Podcasts about acth

Cushing's disease. The adenoma in Cushing's disease causes the pituitary gland to produce an excessive amount of adrenocorticotropic hormone (ACTH), which, in turn, stimulates the adrenal glands to produce more cortisol than the body needs. Additionally, cortisol is produced in response to acute stress, triggering the well-known "fight or flight" response. In both situations, cortisol plays a vital role in regulating blood pressure, mobilizing energy reserves, and temporarily suppressing the immune system to deal with immediate challenges.

Ständig erschöpft. Gereizt ohne Grund. Dauernd unter Strom – kommt dir das bekannt vor? Dann könnte das Stresshormon Cortisol eine Rolle in deinem Leben spielen. Es hilft uns zwar eigentlich, mit Druck und Gefahren umzugehen. Aber wenn es dauerhaft hoch bleibt, wird's kritisch. Denn zu viel Cortisol macht uns auf Dauer krank, ohne dass wir es merken. Wie erkenne ich, dass mein Körper im Stressmodus festhängt? Was kann ich konkret tun, um wieder ins Gleichgewicht zu kommen? Und wie viel Ruhe braucht der Mensch wirklich? In dieser Folge spricht Host Niki Löwenstein mit der Wiener Fachärztin für Innere Medizin und Gastroenterologie Dr. Corinna Geiger, die in ihrer Praxis mit den körperlichen und seelischen Folgen von chronischem Stress konfrontiert ist. Der Körper bleibt im Überlebensmodus Das Hormon Cortisol wird in den Nebennieren produziert und ist Teil unseres körpereigenen Alarmsystems. Es mobilisiert Energiereserven, hält uns wachsam und bereit für schnelle Reaktionen. Ideal, wenn wir in Gefahr sind oder unter Zeitdruck stehen. Doch genau dieses System läuft bei vielen Menschen inzwischen dauerhaft. Der Körper bleibt im „Überlebensmodus“, was langfristig das Immunsystem schwächt, den Schlaf stört, den Blutzucker durcheinanderbringt und sogar Entzündungen fördern kann. Expertin Dr. Corinna Geiger erklärt, wie sich ein hoher Cortisolspiegel auf Schlaf, Verdauung, Energielevel und Stimmung auswirkt – und welche Schritte helfen, um Körper und Kopf runterzufahren. Du erfährst, wie du Stresssymptome besser erkennen kannst, warum dein Bett wirkungsvolle Medizin sein kann – und was wirklich hilft: von Ernährung über Bewegung bis zur bewussten Pause. Eine Folge für alle, die sich nicht nur funktionierend durch den Alltag schleppen, sondern bewusst gut auf Stress reagieren wollen. Was wir außerdem aus dieser Episode mitnehmen: Cortisol & Adrenalin – Best friends? Warum wir im Alter dünnhäutiger werden Wozu wir ACTH brauchen Was Opioid-Rezeptoren mit Cortisol zu tun haben Warum langes Ausschlafen ein Mehr an Stress bedeutet Welche Auswirkungen Stress über lange Zeit hat Warum wir ungesünder essen, wenn wir schlecht schlafen Warum sich bei Stress manchmal der Magen zu Wort meldet Warum Magnesium vor dem Schlafengehen sinnvoll sein könnte Show Notes: Mehr zu Dr. Corinna Geiger erfährst du HIER.

Today, we're talking about how nootropics and peptides like Semax (See-max) and Selank (SEH-lank) work together to support cognitive health, improve focus, and reduce mental fatigue. Let's start with nootropics. These are substances that are designed to support and enhance mental performance. Some work by improving memory, others help with focus, alertness, or reducing brain fog. Nootropics can be: Natural, like L-theanine or Lion's Mane Nutraceuticals, like Alpha-GPC or CDP-Choline, which support neurotransmitter production Or synthetic, like Modafinil or racetams “RASS-uh-tams”, which are often used off-label to promote wakefulness and focus Most nootropics work by affecting levels of key brain chemicals like dopamine, acetylcholine, or norepinephrine. They don't “make you smarter,” but they can improve how efficiently your brain is working—especially under stress or fatigue. Now, let's talk about peptides—specifically Selank and Semax, which are two of the most well-known nootropic peptides. Selank is more about calming and emotional regulation, while Semax leans into cognitive enhancement and brain performance. Think of Selank as the anti-anxiety sidekick and Semax as the mental sharpener. Selank works by boosting GABA activity, which helps calm the nervous system. That's why it's often used to reduce stress and anxiety without causing drowsiness or dependence — unlike traditional anti-anxiety meds. Interestingly, it also slightly increases BDNF, the brain growth factor that supports memory and learning. Semax, on the other hand, has a much stronger impact on BDNF. It's derived from ACTH, but it doesn't raise cortisol levels. Instead, it enhances BDNF, dopamine, and serotonin activity, making it great for improving focus, mental energy, and even mood. And that's what makes them such a powerful combo for some people. Selank helps create a calm, clear mental space — kind of like reducing background noise — while Semax boosts the brain's signal, improving neuroplasticity, motivation, and mental clarity. Together, they offer a full-spectrum brain support: emotional balance and cognitive performance. Whether you're dealing with brain fog, anxiety, or just want to perform at a higher level, these peptides could be worth exploring. Stacking Nootropics with Peptides One of the most popular strategies for cognitive support is to combine or stack peptides with nootropics. For example: Selank pairs well with L-theanine for calming, focused energy. L-theanine, an amino acid found primarily in green tea, promotes relaxation and reduces stress without causing drowsiness by increasing calming neurotransmitters like GABA and serotonin. Lion's Mane mushroom, a natural nootropic found in both wild and cultivated forms, can be stacked with Semax to naturally support memory, focus, and neurogenesis. Semax can be used with Alpha-GPC to support both short-term concentration and long-term brain health. Alpha-GPC (Alpha-glycerophosphocholine) is a choline-containing nutraceutical, often derived from soy or sunflower lecithin, that acts as a powerful nootropic. It increases levels of acetylcholine, a key neurotransmitter involved in learning, memory, focus, and muscle control. Because of its ability to cross the blood-brain barrier efficiently, Alpha-GPC is often used to enhance cognitive function, support brain health and neuroprotection, and improve physical performance by boosting power output and recovery in athletes. Semax can also be used with CDP-Choline for memory support, brain fog, and age-related cognitive decline. It too is a nutraceutical that provides choline, which the brain uses to produce acetylcholine, a neurotransmitter essential for memory, learning, and focus. It also delivers cytidine, which converts into uridine—a compound that supports neuron repair and brain cell membrane synthesis.  Alright, so one question we get a lot is, “What's the difference between CDP-Choline and Alpha-GPC?” It's a good one—because they're both great choline sources, but they work a little differently. Alpha-GPC delivers choline more directly, which means you'll feel that boost in focus and mental energy a bit faster. It's especially handy if you're doing high-intensity brain work or even something athletic. Lastly, I also want to dive into something a lot of people are curious about, Modafinil and racetams (RASS-uh-tams).  Modafinil (Provigil) is a prescription, stimulant medication used to treat sleep disorders (e.g., narcolepsy and obstructive sleep apnea) and shift work disorder. It's also used off-label as a focus-enhancing nootropic. It works by promoting wakefulness in the CNS. Researchers don't know exactly how it works, but it appears to affect areas in the brain that control attention and wakefulness. Racetams (e.g., Piracetam, Aniracetam, or Oxiracetam) are a class of compounds that enhance acetylcholine activity and neuroplasticity, leading to better learning, memory, and focus with subtle, non-stimulant effects.  While Modafinil provides a noticeable surge in alertness and productivity, racetams offer a more gradual cognitive boost that can be ideal for sustained mental performance. Just remember, peptides provide foundational support—helping your brain repair and function better long-term. Nootropics can then layer on immediate effects, like sharper focus or improved mood. Thanks for listening to The Peptide Podcast. If you found this episode helpful, please follow or leave a review. And if there's a topic you'd like to hear more about, feel free to reach out—we'd love to hear from you. As always, have a happy, healthy week! We're huge advocates of elevating your health game with nutrition, supplements, and vitamins. Whether it's a daily boost or targeted support, we trust and use Momentous products to supercharge our wellness journey.  Momentous only uses the highest-quality ingredients, and every single product is rigorously tested by independent third parties to ensure their products deliver on their promise to bring you the best supplements on the market.

In today's episode, we detail the enteric nervous system and regulation of gastrointestinal motility. We discuss factors including dysautonomia, stress, microbial overgrowth, and more, with regards to potential effects upon gastrointestinal motility. We further detail symptoms of altered GI motility. Topics:1. Introduction to Gastrointestinal Motility- Orchestrated contraction of smooth muscles that propel contents along the digestive tract.  - Roles in mixing, absorption, and preventing bacterial overgrowth.- Disruptions in motility. 2. The Enteric Nervous System (ENS) and Its Role- Myenteric and submucosal plexus.- Coordinating contractions and relaxations for effective motility. - Mucosa includes epithelium, lamina propria, and muscle.  - Submucosa houses the submucosal plexus.  - Muscularis externa. - Inner circular and outer longitudinal muscle layers with the myenteric plexus in between.   3. The Role of Interstitial Cells of Cajal (ICCs)- Specialized pacemaker cells in muscular layers  - Generate slow-wave electrical activity to synchronize smooth muscle contractions  - Critical for peristalsis.- Work with neural inputs to fine-tune gut motility   4. Dysautonomia and Its Impact on Gut Motility- Dysfunction of the autonomic nervous system (ANS)  - Motility impacts- Microbial overgrowth, SIBO 5. Gastrointestinal Dysmotility- Neurological dysregulation - Structural abnormalities and smooth muscle dysfunction  - Hormonal imbalances - Microbial overgrowth - Autoimmunity  6. The HPA Axis- Hypothalamus, pituitary gland, adrenal glands  - Central to the stress response and interlinked with gut function  - The amygdala and PVN of the hypothalamus  - CRH stimulates ACTH, leading to cortisol release from adrenal glands   7. Cortisol and Gut Barrier Function- Cortisol is a glucocorticoid that modulates immune function and gut physiology  - Chronic cortisol exposure can impair tight junction (TJ) integrity  - Increases paracellular permeability and allows passage of antigens and endotoxins   8.Stress-Induced Changes in Gut Motility- Slow gastric motility - Increased colonic motility  9. Symptoms of GI Dysmotility10. Addressing Root Cause(s)Thank you to our episode sponsor:1. Shop ⁠⁠⁠⁠⁠⁠⁠Fresh Press Farms⁠⁠⁠'⁠⁠⁠⁠⁠⁠⁠⁠Peach Cider Vinegar⁠⁠⁠⁠ at Sprouts locations nationwide, and check out their full collection ⁠⁠⁠⁠⁠⁠⁠here⁠⁠⁠⁠⁠⁠⁠. Get Chloe's Book Today! "⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠75 Gut-Healing Strategies & Biohacks⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠" Follow Chloe on Instagram ⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠@synthesisofwellness⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠Visit ⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠synthesisofwellness.com⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠

The adrenal glands play a crucial role in keeping horses healthy and resilient.My recent hands-on experience with horse dissections highlighted the importance of the adrenal glands for metabolism, hormone regulation, and stress response in horses. When horse owners learn how the adrenal glands work and how chronic stress affects them, they can become far more effective in supporting the health and well-being of their horses.The Role of the Adrenal GlandsThe adrenal glands produce cortisol, ACTH, and DHEA, which regulate energy, influence immune function, and affect the overall hormone balance in horses. Horses are prey animals, so they tend to be on high alert. That means their adrenal glands are often working overtime. When a horse is under constant stress from its environment, emotions, or physical strain, it can lead to adrenal fatigue, affecting everything from metabolism to immune function.Hormonal Imbalances and Their EffectsHorses with metabolic issues like PPID or insulin resistance often have adrenal dysfunction. High cortisol levels can lead to tissue breakdown, slow healing, and weaken the immune system. The adrenals also play a role in sex hormone production, as DHEA influences testosterone and estrogen levels. So adrenal health can affect everything, including the reproductive cycle of mares and the hormone balance of geldings. Understanding those connections helps horse owners make better health decisions.The Impact of Chronic Inflammation and StressMany horses deal with low-grade inflammation from environmental toxins, poor diet, or chronic illness. With those issues, the adrenal glands keep pumping out cortisol, which, over time, can wear them out. When adrenal function drops, the pituitary gland produces more ACTH, which can contribute to metabolic disorders. To manage that, owners must reduce external stressors, like inadequate stable conditions and poor handling techniques, and internal stressors, such as diet and gut health.Nutritional and Holistic SupportSupporting adrenal health in horses requires a combination of proper nutrition, stress reduction, and careful hormone management. Horses naturally produce vitamin C, but in times of stress, they may require supplementation. Other vital nutrients include minerals that help regulate adrenal function. Maintaining a balanced diet that promotes gut health can also reduce overall stress on the body, and providing horses with an environment that meets their instinctual needs for freedom, forage, and friendship is vital for reducing chronic stress.Recognizing the Signs and Taking ActionAs research into equine adrenal health progresses, more vets and equine professionals recognize the signs of adrenal insufficiency. Symptoms like persistent fatigue, poor coat quality, muscle wasting, and metabolic imbalances can indicate underlying adrenal stress. By taking a proactive approach to adrenal support through dietary improvements, environmental enrichment, and holistic care, owners can help prevent long-term health complications in their horses.Links and resources:Connect with Elisha Edwards on her website Join my email list to be notified about new podcast releases and upcoming webinars.Free Webinar Masterclass: Four Steps to Solving Equine Metabolic Syndrome NaturallyRegister for Resolving Equine Metabolic...

In this episode, we detail the bidirectional relationship between the HPA axis and the intestinal barrier, illustrating how HPA axis dysfunction and cortisol dysregulation can impact intestinal permeability. We further discuss how intestinal dysbiosis can contribute to HPA axis overstimulation. Lastly, we detail some of the roles of short-chain fatty acids (SCFAs) and secretory IgA (sIgA) in this bidirectional relationship.Topics: 1. Overview of the HPA Axis and Gut Bidirectional Relationship- Chronic HPA activation, intestinal permeability, mucosalimmunity, and microbiome composition.   2. Components and Function of the HPA Axis- Hypothalamus, pituitary gland, and adrenal glands.  - Stress signals from the amygdala and prefrontal cortex, CRH release from the hypothalamus.  - CRH stimulates ACTH release from the pituitary.- Cortisol production and release. 3. Structure of the Intestinal Epithelial Barrier- The gut barrier consists of the intestinal lumen, microbiome, mucus layer, epithelial cells, and lamina propria.  - Specialized epithelial cells: goblet cells, enterocytes, enteroendocrine cells, and more.- The lamina propria contains immune cells, blood vessels, and lymphatics, supported by a smooth muscle layer.   4. Intestinal Permeability and Tight Junction Regulation- Transport across the intestinal epithelium: transcellular and paracellular pathways.  - Nutrient absorption and selective permeability.  - Tight junction proteins, such as occludin and claudins.   5. Cortisol's Impact on Gut Barrier Integrity- Cortisol can cross the intestinal microvascular endothelium and enter the lamina propria. - Chronic cortisol exposure and intestinal barrier function.- Increased permeability allows luminal antigens and bacterial endotoxins (e.g., LPS) to infiltrate the lamina propria.   6. Secretory IgA (sIgA) and Gut Immune Function  - Chronic cortisol exposure can reduce sIgA levels, weakening mucosal immunity.  - sIgA neutralizes pathogens, prevents microbial adhesion, and more.  - Lower sIgA levels increase susceptibility to dysbiosis and infections.   7. CRH and Its Role in Intestinal Permeability- CRH is produced in the hypothalamus and also peripherally.- CRH can stimulate mast cells, triggering histamine and inflammatory mediator release.  - Mast cell activation can increase gut permeability. 8. Microbiome's Influence on HPA Axis Regulation- Dysbiosis can disrupt HPA axis function.- IBS and sustained HPA activation.- Dysbiosis reduces SCFA production.  - SCFAs, particularly butyrate, support colonocyte health, tight junction integrity, and anti-inflammatory pathways.  - Inflammation and HPA axis dysfunction. 9. Root Cause Approach & Closing- Chronic cortisol exposure, CRH signaling, and gut barrier dysfunction.  - The microbiome influences stress response and HPA axis activity.  - Roles of SCFAs, sIgA, and tight junction proteins.- Addressing gut dysbiosis and GI-derived inflammation can support HPA axis regulation.  - Root cause approach.Thank you to our episode sponsors:1. Shop ⁠⁠⁠Fresh Press Farms⁠⁠⁠'Peach Cider Vinegar at Sprouts locations nationwide, and check out their full collection ⁠⁠⁠here⁠⁠⁠. 2. Shop the ⁠⁠Scalp Cleanser⁠⁠ and ⁠⁠Scalp Essence⁠⁠ from ⁠⁠T Stem Care. ⁠⁠3. Shop ⁠⁠⁠⁠⁠⁠⁠Ulyana Organics'⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠Tallow Wild Yam Cream⁠⁠⁠⁠⁠⁠⁠, and use code ⁠⁠⁠⁠⁠⁠⁠CHLOE10⁠⁠⁠⁠⁠⁠⁠ 10% off your order.Get Chloe's Book Today! "⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠75 Gut-Healing Strategies & Biohacks⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠" Follow Chloe on Instagram ⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠@synthesisofwellness⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠Visit ⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠synthesisofwellness.com⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠

Send Audrey a Text to get your question answered on the showAnother Q&A Episode ready for you with questions from all corners of the country on: Will keeping a horse under barn/stall lights until 9pm help with PPID seasonal fall ACTH rise?Feeding a PSSM 2 HorseNatural remedies for equine asthma Find the Resource List Here: linktr.ee/equineenergymed

