 And it was a different world back then. Bob Miller 00:23:05 These are some of the triggers. And we’ll get into these, but right now, high fructose corn syrup, And the high-fat diet. High fructose corn syrup only came about in 1968. So now we’re being exposed to high fructose corn syrup. Then… we didn’t have these, these viruses like COVID. Dr. Deb Muth 00:23:26 Yeah. Bob Miller 00:23:27 Now, there’s now pretty strong evidence that COVID Was actually, you know, made as a gain of function. It’s debated, and I’m not taking an opinion on it, but there’s some people who believe Lyme disease was also a part of experimentation. Dr. Deb Muth 00:23:40 Go. Bob Miller 00:23:41 Then we have molds, and it appears as though mold is getting stronger. you know, 20 years ago, when I was seeing folks, mold wasn’t on the radar. I would say 7 out of the 10 folks we speak to today have mold problems. Yeah, 20 years ago, we talked more about mold allergy being an issue versus mold toxicity being an issue. Right. So… I know some folks are, you know, speculating what’s happening, but one of the theories out there is that EMF is strengthening mold. I don’t know if you ever heard that theory, and I don’t… Dr. Deb Muth 00:24:13 I have. Bob Miller 00:24:14 I’m not claiming it’s true, but it’s an interesting theory. Then even, you know, your black mold from water-damaged buildings. Then our air pollution is getting worse. We’re getting more toxic metals. Dr. Deb Muth 00:24:26 You know, if we have a… Bob Miller 00:24:27 You know, we’re gonna look back someday and say, what were we thinking, smearing aluminum into our armpits? The, what were we doing putting mercury in our teeth? Then, you know, glyphosate. When I was a kid, there was no glyphosate. So, all of these herbicides and pesticides. Polychlorinated biphenols, And then EMF. So, we love our cell phones, you know, and I think unless you, or in the middle of the desert, or down in a cave, you’re being exposed to EMF somewhere. So, you know, we have our cell phones with us, we have, We have Wi-Fi, the towers are everywhere. And we don’t know long-term, but we may find that this can… this creates some inflammation. And I don’t know if you get any folks, but do you have any folks that have… are they EMF sensitive? Dr. Deb Muth 00:25:16 Oh yeah, we have a whole bunch of them. Bob Miller 00:25:18 Yeah, and then if you have any TBIs, So, plenty of things here. that will stimulate into the microglia, M1. Now, you could say, well. We’re all pretty much exposed to the same thing. Why do some people get hit harder than others? So here’s where we’re gonna start. There’s an enzyme called Nrf2 and RF2. And Nrf2 is the enzyme that senses when there’s inflammation. And turns on hundreds of anti-inflammatory enzymes. We’ll show when we do the demo, you can have genetic weakness on NERF2. And NERF2 inhibits and slows down microglia M1. supports M2. Now, if it’s not complicated enough, there’s an enzyme called KEEP1. And KEEP1 inhibits NRF2. And you can actually have gain of function on keep 1, that makes Keap 1 stronger. So… A lot of the people who land on my doorstep So… A lot of the people who land on my doorstep Both parents gave a mutation on KEEP1, making it overactive. Both parents gave a mutation on KEEP1, making it overactive. Dr. Deb Muth 00:26:31 Hmm. Dr. Deb Muth 00:26:31 Hmm. Bob Miller 00:26:32 Suppressing Nrf2, nerve 2 might be weak. So, nobody’s putting the brakes on, M1. And by the same token, Nerve 2 supports M2. Then there’s a process called mTOR and autophagy. mTOR stands for mammalian tard of rapamycin, the growth of new cells. And then autophagy, taking our dead cells and recycling them. We need a balance between the two of them. If we didn’t have mTOR, the sperm and the egg would never become the baby, the baby would never become the adult, we wouldn’t make new cells. But our cells are constantly, you know, the old cells dying off. Autophagy is where we take that debris from the cell and recycle it, just like a farmer Plows the crop under at the end of the year. The dead plant then becomes the fuel for the spring, your dead cell becomes the fuel for the spring, and that’s autophagy. So we’re gonna look back someday and say, what were we thinking? We give our animals growth hormones so they get fatter faster. Oh my. So, we consume those animals, and inventory runs faster. Now, for anybody who’s, You know, maybe above 40, 45 years old. Think back when you were 12, and what did girls look like? They were primarily flat-chested little girls. Now they look like 16-year-olds. Because environmentally, we’re jacking up mTOR. So, mTOR stimulates microglia M1, suppresses microglia M2. Probably 80% of the folks we visit with. This is the part of the problem. NRF2 is weak. mTOR is strong. Environmental factors come along. And this guy gets carried away. He doesn’t do that burst and move back. Stays here. We’re calling that How environmental factors create a locked-in, pro-inflammatory. and neurotoxic phenotype. In other words, once it starts, it just keeps… Feeding upon itself. Alright, so what happens now when microglia is overactive. it triggers these 3 enzymes, TNFA, N of kappa B, And