Podcasts about occurring

This week on Watts Occurring Femmes, Manon puts Emma under the spotlight. How do you win Olympic Gold? And how do you even begin to think about backing that up four years later, at your second Olympics? This is a fascinating chat into Emma's mindset and shows just how she's become a world champion and three-time Olympic medallist at such a young age. Watts Occurring Femmes is brought to you by Rouvy, and hosted by Pinarello. Want a free month on ROUVY, on us? Use code FEMMES when you sign up and explore everything ROUVY has to offer. SIGN UP HERE: https://rouvy.com/?utm_source=gtcc&utm_medium=direct-buy&utm_campaign=rouvy-brand&utm_term=femmes-podcast ROUVY connects indoor and outdoor by bringing the real routes from around the world to your home and ROUVY's new Route Creator tool allows users to film, upload and ride their favourite loops on ROUVY. Want to check out your local Pinarello retailer? Visit https://pinarello.com/global/en/store-locator to find your local store today. Oh, and a huge thank you to Arlo & Jacob for Emma and Manon's snazzy armchairs. The girls will be back next week. Learn more about your ad choices. Visit podcastchoices.com/adchoices

You've seen G's personal Tour debrief, but now enjoy Luke and Producer George breaking down the whole race by picking their top 10 riders from this year's journey round France. Live from a windy and rainy Paris, inside the excellent Continental Tyres base on the Champs Elysees, they ran through the riders who've left the biggest impact on the Tour in 2025. Agree? Disagree? Let them know over in the YouTube comments. Watts Occurring is brought to you by Continental Tyres Learn more about your ad choices. Visit podcastchoices.com/adchoices

Well, that's that then. G has raced his final ever Tour de France stage. From the youngest man in the race who finished 140th back in 2007, to the 2018 winner, and now the oldest guy in the race. It's been a truly remarkable journey. Yesterday's ride around Paris was G's 282nd Tour stage. Yes, you are reading that correctly. The rain fell on Paris and put paid to our best laid plans to bring you a finish line pod with G but, once he'd dried off, had a shower and a celebratory beer, he joined Tom for a chat at the team hotel to reflect on a momentous day. Enjoy - and thank you, G. Watts Occurring is brought to you by Continental Tyres. Learn more about your ad choices. Visit podcastchoices.com/adchoices

In this JCO Article Insights episode, Michael Hughes summarizes “International Myeloma Society and International Myeloma Working Group Consensus Recommendations on the Definition of High-Risk Multiple Myeloma" by Avet-Loiseau et al. published on June 09, 2025 along with an interview with author Dr Nikhil C. Munshi, MD. TRANSCRIPT Michael Hughes: Welcome to this episode of JCO Article Insights. This is Michael Hughes, JCO's editorial fellow. Today I am interviewing Dr. Nikhil Munshi on the “International Myeloma Society and International Myeloma Working Group Consensus Recommendations on the Definition of High-Risk Multiple Myeloma” by Avet-Loiseau et al. At the time of this recording, our guest has disclosures that will be linked in the transcript. While some patients with multiple myeloma live for decades after treatment, others exhibit refractory or rapidly relapsing disease irrespective of treatment administered. We term this “high-risk myeloma.” Multiple risk stratification systems have been created, starting with the Durie-Salmon system in 1975 and evolving with the advent of novel therapeutics and novel treatment approaches. In 2015, the Revised International Staging System (R-ISS) was introduced, which incorporated novel clinical and cytogenetic markers and remained, until recently, a mainstay of risk stratification in newly diagnosed disease. Myeloma as a field has, just in the past few years, though, undergone explosive changes. In particular, we have seen groundbreaking advances not only in treatments - the introduction of anti-CD38 agents and the advent of cellular and bispecific therapies - but also in diagnostic technology and our understanding of the genetic lesions in myeloma. This has led to the proliferation of numerous trials employing different definitions of high-risk myeloma, a burgeoning problem for patients and providers alike, and has prompted attempts to consolidate definitions and terminology. Regarding cytogenetic lesions, at least, Kaiser et al's federated