In this episode, we dive into the interplay between the hypothalamic-pituitary-adrenal (HPA) axis and the microbiota-gut-brain (MGB) axis, highlighting their bidirectional communication through endocrine, immune, and neural pathways. We'll explore how gut-derived metabolites like short-chain fatty acids (SCFAs) and endotoxins like LPS influence HPA axis activity; conversely, we explore how dysregulated cortisol can impact gut barrier function, immune signaling, and more. We also discuss testing including stool analysis and DUTCH tests. Topics: 1. HPA Axis and MGB Axis Interaction The HPA axis and microbiota-gut-brain (MGB) axis are bidirectionally connected. Gut microbiota influences the HPA axis via metabolites and more 2. Overview of the HPA Axis and Cortisol Secretion Stress signals activate the hypothalamus to release CRH. Stimulates the anterior pituitary to produce ACTH. ACTH signals the adrenal cortex. The adrenal cortex releases cortisol, which binds to glucocorticoid receptors (GRs). 3. Cortisol Dysregulation Impact on Intestinal Health Intestinal lining anatomy: epithelial cells Tight junction proteins regulate nutrient trafficking and prevent pathogen entry. The mucosa contains epithelial cells, connective tissue (lamina propria), and a thin muscle layer. 4. Glucocorticoid Receptors (GRs) in the Gut GRs are intracellular receptors that modulate gene expression when activated. Cortisol binding causes GRs to translocate to the nucleus and bind DNA at GREs. GRs on epithelial cells. Modified tight junction protein expression. 5. Gut Microbiome's Role in HPA Axis Activity SCFAs, including acetate, propionate, and butyrate, produced by gut bacteria fermenting dietary fiber. SCFAs support gut integrity, reduce inflammation, and act as signaling molecules. A diverse and healthy microbiome can enhances HPA regulation via SCFAs. 6. SCFA Modulation of the HPA Axis SCFAs and cortisol. Research highlights SCFAs' ability to attenuate stress-induced cortisol increases. 7. Dysbiosis - Impact on the HPA Axis Dysbiosis reduces SCFA production, impairing gut barrier integrity and immune signaling. Dysbiosis, intestinal hyperpermeability and LPS. LPS activates inflammatory pathways. 8. Inflammation and Dysregulated HPA Activity Chronic inflammation and cortisol. Inflammatory signals from the gut exacerbate systemic and neural stress responses. 9. Symptoms of HPA Axis Dysfunction Chronic fatigue, disrupted sleep, mood disturbances... 10. Identifying Root Causes Dysbiosis, chonic infection / chronic inflammation... DUTCH Test Stool analysis Thanks for tuning in! "⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠75 Gut-Healing Strategies & Biohacks⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠" Follow Chloe on Instagram ⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠@synthesisofwellness⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠ Follow Chloe on TikTok @chloe_c_porter Visit ⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠synthesisofwellness.com⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠ --- Support this podcast: https://podcasters.spotify.com/pod/show/chloe-porter6/support

2ème épisode / 5, de la série sur les Dysplasies fibreuses. Episode 2 : Maladie rare – Dysplasie Fibreuse des Os / Syndrome de MacCune Albright: les aspects endocriniens chez l'enfant. Invité : Dr Cyril Amouroux, pédiatre endocrinologue, praticien hospitalier au sein du service de pédiatrie multidisciplinaire du CHU de Montpellier, coordonnateur du Centre de Compétences Dysplasie Fibreuse des Os et Syndrome de McCune-Albright affilié à la filière OSCAR, membre du Groupe de Travail de l'actualisation du PNDS sur dysplasies fibreuses des os et syndrome de McCune-Albright. https://maladies-rares.chu-montpellier.fr/fr/les-centres/centre-de-competence-dysplasie-fibreuse-des-os-syndrome-de-mac-cune-albright    1️⃣   Qu'appelle-t-on syndrome de McCune-Albright ? [0'33 – 0'52] ✔️ Le syndrome de McCune-Albright associe dysplasie fibreuse des os et troubles hormonaux. Pour plus d'informations, retrouvez notre page article : https://rarealecoute.com/la-dysplasie-fibreuse-des-os-dfo/ 2️⃣   Quelles sont les atteintes hormonales de cette maladie rare ? [0'53 – 1'27] ✔️ Surproduction hormonale due à l'hyperactivation des gonades (ovaires chez la fille, testicules chez le garçon), de la thyroïde et/ou de l'hypophyse. 3️⃣   Quel est le tableau clinique rencontré chez les patients touchés ? [3'47 -4'20] ✔️ Gonades : puberté précoce, voire très précoce, ✔️ Thyroïde : Hyperthyroïdie (irritabilité, perte de poids, fatigue, goitre), ✔️Hypophyse : hyperproduction de prolactine (galactorrhée), d'ACTH avec excès de cortisol (prise de poids, hypertension), et/ou d'hormone de croissance (croissance accélérée, épaississement osseux). 4️⃣   Quels diagnostics différentiels écarter ? [1'28 – 5'05] ✔️ Puberté précoce idiopathique, tumeurs, maladie de Basedow, adénomes hypophysaires... 5️⃣   Quelle prise en charge proposer aux patients touchés par le syndrome de McCune-Albright ? [5'06 – 7'50] ✔️ Traitements médicamenteux bloquant les surproductions hormonales ✔️ Chirurgie dans certains cas. 6️⃣   Quel suivi proposer et quel pronostic pour ces patients ? [7'51 – 8'59] ✔️ Consultations pluridisciplinaires régulières en centres experts, ✔️ Surveillance des atteintes endocriniennes, avec dosages hormonaux si nécessaire, ✔️Bon pronostic en général, grâce à l'efficacité des traitements.   L'équipe : Virginie Druenne – Ambassadrice RARE à l'écoute Cyril Cassard – Journaliste/Animation Hervé Guillot - Production Crédits : Sonacom ******************************************************************************************************************************* À propos : "RARE à l'écoute" est un podcast dédié à la sensibilisation aux maladies rares et au soutien des personnes touchées par ces affections. Créé par un groupe passionné de professionnels de la santé, le podcast vise à informer les professionnels de santé et fournissant des informations sur les dernières avancées médicales et scientifiques dans le domaine des maladies rares, et inspirer les patients et leurs proches en partageant des histoires de courage et de persévérance. Contenu :

This continuing education activity is provided by AffinityCE and CheckRare CE. This activity provides continuing education credit for physicians. A statement of participation is available for other attendees. Estimated time to complete: 0.50 hoursTo obtain CME credit, go to https://checkrare.com/learning/p-cushings-syndrome-treatment-research-highlights-endo-2024/Commercial SupportEducational Support for this activity was provided by Recordati Rare Diseases, Inc., and Xeris Pharmaceuticals.Learning ObjectiveAfter participating in the activity, learners should be better able to:Describe the latest research being presented to better manage individuals with Cushing's syndrome and its clinical relevance.Share new information with their clinical team. Activity DescriptionThis 30-minute CME program highlights the latest clinical research about Cushing's syndrome and Cushing' disease.Cushing's syndrome is rare endocrine disorder characterized by chronic hypercortisolism. It is often due to a pituitary adenoma producing excessive ACTH leading to hypercortisolism. Symptoms can range from mild to extensive.This CME program, hosted by Maria Fleseriu, MD, FACE, Professor of Medicine and Neurological Surgery, Director of the Pituitary Center at Oregon Health & Science University, provides an overview of the latest clinical research presented at ENDO 20234 involving Cushing's syndrome. FacultyMaria Fleseriu, MD, FACEProfessor of Medicine and Neurological SurgeryDirector of Pituitary CenterOregon Health & Science UniversityPortland, OregonDisclosure StatementAffinityCE and CheckRare CE staff, as well as planning and review committees, have no financial interests to disclose. Faculty EducatorsDr. Fleseriu discloses the following relevant financial relationships with ineligible companies to disclose:Funding to the University as Principle Investigator from Sparrow PharmaceuticalsScientific consultant for Crinetics Pharmaceuticals, Recordati Rare Diseases, Sparrow Pharmaceuticals, and Xeris PharmaceuticalsMitigation of Relevant Financial Relationships AffinityCE adheres to the ACCME's Standards for Integrity and Independence in Accredited Continuing Education. Any individuals in a position to control the content of a CME activity, including faculty, planners, reviewers, or others, are required to disclose all relevant financial relationships with ineligible companies. Method of ParticipationThere are no fees to participate in the activity. Participants must review the activity information including the learning objectives and disclosure statements, as well as the content of the activity. To receive CME credit for your participation, please complete the pre- and post-program assessments. Your certificate will be emailed to you in within 30 days.Participation CostsThere is no cost to participate in this CME session. To receive CME credit for your participation, please complete the pre- and post-program assessments. Your certificate will be emailed to you in within 30 days.CME InquiriesFor all CME policy-related inquiries, please contact us at ce@affinityced.com.Send customer support requests to cds_support+ldrtc@affinityced.com.Copyright© 2024. This CME-certified activity is held as copyrighted © by AffinityCE and CheckRare CE. Through this notice, AffinityCE and CheckRare CE grant permission of its use for educational purposes only. These materials may not be used, in whole or in part, for any commercial purposes without prior permission in writing from the copyright owner(s). 

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In this Horse & Hound Podcast promotional feature with Boehringer Ingelheim, our podcast host Alex Robinson speaks to globally renowned specialist equine vet Professor Andy Durham about the key signs of Equine Cushing's disease in horses and ponies. They also discuss how animals with the condition can be managed to live happy and healthy lives, as well as how you can claim a free* test for your horse this autumn via Boehringer Ingelheim's Care About Cushing's scheme. The educational content of this podcast episode is sponsored by Boehringer Ingelheim Animal Health UK Ltd (“BI”). Further information available from BI, RG12 8YS, UK. Date of preparation: September 2024 UI-EQU-0131-2024. Use Medicines Responsibly *Free basal ACTH test laboratory fees only. Veterinary practices may apply visit, blood sampling and interpretation fees.

Welcome back to A Stride Above! In today's episode, Dr. Colton Ramstrom joins us again to discuss a common yet complex issue in older horses: Equine Cushing's, also known as Pituitary Pars Intermedia Dysfunction (PPID). Dr. Alberto Rullan and Dr. Colton Ramstrom discuss this condition as it often challenges horse owners and veterinarians alike due to its nuanced symptoms and ongoing management needs.In this episode you'll learn about: • What Pituitary Pars Intermedia Dysfunction (PPID) is and insights into how it affects horses.• How to identify classic signs of Cushing's and recognize the symptoms.• What the diagnostic approaches are and exploring the testing options for diagnosing Cushing's, including baseline ACTH levels and stress tests.• What the management and treatment for Cushing's entails- is there a cure?If you'd like to learn even more or have any further questions regarding Cushing's Disease, visit https://www.albertorullan.com/ for more information! Be sure to subscribe, follow and rate this podcast- we appreciate immensely! See you back here next week for more helpful tips and guidance on improving the mindful care of your horse's health.Links For You:• Our Website • Facebook • Instagram • Youtube Dr. Alberto Rullan, VMD• Website• LinkedIn• Instagram

This week, we examine how dopamine affects horses with PPID.There is a significant link between dopamine, diet, lifestyle, nutrition, and the symptoms commonly associated with PPID. So today, I share various lifestyle and nutritional ways horse owners can support dopamine levels in their horses.The Role of DopamineDopamine is a neurotransmitter responsible for motor skills, cognitive abilities, and the reward system, so it is vital for physical and mental health. Low dopamine levels in horses can lead to lethargy, depression, and poor concentration.Dopamine and Its Impact on Hormonal RegulationDopamine plays a significant role in the reward system, and it also controls the overproduction of hormones like ACTH. When dopamine-producing brain cells degenerate, ACTH levels rise, leading to overworked pituitary glands and inflammation. Stress and Lifestyle Factors Contributing to Low Dopamine LevelsStress and lifestyle factors can significantly impact dopamine levels in horses with PPID. Dopamine plays a crucial role in mood regulation, motivation, and overall well-being, so when horses are chronically stressed or have frequent inflammation, dopamine levels can drop. By addressing environmental stressors, changing diet, and providing a stable environment, owners can improve the dopamine levels of their horses.The Role of Gut Health in Dopamine and Hormonal BalanceToxic hindgut conditions, often caused by poor diet and lack of movement, can negatively impact the microbiome of horses, leading to lower dopamine and serotonin levels. Unhealthy gut conditions also contribute to metabolic issues and hormonal imbalances, which can complicate health issues.Connection Between Dopamine, ACTH, Cortisol, and InsulinThere is a relationship between dopamine, ACTH, cortisol, and insulin levels. Low dopamine leads to higher ACTH and cortisol levels, which increases blood sugar and insulin production. That imbalance is particularly problematic for horses with conditions like laminitis, so early intervention is essential to prevent further deterioration.The Importance of Comprehensive ManagementManaging conditions like PPID requires a holistic approach that focuses on diet, lifestyle, and mental and emotional health. As there is no quick fix for those chronic conditions, consistent management practices are essential for preventing disease progression and supporting horse health.Final Thoughts on the Role of Dopamine in PPIDMaintaining dopamine levels through lifestyle changes and reward-based training is crucial. By engaging their horses in learning and activities that stimulate dopamine production, owners can help preserve their brain cell integrity and potentially slow the progression of PPID.Links and resources:Connect with Elisha Edwards on her website Join my email list to be notified about new podcast releases and upcoming webinars.Free Webinar Masterclass: Four Steps to Solving Equine Metabolic Syndrome NaturallyRegister for Resolving Equine Metabolic Syndrome Naturally, nowRiva's RemediesMentioned in this episode:Learn the 4 Steps to Resolving Metabolic Syndrome NaturallySign up for the

This week, we focus on Cushing syndrome, now known as PPID. There is currently an epidemic of horses being diagnosed with this issue. It is a complex condition involving much chemistry and many hormones. So, I will continue exploring it in the next few episodes.Cushing's Syndrome and Pituitary Pars Intermedia Dysfunction (PPID)Even though the term Cushing's Syndrome in the horse health industry recently transitioned to Pituitary Pars Intermedia Dysfunction (PPID), I still prefer referring to it as Cushing's Syndrome, as that term encompasses the complexity of the condition, which involves multiple glands, not just the pituitary gland.A Holistic View Cushing's Syndrome might be defined more accurately as a hormonal imbalance rather than a pituitary issue. It is a complex condition involving many hormones and bodily systems, and many believe that underlying factors such as diet and lifestyle contribute to it, as it cannot be due to random occurrences.Stress and Inflammation as Root CausesStress and inflammation are the key contributors to developing PPID or Cushing's Syndrome. When overstimulated due to stress or inflammation, the pituitary gland produces ACTH, leading to an overproduction of cortisol by the adrenal glands. That hormonal imbalance can lead to various health issues in horses over time.Pituitary Gland and Adenoma DevelopmentIn advanced stages of PPID or Cushing's Syndrome, a growth known as an adenoma may develop on the pituitary gland, which complicates treatment. Addressing the underlying causes, like diet and lifestyle, can sometimes reverse early-stage symptoms and reduce ACTH levels.Holistic Treatment ApproachesA multi-faceted, individualized approach is essential for treating horses with PPID or Cushing's Syndrome. Since symptoms, conditions, and history of horses vary, a one-size-fits-all treatment is ineffective. For that reason, customizing programs to the individual horse is crucial for managing the condition.Hormonal Imbalance and Related SymptomsHorses with PPID often exhibit symptoms related to hormonal imbalances, like changes in shedding patterns, hair coat, excessive sweating, and fatigue. The symptoms can vary from horse to horse, making it essential to assess each case individually.Metabolic and Immune System ImpactPPID affects the metabolism of horses, often leading to weight gain or loss, depending on the stage of the condition. The immune system also gets compromised, making horses more susceptible to infections and other health issues. Long-term elevated cortisol levels can cause muscle wasting and a weakened immune response.Importance of Diet and NutritionDiet plays a significant role in managing PPID, as there is a link between sugar and inflammation in the condition. It is crucial to ensure that horses receive proper nutrition without any inflammatory ingredients. Monitoring and adjusting diet based on individual needs can help manage symptoms and improve overall health.Final Thoughts on Managing PPIDManaging PPID in horses requires a holistic approach that considers the complexity of the condition. By addressing underlying factors such as stress, inflammation, diet, and lifestyle, horse owners can help regulate hormonal imbalances and improve the quality of life of their horses.Links and resources:Connect with Elisha Edwards on her website Join my email list to be notified about new podcast releases and upcoming webinars.Free Webinar...

She had been on a chronic illness journey of several years and despite her efforts to manage her energy levels her FATIGUE was becoming debilitating. Shannon at only 40 years old was running out of options to resolve her health issues and was contemplating the realty of an early death. Luckily when the DAM BROKE her doctor was able to recognize the message her body was sending through all of her various symptoms but mainly through her hyperpigmentation. A skyrocketing ACTH test lead to her medical diagnosis of Addison's Disease. She is approaching this next chapter in her life battling back not just with steroids but with everything else she can control. Nutrition. Exercise. Mental health. Shannon acknowledges for her to find her SWEET SPOT with Addison's Disease to fully thrive at life it will take EFFORT and DETERMINATION. She is ready to take the gently loving steps in the progress of healing after diagnosis. Join Shannon in this fight. Shannon will be your hope and inspiration. If you would like to share your journey on THE PICKLE JAR please go to www.chronicallyfitcanada.com for more information. DISCLAIMER: The information from THE PICKLE JAR represents the experiences of the host Jill Battle and the individual experiences of each guest. No information is intended to provide or replace the medical advice of a medical professional. The host or guests are not liable for any negative consequences from any treatment, action, application or preparation, to any person following the information from the podcast.