interleukin-6. Each one of these can have genetics that make them run stronger. Then it stimulates an enzyme called NLRP3, Which makes what are called inflammasomes. Now, guess what inflammasomes can be? Your best friend or your worst enemy? Because they will, if you’ve got, again, a virus or bacteria, or possibly even some bad cells in the body. They will zap them. Well, that’s good. Unless it’s overactive. Unless it’s overactive. And then what it does, through interleukin-1 beta, makes excess glutamate. And then what it does, through interleukin-1 beta, makes excess glutamate. Anxiety, gut inflammation, OCD, ADD, autism. And, you know, glutamate, we’ll talk about that a little bit, but glutamate makes you intelligent, highly motivated go-getter. but can also be excitatory. And then, look what it does. Let’s see, do I have the drawing tool here? Yes, I do. Okay. So, it comes down through here, Makes the glutamate. Comes back up through here. through the ADORA 2A enzyme, Then we’ve got a feedback loop that feeds upon itself. Then, through interleukin-18, we make histamine. and mast cells. And then through histamine receptor site number 1, we come back and spin it. And now you’ve just got this spinning feedback loop. So, the glutamate will make you anxious, the histamine will give you allergies and make you anxious. And you’re allergic to everything, and you’re feeling horrible. Now, it doesn’t end there, Dr. Dad. It then goes on to make something called gast dermins that creates pyroptosis, where it actually starts punching a hole in the cell membrane. And you’re only going to be as healthy as your cells are. Just a little background. You know, we’re made up of trillions of cells, and each one of them has what’s called a lipid bilayer, made from lipids, which comes from fats. And you’re only going to be as healthy as those membranes are. So that’s why we coined an interesting phrase. Cellular CPR. Construct the cell. Protect the cell. And restore the cell membrane. And we believe that’s going to be revolutionary in the functional medicine world. So… It’s not hard to figure out that if you start punching holes in the cell membrane, that’s not a good thing, okay? Bob Miller 00:31:22 Now… There’s an interesting molecule called NAD. Thicotide adenoside dinucleotide. And anybody who’s in the, you know, listening to the health podcasts and things, they’re… They’re, they’re learning about NAD. And I’m going to show you a chart later, all the good things that NAD does, but For the most part, it helps what’s called sirtuins. And sirtuins are quite interesting. If anybody’s looking at longevity. The sirtuins is where they’re looking at.Because sirtuins turn on good things. Turn off bad things. And I’ll show some charts on that later. So for right here, this sirtuin uses NAD, to slow down NF-kappa-B. CERT 2 uses NAD to slow down an ORP3. So, if we’ve got genetic weakness on these, or we don’t have enough NAD, We don’t hold this pathway back. Make sense? Dr. Deb Muth 00:32:24 Yeah, makes perfect sense. Bob Miller 00:32:25 Now, I’ll show this a little bit later. So, people are like, oh, well, I’m gonna start taking some NAD. Dr. Deb Muth 00:32:31 Right. Bob Miller 00:32:32 And there’s functional doctors who give NAD intravenous. It was just this morning, I was talking to a woman who said, Oh my gosh. I went and got intravenous NAD, and it took me a month to recover from that. Dr. Deb Muth 00:32:45 Hmm. Bob Miller 00:32:46 what happens is, and I’ll show this in a little more detail, there’s an enzyme called CD38, that’s stimulated by NF-kappa-B. And it takes NAD, To make intracellular calcium. that stimulates NLRP3 and actually makes things worse. So, if we have this guy upregulated, and I’ll show a chart what does that. taking NAD will make you worse. Again, when I go into the software, I’ll show you that whole pathway, so… I would encourage people, you know, just don’t go out and start taking massive amounts of NAD, you know, stick your toe in the water, see how you do. Because everything you’ve heard about, how good it is, is true, unless this guy says, oh, thank you very much, let me make more inflammation. Now, this might be part of our innate immune system, that if we have some pathogen that’s gonna kill us. By golly, we want that to happen. But if this is happening by environmental factors, Then it’s detrimental. So the immune system that protected us a thousand years ago now might be turning on us because of the environmental factors that we showed earlier. All right. Then there’s an enzyme called PARP that’s NAD-dependent, and that actually repairs strain breaks in your DNA. Now, the next thing that happens… is there’s an enzyme called NADPH oxidase that gets stimulated. and something called INOS. Now, I’m sure most people know about nitric oxide. It’s a gas that dilates your blood vessels. That’s why sometimes they’ll even give people drugs, nitroglycerin, to boost their nitric oxide. That’s why people are doing beetroots and other things to boost their nitric oxide. But there’s an OS3 enzyme that makes the nitric oxide that’s good for blood flow. But there’s an INOS That makes nitric oxide to kill pathogens. probably might be the third or fourth time I’ve said this. That’s a good thing, unless it isn’t. So, if it’s killing some pathogen, great. It was just misfiring. it combines… With superoxide that’s made by this enzyme, and makes something called peroxynitrite, which is one nasty free radical that chews you up and spits you out. So, the NOx enzyme, NADPH oxidase, uses NADPH, To make this free radical called superoxide. If we have time, we’ll get into it. NADPH is what your body needs to recycle your antioxidants.So, I coined the phrase, the NADPH steel. Where the NOX enzyme takes this very important NADPH, And rather than being useful, makes superoxide. Now, again, is that fine if you’ve got some bacteria to kill? Of course. But if it’s just chronically running, it’s just making all this chronic inflammation. Then it makes something called hydrogen peroxide. And we need to clear hydrogen peroxide by 3 enzymes, catalase, thyroid reduction. And glutathione peroxidase. If we have genetic issues on here, or we don’t have the cofactors. There’s something called the Fenton reaction, discovered in 1895 by Dr. Fenton. Where hydrogen peroxide combines with iron to make what are called hydroxyl radicals. And guess what they do? They create lipid peroxides, That damages your cell membranes. Now, again, the body’s pretty darn amazing. We have glutathione, And here’s where your body’s taking glutathione and recycling it. But look who’s needed to recycle it. NADPH. So, if this guy up here is chewing it up, We don’t recycle our glutathione. And then an enzyme called glufon peroxidase 4, Takes this damaged lipid and repairs it. So, here we’ve got this protecting, we want to protect it by not having this happen. But then we also need this guy to do the restoration. So, there’s a lot that can go wrong in here, Dr. Deb. Dr. Deb Muth 00:37:07 There’s a lot that could go wrong. And I can imagine some of my listeners are thinking that lipid peroxidase, is that the same thing as what they’re thinking of when we talk about lipids and cholesterol? Is that the same process that’s happening there? Bob Miller 00:37:22 Well, no, no, the lipids can be used to make cholesterol, but here we’re talking about where they’re going to build the cell membrane. And they’re being… and they’re being, destroyed. If anybody would like to see a visual representation of this, just go on YouTube. And type in, ferrooptosis Animation. cool little video, it’s about 3 minutes long, and it shows the lipids coming over, being oxidized, and now GPX4 fixes them, so… YouTube, Pharaoptosis Animation, cute little video. It’s just that really… Shows vividly what we’re… what we’re talking about here. Now, this is… Dr. Deb Muth 00:37:59 And so this is very common, too. Like, a lot of people do hydrogen peroxide IVs. Dr. Deb Muth 00:38:04 And so, if somebody doesn’t know their genetics, they could have a problem with doing those, just like they could doing the NADHIVs, correct? Bob Miller 00:38:13 Sure, yeah, yeah, yeah. So, I’ve talked to so many, you know, of course, the hydrogen peroxide kills pathogens. I mean, that’s what it does. So… but I’ve spoken to so many people that said. I had one client that said they’ve never been the same after having one hydrogen peroxide infusion. Dr. Deb Muth 00:38:30 Interesting. Bob Miller 00:38:31 Yeah. So… it can be… I see why people use it, because it. Bob Miller 00:38:36 pathogens, But on the other hand. And now’s a good time to speak about… I don’t have it on here, but there’s a, there’s an enzyme called the HFE gene. And that is what causes you to absorb iron. And there’s mutations in it that cause something called hemochromatosis. Were you overabsorb iron? Now, true hemochromatosis is when both parents give you a mutation. But there’s now growing evidence even a heterozygous can cause a little bit more iron absorption, not to the human chromatosis point, but overabsorption. So, if you overabsorb iron, And you have too much hydrogen peroxide that’s not cleared, All kinds of inflammation. Now, what’s happened is sometimes this inflammation Will damage the red blood cells. And some well-meaning doctor says, oh, you need some iron. And they take iron and it makes it worse. So, can’t tell you how many people I’ve said, you’ve got the overabsorption of iron, and they say, well, that can’t be right, because I’m low in iron. Well, that could be because it’s being chewed up here. Dr. Deb Muth 00:39:40 Sure. GPX1 and TXN turn it into, to water. The, catalase turns it into water and oxygen. Dr. Deb Muth 00:39:58 Now, I see a lot of my clients who have mutations or SNPs on that GPX gene, on that glutathione gene. And they really struggle to clear a lot of their toxins. Bob Miller 00:40:12 Sure. Dr. Deb Muth 00:40:14 Yeah, absolutely. Well, GPX4. Bob Miller 00:40:18 is what, repairs, but you can see GPX1 Is what uses glutathione. To turn hydrogen peroxide. So, but it all depends upon having enough glutathione. Dr. Deb Muth 00:40:30 Yeah. Bob Miller 00:40:31 Well, guess who controls making a glutathione? Dr. Deb Muth 00:40:34 Nerf 2. Bob Miller 00:40:37 So, if you have a keep one weakness, or strength to two… I’m sorry, keep one is too strong. Nrf2 is too weak. You don’t