Episode 321: Pharmacology 101: CYP17 Inhibitors “I think we're in a scientific golden age for prostate cancer and probably cancer as a whole, but we're talking about prostate cancer today. So I'm excited to be sitting on the front lines, seeing the new ways that we can help our patients. But I do still think CYP17 inhibitors will continue to be one of our main weapons against prostate cancer for a very long time,” Andrew Ruplin, PharmD, clinical oncology pharmacist at Fred Hutchinson Cancer Center in Seattle, WA, told Jaime Weimer, MSN, RN, AGCNS-BS, AOCNS®, manager of oncology nursing practice at ONS, during a conversation about the CYP17 inhibitor drug class. Music Credit: “Fireflies and Stardust” by Kevin MacLeod Licensed under Creative Commons by Attribution 3.0  Earn 0.5 contact hours of nursing continuing professional development (NCPD) by listening to the full recording and completing an evaluation at myoutcomes.ons.org by July 19, 2026. The planners and faculty for this episode have no relevant financial relationships with ineligible companies to disclose. ONS is accredited as a provider of NCPD by the American Nurses Credentialing Center's Commission on Accreditation. Learning outcome: The learner will report an increase in knowledge related to CYP17 inhibitors. Episode Notes  Complete this evaluation for free NCPD.  Oncology Nursing Podcast episodes: Pharmacology 101 series Episode 242: Oncology Pharmacology 2023: Today's Treatments and Tomorrow's Breakthroughs Episode 154: New Drug Approvals for Metastatic Castration-Sensitive Prostate Cancer ONS Voice article: The Case of the Genomics-Guided Care for Prostate Cancer ONS course: Safe Handling Basics ONS books: Chemotherapy and Immunotherapy Guidelines and Recommendations for Practice (second edition) Safe Handling of Hazardous Drugs (fourth edition) Clinical Journal of Oncology Nursing article: Navigating Treatment of Metastatic Castration-Resistant Prostate Cancer: Nursing Perspectives Oncology Nursing Forum articles: Interventions to Support Adherence to Oral Anticancer Medications: Systematic Review and Meta-Analysis ONS Guidelines™ to Support Patient Adherence to Oral Anticancer Medications ONS Huddle Card: Hormone Therapy ONS Biomarker Database (refine by prostate cancer) ONS Learning Libraries: Cancer of the Genitourinary Tract Oral Anticancer Medication Oral Chemotherapy Education Sheets To discuss the information in this episode with other oncology nurses, visit the ONS Communities. To find resources for creating an Oncology Nursing Podcast™ Club in your chapter or nursing community, visit the ONS Podcast Library. To provide feedback or otherwise reach ONS about the podcast, email pubONSVoice@ons.org. Highlights From This Episode “Identification of CYP17 as a target to decrease androgen production led to the first synthesis of a dedicated inhibitor of CYP17 named abiraterone acetate in the 1990s. But it would also not be until 2011, when there was sufficient evidence through clinical trials, for the [U.S. Food and Drug Administration] to approve abiraterone as treatment for castrate-resistant prostate cancer. And since then, abiraterone has been studied in many different stages of prostate cancer and has demonstrated clear benefits to survival for patients with metastatic or nonmetastatic prostate cancer and in the castrate-sensitive setting, as well.” TS 3:07 “Patients on abiraterone, regardless of the formulation that they get, they also have to receive an oral steroid every day while undergoing treatment due to the risk of that mineralocorticoid excess. … CYP17 inhibition by abiraterone leads to the loss of negative feedback on the adrenocorticotropic hormone, or ACTH, through a relative cortisol deficiency, which then results in higher levels of ACTH, which then cause the formation of excess precursors, including those mineralocorticoids that are upstream of the CYP17 inhibition step of androgen formation.” TS 14:04 “I recommend that patients take the standard formulation of abiraterone on an empty stomach. Conversely, I do recommend patients take their steroids with food to reduce the chances of [gastrointestinal] upset from their steroids. And so, I emphasize to these patients that abiraterone and the steroid do not need to be taken together at the same time, even though they are both a component of their treatment, and that they probably should, in fact, take them a little bit separately.” TS 23:00 “Now we're really in the phase of studying combination treatments, and we've had some really good results so far. So, one of the combinations that made a splash a few years ago is what we call triplet therapy, so abiraterone plus docetaxel plus [androgen-deprivation therapy], docetaxel being a traditional cytotoxic chemotherapy that's been used in prostate cancer for several decades now. But now we're combining it with CYP17 inhibitors and other novel hormonal therapies, which has been exciting. So, this has been implemented into the standard of care for metastatic hormone-sensitive prostate cancer.” TS 27:26  

At one point Dawn from a small town in Alberta couldn't walk to the end of her driveway without being winded. She has now conquered her diagnosis in 2020 with secondary adrenal insufficiency and now walks thousands of kilometres a year. Dawn's secondary adrenal insufficiency was caused by the removal of a pituitary tumour that was producing ACTH hormone. But her journey started years before SAI with a life full of illness, steroids, autoimmune disorders, asthma and migraines. She has learned to set boundaries, manage her medication, improve her overall wellness and live a life with SAI. SAI is not stopping Dawn from living her life and she is ready to conquer any challenge SAI gives her. We are a family and as a family, we can make a difference. THE PICKLE JAR PODCAST through donations at:https://www.gofundme.com/f/thepicklejarpodcast If you would like to share your journey on THE PICKLE JAR please go to www.chronicallyfitcanada.com for more information. DISCLAIMER: The information from THE PICKLE JAR represents the experiences of the host Jill Battle and the individual experiences of each guest. No information is intended to provide or replace the medical advice of a medical professional. The host or guests are not liable for any negative consequences from any treatment, action, application or preparation, to any person following the information from the podcast.

Kevin's journey with ADDISON'S DISEASE starting at day 1 is far from typical. Everything from his symptoms to diagnosis and the amazing things he has accomplished since diagnosis Kevin will leave you re-evaluating your disease management, leave you with a list of questions for your medical team and have you setting higher standards for your quality of life. While most diagnosed with adrenal insufficiency fight for years with medical doctors not recognizing the symptoms, Kevin was fortunate enough to have an endocrinologist who quickly did a complete series of tests, including the ACTH stimulation test and discovered this UNWELL man had ADDISON'S DISEASE. It was a 10-year progression of a slow decline in health as exercise recovery time increased, daily living became a struggle and Kevin's "LIFE GOT SMALL" Having led a full active lifestyle with regular exercise, Kevin and his new wife started a slow and steady process of learning how to manage his medication with his active levels. Disease management, planning, proper recovery, and common sense built Kevin's confidence to accomplish amazing things with Addison's Disease. Kevin is now in his mid-50s and with a supportive wife runs marathons. ADDISON'S SELF HELP GROUP UKhttps://www.addisonsdisease.org.uk/BOOK "LIVING WITH ADDISON'S DISEASE"Please comment on the video below and help make our voices heard! We are a family and as a family, we can make a difference. THE PICKLE JAR PODCAST through donations at: https://www.gofundme.com/f/thepicklejarpodcast If you would like to share your journey on THE PICKLE JAR please go to www.chronicallyfitcanada.com for more information. DISCLAIMER: The information from THE PICKLE JAR represents the experiences of the host Jill Battle and the individual experiences of each guest. No information is intended to provide or replace the medical advice of a medical professional. The host or guests are not liable for any negative consequences from any treatment, action, application or preparation, to any person following the information from the podcast.

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Contributor: Ricky Dhaliwal MD Educational Pearls: Primary adrenal insufficiency (most common risk factor for adrenal crises) An autoimmune condition commonly known as Addison's Disease Defects in the cells of the adrenal glomerulosa and fasciculata result in deficient glucocorticoids and mineralocorticoids Mineralocorticoid deficiency leads to hyponatremia and hypovolemia Lack of aldosterone downregulates Endothelial Sodium Channels (ENaCs) at the renal tubules Water follows sodium and generates a hypovolemic state Glucocorticoid deficiency contributes further to hypotension and hyponatremia Decreased vascular responsiveness to angiotensin II Increased secretion of vasopressin (ADH) from the posterior pituitary An adrenal crisis is defined as a sudden worsening of adrenal insufficiency Presents with non-specific symptoms including nausea, vomiting, fatigue, confusion, and fevers Fevers may be the result of underlying infection Work-up in the ED includes labs looking for infection and adding cortisol + ACTH levels Emergent treatment is required 100 mg hydrocortisone bolus followed by 50 mg every 6 hours Immediate IV fluid repletion with 1L normal saline The most common cause of an adrenal crisis is an acute infection in patients with baseline adrenal insufficiency Often due to a gastrointestinal infection References 1. Bancos I, Hahner S, Tomlinson J, Arlt W. Diagnosis and management of adrenal insufficiency. Lancet Diabetes Endocrinol. 2015;3(3):216-226. doi:10.1016/S2213-8587(14)70142-1 2. Bornstein SR, Allolio B, Arlt W, et al. Diagnosis and Treatment of Primary Adrenal Insufficiency: An Endocrine Society Clinical Practice Guideline. J Clin Endocrinol Metab. 2016;101(2):364-389. doi:10.1210/jc.2015-1710 3. Cronin CC, Callaghan N, Kearney PJ, Murnaghan DJ, Shanahan F. Addison disease in patients treated with glucocorticoid therapy. Arch Intern Med. 1997;157(4):456-458. 4. Feldman RD, Gros R. Vascular effects of aldosterone: sorting out the receptors and the ligands. Clin Exp Pharmacol Physiol. 2013;40(12):916-921. doi:10.1111/1440-1681.12157 5. Hahner S, Loeffler M, Bleicken B, et al. Epidemiology of adrenal crisis in chronic adrenal insufficiency: the need for new prevention strategies. Eur J Endocrinol. 2010;162(3):597-602. doi:10.1530/EJE-09-0884  Summarized by Jorge Chalit, OMSII | Edited by Meg Joyce & Jorge Chalit  

In this episode we discuss adrenal insufficiency  You can have either primary, secondary, or tertiary adrenal insufficiency. Primary adrenal insufficiency is also called Addison's disease. When you have this type, your adrenal glands are damaged and can't make the cortisol you need. They also might not make enough aldosterone. Secondary adrenal insufficiency is more common than Addison's disease. The condition happens because of a problem with your pituitary gland, a pea-sized bulge at the base of your brain. It makes a hormone called adrenocorticotropin (ACTH). This is the chemical that signals your adrenal glands to make cortisol when your body needs it. If your adrenal glands don't get that message, they may eventually shrink.  This is the type our guest on this week's episode is dealing with. Tertiary is due to hypothalamic disease and a decrease in the release of corticotropin releasing hormone (CRH). Causes can include brain tumors and sudden withdrawal from long-term exogenous steroid use (which is the most common cause overall) The most common cause of Addison's disease today is an autoimmune problem, when your immune system malfunctions and attacks and damages your own body, in this case, your adrenal glands.

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As we begin a new year, it's crucial to understand how the Cortisol Awakening Response (CAR), which is closely tied to our sleep patterns and overall well-being, can impact our ability to wake up refreshed and ready to tackle the day. We'll explore the intricate biochemical processes that govern the CAR, the factors that can lead to its dysregulation, and practical strategies to reset cortisol's diurnal rhythm for optimal energy and productivity (so you can go above and beyond with your goals in 2024). Topics: 1. Introduction - Importance of discussing the cortisol awakening response - Connection between cortisol awakening response and sleep regulation - Overview of the cortisol-melatonin diurnal cycle 2. Retinal Ganglion Cells (RGCs) and Light Response - Role of photoreceptor cells in the retina - Specialized cells - Retinal Ganglion Cells (RGCs) - Melanopsin in RGCs and its light sensitivity - Generation of electrical signals in response to light - Transmission to the suprachiasmatic nucleus (SCN) 3. Suprachiasmatic Nucleus (SCN) and Light Signals - Integration of light signals by SCN - SCN's role in assessing day-night cycle - Adjustment of the body's internal clock 4. Intracellular Signaling in SCN - Activation of intracellular signaling pathways - Role of CREB (transcription factor) - Transcription and translation of CRH within SCN neurons - Release of CRH into the bloodstream 5. Adrenocorticotropic Hormone (ACTH) Release - Travel of CRH to the anterior pituitary gland - Binding of CRH to corticotroph cells - Increase in cyclic adenosine monophosphate levels - Stimulation of ACTH synthesis and release 6. Cortisol Production - ACTH reaching the adrenal glands - Stimulation of cortisol production - Importance of cortisol in the context of discussion 7. Dysregulation of Cortisol Awakening Response - Factors leading to high or low Cortisol Awakening Response - Impact on energy levels and waking up - Focus on the case of chronic fatigue 8. Addressing Dysregulated Cortisol Awakening Response - Assumption of no underlying root causes - Strategies for resetting cortisol's diurnal rhythm - Aligning light exposure with natural environment - Increasing morning light exposure - Incorporating physical activity, including high-intensity exercise earlier in the day - Cold therapy as a stimulatory strategy for the morning - Avoiding overstimulation at night (caffeine, intense exercise, loud sounds, alcohol, LIGHT) 9. Supporting Melatonin for Cortisol's Diurnal Rhythm - Importance of melatonin in sleep regulation - Consuming foods rich in melatonin or precursors - Exploring endoluten, a pineal peptide bioregulator Thanks for tuning in! ⁠⁠⁠⁠Book An Intro Coaching Call with Chloe Porter⁠⁠⁠⁠ Get Chloe's Book Today! "⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠75 Gut-Healing Strategies & Biohacks⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠" If you liked this episode, please leave a rating and review or share it to your stories over on Instagram. If you tag @synthesisofwellness, Chloe would love to personally thank you for listening! Follow Chloe on Instagram ⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠@synthesisofwellness⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠ Follow Chloe on TikTok ⁠⁠⁠⁠@chloe_c_porter⁠⁠⁠⁠ Visit ⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠synthesisofwellness.com⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠ to purchase products, subscribe to our mailing list, and more! Or visit ⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠linktr.ee/synthesisofwellness⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠ to see all of Chloe's links, schedule a BioPhotonic Scanner consult with Chloe, or support the show! Thanks again for tuning in! --- Support this podcast: https://podcasters.spotify.com/pod/show/chloe-porter6/support

This week, I will be covering the fall flare-up.Horses tend to face their most significant health struggles in spring and fall. It happens in spring because the grass sugars increase as the grasses transition from hay, heightening the risk of flare-ups for horses with metabolic conditions like laminitis. Yet, fall could trigger even more issues- especially in horses with pre-existing imbalances or health problems.Fall Hormonal Shifts and Their Impact on Metabolic ConditionsAs we transition into the fall, I have noticed a surge in health issues, particularly in horses diagnosed with PPID or Cushing's disease. The fall season brings about a natural rise in ACTH levels, exacerbating those conditions in horses already grappling with hormonal imbalances. That surge in ACTH also leads to elevated cortisol levels, which, if prolonged, can pose various health risks, from muscle wasting to laminitis. That highlights the need for proactive management strategies, and makes it essential for anyone owning horses predisposed to metabolic conditions to understand those hormonal shifts.Laminitis Challenges in the FallPreventive measures are essential for mitigating the risk of laminitic flare-ups during the seasonal transition. Horses that have enjoyed a seemingly healthy summer outdoors sometimes experience acute episodes of laminitis as the fall sets in. The trim plays a crucial role in preventing that, as an unhealthy trim could compound the impact of hormonal triggers.Dietary Changes in the Transition from Grass to HayFall can bring significant dietary challenges, particularly for horses transitioning from grass to hay. Without proper management, an abrupt shift from grass to hay could impact the digestive system and trigger other health issues. A gradual transition- especially for horses prone to metabolic conditions, will ensure a much smoother adjustment. That is why horse owners who want to prevent laminitic episodes must know about the higher sugar concentrations in the fall grass.Supplementation and Maintaining a Low-sugar DietSupplementing essential fatty acids and maintaining a low-sugar diet will go a long way in contributing to the overall nutritional support of a horse during its dietary transition in the fall.Environmental Allergies and Respiratory ConditionsIn the fall, there is a rise in environmental particulates, like pollen, which may exacerbate equine respiratory conditions, especially in horses with pre-existing issues like COPD. Switching to round bales or using hay nets could also contribute to dust inhalation and further impact any existing respiratory health issues. Strategies like adjusting feeding setups and using netting to minimize dust exposure, are essential for horses susceptible to respiratory allergies.Temperature Fluctuations and Circulatory ImpactDrastic temperature fluctuations are common in the fall and could challenge a horse's ability to regulate its body temperature. Older horses or those with existing metabolic challenges may struggle with those temperature fluctuations, potentially leading to compromised circulation. That, in turn, could contribute to winter laminitis. Proactive measures, including proper hoof care and trimming, help to maintain healthy circulation and prevent temperature-related complications.Strategies for Prevention and Well-beingA holistic approach is essential for navigating the challenges of fall flare-ups. Prioritizing digestive system support through gradual dietary transitions, probiotic supplementation, and essential fatty acids are needed for a horse's overall well-being. Managing their stressors, maintaining the three Fs (forage, freedom, and friendship), and promptly addressing any signs of distress will help to reduce their stress. Taking a...

*Drought conditions are improving in many areas of Texas.   *Three agriculture professionals from East Texas have been named finalists for the Texas Farm Bureau Excellence in Agriculture award.  *A federal appeals court has struck down the Environmental Protection Agency's ban on chlorpyrifos.  *Texas High Plains farmers are wrapping up a season that had a promising start, but a disappointing finish.  *Texas has a new state veterinarian.  *Coastal Bend agricultural organizations have been busy informing elementary students about the importance of agriculture.  *ACTH is a hormone that is tested to determine if horses have Cushing's disease.  *Parks and wildlife is gathering input from the public on the future of light goose management in Texas.

Let's talk about the health benefits of magnesium. Magnesium is a fascinating and important mineral that's involved in over 350 enzymes in the body. Enzymes speed up the chemical reactions in the body, and they don't deplete their energy in the process. Well-known benefits of magnesium: • It supports the heart • It may help with muscle cramping • It supports sleep • It may help reduce anxiety • It may help promote relaxation • It supports the flexibility of the arteries • It may help with headaches • It may help with problems related to the nerves and muscles Surprising benefits of magnesium: 1. It may help regulate LDL cholesterol and triglycerides and increase HDL 2. It helps make ATP (energy in the body) 3. It helps regulate adrenaline, cortisol, and ACTH—and counters oxidative stress from these hormones 4. It's involved in enzymes related to lecithin (the antidote to cholesterol) 5. It's a natural calcium channel blocker, beta blocker, and antithrombotic 6. It helps regulate blood sugar levels 7. It's involved in making DNA Many people don't consume enough magnesium, which can cause a magnesium deficiency and lead to various health issues. Magnesium-rich foods: • Foods high in chlorophyll (dark leafy green vegetables) • Nuts and pumpkin seeds • Dark chocolate (sugar-free) • Sea kelp • Avocado • Low-sodium sea salt Here are the top things that can cause you to become magnesium deficient: • Refined sugar and refined carbs • Alcohol • Diuretics • Diarrhea • Low stomach acid • Certain gene variations The type of magnesium supplement I would take, if needed, is magnesium glycinate.