make glutathione. So, when a lot of people do that, it’s like, well, I’m gonna take glutathione. Dr. Deb Muth 00:40:51 Right. Bob Miller 00:40:52 And some do great, and some do poorly. You know, because… and I’ll show this on one of the other charts. You can see here that the, The glutathione has to be recycled. And if we don’t recycle it, it actually turns into superoxide free radical. So… NADPH are the cofactors, For taking the oxidi… here’s oxidized glutathione, here’s reduced. So, this is a good glutathione. After it does its job, you can see it becomes oxidized.We need to recycle it. Well, if we have weakness on the enzyme that does that, or a weakness in Nrf2, or not enough NADPH. The oxidized glutathione never gets recycled. So, I’ve talked to a lot of people who said, oh, glutathione made me so sick, and say, well. Dr. Deb Muth 00:41:43 Yeah. Bob Miller 00:41:44 You need it, but you need to recycle it. Dr. Deb Muth 00:41:46 Can you speak for just a brief moment, too, about MTHFR? That is a very popular gene, it’s all over social media as the major gene, but can you speak to a little bit about that, and how that fits into this whole process of things? Because it is just such a small piece. Dr. Deb Muth 00:42:04 understanding genetics. Bob Miller 00:42:06 Yeah, to be honest, it drives me nuts. Dr. Deb Muth 00:42:08 Me too. Bob Miller 00:42:11 Alright, so… You know, there are people on social media I won’t say what I think, I’ll be kind. But… But the, And, you know, they might mean well. But they talk about, if you have MTHFR and COMT and PEMT, that’s… oh my goodness, that’s horrible, and we’ll fix that for you, and you’ll be fine. Bob Miller 00:42:36 it just irritates me to no end. And it really could get anybody who’s doing this legitimately in trouble. I mean, I’m afraid someday, you know, there might be some cracking down on this kind of nonsense. Now, to answer your question about MTHFR. Dr. Deb Muth 00:42:51 I mean, it really is, but I’ll tell you what, why don’t we hold that thought until I go to another map and I can actually… Okay. Bob Miller 00:42:56 But the real… the cliff notes is the MTHFR puts a methyl group on your folate, which is needed, but it has gotten way, way, way too much attention. And people learn they have MTHFR, and they start taking a multivitamin with methylfolate, then they take a B vitamin with methylfolate. Dr. Deb Muth 00:43:13 And they’re pushing it too hard. Bob Miller 00:43:15 Yeah. So I can’t tell you how many people I’ve helped by saying, stop it. Dr. Deb Muth 00:43:20 Yeah, take less of it. Bob Miller 00:43:21 Take less of it, yeah. So, yeah. Yeah, there’s a… If somebody, say, ranked the enzymes at their level of importance, MTHFR might be 40 or 50 on a scale of 100, you know. Keep one Nerf two. big deals. Dr. Deb Muth 00:43:40 deals. Bob Miller 00:43:41 NQO1 that I didn’t even talk about yet, NQO1, takes your, NA… your NAD goes into NADH, To make electrons for the electron transport chain. you need NQ01 to bring that back. If that’s not working, and I’ll show you on the NAD map how disastrous that can be. Now, the next piece is here, and I think You know, if you talk to any school teachers and say, if you’ve taught for more than 10 years, how are the kids today? Every one of them says, more ADD, ADHD, more autism. Just look at human beings, we’ve never been so agitated. You know, everybody, and it might be a social media thing, but people take a position on something, and if anybody doesn’t share that position, they view them as the enemy. Dr. Deb Muth 00:44:29 And it’s kind of scary what’s happening to us. Bob Miller 00:44:33 So, we can’t agree to disagree anymore. We see anybody who has a differing opinion as the enemy. And, you know, there was… there’s people that didn’t have Christmas dinners together, because they had political differences, like… Dr. Deb Muth 00:44:44 Excuse me. Bob Miller 00:44:45 can’t you put your political differences aside to have Christmas together, you know? Dr. Deb Muth 00:44:49 Right? Bob Miller 00:44:50 become that, you know, no matter what your position is, and I’m not saying anyone’s right or wrong, I’m just saying. You know, in the old days, they used to say that the Republicans and Democrats in Congress would argue policy and then go have dinner together. And now everybody’s all up in arms, angry. Dr. Deb Muth 00:45:05 Yeah. Bob Miller 00:45:06 So… There’s likely multiple reasons for that. But let me show you one of them. That, you know, to what degree this is… very important, we don’t know, but I think We’re beginning to believe this is very important. So, there’s something… there’s a neurotransmitter called GABA. And God buys the don’t worry, relax, be happy. Chill. Okay. Dr. Deb Muth 00:45:31 Nobody has enough of that anymore. Bob Miller 00:45:33 Well, yeah, you’ll be surprised what I’m gonna show you. So, let me see if I can find a, Let me see if I can find the right slide here. Let me look for it here. So, there’s something called a GABA receptor site. And here you can see… This is a neuron, and this is where you, The neuron normally is excitatory. However, there’s normally low chloride in the neuron. Dr. Deb Muth 00:46:09 Hmm. Bob Miller 00:46:10 So, GABA itself is neither relaxing. For excitatory, all GABA does, it opens up what’s called a chloride channel. And then chloride, which has a negative charge, will flow into the neuron. Follow me there? Dr. Deb Muth 00:46:26 Yep. Bob Miller 00:46:27 And as it does, it changes this from a positive charge to a negative charge, And it’s relaxing. and inhibitory. Dr. Deb Muth 00:46:34 Hmm. Bob Miller 00:46:36 Now, on the other hand, there’s enzymes called NKCC1, That will push chloride in. and KCC2 that will bring chlor… oops and bring chloride out. And then there’s a sodium channel. And, sodium has a positive charge. And glutamate will push that in. So, as long as this is happening. And GABA says, receptor sites, open, chloride goes in, Chill. However, If NKCC1 Pushes extra chloride in. KCC2 doesn’t pull it out. and GABA hits the receptor site, the GABA comes flowing out, Sodium comes in, And now it’s excitatory. So Gabba didn’t change. GABA just opened the receptor site, that’s all it does. Dr. Deb Muth 00:47:33 Yeah. Bob Miller 00:47:34 But it’s the chloride balance that’s going to determine whether this is relaxing or not. Now, these are the things that go along with when they lose that KCC2 or gain NKCC1. Pain and sensitivity, burning electrical, neuropathic pain. Normal touch hurts. Sound and light sensitivity. Tinnitus can flare. Headaches and migraines. Seizure tendency. Body jolts. Spasticity, cramps, stiffness, startle reflex. Trouble falling asleep, non-restorative sleep. Anxiety, stress, reactivity, that’s what we have now. Hyperarousal, panic-like surges, irritability, racing thoughts. Brain fog, slowed processing, working memory slip-ups. Mental fatigue. Episodes of racing hearts, sweaty palms, guts on edge. Those are all the things that happen when this GABA switch occurs. Now, here’s what happens, and this is what I’m going to be presenting at an autism conference. When you have a newborn, they need that NKCC dominant to develop. By early childhood, it should… or, sorry, early adulthood. we should move over to the KCC dominant, that’s the taking the chloride out. Nice-looking 25-year-old boys, functioning very well. However, when we get microglia M1 upregulated. Because of environmental toxins, processed foods, Tylenol, aluminum. they stay in NKCC1 dominant, and there’s ADD, ADHD, Autism, the whole spectrum. because… They’ve not moved over to the… They’ve not moved over to the KCC2. And again, this is caused by… Environmental factors. Stimulating the microglia. And then, interleukin-1, interleukin-18 weakens KCC2, interleukin-1 beta, Strengthens NKCC1. high chloride. We open up the chloride channel, In Rebell Excitatory. So, I think when, When the pediatricians get ahold of this, they’re going to be very excited to know that This could be why we’re seeing such a rise, and not just autism, but ADD, ADHD, anxiety, the whole shit mess. Dr. Deb Muth 00:49:58 thing. Bob Miller 00:49:59 Yeah, so… and you can see NF-kappa-B stimulates that. These stimulate it, and I think that’s why everyone’s getting so anxious. Now, there’s a little bit more to it, and we’ll get into this when we look at some of the maps, but… The, the glutamate, Which is excitatory. will stimulate the NMDA receptor, make more glutamate, And glutamate will inhibit KCC2. And then we also need an astrocyte To, take both ammonia And glutamate, and… Turn them back into glutamine. And I’m going to talk to you a little bit about arachidenic acid, and if we have too much arachidenic acid. or TNFA is upregulated, that doesn’t happen. Ammonia goes up, and there may be multiple reasons for this, but this is a reason why some of the autistic kids do flapping. Dr. Deb Muth 00:50:49 Hmm. Bob Miller 00:50:50 Because they’re not clearing their ammonia. And you can tell if somebody has high ammonia by… they get that old person smell, you know. Dr. Deb Muth 00:51:00 Yup. Bob Miller 00:51:01 your vehicle cycle’s not taking out the, the ammonia. Now, last pathway here. There’s growing interest in mast cell activation. So, back here, we talked about peroxynitride. And that will stimulate mast cells, and those are white blood cells that are your best friend, unless they’re your worst enemy. Then it’ll make histamine. And there’s enzymes called histidine decarboxylase that’ll make more. Dr. Deb Muth 00:51:28 I’m sure everybody’s heard of DAO, the enzyme that degrades histamine. Yep. Bob Miller 00:51:31 We can have genetic weakness, we don’t make that. There’s an enzyme called histamine and methyltransferase, That, That breaks down the histamine. Then if we don’t do that, it’ll get stuck in the histamine receptor site. And then it’ll make something called, renin. Which will cause angiotensinogen to turn into angiotensin. One, that turns into angiotensin II,And that’s where people make aldosterone, where they’ll get the, The swollen ankles and high blood pressure. But interestingly, there’s an enzyme called ACE2, that takes this guy and turns it into angiotensin 1-7, Which is anti-inflammatory and also inhibits… TNFA. Now, you can have weakness on ACE2, But… and anybody’s saying, that sounds familiar? Dr. Deb Muth 00:52:25 That’s where COVID comes