Send us a Text Message.Dr. Xenia Zawadzkas (Dr. Z) returns as our special guest for an eye-opening episode dedicated to Addison's disease in dogs. In this in-depth conversation, Dr. Z sheds light on the complexities of Addison's disease in dogs. With Dr. Z's expertise, you'll gain a deeper understanding of how Addison's affects your canine companions and why timely intervention is crucial.Throughout the episode, Dr. Z walks us through the diagnostic process, highlighting the nuances of interpreting baseline cortisol levels and sodium-to-potassium ratios. You'll also discover why the ACTH stimulation test is the gold standard for diagnosing Addison's.Once diagnosed, Dr. Z shares valuable insights into treatment options, particularly the use of Zycortal injections and prednisone. You'll learn how to tailor the treatment plan to your dog's needs, ensuring they enjoy a high quality of life. Whether your dog is young or elderly, large or small, this episode equips you with the knowledge and confidence to provide them with the best care possible.What You'll Learn:Recognize the subtle symptoms of Addison's disease in dogs, such as lethargy, vomiting, and diarrhea.Understand the prevalence of Addison's disease across countless dog breeds.Explore the diagnostic challenges veterinarians face in differentiating Addison's disease from other conditions.Discover the gold standard diagnostic test for Addison's disease: the ACTH stimulation test.Gain insights into how baseline cortisol levels and sodium-to-potassium ratios play a crucial role in diagnosis.Learn about atypical cases of Addison's disease and their potential transition to typical Addison's.Explore the treatment options available for dogs diagnosed with Addison's, including Zycortal injections and prednisone.Understand the importance of tailoring treatment plans to individual dogs' needs and monitoring their progress.Discover why timely intervention and collaboration with veterinarians are key to managing Addison's disease effectively.Gain confidence in providing the best care for dogs with Addison's disease, whether they're young, old, large, or small.Support the Show.Connect with me here: https://www.vetsplanationpodcast.com/ https://www.facebook.com/vetsplanation/ https://www.twitter.com/vetsplanations/ https://www.instagram.com/vetsplanation/ https://www.tiktok.com/@vetsplanation/ https://youtube.com/@Vetsplanationpodcast https://www.youtube.com/playlist?list=PLVbvK_wcgytuVECLYsfmc2qV3rCQ9enJK Voluntary donations and Vetsplanation subscription: https://www.paypal.com/donate/?hosted_button_id=DNZL7TUE28SYE https://www.buzzsprout.com/1961906/subscribe

This Week In Wellness a new study has shown that commonly used birth-control pills can negatively impact women’s stress response, in particular the ability to reduce their levels of the stress hormone ACTH when the stress has been removed. https://www.news-medical.net/news/20230707/Birth-control-pills-disrupt-womens-stress-response-study-shows.aspx https://linkinghub.elsevier.com/retrieve/pii/S0166432823002681

This Week In Wellness a new study has shown that commonly used birth-control pills can negatively impact women's stress response, in particular the ability to reduce their levels of the stress hormone ACTH when the stress has been removed. https://www.news-medical.net/news/20230707/Birth-control-pills-disrupt-womens-stress-response-study-shows.aspx https://linkinghub.elsevier.com/retrieve/pii/S0166432823002681

Welcome back into THE PICKLE JAR our inspiring friend Belinda. In November of 2022, Belinda shared her LIFE-LONG JOURNEY to adrenal insufficiency diagnosis at the age of 49. This was a journey that should have been started at the age of 14 when Belinda's health issues led to an ACTH stimulation test that indicated she has primary Addison's Disease. However, this diagnosis was set aside and the doctors choose to focus on Belinda's GI issues and treat her suspecting she had Crohn's Disease. Years of 'treating' a misdiagnosed Crohn's disease with steroids avoid any major adrenal crisis and managed her adrenal insufficiency. Eventually, that treatment was not enough to sustain life and in 2017 low cortisol levels flagged that there was certainly something more serious going on. After diagnosis, Belinda has a MAJOR ADRENAL CRISIS leading to a minor stroke and making her WORK HARD to regain her quality of life. That HARD WORK paid off. Belinda recaps her journey with us and updates us on being able to return to work full-time and manage her illnesses. She has learned to PLAY BY HER NEW RULES...and she is winning the game of life. Boundaries, self-love, communication with her advocates and so much more you will take from this episode. And of course, the LOVE OF A DOG to keep her motivated and moving. Listen to Belinda's original episode E43 - Belinda's Long Journey to Addison's Disease. OR watch on YouTube "CHRONICALLY FIT CANADA" Watch this episode on YouTube at CHRONICALLY FIT CANADA. https://www.youtube.com/chronicallyfitcanada Social media is one of the best means to help our voice with adrenal insufficiency be heard so please share this podcast and subscribe. Help our voice be LOUD and CLEAR...we are here and we deserve support in our illness. THE PICKLE JAR Podcast is running on love and determination. If you would like to make a contribution to cover costs it would be greatly appreciated.     https://gofund.me/155401bb If you would like to share your journey on THE PICKLE JAR please email me at thepicklejar@rogers.com DISCLAIMER: The information from THE PICKLE JAR represents the experiences of the host Jill Battle and the individual experiences of each guest.  No information is intended to provide or replace the medical advice of a medical professional.  The host or guests are not liable for any negative consequences from any treatment, action, application or preparation, to any person following the information from the podcast.

Episode 141: Adrenal Insufficiency BasicsFuture doctor Wilson explains how to recognize an acute adrenal insufficiency and explains how to treat it. Also, chronic adrenal insufficiency is explained. Dr. Arreaza adds comments about congenital adrenal hyperplasia.Written by Candace Wilson, MSIV, American University of the Caribbean. Comments by Hector Arreaza, MD.June 2, 2023.You are listening to Rio Bravo qWeek Podcast, your weekly dose of knowledge brought to you by the Rio Bravo Family Medicine Residency Program from Bakersfield, California, a UCLA-affiliated program sponsored by Clinica Sierra Vista, Let Us Be Your Healthcare Home. This podcast was created for educational purposes only. Visit your primary care provider for additional medical advice.Introduction: After having seen patients with adrenal insufficiency when I did a rotation in ICU, I saw how important it is to be able to recognize it quickly to ensure that patients receive appropriate treatment as quickly as possible. Arreaza: AI is adrenal insufficiency but also AI stands for Artificial intelligence, so we had the idea to ask Chat GPT what are the adrenal glands and this is what we got: “The adrenal glands are small endocrine glands located on top of each kidney. They are small in size, but they play a vital role in producing and secreting essential hormones.” (end of quote)Glucocorticoids play an important role in the mobilization of energy reserves by increasing gluconeogenesis, glycogen synthesis, protein catabolism, lipolysis, appetite, and insulin resistance. Each adrenal gland is composed of two main parts: the outer region called the adrenal cortex and the inner region called the adrenal medulla. These two regions have distinct structures and functions.” The adrenal cortex has three zones, Zona glomerulosa (mineralocorticoids, mainly aldosterone), Zona fasciculata (cortisol), and Zona reticularis (androgens). Mineralocorticoids are a class of steroid hormones produced by the Zona glomerulosa of the adrenal gland that influence electrolyte and water balance through modifying renal absorption of sodium and potassium.Definition of AI: AI is “inadequate functioning of the adrenal glands”. Adrenal gland hormones: glucocorticoids, mineralocorticoids, and sex hormones.Primary vs. secondary adrenal insufficiency.Candace: Primary adrenal insufficiency is caused either by the abrupt destruction of the adrenal gland or by progressive destruction/atrophy, whereas secondary adrenal insufficiency is due to conditions that impair the hypothalamic-pituitary-adrenal axis leading to decreased ACTH production. Causes of primary adrenal insufficiency includes autoimmune adrenalitis (which is the most common cause in the US); infectious adrenalitis (tuberculosis being the most common cause worldwide); adrenal hemorrhage; infiltration of the adrenal gland by tumors, amyloidosis, or hemochromatosis; adrenalectomy; cortisol synthesis inhibitors (such as rifampin, fluconazole, phenytoin, ketoconazole); 21B-hydroxylase deficiency; and vitamin B5 deficiency. Fluconazole is commonly used to treat pulmonary cocci (Valley Fever in our community). What about secondary causes?Causes of secondary adrenal insufficiency include sudden discontinuation of chronic glucocorticoid therapy; stress (such as infection, trauma, or surgery) during prolonged glucocorticoid therapy; and hypopituitarism. Clinical presentation of adrenal crisis.Adrenal insufficiency can present acutely or chronically with more insidious symptoms. We will first discuss the acutemanifestation of adrenal insufficiency, also known as adrenal crisis. In any patient who demonstrates vasodilatory shock, unexplained severe hypoglycemia, or unexplained hyponatremia whether or not the patient is known to have adrenal insufficiency, adrenal crisis should be considered a possibility. Adrenal crisis is a life-threatening emergency that requires immediate medical treatment and can occur in either primary or secondary adrenal insufficiency, though it is most common in patients with primary adrenal insufficiency. The main feature of adrenal crisis is shock, but patients may also have vague symptoms such as anorexia, nausea, vomiting, abdominal pain, weakness, fatigue, lethargy, fever, confusion, or coma. In patients with adrenal crisis from primary adrenal insufficiency, volume depletion and hypotension are the major clinical features, resulting from mineralocorticoid deficiency. In contrast, the patients with adrenal crisis from secondary adrenal insufficiency (which is an isolated glucocorticoid deficiency) will have hypotension secondary to decreased vascular tone without volume depletion.Treatment of adrenal crisis.Signs of an adrenal crisis should be recognized quickly, and management should be started as quickly as possible. When adrenal crisis is suspected, do not wait for laboratory results before initiating treatment as this is a life-threatening medical emergency. After all necessary laboratory tests have been collected (including serum electrolytes, glucose, routine measurement of plasma cortisol and ACTH) and IV access has been established, infuse 2-3L of isotonic saline or 5% dextrose in isotonic saline as quickly as possible and give bolus of hydrocortisone 100mg IV followed by 50mg IV every 6 hours or 200mg/24 hours as a continuous IV infusion for the first 24hrs. The answer to many endocrine emergencies is IV fluids, in this case, you also add hydrocortisone and mineralocorticoids.Alternative glucocorticoids if hydrocortisone is unavailable include methylprednisolone and dexamethasone. While patient is hemodynamically unstable, it is important to frequently monitor vital signs and serum electrolytes to avoid iatrogenic fluid overload. When the patient has stabilized, continue IV isotonic saline at a slower rate for 24-48 hours, and for patients with primary adrenal insufficiency, begin mineralocorticoid replacement with fludrocortisone 0.1mg orally daily when saline infusion is stopped. If there is concern for infectious precipitating cause of the adrenal crisis, perform an extensive infectious workup. Addison's disease.Early symptoms of chronic adrenal insufficiency can be vague and nonspecific (such as fatigue, weight loss, and GI complaints), making the clinical diagnosis more difficult than acute adrenal insufficiency. Diagnosis must be confirmed with a thorough endocrine evaluation to determine the type and cause of the adrenal insufficiency, but treatment should be started before the diagnosis is established in acutely ill patients. Primary and secondary adrenal insufficiency shares some common clinical manifestations, such as fatigue, weight loss, anorexia, nausea, vomiting, abdominal pain, amenorrhea, diffuse myalgia, arthralgia, confusion, delirium, stupor, depression, psychosis, mania, anxiety, disorientation, and hallucinations.Clinical manifestations of indicative of primary adrenal insufficiency include orthostatic hypotension, salt craving, hyperpigmentation especially of areas not typically exposed to sunlight (such as palmar creases, mucous membrane of the mouth), vitiligo (though hyperpigmentation is more common), hypotension, and auricular calcifications. Lab findings.Laboratory results will show electrolyte disturbances (such as hyponatremia, hyperkalemia, and hypercalcemia), azotemia, normocytic anemia, eosinophilia, increased renin, normal anion gap metabolic acidosis, hypoglycemia, increased ACTH, low cortisol, low aldosterone, increased cortisol releasing hormone, and decreased DHEA-S.Clinical manifestations of secondary adrenal insufficiency is similar to those in primary adrenal insufficiency with the notable exceptions of: hypotension (which is less prominent than in primary AI), absence of dehydration, pale skin as opposed to hyperpigmentation. Laboratory results in secondary adrenal insufficiency will show normal aldosterone, sodium, potassium, and renin; decreased ACTH and cortisol; and increased cortisol-releasing hormone.Treatment of chronic adrenal insufficiency. Treatment of primary adrenal insufficiency focuses on replacing hypocortisolism with glucocorticoids and hypoaldosteronism with mineralocorticoids. In contrast, the treatment of secondary adrenal insufficiency focuses on the replacement of hypocortisolism with glucocorticoids without the need to supplement aldosterone. Short-acting glucocorticoids (such as hydrocortisone) are the preferred medication for treatment since they roughly mimic the normal diurnal rhythm. Intermediate-acting (such as prednisone or prednisolone) and long-acting glucocorticoids (such as dexamethasone) are acceptable alternatives, especially in patients who are non-compliant with multiple-day dose schedules or those with severe late-evening or early-morning symptoms, but due to variable inter-individual metabolism of dexamethasone, be cautious of over-treating patients. Whether the patient is receiving short-acting, intermediate-acting, or long-acting, ensure that patients receive the lowest glucocorticoid dose that relieves symptoms while avoiding signs and symptoms of glucocorticoid excess (such as weight gain, facial plethora, truncal obesity, osteoporosis, etc.).Summary: Primary = Glucocorticoids and mineralocorticoids. Secondary = Glucocorticoids. Glucocorticoids can be short, intermediate, and long-acting. What about mineralocorticoids?Fludrocortisone 0.1mg/day is the preferred agent for mineralocorticoid replacement in patients with primary adrenal insufficiency, though patients who are receiving hydrocortisone therapy in conjunction may require a lower dose of 0.05mg/day. Mineralocorticoid therapy may need to be increased during the summer due to salt loss in perspiration. As a reminder, aldosterone works by controlling the reabsorption of sodium and excretion of potassium. It influences water reabsorption. It is part of the renin-angiotensin-aldosterone system (RAAS) to maintain blood pressure. In addition, it is important that patients receive adequate education about their medical condition and causes, whether it is primary or secondary adrenal insufficiency, especially the maintenance of medication, adjustment during minor illnesses, and when to consult a clinician.Bottom line: Adrenal insufficiency can be acute or chronic, primary or secondary. In primary adrenal insufficiency, laboratory results will show electrolyte abnormalities, such as hyponatremia and hyperkalemia, with increased ACTH. Whereas in secondary adrenal insufficiency, electrolytes will be normal, and ACTH will be decreased. Both primary and secondary adrenal insufficiency require treatment with glucocorticoid, but a mineralocorticoid should be added in the setting of primary adrenal insufficiency. _________________________Conclusion: Now we conclude episode number 141, “Adrenal Insufficiency Basics.” We encourage you to recognize acute adrenal insufficiency promptly and start IV fluids and glucocorticoid stat. Candace reminded us that chronic adrenal insufficiency presents with vague and insidious symptoms, including hypotension, fatigue, weight loss, anorexia, hyperpigmentation of the skin, and even vitiligo. Make sure to include our colleagues from endocrinology if you have concerns.   This week we thank Hector Arreaza and Candace Wilson. Audio editing by Adrianne Silva.Even without trying, every night you go to bed a little wiser. Thanks for listening to Rio Bravo qWeek Podcast. We want to hear from you, send us an email at RioBravoqWeek@clinicasierravista.org, or visit our website riobravofmrp.org/qweek. See you next week! _____________________References:Nieman, L. K. (n.d.). Diagnosis of adrenal insufficiency in adults. UpToDate. https://www.uptodate.com/contents/diagnosis-of-adrenal-insufficiency-in-adults. Accessed June 2, 2023.Nieman, L. K. (2022, October 25). Clinical manifestations of adrenal insufficiency in adults. UpToDate. https://www.uptodate.com/contents/clinical-manifestations-of-adrenal-insufficiency-in-adults . Accessed June 2, 2023.Nieman, L. K. (2022a, October 19). Treatment of adrenal insufficiency in adults. UpToDate. Treatment of adrenal insufficiency in adults - UpToDate. Accessed June 2, 2023.Royalty-free music used for this episode: "Latina Havana Boulevard." Downloaded on October 13, 2022, from https://www.videvo.net/ 

Lauren and JJ are back with a case to kick off season 4 of the podcast! What is causing weakness, decreased appetite, and weight loss in this canine patient? The episode includes a review of the diagnosis and management of hypoadrenocorticism in the dog, as well as important information about accurate diagnosis in patients who have already received steroids. Special thanks to Ellen Behrend, VMD, PhD, DACVIM for agreeing to be featured on this episode! Sources: (1) Behrend, E., Rothrock, K., & Shell, L. (2022). Hypoadrenocorticism (canine). VINcyclopedia. www.vin.com (2) Lobetti, R., Lindquist, E., Frank, J., Casey, D., Marek, K., & Timon, T. (2016). Retrospective study of adrenal gland ultrasonography in dogs with normal and abnormal ACTH stimulation test. Journal of Veterinary Clinical Practice and Petcare, 1(1), 1-6. (3) Wenger, M., Mueller, C., Kook, P. H., & Reusch, C. E. (2010). Ultrasonographic evaluation of adrenal glands in dogs with primary hypoadrenocorticism or mimicking diseases. Veterinary Record, 167(1), 207-210. Special Guest: Ellen Behrend.

In this episode, host Dr. Aparna Baheti interviews Dr. Fritz Angle about adrenal vein sampling, including indications, workup, and his technique for accessing the right adrenal vein. --- CHECK OUT OUR SPONSOR RADPAD® Radiation Protection https://www.radpad.com/ --- SHOW NOTES Dr. Fritz Angle is the Director of Interventional Radiology at the University of Virginia. He frequently performs adrenal vein sampling for primary hyperaldosteronism, and has developed a specific technique. The patient is usually referred from an endocrinologist or primary care doctor. The IR should review the labs to verify the aldosterone-to-renin ratio is greater than 20. Additionally, it is important to review medications and stop all potassium sparing diuretics at least two weeks before the procedure. If they haven't had a CT scan, the IR should order one to assess the position of the right adrenal vein, the hardest to access due to its variable anatomy.  The morning of the procedure, Dr. Angle always checks a potassium level to know whether to give potassium supplements. He gets dual femoral access, so that he can obtain both non-stimulated and ACTH-stimulated samples. He obtains the sample from the left adrenal vein first. For the right side, he starts with a C2 catheter, to which he adds side holes using a biopsy needle. The left adrenal vein is almost always one vertebral body above the right renal vein, so he begins here, with the catheter pointing directly posterior. He searches around the entire back wall of the IVC by puffing contrast and rotating the catheter. He moves up and down by half a vertebral level. If he still cannot locate it, he begins looking to the left and right. When injecting, it is important to be gentle. To do this, he inserts an 014 wire through his catheter, then does a dry scan to see if the vein is pointing toward the liver or the right adrenal gland. If the vein is injected too hard, it can cause a venous infarct and adrenal insufficiency. The right adrenal vein forms an upside down Y shape. Dr. Angle draws two sets each from the right and left adrenal veins and two peripheral samples.  To interpret results, look for a cortisol of 2-3x greater (3-4x greater in stimulated samples) compared to the peripheral blood to confirm correct placement in the adrenal veins. Once you correct aldosterone levels to cortisol levels, the aldosterone-to-cortisol ratio should be about 5x greater on one side (compared to the other side) to confirm the diagnosis and lateralize the hyperaldosteronism to one side. About 2 ⁄ 3 cases lateralize, but Dr. Angle has found many patients' symptoms are actually due to bilateral adrenal hyperplasia. Finally, Dr. Angle emphasizes that this is an easy, safe procedure that all IRs should offer.