in, using ACE2. Bob Miller 00:52:28 And now we just found there’s literature that if you get COVID long enough, it can actually make ACE2 not be able to work as well. So look what it does. It comes down here, stimulates the NADPH oxidase, More superoxide. More peroxynitrite. And we’re on a cycle here. We’ve actually named this the Home Cycle Hypothesis, the proposed feed-forward loop. That just keeps feeding on itself. All being caused by… Primarily, The environmental factors. But hitting those who have genetic weakness the hardest. That’s why. Dr. Deb Muth 00:53:08 To the people. Bob Miller 00:53:09 Don’t live in a moldy house. One person is sick as can be, and the other person says, well, you must be imagining things, because I don’t feel anything. Dr. Deb Muth Yeah. Same thing with long haul, right? Two people can both get sick, one gets sick and never seems to recover, and somebody else gets sick, and they have absolutely no problems with it at all. Bob Miller 00:53:30 Sure. Well, think about it, if you get COVID, and ACE2 is weak, and some of this other stuff is going on. This thing just starts feeding upon itself. Dr. Deb Muth 00:53:38 Keep creating more inflammation, more complications, nothing’s calming down. Bob Miller 00:53:43 Yeah. Now, you, you ask about, MTHFR. So, this is the, this is the, the software called Functional Genomic Analysis. There’s a demo report we have. So, let’s talk a little bit about, MTHFR. So, we actually have a map called a methylation map. Now, what happens is, when you do your saliva test, you, you know, you spit, you put some saliva. in a collection kit, goes to a lab, takes out the DNA data, sends it to the computer, and now you can actually see it visually. Okay. So, it’s gonna take a second for this, data to load up, it’s, and each of these Circles, each of these ovals, is an enzyme. And the data gets loaded up to see where it is. So, until it gets loaded up here, I didn’t preload this. There it goes. So… The primary thing about methylation is There’s a nasty substance called homocysteine that, if it’s too high, can really be detrimental. The body takes methylfolate, and combines with methyl B12, To bring this back up to methionine. And then through the MAT genes, we make SAMI, S-adml methionine. Which is involved in so many processes. Then after it does its thing, it turns back into homocysteine. And this thing needs to keep spinning around. That’s why, you know, it’s a good idea to keep homocysteine at, do you have a number that you’d like? 7, 8? What do you like for a number? Dr. Deb Muth 00:55:24 Yeah, I like mine below 7. Bob Miller 00:55:26 Yeah. So if the homocysteine goes too high. It, caused all kinds of problems. So, here’s where you ask about the MTHFR. So, here you can see on this individual. I click on MTHFR, and you can see it comes up here, here’s the C677. And you can see here where it says, variants. I’ll… I’ll draw in case somebody’s having a hard time seeing that. So, you can see there’s nothing in there. That means there’s no genetic mutations. If one parent would have given a mutation, there’d be a 1. If both parents did, there’d be a 2. Now, here’s why Yes, methylation is important, I’m not saying it isn’t important, but look at this MTHFRC677. In my software. Only 42.5% of the population does not have a mutation. 44.7% have won. 12.9 have 2. So, this isn’t some rare, oh my god, I’m gonna die… Kind of thing, yeah. Dr. Deb Muth 00:56:27 Right. Bob Miller 00:56:28 So, And then what happens is that, and again, I’m not dismissing methylation, I… we could do a whole show on methylation. Bob Miller 00:56:36 get it. But I think that what people are doing is they’re, they’re learning about MTHFR, they get it measured, they panic. They start taking massive amounts of methylfolate, which many times is to their detriment. Dr. Deb Muth 00:56:50 Well, it’s… and isn’t it true, too, with MTHFR, like, you have to also look at MTR, MTRR, and the more we stack up of those, the more complicated than MTHFR can be. It’s not… it’s not as simple as just saying MTHFR 677 versus 1298. It’s more complex than that, kind of like what you’ve already shown with some of the other things. There’s more to it than just that one little sliver. Bob Miller 00:57:17 Oh, sure, well, let’s take a look. So, remember I said there’s a cofactor? One of the cofactors is called FAD. Just a Bob Miller observation, that’s all. But when people have trouble with their riboflavin and they don’t have enough FAD, They’re doing much worse than people who have just a C677. So, right here, you could have perfect C677th. And if you don’t have the cofactor, it’s not gonna work, okay? Dr. Deb Muth 00:57:48 And as you said, there’s an MTR enzyme. Bob Miller 00:57:51 that takes methylfolate and methyl B12, to spin it around. So, here on this individual. here’s your… here’s your B vitamins, or I’m sorry, your B12s. There’s an enzyme called TCN1 that takes it from the stomach into the blood. Then there’s other enzymes that take it from the blood into the tissue. And if you’re having trouble here. Well, then you’re not going to have this working, so… Even if you don’t have MTHFR, And you have MTR, like this, no, I’m sorry, this person doesn’t. But they have the MTRR, and then they don’t have enough B12, this isn’t gonna work, aside from that. And then there’s a middle pathway. And then there’s enzymes called the MAT1. they take the methionine to the salmon. If that’s not working, we stick… we get stuck in methionine. So, it’s, it’s not just an MTHFR. And then, one of the things that people forget about. is through these CBS enzymes and CTH, We make cysteine, which is needed to make glutathione. The master antioxidant. So, it really is that… I call it the, The 3D chess game played underwater. Dr. Deb Muth 00:59:07 It really is. I mean, I see people who have CVS, COMT, glutathione, MGHFR genes. And some of them function just fine. Like, they have Like, I look at this person and I’m like, oh my gosh, I don’t know how they’re functioning because they’re double mutated on so many pathways, but yet they don’t have a lot of symptoms, they don’t have a lot of complications. Somehow their body has figured out a way to adapt to what it has so it can stay alive and it can function at a high functioning level. Bob Miller 00:59:36 Yeah, and they may be, you know, eating right? Yeah. Staying out of a moldy house. reducing stress. So, it’s diet, it’s stress, it’s genetics, environmental factors. So, yeah, we can’t just say somebody’s gonna be good or somebody’s gonna be bad. You know, some people get scared, oh, I got all these, it’s like, well… Bob Miller 00:59:56 Are you living in a moldy house? You know, and if you live in a moldy house and your glucuronidation pathway doesn’t do well, or if you’re, you know, a smoker, or you’re constantly eating junk food, I mean, all. Bob Miller 01:00:07 things come together. Although, you know, when we focus on genetics, we’re well aware that this is just a piece of it. You know, you could have identical twins, Genetically, and if one… Is exposed to mold and smokes and drinks and stressed out. They’re gonna be a whole lot sicker than their sibling. Bob Miller 01:00:28 Yep. Dr. Deb Muth 01:00:29 Yeah, it’s that concept of taking twins, and one gets raced with one family, and one gets raced with another family, and they don’t have the same… problems that… that each other have, you know? It’s a very unique situation, we don’t think about that enough. Bob Miller 01:00:44 Alright, so again, genetics loads the gun, environment pulls the trigger. So, if you’ve got a loaded gun, but you don’t have the triggers, you’re okay. Dr. Deb Muth 01:00:53 Yeah. Bob Miller 01:00:54 Yeah. So, remember I said I was going to talk about NAD? So, here’s NAD, and what it does, it turns into NADH. And what NADH does, it, Comes down this pathway, what’s called the electron transport chain. And that makes your ATP, that’s your energy. So, if this wasn’t working, we wouldn’t be alive, because we wouldn’t have energy. So it donates an electron, that’s why it’s called electron transport chain. So, we need NAD, To make this, to make the energy. But remember I said that NQ01, this would probably be, like, on my top 10 list of… Bob Miller 01:01:36 Much more important than MTHFR. This one takes NADH back to NAD. If we’re stuck over here, We’re low in this NAD+, But what happens is, NQO1 also provides CoQ10. And CoQ10 Is what’s needed for the electron transport chain to flow. So if we get too many electrons up here. And they don’t turn them into energy. They make a nasty free radical called superoxide. Okay. Now, NAD plus also makes NADPH, And that is needed. Remember I said we need to recycle our antioxidants. So, if we have a problem with FAD from riboflavin. Yeah, we don’t have enough NADPH, Glutathione’s not getting recycled, and you’re gonna be inflamed. And you take glutathione, you’ll feel worse. There’s another enzyme called thimoredoxin. Same thing, needs NADPH and FAD. And same way with your nitric oxide, there’s an enzyme called NOS3, That makes the nitric oxide that dilates your blood vessels. And if we don’t have enough NADPH or fat, You’re gonna make superoxide. Rather than nitric oxide. Now, remember

En este episodio, converso con Carlos Henao sobre una experiencia que transformó profundamente su manera de ver la vida, el trabajo, el éxito y las prioridades.Carlos comparte su historia personal tras enfrentar un tumor cerebral, desde el impacto inicial del diagnóstico hasta el proceso de cirugía, recuperación y reeducación del cuerpo. También hablamos sobre resiliencia, familia, liderazgo, espiritualidad, humor en momentos difíciles y la forma en que una experiencia límite puede cambiar la relación con el futuro, la ambición y la muerte.Una conversación honesta sobre aceptar lo que no controlamos, encontrar perspectiva en medio de la incertidumbre y recordar qué es verdaderamente importante.Capítulos:00:00 Introducción a momentos transformadores01:37 La historia de Carlos: de Venezuela a Barcelona09:05 El camino hacia el marketing y la creatividad17:24 Decisiones de vida: cambios y oportunidades25:30 El impacto del tumor cerebral en la vida de Carlos28:47 La llegada de la familia y el apoyo emocional29:50 Reflexiones sobre la vida y la muerte31:16 La dificultad de compartir el proceso con los seres queridos32:48 La perspectiva espiritual y estoica de la experiencia35:08 Lecciones de vida y la aceptación de la mortalidad37:35 El impacto del pasado familiar en la experiencia actual40:05 La experiencia de la cirugía y el humor en momentos difíciles42:18 El proceso de recuperación y la reeducación del cuerpo44:57 El lado emocional y la descalibración tras la experiencia46:57 Cambios en la perspectiva y la planificación futura48:18 Compartiendo aprendizajes y el deseo de ayudar a otrosConecta:LinkedIn de Carlos: https://www.linkedin.com/in/chenao/ This is a public episode. If you would like to discuss this with other subscribers or get access to bonus episodes, visit becomingschool.substack.com