Noradrenaline (norepinephrine) is a neurotransmitter and hormone that plays a role in the body's "fight or flight" response.  Acetylcholine is a neurotransmitter (“brain” +” across” + “to send”) that helps transmit signals in the brain and body. Its name comes from its chemical structure, an acetate group and a choline molecule.  Dopamine is a neurotransmitter that plays a role in motivation, reward, and movement. Its name comes from its chemical structure, a combination of two molecules called dihydroxyphenylalanine and dopamine. Adrenaline (epinephrine) is a hormone and neurotransmitter that helps the body respond to stress. Its name comes from its source, the adrenal glands.  Serotonin is a neurotransmitter that is involved in mood, appetite, and sleep. Its name comes from its chemical structure, a combination of sero- (meaning "serum") and -tonin (meaning "tonic" or "substance that modifies").  Corticotropin-releasing hormone (CRH) is a hormone that stimulates the release of cortisol, a stress hormone. The name comes from its function of stimulating the release of corticotropin, a hormone that stimulates the adrenal glands. Also, it gets its name from its role in stimulating the release of adrenocorticotropic hormone (ACTH) from the pituitary gland, which in turn stimulates the release of cortisol from the adrenal gland. Vasopressin is a hormone that regulates water balance in the body. Its name comes from its ability to constrict blood vessels (vasoconstriction) and increase blood pressure. Vasopressin, also known as antidiuretic hormone (ADH), is so named because it regulates water balance by causing the kidneys to reabsorb water. Thyrotropin-releasing hormone (TRH) is a hormone that stimulates the release of thyroid-stimulating hormone (TSH), which regulates the thyroid gland. Its name comes from its function of stimulating the release of thyrotropin.  Oxytocin is a hormone that is involved in social bonding, childbirth, and lactation. Its name comes from its ability to stimulate uterine contractions (oxytocic) and milk ejection (lactogenic).  Gonadotropin-releasing hormone (GnRH) is a hormone that stimulates the release of luteinizing hormone (LH) and follicle-stimulating hormone (FSH), which regulate the reproductive system. Its name comes from its function of stimulating the release of gonadotropins.  Growth hormone–releasing hormone (GHRH) is a hormone that stimulates the release of growth hormone (GH), which regulates growth and metabolism. Its name comes from its function of stimulating the release of growth hormone.  Catecholamines are a group of hormones and neurotransmitters that includes adrenaline, noradrenaline, and dopamine. Their name comes from their chemical structure, which includes a catechol group and an amine group.  Histamine is a neurotransmitter and hormone that is involved in inflammation, allergies, and gastric acid secretion. ACTH (adrenocorticotropic hormone) is a hormone that stimulates the release of cortisol from the adrenal glands.  Orexin (hypocretin) is a neurotransmitter that is involved in wakefulness and appetite. Its name comes from its discovery in the hypothalamus and its ability to stimulate food intake (orexigenic).  Glutamic acid (glutamate) is a neurotransmitter that is involved in learning, memory, and neural plasticity. Its name comes from its chemical structure, a combination of glutamine and an acid group.  Galanin is a neuropeptide that is involved in pain perception, mood, and appetite. Its name comes from its discovery in the galanin-containing neurons of the hypothalamus.  Neurotensin comes from the words "neuro," meaning related to nerves, and "tensin," which refers to its ability to cause contraction in smooth muscle. Neurotensin is a neuropeptide that is found in the central nervous system and gastrointestinal tract. --- Support this podcast: https://podcasters.spotify.com/pod/show/liam-connerly/support

Welcome to this edition of Aphasia Access Aphasia Conversations Podcast. My name is Janet Patterson. I am a Research Speech-Language Pathologist at the VA Northern California Healthcare System in Martinez, California, and a member of the Aphasia Access Podcast Working Group. Aphasia Access strives to provide members with information, inspiration, and ideas that support their efforts in engaging with persons with aphasia and their families through a variety of educational materials and resources. I am today's host for today's episode that will feature Dr. Jacqueline Laures-Gore. These Show Notes accompany the conversation with Dr. Laures-Gore but are not a verbatim transcript.     Dr. Jacqueline Laures-Gore     Dr. Laures-Gore is a professor in the Department of Communication Sciences and Disorders at Georgia State University in Atlanta, where she directs the Aphasia and Motor Speech Disorders Laboratory. Jacqueline's work spans topics in aphasia and motor speech disorders. For the past several years she has investigated the relationship between integrative health practices and aphasia rehabilitation.     In today's episode with Dr. Laures-Gore you will hear about: the relationship among stress, resilience, and coping skills, recognizing and measuring physiological stress and perceived, self-reported stress, the interaction of stress, anxiety, and fear, and the role integrative health practices can have in daily life and in aphasia rehabilitation.     Dr. Janet Patterson: Welcome to this edition of Aphasia Access Conversations. Today I am delighted to be speaking with my friend and colleague, Dr. Jacqueline Laures-Gore. Jacqueline is a professor in the Department of Communication Sciences and Disorders at Georgia State University in Atlanta, where she directs the Aphasia and Motor Speech Disorders Laboratory. Jacqueline's work spans topics in aphasia and motor speech disorders, including investigating working memory in persons with aphasia. In motor speech disorders, she and colleagues examined topics such as intelligibility in people who have dysarthria, and speaker and listener perceptions of speech in persons with dysarthria. She is a co-creator of the Atlanta Motor Speech Disorders Corpus, which is a comprehensive spoken language dataset from speakers with motor speech disorders in Atlanta, Georgia. This collaborative project gathered speech samples from non-mainstream, American English speakers residing in the southeastern United States in order to provide a more diverse perspective of motor speech disorders.   For over two decades, Jacqueline has been interested in how personal, physiological, and psychological factors affect people with aphasia, and aphasia rehabilitation. She has investigated topics such as stress, depression, mental health concerns, and how to assess their presence and influence. With her colleague, Ken Rice, she recently published the Simple Aphasia Stress Scale in the Journal of Speech, Language, and Hearing Research. The SASS is a single item self-report measure of acute stress in adults with aphasia.   Dr. Laures-Gore's work also investigated the power of laughter, mindfulness, meditation, spirituality, yoga, and integrative health practices for persons with aphasia. I am pleased to welcome Jacqueline to Aphasia Access Conversations today and look forward to talking with her about her clinical and research experience considering how integrative medicine can influence a person with aphasia and their rehabilitation, and the powerful effects that mindfulness, laughter, and yoga can have on life outlook, participation, and rehabilitation.   Welcome, Jacqueline. I appreciate your time today in talking with me about these fascinating and important topics.   Dr. Jaqueline Laures-Gore: I am very happy to be here, Janet, and very honored. I look forward to a very lively and fun conversation with you today.   Janet: Jacqueline I would like to start by asking you about the aspect of your aphasia research interests that includes important topics such as depression in persons with aphasia, stress, laughter, and spirituality. In fact, I believe you are among the first to write about the value of integrated health practice in aphasia. How did your career path and learning curve about aphasia take you to this line of inquiry?   Jacqueline: There's quite a bit of time that I spent with people with aphasia through my clinical work, and even early on before I became a speech-language pathologist and worked in a geriatric setting. There was a gentleman there who had aphasia and we did not really know how to communicate with him. He was very isolated. He sat by himself most of the time, was very alone. That image of him and what he must have been experiencing, and our inability to really know how to communicate with him, stuck with me over the years and definitely drove me toward a career in speech-language pathology, and specifically working with people with aphasia. Then, after becoming a speech-language pathologist, and working full time in rehab settings, it became very obvious that people with aphasia were more than the problems with phonology and semantics, and so forth. There was a bigger picture here, and there was oftentimes frustration. I watched and tried to provide some help to reduce frustration during some of the language tasks that people would be doing in clinic. But as I tried to look in the literature about well, what do we know about this frustration? What do we know about stress and the language system? What do we know about ways to facilitate language through the stress mechanism? What do we know about relaxation, and its effect on language, and so forth. All of those things really seem very under-explored in our aphasia literature. My curiosity definitely drove me to looking then, into a Ph.D., and having some great mentors who encouraged me to continue down this path of the fringe group. There weren't a lot of people who were very interested at the time in stress and thinking about what happens with the language system, or of mindfulness, meditation, and so forth. By far, I'm not the first to consider these things. McNeil and Prescott had a meditation paper, I think it was back in the 1970s. Cynthia Thompson had a paper on hypnosis, I think it was in the 1980s. There have been others, too.   Janet: I'm listening to you and thinking, we probably all had some sort of thoughts about this, as we see patients. I'm envisioning the patient that you saw in the geriatric center, we probably all have had patients like that. I'm impressed that you didn't forget, that you kept that in your mind as you moved forward. I think many of us didn't know what to do with it, didn't know how to think about this. Other things present themselves and we get busy with our worlds and our learning about phonology, or semantics, or syntax. It's hard to remember. I'm glad that you remembered and also, that you were brave enough to stay out there on that fringe, because not everybody is that brave.   Jacqueline: Oh, it's hard! It has been hard. It's gotten easier now, and hopefully, it will be easier for the next generation of researchers on this topic. Definitely my longtime collaborator, Rebecca Shisler Marshall, and I had difficulty getting things published. Thinking too, about research design, and approaching the topic with this particular group of individuals with communication disorders, it's a unique population. There's still a lot of growth regarding research design and establishing clinical trials, and we're just at the early phase of really investigating this.   I love that you were pointing out that oftentimes people forget that first person that they encounter with a specific communication disorder, and in this case with aphasia. I was 17, and I'm a few years older than 17 now, but I think, though, that for some individuals, there's a catalyst. It could be a personal experience, I hear lots of times when we have students coming through our program, “Oh, I had a family member who (fill in the blank) and had to have speech therapy”, or “I myself had to have some kind of speech therapy, and that's why I want to do this”. For me, at least, it was this individual that I was tasked to care for, and not really knowing how to care for that person. Definitely an emotional component there, and a feeling of responsibility.   Janet: I have visions of some of my patients when I was first starting out, boy do I wish I could have a do over!   Jacqueline: Oh yeah, obviously, I hear you.   Janet: This leads me to my next question. Your research has investigated some of the challenges that all of us, including persons with aphasia, experience such as depression or stress or mental health concerns, or coping with life's challenges, whether they're small challenges or large challenges. These words and concepts, I think they appear commonly in our conversations, and while people may believe they understand their definitions at a broad level, I believe that that may not be the case when we consider them in the context of treating our clients who have aphasia. How do you think about these concepts as they relate to persons with aphasia and their family members? And to our treatment programs? Could you give us some sort of guidance about how we might define and use these terms in our clinical work?   Jacqueline: Let's start with stress. Something that I have been talking a lot about lately, and especially with my doctoral student right now, is defining stress, defining anxiety, defining fear, and the differences between those three. When we think about stress, stress is really that threat in the moment. There are different ways in which we respond to that in-the-moment threat. One way is physiologic, and we have two biological arms of the physiologic stress response. One is the sympathetic adrenal medullary system, and the other is the hypothalamic pituitary adrenal axis. The first one, the sympathetic one, or the SAM, shows up with our heart rate and sweating, changes in our digestive system, and pupil dilation. The other one, the hypothalamic pituitary adrenal axis, that one will show up more with the changes in ACTH [adrenocorticotropic hormone] and downstream cortisol. All of those, though, have different effects on our body, and we can measure them with different techniques.   The physiologic stress response is adaptive, and stress is not always a bad thing. From an evolutionary perspective, having that stress response has been very beneficial for us, as humans. Now, when that stress response is consistently engaged, then it becomes problematic and oftentimes can become some type of illness or disease. In the short term in helps us to adapt to a potentially negative situation.   The other stress is more of a perceived stress. Perceived stress is the perception that there is a stressor, there is something in my environment that is creating this feeling of dis-ease. That perception of stress is reliant also on whether you feel you have, or you have coping resources. Do you have the support around you to help you deal with this stressor? For instance, do you have the financial means to help yourself, and some people rely on religious practices or spiritual practices to help them cope.   Anyway, so we have that self-perception of stress, and then we also have the physiologic stress, and the two do not have to match. Oftentimes, we can have somebody who reports themselves as perceiving stress and having a high level of perceived stress, but physiologically, it's not showing up. That makes it always a little bit tougher to study stress, and clinically to even assess stress. I'm not sure which is more important. Is it more important to not be perceiving stress? Or is it more important not to be feeling stress physiologically? I don't have the answer to that.   One of the things that's very exciting clinically though, is that there are more wearables now that can detect changes in heart rate, changes in skin conductance or skin response. I think that is going to be helpful eventually for clinicians who are trying to determine how stressful a certain situation is as far as a language task or a communication task.   We're also seeing more self-report measures of stress. We have the SASS, as you had mentioned, which is an acute measure. It's just one question and it's on a scale. Rebecca Hunting Pompon and colleagues created the Modified Perceived Stress Scale, which looks at stress over the last month, more of a chronic stress assessment.   You'd mentioned depression. We're seeing a lot more work in post stroke depression in people with aphasia in the last ten years or so. With that attention to the mental health of people with aphasia, we're seeing more scales that are at least being looked at, to help measure depression in people with aphasia, whether it be modifications of stroke depression scales that are already there but for the general population, or specific to people with aphasia. I see those as becoming more accessible clinically and us figuring out more about what we can be using in the clinic to look at depression.   Janet: This is fascinating, and I would love to spend hours talking with you in more detail about some of these measures.   In preparing to talk with you, I did a literature search of some of these terms like stress or depression, as they are linked with aphasia. I noticed that there were a few papers on the topic 30 or more years ago, but not many. In the last decade or so, as you mentioned, there has been an increasing number of papers that describe something about stress or depression, or how to measure it, or what to do about it. I think that this is a good trend, and it's certainly consistent with LPAA principles that seek to maximize the life experience of persons with aphasia. That said, I was challenged to draw consistent conclusions from the evidence that I saw. I'm wondering if you could summarize some of the findings from your research and experience and help us place this work in the greater context of evidence informed practice for aphasia.   Jacqueline: We know more about depression and functional outcomes, how post stroke depression can have a negative effect on functional outcomes in persons with aphasia. The problem is that the amount of literature is fairly small. Primarily, it's because that in the past, people with aphasia have been excluded from some of those studies. I see that changing now, where there is more inclusion of persons with aphasia. Then when it comes to stress, that literature is really, really just beginning, as far as empirical data to direct clinical care. In my work, what I've been able to show is that there are definitely some correlations, some associations between self-reported stress, and some aspects of discourse. I've been setting, at least most recently, picture description, for instance, or some type of narrative, and then looking at the discourse production to see if there's any kind of association with different aspects of self-reported stress. We found some things but nothing necessarily consistent. There's been some association with pausing, such as filled pause and unfilled pauses. We've seen that perceived stress can be either negatively or positively associated with those aspects of discourse. I think that right now, the evidence is a little unclear about what the effect of stress is on language.   I also always want to tell people that we really need to not always think about stress negatively. We need to think too about stress as an adaptive process. It may be that sometimes stress and language work together very nicely, and stress may give language a little boost. There was a 2019 paper that we had out looking at cortisol awakening response and diurnal variation, and we saw some differences between people with aphasia, and people without stroke and aphasia. The people who did not have a stroke and aphasia had a cortisol awakening response, which is that when we first wake up, the cortisol which is always in our body and is that very endpoint of hypothalamic pituitary adrenal axis, it releases glucose in our system and gives us sugar which gives us energy. For the most part, when people wake up, they have a lower level of cortisol. Then about 30 minutes later it starts peaking and then it continues to climb throughout the day. It's thought that that energy at the early onset of the day gives us a little bit of energy to get us going. In that 2019 paper, we didn't see that people with aphasia were following that pattern. That made us wonder if maybe there's an energy source that isn't fully functioning for people with aphasia, or at least isn't fully engaged in people with aphasia, and that could be contributing to language. There are a lot of things with that paper, too, that left us with more questions than answers. I think that's where we're at as a whole, with stress, with depression, with integrative health practices, is a lot more questions than answers still.   I do think that there's a sweet spot that maybe I won't, it will probably be maybe the next generation, I don't know if it'll stick around with my generation, or with me at least, but I'm trying to figure out what that sweet spot is for individuals. How much stress is too much stress, how much stress is just enough stress. Also, there's probably a big component of just inter- and intra-individual variability. What works for me, Janet, may not work for you. I think that's when clinical care really takes on that art piece, too, tuning into the person that you're helping and finding out what works for them.   Janet: I think you've said that so, so well. One of my fears is that this larger idea of the work that you're doing, people may see it as a bandwagon to jump on without really understanding the work behind it, the data behind it. So hearing you say, yes, we think there are some effects, but there's not enough evidence yet for us to say exactly what, in what way, for whom, all the time, under what conditions. Also bringing the ideas back into the art of the clinical work to pay attention to your patient, not just the responses that they're making linguistically, but also nonverbally, what they're showing you or telling you. Maybe take a step back to talk about, are they having a moment of stress? Or is something going on in their life that can be affecting their performance today? I think that's a good thing.   Let me turn a little bit in a different direction, because in addition to talking about and measuring stress and depression, your work is also focused on behaviors that can benefit all of us. Behaviors or activities such as mindfulness, yogic breathing, meditation, yoga. How did you become convinced that these activities can have a positive effect on a person with aphasia?   Jacqueline: Well, I don't know if I'm convinced. I am exploring.   Janet: Good point.   Jacqueline: It is yeah. I'm not convinced. I think, again, that there are differences between people and so that not everybody has a good experience with yogic breathing,  or is it maybe not appropriate for some individuals. Mindfulness can be very beneficial for people who are not necessarily aware of a certain behavior. But at the same time, when one becomes more mindful, there may be other emotions that come up. When you're introducing mindfulness into therapy you have to be aware that there may be some negative parts to introducing that and be prepared for some other emotions that may come up.   Stacy Silverman McGuire is a student of mine, and she did a thesis on laughter, yogic laughter. In that paper, we give a little qualitative piece to some of what she had studied and there were some people who just really enjoyed laughing and wanted to have more laughter in therapy. One person specifically commented that there's just not enough laughing that goes on in aphasia therapy. Another comment was that it was just weird; their experience was that this was kind of weird. People have different things that work for them, and some people don't like them. I think what we'll continue to find in this line of work is, again, that individual piece of what may work for some may not work for others.   When we look at some of these integrative health practices, many of them have roots in ancient medicines, whether it be ayurvedic medicine, traditional Chinese medicine, indigenous medicines, there's a long, long history. Some of the practices have become more secularized. Some of the practices have, I should say, religious roots to them, and in the western world have become a bit more secularized. For some people that we may be caring for, they may not be comfortable with some of these integrative health practices because of religious beliefs, or they may prefer more conventional medicine. So how's that, clear as mud?   Janet: It is more clear than mud, actually. Because it's what you said earlier. I don't think this is a fringe topic any longer, but it certainly is an unexplored topic. It's messy, it's difficult to examine. You talked about your challenges in thinking about research design, for example. And then, of course, there's the personal comfort with any aspect of this. It's not just the person with aphasia, but I'm thinking about if you're a clinician, how do you get to a comfort level where you can talk about mindfulness, or talk about spirituality? If you're not comfortable, then it's probably not a good thing for you to do, because your level of discomfort will spill over onto the client, who will certainly be aware that you're not comfortable talking about this. That may affect the interaction.   Do you have any thoughts or any advice or guidance you might give to clinicians as we think about this large, messy topic, if you will, and how we might be thinking about incorporating any of these things into our worlds?   Jacqueline: Yeah, I think a really good aspect of all of this is clinician comfort, and thinking about clinician comfort, even getting away from just the standard, traditional model of therapy, where we show a picture, and then we work on naming that picture. When there's been the movement since the late 1990s of the Life Participation Approach to Aphasia, and getting outside of just the impairment focus, and looking at life participation, and so forth. That goes along with A-FROM and all of that wonderful work that people before me have done. Clinicians had to feel comfortable with that, too, of looking at the bigger, broader picture. Now this adds another dimension as well, that I think feeds in very nicely to LPAA, and A-FROM and so forth.   When we think about things like meditation, awareness, even just doing something, not necessarily labeling it as meditation, but labeling it, as “Let's just focus on your breath for a moment. Slow down, and just breathe.” You can have a few deep breaths, and help that person get back into a state where maybe they are not over aroused with their stress system.   As far as the religion and spiritual aspect, it's part of one's culture. As we work with people who are culturally diverse, we are as speech-language pathologists, really responsible for becoming more comfortable with acknowledging all of the aspects of culture, which includes religion and spirituality. One's religious practices can have an immense effect on their perspective about therapy, about aphasia, about recovery. That is an area that we're learning more about specifically with aphasia. When we look at religious practices and healthcare in general, and there's a much larger literature out there than looking here, just within aphasia rehabilitation. So, again, I think we're going to be learning a lot more in the coming years about that aspect. But again, it is recognizing an important piece of one's culture.   I feel like I'm kind of just like rambling on.   Janet: Well, first of all, you're not rambling on. It's a winding road topic, if you will, it's not a straight-line topic. There are perspectives from all over that we have to consider. As you were talking, part of what I began to think was that there's a difference between acknowledging and respecting someone else's beliefs or spirituality or their culture, even if you don't understand it, or perhaps you don't personally practice it or personally agree with it. But you acknowledge it, you accept it, and put yourself in a comfortable position so that you can have a clinical relationship with the patient, and then achieve the goals that you want. That's what it seems to me like you're saying, or you're advocating for?   Jacqueline: Yeah, I think the hit the nail on the head.   Janet: Let me ask you a little bit more about your work on stress. You talked about two terms, self-reported perceived stress, and then stress, or maybe physiological stress. Could you define these terms a little bit more deeply, and give us some examples of how they appear in the lives of persons with aphasia, and without aphasia?   Jacqueline: Well, physiologic stress, again, can manifest differently throughout the body, because of the two different biological arms of the stress response. There is such a huge literature now on all of the stress-related illnesses that we have here and globally, and of course, stressors are different. They can be related to family situations, they can be related to income level, they can be related to health, political issues, wars. There can be the big things. Then that physiologic stress may be engaged with the smaller day to day things, such as a coworker, that is really hard to deal with, or a situation with a spouse or a sibling, or so forth.   And then there's the perception of stress, which I think is so incredibly important. Sometimes you may, Janet, have met somebody, or maybe you yourself are that person, who doesn't seem to get too worried about things. They seem to have a perspective that, “I can handle this, I got this, It'll turn out just fine”. They can kind of roll along with life. Then there are individuals where the cup of water spills and it's the end of the world. There's concern about little things. How we perceive stress is based on, I think, early life experiences. It's based on what we come into this world with and the modifiers in the environment, and then from there, form those who perceive stress and those who don't perceive a lot of stress. It gets back to coping. Some individuals have the ability to cope much better than other individuals and have a lot more to rely on in times of stressful events than others?   Janet: I think the coping that you mentioned is so important. A big part of our job is probably supporting that throughout our treatment, the rehabilitation program, so the patient can continue to cope with the challenges of aphasia.   Jacqueline: I agree, finding out how an individual's coping. We've been working on trying to develop a coping questionnaire for people with aphasia for a few years now. We're data collecting with that and hoping to have that available to clinicians. Right now, we don't have one that's aphasia friendly. We don't have a coping questionnaire to find out how are people coping? What are they relying on? Are they relying on maladaptive behaviors to cope? Are they drinking a lot? Are they abusing other substances? Or, are they reaching out to friends? Are they getting some exercise. There are some very positive ways of coping, and there are some natural, healthy ways of coping. Finding that out is very important clinically, and how do we do that? My answer is we need to develop a good questionnaire that's psychometrically valid, and so forth. Until then, clinicians can definitely ask, and use supported communication techniques, I should say, in order to get those answers to, “What do you do when you get really frustrated?”, and then have some pictures to point to perhaps, or words to point to whatever that person is able to best communicate with?   Janet: That's a great idea.   Jacqueline: Yeah. First of all, understand what their coping mechanisms are and strategies, and then help them to develop more or, through the Life Participation Approach, how do we help them to have access to those things that might help them to cope? If they were really engaged in group activities prior to their stroke and living with aphasia, then how can they get back to that? How can we have them engage again?   Janet: Well, you've just actually given a partial answer to the next question I want to ask you, which is how we can, as clinicians, incorporate some of these positive experiences or helpful experiences into our clinical activities. The thing is, like many of us, we may not be experienced at, say, incorporating mindfulness or yoga into our own lives, not to mention putting them into treatment. And so we likely have no idea how to start. Based on your research, and again, on your clinical experience, what advice can you give our listeners who may wish to add some of these ideas or some of these activities to our practice? Where do we start?   Jacqueline: I think getting back to that comfort level. What is the clinician comfortable with? And as you had pointed out, that if you're don't have that internal self-comfort of “I can have the person that I'm working with, kind of slow down, take a deep breath, maybe take four breaths in and out slowly”. If I don't feel comfortable doing that, then don't do it, because it's going to come off kind of odd. Having some comfort, whether it be practicing with oneself, or practicing with others before you get into therapy, I think that's really important.   Janet: There are practices such as yoga, for example. I think if you're going to incorporate yoga, you have to know what you're doing. You have to understand yoga, or you have to be able to do it or to instruct it. If you're not at that instructor level, there can be problems in the therapy session. So you wouldn't want to incorporate yoga, unless you are really skilled at it and know what you're doing. But there have to be some positive practices that are relatively easy to incorporate, maybe laughter or even a discussion of spirituality. I'm thinking about, sort of, the term Monday morning practice. What can clinicians do on Monday morning, without having to do a lot of learning about yoga or practicing yoga? What can they do on Monday morning, when they see clients that might help them begin on this path of integrative health practices or thinking about the other aspects of our aphasia rehabilitation? Does that makes sense?   Jacqueline: Yeah, yeah. Yeah. It is the “rubber hitting the road” sort of thing to all of this?   Janet: Exactly.   Jacqueline: There is adaptive yoga that Amy Dietz and Laura Bislick and colleagues had published in AJSLP, a couple of years ago. There are some postures that are presented that are accessible to clinicians. So they could look at those. There are some adaptive yoga techniques that are clinically accessible. Some very simple breathing activities. These are not complicated. It is just a matter of “Close your eyes; and for a moment, go ahead and take a nice deep breath in and out.” Recognizing that the breath really anchors everyone to the moment. When you have an individual that you're working with that seems to be over stressed and it's working against them in what you're trying to have accomplished in your therapy session, taking a moment, closing the eyes, and breathing will bring them back to that moment, moment of relaxation or to the present where they can approach the task with a different perspective.   Janet: It makes so much sense to me and even just doing it with you - for those few seconds, closing my eyes taking a deep breath, I felt a difference in my own self, just in the in the course of this conversation. I can imagine that it will produce a similar effect, resetting, if you will, the clinical environment, resetting the goals, and reducing perhaps any negative perceived stress that the patient might have. If they're thinking that they're not doing what they're supposed to, or they're not meeting goals, or they're having troubles. It's great idea.   As we bring this conversation to a close Jacqueline, are there any other pearls of wisdom or lessons learned in thinking about the influences of integrative health behaviors on language and communication, rehabilitation, not just for the people with aphasia, but also for their families, their friends, and for clinicians,   Jacqueline: I think lessons learned is keeping an open mind and really approaching aphasia, with the perspective that there is the language impairment, but there's also a bigger picture here. There are different approaches to recovery that can stem from traditional ancient medical beliefs that may help us during this modern time that we're in. I think keeping an open mind, but yet, maintaining some skepticism, too. We do want to continue to have science guide our therapies, as well as our clinical experience. It can be hard to have a convergence of the two at times. But I think that we can't ignore that there is more than just the language impairment going on.   Janet: We cannot ignore it. You're right, especially if we are proponents of the LPAA model, which incorporates the whole individual in living their life. I agree with everything that you've said and I'm finding myself thinking of that balance, too, between there is some stress that can be good, but don't have too much stress, because you don't want it to be a bad thing, and keep an open mind but have healthy skepticism. All of that's a good thing for all of us to practice.   Jacqueline: Not easy, it's hard to do, but it's a good thing.   Janet: Today's conversation has been, for me at least, thought provoking and enlightening and I hope it has been for our listeners as well. Realizing that additional work is necessary to provide an evidence informed foundation for incorporating many of the activities such as yoga practice, or mindfulness into aphasia rehabilitation, I believe that this is an avenue well worth pursuing in both clinical and research activities. I would like to thank my guest, Dr. Jacqueline Laures-Gore for sharing her thoughts and experience in this important area of clinical research and practice, Jacqueline, I greatly appreciate you taking the time to speak with me today, and for providing our listeners with the foundation and how to think about integrative medicine.   Jacqueline: You are very welcome. This was very fun. Thank you, Janet, for asking me.   Janet: Oh, you're welcome.   I would also like to thank our listeners for supporting Aphasia Access Conversations by listening to our podcasts. For references and resources mentioned in today's show, please see our Show Notes. They are available on our website, www.aphasia.access.org. There you can also become a member of our organization, browse our growing library of materials and find out about the Aphasia Access Academy. If you have an idea for a future podcast episode, email us at info@aphasiaaccess.org. For Aphasia Access Conversations, I am Janet Patterson and again, I thank you for your ongoing support of aphasia access                       References Aphasia Access Conversations Episode #98: An Aphasia Journey Through Linguistics, Neuroplasticity, Language Treatment, Counseling, and Quality of Life: A Conversation with Chaleece Sandberg Episode #95: Supporting Psychological Well-Being: A Conversation with Jasvinder Sekhon Episode #89: Aphasia is a Complex Disorder: Mental Health, Language, and More – A Conversation with Sameer Ashaie Episode #69: Motivation and Engagement in Aphasia Rehabilitation: In Conversation with Michael Biel Episode #67: Considering Depression In People Who Have Aphasia and Their Care Partners: In Conversation with Rebecca Hunting Pompon   Scholarly papers Bislick, L., Dietz, A., Duncan, E. S., Garza, P., Gleason, R., Harley, D., ... & Van Allan, S. (2022). Finding “Zen” in Aphasia: The benefits of yoga as described by key stakeholders. American journal of speech-language pathology, 31(1), 133-147. https://doi.org/10.1044/2021_AJSLP-20-00330 Hunting Pompon, R, Amtmann, D., Bombardier, C., & Kendall, D. (2018). Modifying and validating a measure of chronic stress for people with aphasia. Journal of Speech, Language and Hearing Research, 61(12):2934-2949. https://doi.org/10.1044/2018_JSLHR-L-18-0173  Kagan, A., Simmons‐Mackie, N., Rowland, A., Huijbregts, M., Shumway, E., McEwen, Threats, T., & Sharp, S. (2008) Counting what counts: A framework for capturing real‐life outcomes of aphasia intervention, Aphasiology, 22(3), 258-280. https://doi.org/10.1080/02687030701282595 Laures-Gore, J., Cahana-Amitay, D., & Buchanan, T. (2019). Diurnal cortisol dynamics, perceived stress, and language production in aphasia. Journal of Speech, Language, and Hearing Research, 62, 1416-1426. https://doi.org/10.1044/2018_JSLHR-L-18-0276 Laures-Gore, J., & Rice, K. (2019). The Simple Aphasia Stress Scale. Journal of Speech, Language, and Hearing Research, 62, 2855–2859. https://doi.org/10.1044/2019_JSLHR-L-19-0053 Laures-Gore, J., Russell, S., Patel, R., & Frankel, M. (2016). The Atlanta Motor Speech Disorders Corpus: Motivation, Development, and Utility. Folia-Phoniatrica-et-Logopaedica 68(2):99-105. https://doi.org/10.1159/000448891 McGuire, S.S., Laures-Gore, J., Freestone, E.J., & van Leer, E. (2021). Simulated laughter, perceived stress, and discourse in adults with aphasia, Aphasiology, 35:9, 1207-1226. https://doi.org/10.1080/02687038.2020.1787944  McNeil, M., Prescott, T., & Lemme, M. (1976). An application of electromyographic feedback to aphasia/apraxia treatment. Proceedings of the Clinical Aphasiology Conference, 151-171. http://aphasiology.pitt.edu/21/1/06-11.pdf Thompson, C.K., Hall, H.R., & Sison, C.E. (1986). Effects of hypnosis and imagery training on naming behavior in aphasia. Brain and Language, 28(1), 141-153. https://doi.org/10.1016/0093-934x(86)90097-0   urls Aphasia & Motor Speech Disorders Lab, Georgia State University  https://education.gsu.edu/csd/csdresearchoutreach/aphasia/?fbclid=IwAR1x5-CQxmiXkV4ZVcDbbt5oZmYw5VhZLKsmmw62xmh9XyC6O9sEzqV0mvU#stress-and-aphasia and https://www.facebook.com/gsuaphasia