Unprocessed red meat and cancer risk remains one of the most debated topics in nutrition science, partly because the evidence is often presented in overly simplistic terms. The key question is not whether to adopt a vague "balanced" position on red meat, but whether the evidence clearly identifies intake levels at which colorectal cancer risk increases and whether controlled human trials support plausible mechanisms for that risk. A second issue is whether claims that fibre, vegetables, or an otherwise "healthy diet" can neutralise high red meat intake are actually supported by the mechanistic evidence, or whether they overstate what dietary context can plausibly offset. In this episode, Danny and Alan examine the evidence base by moving beyond the usual epidemiology-only debate. They discuss why regional intake patterns and dose thresholds matter, then explore controlled human feeding studies showing how higher red meat intake can increase endogenous N-nitroso compound formation, faecal water genotoxicity, and other mechanistic biomarkers linked to colorectal carcinogenesis. Timestamps: [01:11] Defining the exposure and outcome [02:34] Carcinogen labels explained [07:54] Epidemiology and dose thresholds [14:04] Interpreting null findings [19:09] Bingham 1996 nitroso study [25:20] Hughes dose response trial [33:49] Cross 2003 heme iron mechanism [42:55] Fecal water genotoxicity [55:42] Tumor mutational signatures [59:38] What we can conclude now [01:04:10] Practical intake recommendations [01:08:41] Key ideas segment (premium-only) Links: Go to episode page (includes links to studies mentioned) Subscribe to Sigma Nutrition Premium Join the Sigma newsletter for free Enroll in the next cohort of our Applied Nutrition Literacy course

Featuring perspectives from Prof Thomas Powles, including the following topics: Circulating tumor DNA (ctDNA) analyses with adjuvant nivolumab for MIBC in the CheckMate 274 study (0:00) Use of ctDNA to guide response-adapted bladder preservation for patients with MIBC (2:27) ctDNA response-adapted treatment de-escalation for patients with metastatic urothelial carcinoma: The CT-READ trial (10:26) Emerging data and studies regarding urinary tumor DNA (18:04) CME information and select publications

In this podcast, experts Manmeet Ahluwalia, MD, MBA; and Ashley S. Margol, MD, MS; discuss targeted therapies for adult and pediatric low-grade gliomas, pediatric diffuse midline glioma, and adult glioblastoma.

Sheinbaum apuesta por el diálogo con la CNTE Continúan cerradas estaciones de la Línea 2 del STC MetroAlbania acusa injerencia de Irán en protestasMás información en nuestro podcast#grc

Interview conducted with Prof Bernd Kasper on March 5, 2026, by Dr Neil Love, including the following topics: Current management of desmoid tumors: A review from the Desmoid Tumor Working Group (0:00) Long-term nirogacestat treatment in adult patients with desmoid tumors: Updated efficacy and safety from the Phase III DeFi trial (8:26) Phase IV trial of nirogacestat in adult premenopausal women with desmoid tumors (17:35) CME information and select publications here.

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An upcoming resupply mission will carry tumor samples to the International Space Station for research. Experiments in microgravity have yielded shocking results: Some tumors triple in size in just 10 days—the kind of growth that could take 10 years on Earth. What does that mean for science, and for astronauts?  Joining Ira to discuss this new frontier in cancer research are hematologist Catriona Jamieson and aerospace engineer Meenal Datta. Guests:  Dr. Catriona Jamieson is a hematologist at the UC San Diego Health Moores Cancer Center in California. Dr. Meenal Datta studies the physics of cancer at the University of Notre Dame's College of Engineering in Indiana. Other episodes you may enjoy: How A Fringe Idea Led To Lifesaving Cancer Treatments To Get Ready For Mars, NASA Studies How The Body Changes In Space Want SciFri gear? Check out our new shop! Transcripts for each episode are available within 1-3 days at sciencefriday.com. Subscribe to this podcast. Follow our show on Instagram, TikTok, Facebook, and Bluesky @scifri and sign up for our newsletters. Got a science question that's keeping you up at night? Call us: 877-4-SCIFRI Hosted by Simplecast, an AdsWizz company. See pcm.adswizz.com for information about our collection and use of personal data for advertising.

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