In today's episode, we discuss the cortisol awakening response, which is a salivary test that's part of the Dutch test and other hormone tests. We'll be looking at the patterns of this response and discussing what can cause it to go out of balance. This test, along with urine-based metabolite measurements, provides a beautiful picture of your overall cortisol levels. If you're interested in learning more about the importance of cortisol testing and how it can benefit your health, listen to the full episode.IN THIS EPISODE:Cortisol Awakening Response TestThe Cortisol Awakening Response (CAR) is a natural biological process in which the hormone cortisol is released by the adrenal glands upon awakening in the morning. The CAR typically occurs within the first 30-45 minutes after waking and is responsible for preparing the body for the day ahead. The Cortisol Awakening Response Test measures the amount of cortisol in the saliva at awakening. It is used in conjunction with the urine metabolite testing to evaluate response to stress. When used with metabolite testing, it allows you to see the dips and peaks throughout the day to see if there are any imbalances. If the cortisol awakening response is too low or too high, that is a sign that we need to ask more questions about this client's lifestyle. Why Timing The Cortisol Awakening Response MattersThe cortisol awakening response is a natural physiological pattern where cortisol levels increase rapidly within 30-45 minutes after waking up in the morning. When testing, it is crucial to test immediately upon awakening, within the first 5 minutes at most. Once a person starts moving around we are no longer going to see the baseline amount. The timing of the cortisol awakening response is critical because it sets the tone for the body's stress response levels throughout the day. If cortisol levels are not elevated in the morning, it can impact our ability to cope with stressors, increase our risk for diseases, and affect our mood and energy levels for the rest of the day.The HPA Axis and Blood Sugar DysregulationThe HPA (hypothalamic-pituitary-adrenal) axis is a complex neuroendocrine system that regulates the body's response to stress. When we encounter a stressful situation, the hypothalamus in the brain signals the pituitary gland to release adrenocorticotropic hormone (ACTH), which then stimulates the adrenal glands to produce cortisol. Cortisol is a hormone that helps the body to respond to stress, but chronic stress can cause dysregulation of the HPA axis and lead to various health problems. One of these problems is blood sugar dysregulation, which occurs when cortisol raises blood sugar levels in response to stress. Over time, this can lead to insulin resistance and type 2 diabetes. Additionally, high levels of cortisol can cause the body to store fat, particularly in the abdominal area, which can further contribute to blood sugar dysregulation and other health issues.RESOURCES:Read through our FREE Resource Adrenal Guide.Get our FREE Guide to Taking a Detailed Health History that gets you to root causes with ease. Access Additional Resources for Practitioners ready to improve clinical outcomes through our Nutritional Endocrinology Practitioner Training. Watch our recorded Thyroid Adrenal Workshop here.

Who feels like Cushing's is a nice disease to diagnose and manage? Like, how often do you feel like your hyperadrenocorticism patients are really doing REALLY well? My guess is: not that often. This episode will change that. Dr Sue Foster is a registered specialist in Feline Medicine and Senior Lecturer in Small Animal Medicine at Murdoch University in Western Australia. She's also a medical consultant for Vetnostics and ASAP Laboratory, where a large part of her role is interpreting cortisol test results and supporting veterinarians in their clinical decision-making. In this conversation, Dr Sue challenges the belief that Cushing's is to some degree a 'lifestyle' disease that doesn't always need to be treated, we discuss the subtle ways that it can present, and of course we take a deep dive into those slippery cortisol tests, which should feel a lot less slippery after this episode. Dr Sue also presents a paradigm shift in how we think about treating these cases. Topics: 0:00 Understanding the cortisol lab tests.  4:40 ACTH stim vs LDDT - which is better?  10:28 The TRUE significance of ALP in diagnosing Cushing's. 13:30 Fasting triglycerides - your friend in Cushing's screening?  16:26 Deciding when to test for Cushings . 18:27 More on triglycerides and lipaemia  23:52 Why Cushing's cases don't all have to have pu/pd.  26:04 The many different faces of Cushing's - spotting the sneaky hyperA case . 29:42 Why we should consider treating Cushing's even if they aren't textbook cases.  31:41 Cushing's and anxiety. 35:40 The dog with the high ALP but no clinical signs of Cushing's. 39:44 Treatment trials for the ‘undiagnosable' Cushing's case. 45:13 Monitoring Cushing's therapy with ACTH stim testing.  52:30 The quick and easy ACTH stim test.  56:20 Treating Cushing's like a pro.  This episode is supported by the SVS Pathology Network. QML/TML Vetnostics (QLD & Tas): 1300 838 765 vetnostics@qml.com.au Vetnostics (NSW & ACT): 02 9006 7468 enquiries@vetnostics.com.au ASAP Laboratory (VIC): 1300 838 522 admin@asaplab.com.au Vetpath (WA): 08 9317 0777 admin@vetpath.com.au Join our community of Vet Vault Nerds to lift your clinical game and get your groove back with our up to date easy-to-consume clinical episodes at vvn.supercast.com, visit thevetvault.com for the show notes and resources for this episode, and connect with us through our online Vet Vault Network. for episode highlights, discussions, questions and support. Join us at Vets on Tour in Wanaka, New Zealand on 13 - 18 August 2023 for great CE, live podcasting and snow... lots of snow! --- Send in a voice message: https://podcasters.spotify.com/pod/show/vet-vault/message

The term hypothalamus originates from the Greek words "hypo" and "thalamus," which mean "below" and "chamber," respectively. This term was first coined by German anatomist Johann Christian Reil in 1809. The hypothalamus is a small region of the brain located at the base of the brain, just above the brain stem. It is responsible for regulating homeostasis and controlling many of the body's automatic responses such as hunger, thirst, body temperature, and hormones. It also plays a role in emotion and behavior. The hypothalamus is responsible for releasing hormones that help to regulate other systems in the body, such as the endocrine and autonomic nervous systems. It is connected to the pituitary gland, which helps to control the release of hormones from the hypothalamus. 1. Corticotropin-Releasing Hormone (CRH): A peptide hormone produced by the hypothalamus that stimulates the release of adrenocorticotropic hormone (ACTH) from the pituitary gland. Etymologically, its name is derived from the Greek words ‘kortiko', meaning ‘outer' and ‘tropin', which means ‘to turn'. 2. Gonadotropin-Releasing Hormone (GnRH): A peptide hormone released by the hypothalamus that stimulates the release of luteinizing hormone (LH) and follicle-stimulating hormone (FSH) from the pituitary gland. Its name is derived from the Greek words ‘gonad', meaning ‘ovaries' and ‘tropin', meaning ‘to turn'. 3. Thyrotropin-Releasing Hormone (TRH): A peptide hormone produced by the hypothalamus that stimulates the release of thyroid-stimulating hormone (TSH) from the pituitary gland. Its name is derived from the Greek words ‘thyro', meaning ‘thyroid' and ‘tropin', meaning ‘to turn'. 4. Growth Hormone-Releasing Hormone (GHRH): A peptide hormone produced by the hypothalamus that stimulates the release of growth hormone (GH) from the pituitary gland. Its name is derived from the Greek words ‘growth' and ‘tropin', meaning ‘to turn'. 5. Prolactin-Releasing Hormone (PRH): A peptide hormone produced by the hypothalamus that stimulates the release of prolactin (PRL) from the pituitary gland. Its name is derived from the Greek words ‘pro', meaning ‘in front of' and ‘lactin', meaning ‘milk'. 6. Oxytocin: A peptide hormone produced by the hypothalamus that stimulates the contraction of the uterus and milk production. Its name is derived from the Greek words ‘oxys', meaning ‘swift' and ‘tocos', meaning ‘birth'. 7. Vasopressin (ADH): A peptide hormone produced by the hypothalamus that regulates water balance in the body and increases blood pressure. Its name is derived from the Latin words ‘vas', meaning ‘vessel' and ‘press', meaning ‘to press'. --- Support this podcast: https://podcasters.spotify.com/pod/show/liam-connerly/support

Knowing which MS changes are significant enough to warrant speaking up can be hard. Relapses can occur every 1-2 years without treatment, but much less frequently on disease-modifying treatment. Distinguishing between an actual relapse, a pseudorelapse or just brief worsening of symptoms (Uhthoff's phenomenon) explained. Options for relapses such as steroids, plasmapheresis and ACTH are reviewed. Importance of MRI monitoring addressed since most new MS lesions pop up on MRI scans without actual symptoms. Slow progression of disability can be challenging to detect. Physical changes can include slower walking, worsening balance and more hand coordination problems. Cognitive worsening may be noticeable due to short-term memory loss, word-finding issues and multitasking challenges. Tools to improve monitoring for disease progression highlighted such as in-office testing, remote electronic monitoring and biomarker blood testing. Why multiple sclerosis disability can worsen without MRI change explained. Ways to better advocate for prompt care of worsening MS shared. Barry Singer MD, Director of The MS Center for Innovations in Care, interviews Jacqueline Nicholas MD, System Chief of Neuroimmunology & Multiple Sclerosis at the OhioHealth Multiple Sclerosis Center and James Bowen MD, Medical Director of the Multiple Sclerosis Center at Swedish Neuroscience Institute in Seattle.  

Epilepsy is a frequent co-morbidity in those with autism spectrum disorder (ASD). Maria Augusta Montenegro, M.D., Ph.D., discusses how cognitive abilities, motor deficit, and other associated symptoms can be factors, how epilepsy can be diagnosed, and recommended treatment options. Series: "Autism Tree Project Annual Neuroscience Conference" [Health and Medicine] [Show ID: 38389]

Epilepsy is a frequent co-morbidity in those with autism spectrum disorder (ASD). Maria Augusta Montenegro, M.D., Ph.D., discusses how cognitive abilities, motor deficit, and other associated symptoms can be factors, how epilepsy can be diagnosed, and recommended treatment options. Series: "Autism Tree Project Annual Neuroscience Conference" [Health and Medicine] [Show ID: 38389]

Epilepsy is a frequent co-morbidity in those with autism spectrum disorder (ASD). Maria Augusta Montenegro, M.D., Ph.D., discusses how cognitive abilities, motor deficit, and other associated symptoms can be factors, how epilepsy can be diagnosed, and recommended treatment options. Series: "Autism Tree Project Annual Neuroscience Conference" [Health and Medicine] [Show ID: 38389]

In this podcast Dr. Rodney and Karen talk about the health and longevity benefits of cold exposure.  This practice definitely gets most of us out of our comfort zone. Here are a few of the reasons to give it a try:1. Raises your metabolic rateThis has to be one of the most compelling because cold exposure increases your BAT - Brown Adipose Tissue which in turn increases your metabolic rate. That means you can eat more without gaining weight and have more energy. 2. Improves fat burningCold exposure ramps up fat burning as the body makes the attempt to keep your body warm. Some have even called it a "weapon" to combat obesity. Are you ready to turn the thermostat down a few degrees?3. Boosts glycemic control and insulin sensitivityWhen you activate BAT it can increase blood glucose so that it is burned as fuel or stored as glycogen (for use later) rather than fat.  When insulin sensitivity goes up it improves metabolic health  and has an anti-diabetic effect. 4.  Diminishes inflammation and painCold exposure is often used to alleviate musculoskeletal pain and inflammation in conditions like arthritis and fibromyalgia.  In one study, participants with inflammatory arthritis who took a two-minute cold shower each day for a week experienced significant reductions in pain.  Cold exposure leads to vasoconstriction and reduces blood flow, which in turn reduces inflammation in tissues within and around injured sites. 5. Boosts moodResearchers believe these beneficial effects may be tied to cold exposure initiating an endocrine response and increasing hormones like cortisone, epinephrine, norepinephrine, adrenocorticotropic hormone (ACTH),  pro-opiomelanocortin (POMC),and endorphins. On top of that, cold exposure may activate the body's own pain control system.6. Promotes better sleep qualityCooler temperatures (between 60 and 67°F) help lower core temperature, which facilitates sleep. Also, body temperature is a strong driver of circadian rhythms. In fact, similar to light, temperature is one of the environmental cues that's able to reset the body's circadian clocks. Turn down the thermostat or take a cold shower.7. Raises alertness & sharpens focusA cold shower can wake you and your body up, promoting a higher state of alertness. The cold also stimulates deeper breathing, helping increase oxygenation of the body's tissues.8. Builds resilienceAs you get acclimated to the cold your stress response (fight or flight) is blunted after repeated exposure. This is what hormetic stress is all about—exposure to small, transient stress leads to adaptation. This improved stress tolerance applies then to other areas of life through greater willpower and remaining cool-headed.9. Enhances cognitive functionConsidering the benefits on hormones (both stress & feel-good chemicals) and the enhancement in resiliency, it should not surprise you that cold exposure can also be good for the brain leading to better brain function. Repeated cold exposure is likely to be beneficial and neuroprotective because it regulates the release of inflammatory cytokines and nitric oxide.10. Connects to your true selfCold exposure therapy builds mental toughness and provides a place where your worries disappear. As you learn to control your breathing your mind clears and focus ensues. You just might also find yourself.Get started with cold exposure:Turn down the thermostatCold and contrast showersCold-water immersion (e.g., cold pools, ice baths, etc.)Go outside in cold temperaturesFollow us on Instagram and Facebook.

Amy sat down with her friend, Meredith Lile, to talk about the benefits of float therapy. Meredith first started floating to help with her anxiety and she loved it so much that she decided to open two studios of her own in the Nashville area: Pure Sweat + Float Brentwood and Pure Sweat + Float Cool Springs.   Meredith explains what float therapy is and the benefits (sleep being one of them because of all the magnesium that's in the float tub!!) She also shares 4 things she's thankful for (one of the things being her husband's sobriety…which is such a blessing!)    FLOAT THERAPY BENEFITS: The buoyancy and healing effects created by the dense Epsom salt solution removes the feeling of gravity on the body, relieves all pressure and stress that gravity normally places on one's muscles and joints, aiding in pain relief. The reduction of environmental stimulation - such as sight, talk, interruption and noise - enables the mind to become tranquil and clear.    Provides Deep Relaxation Lowers Blood Pressure + Heart Rate Reduces Stress on Spine, Hips + Joints Relieves Pain + Muscle Soreness Boosts Hair + Skin Health Restores Magnesium + Sulfate Lowers Cortisol, Acth, Lactic Acid + Adrenaline Improves Circulation Distributes Oxygen + Nutrients Increases Endorphins Aids in Visualization + Creativity Boosts Performance Relieves Insomnia, Fatigue + Jet Lag   PS+FS Brentwood: https://www.puresweatfloatstudio.com/brentwood    PS+FS CoolSprings: https://www.puresweatfloatstudio.com/coolsprings    Best places to find more about Amy: RadioAmy.com + @RadioAmy   Tickets to Amy's 4 Things LIVE Event In Wichita, Kansas: https://selectaseat.com/amy See omnystudio.com/listener for privacy information.

The seasonal rise of ACTH in the fall can throw many PPID horses into laminitis. How can we better manage this? How do we take care of our metabolic horses to prevent laminitis and founder? Dr. Jaini Clougher and Dr. Kathleen Gustafson, both who have worked with ECIR, discuss how to best manage metabolic horses so they can not just survive, but thrive. For more information, visit:  ecirhorse.orgSupport the show

The seasonal rise of ACTH in the fall can throw many PPID horses into laminitis. How can we better manage this? How do we take care of our metabolic horses to prevent laminitis and founder? Dr. Jaini Clougher and Dr. Kathleen Gustafson, both who have worked with ECIR, discuss how to best manage metabolic horses so they can not just survive, but thrive.  For more information, visit:  ecirhorse.org

Videos : Those who speak out are shouted down until they are proved right, says Neil Oliver – 10:06 Gad Saad: Why Rational People Fall for ‘Parasitic' Ideas | American Thought Leaders CLIP – 9:11 Scientist Carl Sagan testifying to the U.S. Senate in 1985 on the greenhouse effect: – 2:44 Parent Eviscerates School Board Over Censorship– 4:59 Vitamin C supplementation associated with improved lung function in COPD Medical College of Lanzhou University (China), September 23 2022. The International Journal of Chronic Obstructive Pulmonary Disease published a systematic review and meta-analysis of clinical trials that found improvement in lung function among chronic obstructive pulmonary disease (COPD) patients who received vitamin C. The disease is characterized by airflow limitation and persistent respiratory symptoms. Ting Lei of Medical College of Lanzhou University in Lanzhou, China and associates identified 10 randomized, controlled trials that included a total of 487 adults with COPD for the meta-analysis. The trials compared lung function and/or antioxidant enzyme or nutrient levels of COPD patients who received vitamin C to a placebo or control group. The meta-analysis found improvement in forced expiratory volume in one second as a percentage (FEV1%, a measure of lung function) in association with vitamin C supplementation. When dosage was analyzed, it was determined that consuming more than 400 milligrams vitamin C per day was needed experience a significant benefit. The ratio of FEV1 to forced vital capacity (another lung function assessment), and levels of vitamin C and glutathione, both of which are antioxidants, also improved among participants who received vitamin C supplements. The authors remarked that oxidative stress, which is a disturbance of the oxidant to antioxidant balance, has been suggested as playing a role in the development of COPD. The current investigation is the first systematic review and meta-analysis to assess the effect of vitamin C supplementation in people with COPD. “We found that supplementing vitamin C to patients with COPD demonstrated vital clinical significance,” Lei and associates concluded. “Vitamin C supplementation could increase the levels of antioxidation in serum (vitamin C and glutathione) and improve lung function (FEV1% and FEV1/FVC), especially in patients treated with vitamin C supplementation greater than 400 mg/day.” Single Flavanoid (Found in 6 Foods) Reduces Cognitive Impairment Drastically Fourth Military Medical University (China), September 19, 2022 A singular flavanoid can protect the brain against cognitive deficit and other cellular damage, according to studies from the Fourth Military Medical University. The news comes from Xi'an, People's Republic of China, and shows great promise for those suffering from mental impairment due to Alzheimer's disease, vascular dementia, and other debilitating cognitive conditions. The study abstract concludes: “Our results provide new insights into the pharmacological actions of rutin and suggest that rutin has multi-targeted therapeutical potential on cognitive deficits associated with conditions with chronic cerebral hypoperfusion such as vascular dementia and Alzheimer's disease.” Rutin is a biologically active flavonoid found in the following foods:  Buckwheat – Possibly the best source of rutin, and much better than boiled oats, uncooked buckwheat leaf flower offers about 675 mg in a 1.1 cup serving. Uncooked buckwheat groats contain 230 mg of rutin per 1 kg, dark buckwheat flour has 218 mg per 1 kg and buckwheat noodles provide 78 mg. Elderflower Tea – When dried, the white flowers of the elderflower make a delicious and rutin-filled tea. According to the Czech Journal of Food Science, elderflower tea contains approximately 10.9g/kg of rutin per brewed cup. Amaranth Leaves – In Western cultures, most people are familiar with the edible seeds of amaranth, though in Chinese and Southeast Asian cooking the leaves are also gaining traction, partly due to their high rutin content. You can expect around 24.5g/kg from the dried leaves. Seeds only contain trace amounts of the important nutrient. Unpeeled Apples – Keep the peel on your apples to enjoy lots of rutin. Just be sure that they are organic, since apple peels are especially prone to pesticide build-up. Apple skins are 6x as powerful as the flesh at preventing high blood pressure due to this flavanoid, too. • Unfermented Rooibos Tea – While rooibos tea contains fewer antioxidants than black or green teas, it is a good source of rutin, providing around 1.69 mg/g. • Figs – These little gems contain about the same amount of rutin as apples, so be sure to add them to your diet. The scientists found that rutin works primarily through anti-inflammatory mechanisms, and reducing hypofusion in the brain. Resistance-breathing training found to lower blood pressure University of Colorado and University of Arizona, September 23, 2022 A team of researchers with members from the University of Colorado, the University of Arizona and Alma College, has found that resistance-breathing training can lower blood pressure as much as some medicines and/or exercises. The study is published in the Journal of Applied Physiology. Hypertension, also known as chronic high blood pressure, can lead to a wide variety of health problems, from loss of vision to strokes and heart attacks. For that reason, doctors take it seriously. Typically, patients are directed to modify their diet and to exercise more. If that does not fix the problem, medications are prescribed. In this new effort, the researchers looked into a new type of therapy to reduce blood pressure levels—resistance-breathing training. Resistance-breathing training involves breathing in and out of a small device, called, quite naturally, a POWERbreathe, every day for several minutes. The device forces the patient to use their breathing muscles to push and pull air through it, making them stronger. And that, the researchers found, also reduces blood pressure. The device has been in use for several years as a means to assist athletes, singers and people with weak lung muscles. Several groups of healthy volunteers practiced the training for a few minutes every day for six weeks. Each was breathed in and out with the device 30 times each session. Each of the volunteers had their blood pressure measured before and after the training. The researchers found a sustained average drop of 9 mmHg in systolic blood pressure (the top number in blood pressure readings)—normal pressure is defined as 120/80. They describe the change as significant, as much as some patients see with medication. They also note that it is similar to changes in many patients who begin an aerobic exercise regimen, such as walking, cycling or running. They suggest such training could be used by patients of all ages who are unable to exercise to lower their blood pressure. How To Maintain Peak Brain Health: Scientists Say It Comes Down To These 3 Factors Norwegian University of Science and Technology, September 23, 2022 What's the best way to maintain peak brain health as we age? There are countless studies detailing ways to prevent cognitive decline, so scientists in Norway sought to simplify the science of managing strong brain health to three recommendations. This report is something of a summation covering modern science's current understanding of how best to cultivate robust brain health. The team at NTNU cite 101 references to prior articles in this latest theoretical perspective paper. “Three factors stand out if you want to keep your brain at its best,” Prof. Sigmundsson adds. The three identified keys to strong brain health are: Physical exercise Social activity Strong, passionate interests and hobbies It's common knowledge that spending all day on the couch isn't healthy for the body, but physical activity is also key to brain health. “An active lifestyle helps to develop the central nervous system and to counteract the aging of the brain,” according to study authors. Researchers add that consistency is essential. Do your best to get in at least a little movement each and every day. Even if you work a sedentary job that requires lots of sitting, get moving every hour or so for just a few minutes at the very least. Some people are naturally more social than others, but researchers stress that no one is an island. Even if you prefer a quiet night in to attending a party, make an effort to stay in touch with the people who matter to you. Our brains thrive on social interactions and connections. “Relationships with other people, and interacting with them, contribute to a number of complex biological factors that can prevent the brain from slowing down,” Prof. Sigmundsson explains. Just like bicep curls help us build muscle, keeping the brain active promotes strong lifelong cognition. Consider taking up a new hobby, or learning a new skill. Perhaps most importantly, though, don't force it; find something you're actually passionate about. It's never too late in life to learn something new! “Passion, or having a strong interest in something, can be the decisive, driving factor that leads us to learn new things. Over time, this impacts the development and maintenance of our neural networks,” Prof. Sigmundsson says. “Brain development is closely linked to lifestyle. Physical exercise, relationships and passion help to develop and maintain the basic structures of our brain as we get older,” Prof. Sigmundsson concludes. Calcium supplements may support a healthy colon: Harvard study Harvard School of Public Health, September 18, 2022 Supplements of calcium or non-dairy products fortified with the mineral may reduce the risk of colorectal cancer, according to meta-analysis of prospective observational studies by researchers at Harvard School of Public Health. For every 300 mg increase in calcium from supplements was associated with a 9% reduction in risk, wrote NaNa Keum and her co-authors in the International Journal of Cancer . Every 300 mg increase in total calcium was associated with a similar reduction in risk (8%), they added. “Our findings have several important clinical and public health implications,” they explained. “First, according to the 2003 to 2006 National Health and Nutrition Examination Survey, a nationally representative cross-sectional survey in the U.S., median total calcium intake of adults aged over 50 years was approximately 650 mg/day for no calcium-supplement users and 1,000 mg/day for calcium-supplement users. “As the benefit of calcium intake on CRC is expected to continue beyond 1,000 mg/day, not only non-supplement users but also supplement users may further reduce their CRC risk through additional calcium intake.” “Second, while dairy products, especially milk, are the major sources of calcium in many countries, they are a substantial source of calories and contain potentially harmful factors such as saturated fat, hormones, and casein proteins. Since our analyses provide evidence for an equivalent benefit of dietary and supplementary calcium, the benefit of calcium on CRC risk may be obtained through supplements and non-dairy products fortified with calcium.” The Boston-based scientists conducted dose-response meta-analyses of 15 studies involving 12,305 cases of colorectal cancer and calcium intakes ranging from 250-1,900 mg/day. The studies varied in duration from 3.3 to 16 years. The data indicated that both total and supplemental calcium were associated with reductions in the risk of colorectal cancer. “In conclusion, both dietary and supplementary calcium intake may continue to decrease colorectal cancer risk beyond 1,000 mg/day,” wrote Keum and her co-authors. Yoga's Age-Defying Effects Confirmed by Science Defence Institute of Physiology and Allied Sciences (India), September 21st 2022 While yoga's longevity promoting effects have been the subject of legend for millennia, increasingly modern science is confirming this ancient technology for spiritual and physical well-being actually can slow aging and stimulate our regenerative potential. One particularly powerful study published lin the journal Age titled, “Age-related changes in cardiovascular system, autonomic functions, and levels of BDNF of healthy active males: role of yogic practice”, found that a brief yoga intervention (3 months) resulted in widespread improvements in cardiovascular and neurological function. Indian researchers studied healthy active males of three age groups (20-29, 30-39, and 40-49 years) by randomly assigning them to practice one hour of yoga daily for 3 months. The observed significant differences between the younger and older participants in the study, specifically: “Significantly higher values of heart rate (HR), blood pressure (BP), load in heart (DoP), myocardial oxygen consumption (RPP), and total cholesterol (TC) were noted in senior age group.” The yogic practice resulted in significant reductions in all of these parameters (HR, BP, DoP, RPP and TC). Also observed in the older participants were decreases in high frequency (HF), total power (TP), all time domain variables of heart rate variability (HRV), and skin conductance (SC) — all of which increased following yogic practice. Higher levels of catecholamines (“stress hormones”) and low frequency (LF) power of HRV were noted in advancement of age, both of which decreased following yogic practice. Additionally, the senior age group had highest levels of cortisol and adrenocorticotrophic hormone (ACTH), both of which decreased following yogic practice. Finally, brain-derived neurotropic factor (BDNF), serotonin, and dopamine were low in higher age group, but these increased following yogic practice; an indication of improved brain function and cognition. The researchers concluded: ‘This study revealed that yogic practices might help in the prevention of age-related degeneration by changing cardiometabolic risk factors, autonomic function, and BDNF in healthy male.” There are a number of promising studies revealing the age-defying potential of this ancient practice. Here are some additional benefits confirmed in 2014 alone: Age-Related Respiratory Problems: A 2014 study from the journal of Human Kinetics found that a 3 month yoga intervention in 36 elderly women (average age 63.1) significantly improved pulmonary (respiratory) function. Age-Related Brain Cognitive Decline: A review in the Journals of Gerontology, involving a two month Hatha yoga intervention in the elderly (average age 62.0) resulted in significant improvements in “executive function measures of working memory capacity and efficiency of mental set shifting and flexibility compared with their stretching-strengthening counterparts.” Age-Related Hormone Insufficiency: A study published in Evidence Based Complementary and Alternative Medicine found that a 3 month yogic intervention in men (average age 42.8) and women (average age 44.75) resulted in improvements in the level of growth hormone and DHEAS, two essential hormones that drop off precipitously as we age. Age-Related Sleep Problems: Astudy published in Alternatives Therapies in Health and Medicine found a 12 week yogic intervention (yoga 2x a week) resulted in significant improvements in the quality of sleep in older individuals (average age 60). Age-Related Depression: From the Chinese Journal of Nursing found that not only did yoga improve sleep as found in the study above but also significantly reduced the depressive symptoms of elderly participants…after 6 months. “ This is just a small sampling of the literature. There is older research revealing that yoga has even more benefits for aging populations.

Hmmmmmm....do you know why people with Addison's Disease look tanned especially pre-diagnosis. It is from the hormone ACTH released from the brain. If you are in the process of being diagnosed this is an important episode for you to tune in to. If ANYTHING in this episode resonates with you. PLEASE subscribe, review and share the podcast. We need to connect as a community and build awareness. Looking for more information about Addison's Disease. Please visit www.facebook.com/teamaddisoncanada DISCLAIMER: The information from THE PICKLE JAR represents the experiences of the host Jill Battle and the individual experiences of each guest. No information is intended to provide or replace the medical advice of a medical professional. The host or guests are not liable for any negative consequences from any treatment, action, application or preparation, to any person following the information from the podcast.

Episode 105: Renal Cell Carcinoma. Manpreet and Jon-Ade explain how to diagnose renal cell carcinoma. Introduction about age and kidney transplant by Dr. Arreaza and Dr. Yomi. Introduction: Too old for a new kidney?By Hector Arreaza, MD. Discussed with  Timiiye Yomi, MD.Today we will be talking about the kidneys, those precious bean-shaped organs that detoxify your blood 24/7. Amazingly, we can live normal lives with one kidney, but when the kidney function is not good enough to meet the body's demands, patients need to start kidney replacement therapy. Modern medicine has made a lot of advances with dialysis, but the perfection of a kidney has not been outperformed by any machine yet. That's why kidney transplant is the hope for many of our patients with end-stage kidney disease.The need for a kidney transplant is growing, likely due to increasing chronic diseases such as diabetes and hypertension, and also because of an increase in elderly population. About 22% of patients on the kidney transplant waiting list are over age 65. A cut-off age to receive kidney transplant has not been established across the globe. Different countries use different criteria for the maximum age for transplant. The American Society of Transplantation's guidelines states “There should be no absolute upper age limit for excluding patients whose overall health and life situation suggest that transplantation will be beneficial.” So, if your patient is older than 65 and needs a kidney, they may qualify for a transplant, and age should not be an absolute contraindication to receive it. Actually, older patients may have lower risk of rejection due to a theoretically weaker immune system. A live donor is likely to be a better option for elderly patients. A condition that would make your elderly patient a poor candidate for kidney transplant would be frailty. Common contraindications to kidney transplant include active infections or malignancy, uncontrolled mental illness, ongoing addiction to substances, reversible kidney failure, and documented active and ongoing treatment nonadherence.So, remember to take these factors into consideration when deciding if you need to refer your elderly patients for a kidney transplant, there is no such thing as being too old for a new kidney if your patient meets all the criteria for a transplant.This is Rio Bravo qWeek Podcast, your weekly dose of knowledge brought to you by the Rio Bravo Family Medicine Residency Program from Bakersfield, California. Our program is affiliated with UCLA, and it's sponsored by Clinica Sierra Vista, Let Us Be Your Healthcare Home. This podcast was created for educational purposes only. Visit your primary care physician for additional medical advice. Renal Cell Carcinoma. By Manpreet Singh, MS3, Ross University School of Medicine, and Jon-Ade Holter, MS3 Ross University School of Medicine. Moderated by Hector Arreaza, MD. Definition:Renal cell carcinoma is a primary neoplasm arising form the renal cortex. 80-85 percent of renal tumors are renal cell carcinomas followed closely by transitional cell renal cancer and Wilms tumor.  Epidemiology: In 2022, 79,000 new cases of kidney cancer were diagnosed with almost 14,000 mortalities. There is a 2:1 male to female ratio and the average age is 64 and normally 65-74. African Americans and American Indians have a higher prevalence rate compared to other racial groups. The lifetime risk for developing kidney cancer in men is about 1 in 46 (2.02%) and 1 in 80 (1.03%) in women.  Risk Factors associated with RCC: Anything that causes assault to the kidneys and affects its function would cause increased demand, injury, and inflammation. This assault can lead to cell derangement and lead to cancer. The risk factors that have been associated with RCC are smoking, obesity, HTN, family history of kidney cancer, Trichloroethylene (a metal degreaser used in large manufacturing factories), acetaminophen, and patients with advanced kidney disease needing dialysis. Patients with syndromes that cause multiple types of tumors: VHL (von Hippel-Lindau) deficiency, a tumor suppressor, gives rise to clear cell renal cell carcinoma. Familial inheritance of VHL deficiency is mostly found in patients that have RCC at a very young age, before 40 y/o. Other tumors can be found in the eye, brain, spinal cord, pancreas, and pheochromocytomas.Hereditary leiomyoma-renal cell carcinoma due to FH gene mutations causing women who have leiomyomas to have a higher risk of developing papillary RCC.Birt-Hogg-Dube (BHD) syndrome mutation in FLCN gene who develop various skin and renal tumors.Cowden syndrome is a mutation in the PTEN gene giving rise to cancers associated with breast, thyroid , and kidney cancers.Tuberous sclerosis causes benign tumors of the skin, brain, lungs, eyes, kidneys, and heart. Although kidney tumors are most often benign, occasionally they can be clear cell RCC. Screening For RCC:Screening is unnecessary because of the low prevalence of this cancer in the general population, though certain groups require annual repeat imaging via US, CT, or MRI. Inherited conditions that are associated with RCC such as VHL syndrome or Tuberous SclerosisESRD patients who have been on dialysis for 3-5 yearsFamily history of RCCPrior kidney irradiation Clinical Picture: Most patients with RCC are asymptomatic until cancer grows large enough to cause disruption of local organs, such as the kidney, bladder, or renal vein, and dysregulates other organs via metastasis. Therefore, it's important to look at other signs and symptoms caused by RCC.  The patient most likely will be an older male who presents with the classic triad of: Flank pain: caused by rapid expansion and stretching of the renal capsule.Hematuria: occurs from the invasion of the neoplasm into the collecting duct.Palpable abdominal mass: mass tends to be homogenous and mobile with respirations. Though this presents only in 9% of patients during the presentation, having physical symptoms is a sign of advanced disease and 25% of patients with these signs tend to have distant metastasis.  Anemia: normally associated with anemia of chronic disease. It precedes the disease by at least 8 months to 1 year. Males can develop varicoceles because of decreased emptying due to neoplasm obstruction. Patients normally develop varicoceles on the left due to the spermatic vein emptying in the higher resistance left renal vein, which causes backup of the blood in the pemphigus plexus. Though a right-sided varicocele should raise a higher suspicion of obstruction due to the spermatic vein draining directly into the IVC which is lower in resistance. A right-sided varicocele is seen in approximately 11 percent of patients. The paraneoplastic syndrome can also arise from RCCEpo: Erythrocytosis with symptoms of weakness, fatigue, headache, and joint pain.PTHrP: PTH-related peptide acts like PTH which gives rise to hypercalcemia with the prevalent symptoms of arthritis, osteolytic lesions, confusions, tetany, ventricular tachycardia, shortened QTc, and nausea and vomiting.Renin: overproduction from the juxtaglomerular cells can cause disarrangement of the RAAS system causing hypertension.Others also like ACTH and beta-HCG. Other disorders present include hepatic dysfunction, cachexia, secondary amyloidosis, and thrombocytosis. Workup If a patient comes in with painless hematuria, then the first test should be abdominal CT or abdominal ultrasound. A CT is more sensitive than the US but it can quickly indicate if the abdominal mass felt can be a cyst or a solid tumor.  US of kidneys should show if it's a simple cyst:-The cyst is round and sharply demarcated with smooth walls- It's anechoic – appears solid black-There is a strong posterior wall echo-Use the Bosniak classification to classify mass  Bosniak I: benign simple cyst with thin wall less than equal to 2mm, no septa or calcifications. No future workup is needed. Bosniak II: benign cyst, 3 cm diameter, requires f/u with US/CT/MRI at 6 months, 12 months, and annually for the next 5 years. Chance of malignancy: 5%.  Bosniak III: indeterminate cystic mass with thick, irregular or smooth walls. This requires nephrectomy or radiofrequency ablation. Chance of malignancy: 55%  Bosniak IV: Clearly a malignancy its grade III with enhancing soft tissue components that its independent from the wall or septum. Requires total or partial nephrectomy. Chance of malignancy 100%.  CT of the kidneys for a neoplasm should show:-Thickened irregular walls or septa -Enhancement after contrast injection are suggestive of malignancy-CT can also help detect invasion in local tissue areas such as renal vein and perinephric organs  MRI is used if the patient cannot use contrast or kidney function is poor. MRI can also evaluate the growth of the cancer. Other imaging studies:Other imaging studies that may be useful for assessing for distant metastases include bone scan, CT of the chest, magnetic resonance imaging (MRI), and positron emission tomography (PET)/CT. Treatment and staging Nephrectomy, partial or total, will be used as the initial tissue collection for pathology. If the patient is not a surgical candidate, you can also obtain a percutaneous biopsy. The nephrectomy is preferred because first, it serves as a definitive treatment option, but also it allows for definitive staging of the cancer with tumor and nodal staging. Regardless of the size, any solid mass may indicate malignancy and point towards RCC, requiring resection.   TNM staging Stage I: Tumor is 7cm across or smaller and only in the kidney with no lymph nodes or distant mets. T1N0M0 Stage IIa: Tumor size is larger than 7cm but still in the kidney but no invasion of lymph node or mets. T2N0M0 Stage IIb: Tumor is growing into the renal vein or IVC, but not into neighboring organs such as adrenals or Gerota's fascia and still lacks lymph node invasion and mets. T3N0M0.  Stage III: Tumor can be any size but has not invaded outside structures such as adrenals, though nearby lymph node invasion is present but not distant. There is no distant mets. T3N1M0. Stage IV:  The main tumor is beyond the Gerota's fascia and may grow into the adrenal gland . It may or may not spread to the lymph nodes or may not have distant mets. Stage IV also consists of any cancer that has any number of distant mets. T4 Adjuvant therapy can be done with immune therapy. Conclusion: Now we conclude our episode number 105 “Renal cell carcinoma.” This type of cancer may be asymptomatic until it is large enough to cause symptoms. Keep it on your list of differentials on patients with hematuria, flank pain, weight loss, and abnormal imaging. Keep in mind the features of simple kidney cysts vs complex cysts when assessing kidney ultrasounds. Your patient will be grateful for an early diagnosis of RCC and a prompt treatment. Even without trying, every night you go to bed being a little wiser.This week we thank Hector Arreaza, Timiiye Yomi, Manpreet Singh, Jon-Ade Holter. Thanks for listening to Rio Bravo qWeek Podcast. If you have any feedback, contact us by email at RioBravoqWeek@clinicasierravista.org, or visit our website riobravofmrp.org/qweek. Audio edition: Suraj Amrutia. See you next week!  Bibliography: Is There a Cut Off Age for Kidney Transplant?, Mayo Clinic Connect, Jul 18, 2017, https://connect.mayoclinic.org/blog/transplant/newsfeed-post/is-there-a-cut-off-age-for-kidney-transplant/ Atkins, Michael. “Clinical Manifestations, Evaluation, and Staging of Renal Cell Carcinoma.” UpToDate, January 21. https://www.uptodate.com/contents/clinical-manifestations-evaluation-and-staging-of-renal-cell-carcinoma American Cancer Society. “Key Statistics About Kidney Cancer”. Cancer.Org, 2022, https://www.cancer.org/cancer/kidney-cancer/about/key-statistics.html. Escudier B, Porta C, Schmidinger M, Rioux-Leclercq N, Bex A, Khoo V, Grünwald V, Gillessen S, Horwich A; ESMO Guidelines Committee. Electronic address: clinicalguidelines@esmo.org. Renal cell carcinoma: ESMO Clinical Practice Guidelines for diagnosis, treatment and follow-up†. Ann Oncol. 2019 May 1;30(5):706-720. doi: 10.1093/annonc/mdz056. PMID: 30788497. https://pubmed.ncbi.nlm.nih.gov/30788497/. Gaillard, F., Bell, D. Bosniak classification system of renal cystic masses. Reference article, Radiopaedia.org. (accessed on 20 May 2022) https://doi.org/10.53347/rID-1006. Kopel J, Sharma P, Warriach I, Swarup S. Polycythemia with Renal Cell Carcinoma and Normal Erythropoietin Level. Case Rep Urol. 2019 Dec 11;2019:3792514. doi: 10.1155/2019/3792514. PMID: 31934488; PMCID: PMC6942735. https://pubmed.ncbi.nlm.nih.gov/31934488/. Leslie SW, Sajjad H, Siref LE. Varicocele. [Updated 2022 Feb 14]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2022 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK448113/. Maguire, Claire. “Understanding Endoscopic Ultrasound and Fine Needle Aspiration.” Educational Dimension, Educational Dimensions, 1 Jan. 2007, educationaldimensions.com/eLearn/aspirationandbiopsy/eusterm.php. Maller, V., Hagir, M. Renal cell carcinoma (TNM staging). Reference article, Radiopaedia.org. (accessed on 20 May 2022) https://doi.org/10.53347/rID-4699. Palapattu GS, Kristo B, Rajfer J. Paraneoplastic syndromes in urologic malignancy: the many faces of renal cell carcinoma. Rev Urol. 2002 Fall;4(4):163-70. PMID: 16985675; PMCID: PMC1475999. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1475999/.