meta-analysis of 24 therapeutic trials, published here in the JCO in February of 2025 and recently podcasted in an interview with associate editor Dr. Suzanne Lentzsch, posited a new cytogenetic classification system to realize a shared platform upon which we might contextualize those trial results. This article we have here by Dr. Avet-Loiseau, Dr. Munshi, and colleagues, published online in early June of this year and hot off the presses, is the definitive joint statement from the International Myeloma Society (IMS) and the International Myeloma Working Group (IMWG). What is high-risk multiple myeloma for the modern era? The IMS and IMWG Genomics Workshop was held in July 2023 and was attended by international myeloma experts, collaborating to reach consensus based on large volumes of data presented and shared. The datasets included cohorts from the Intergroupe Francophone du Myélome (IFM); the HARMONY project, comprised of multiple European academic trials; the FORTE study, findings from which solidified KRd as a viable induction regimen; the Grupo Español de Mieloma Múltiple (GEM) and the PETHEMA Foundation; the German-Speaking Myeloma Multicenter Group (GMMG); the UK-based Myeloma XI, findings from which confirmed the concept of lenalidomide maintenance; Emory 1000, a large, real-world dataset from Emory University in Atlanta; the Multiple Myeloma Research Foundation Clinical Outcomes in Multiple Myeloma to Personal Assessment of Genetic Profile (CoMMpass) dataset; and some newly diagnosed myeloma cohorts from the Mayo Clinic. Data were not pooled for analyses and were assessed individually - that is to say, with clear a priori understanding of whence the data had been gathered and for what original purposes. Consensus on topics was developed based on the preponderance of data across studies and cohorts. In terms of results, substantial revisions were made to the genomic staging of high-risk multiple myeloma, and these can be sorted into three major categories: A) alterations to the tumor suppressor gene TP53; B) translocations involving chromosome 14: t(14;16) (c-MAF overexpression), t(14;20) (MAFB overexpression), and t(4;14) (NSD2 overexpression); and C) chromosome 1 abnormalities: deletions of 1p or additional copies of 1q. In terms of category A, TP53 alterations: Deletion of 17p is present in up to 10% of patients at diagnosis and is enriched in relapsed or refractory disease. This is well-documented as a high-risk feature, but the proportion of the myeloma cells with deletion 17p actually impacts prognosis. GEM and HARMONY data analyses confirmed the use of 20% clonal cell fraction as the optimal threshold value for high-risk disease. That is to say, there must be the deletion of 17p in at least 20% of the myeloma cells on a FISH-analysis of a CD138-enriched bone marrow sample to qualify as high-risk disease. TP53 mutations can also occur. Inactivating mutations appear to have deleterious effects similar to chromosomal losses, and the biallelic loss of TP53, however it occurs, portends particularly poor prognosis. This effect is seen across Myeloma XI, CoMMpass, and IFM cohorts. Biallelic loss is rare, it appears to occur in only about 5% of patients, but next-generation sequencing is nevertheless recommended in all myeloma patients. Category B, chromosome 14 translocations: Translocation t(14;16) occurs in about 2% to 3% of patients with newly diagnosed disease. In the available data, primarily real-world IFM data, t(14;16) almost always occurs with chromosome 1 abnormalities. Translocation t(4;14) occurs in about 10% to 12% of newly diagnosed disease, but only patients with specific NSD2 alterations are, in fact, at risk of worse prognosis, which clinically appears to be about one in every three of those patients. And so together, the CoMMpass and Myeloma XI data suggest that translocation t(4;14) only in combination with deletion 1p or gain or amplification of 1q correlates with worse prognosis. Translocation t(14;20) occurs in only 2% of newly diagnosed disease. Similar to translocation t(4;14), it doesn't appear to have an effect on prognosis, except if the translocation co-occurs with chromosome 1 lesions, in which case patients do fare worse. Overall, these three translocations - t(14;16), t(4;14), and t(14;20) - should be considered high-risk only if chromosome 1 aberrations are also present. In terms of those chromosome 1 aberrations, category C, first deletions of 1p: Occurring in about 13% to 15% of newly diagnosed disease, deletion 1p eliminates critical cell checkpoints and normal apoptotic signaling. In the IFM and CoMMpass dataset analyses, biallelic deletion of 1p and monoallelic deletion of 1p co-occurring with additional copies of 1q denote high-risk. In terms of the other aberration in chromosome 1 possible in myeloma, gain or amplification of 1q: This occurs in up to 35% to 37% of newly diagnosed disease. It upregulates CKS1B, which is a cyclin-dependent kinase, and ANP32E, a histone acetyltransferase inhibitor. GEM and IFM data suggest that gain or amplification of 1q - there was no clear survival detriment to amplification - is best considered as a high-risk feature only in combination with the other risk factors as above. Now, in terms of any other criteria for high-risk disease, there remains one other item, and that has to do with tumor burden. There has been a consensus shift, really, in both the IMS and IMWG to attempt to develop a definition of high-risk disease which is based on biologic features rather than empirically observed and potentially temporally dynamic features, such as lactate dehydrogenase. Beta-2 microglobulin remains an independent high-risk indicator, but care must be taken when measuring it, as renal dysfunction can artificially inflate peripheral titers. The consensus conclusion was that a beta-2 microglobulin of at least 5.5 without renal failure should be considered high-risk but should not preclude detailed genomic profiling. So, in conclusion, the novel 2025 IMS-IMWG risk stratification system for myeloma is binary. It's either high-risk disease or standard-risk disease. It's got four criteria. Number one, deletion 17p and/or a TP53 mutation. Clonal cell fraction cut-off, remember, is 20%. Or number two, an IGH translocation - t(4;14), t(14;16), t(14;20) - with 1q gain and/or deletion of 1p. Or a monoallelic deletion of 1p with 1q additional copies or a biallelic deletion of 1p. Or a beta-2 microglobulin of at least 5.5 only when the creatinine is normal. This is a field-defining work that draws on analyses from across the world to put forward a dominant definition of high-risk disease and introduces a new era of biologically informed risk assessment in myeloma. Now, how does this change our clinical approach? FISH must be performed on CD138-enriched samples and should be performed for all patients. Next-generation sequencing should also be performed on all patients. Trials will hopefully now begin to include this novel definition of high-risk multiple myeloma. It does remain to be seen how data from novel therapeutic trials, if stratified according to this novel definition, will be interpreted. Will we find that therapies being evaluated at present have differential effects on myelomas with different genetic lesions? Other unanswered questions also exist. How do we go about integrating this into academic and then community clinical practice? How do we devise public health interventions for low-resource settings? To discuss this piece further, we welcome the esteemed Dr. Nikhil Munshi to the podcast. Dr. Munshi is a world-renowned leader in multiple myeloma and the corresponding author on this paper. As Professor of Medicine at Harvard Medical School, Director of the Multiple Myeloma Effector Cell Therapy Unit, and Director of Basic and Correlative Science at the Jerome Lipper Multiple Myeloma Center of the Dana-Farber Cancer Institute, he has presided over critical discoveries in the field.  Thank you for joining us, Dr. Munshi. Dr. Nikhil Munshi: Oh, it's my pleasure being here, Michael, to discuss this interesting and important publication. Michael Hughes: I had a few questions for you. So number one, this is a comprehensive, shall we say, monumental and wide-ranging definition for high-risk myeloma. How do you hope this will influence or impact the ways we discuss myeloma with patients in the exam room? And how do we make some of these components recommended, in particular next-generation sequencing, feasible in lower-resource settings? Dr. Nikhil Munshi: So those are two very important questions. Let's start with the first: How do we utilize this in our day-to-day patient care setting? So, as you know well, we have always tried to identify those patients who do not do so well with the current existing treatment. And for the last 30 years, what constitutes a myeloma of higher risk has continued to change with improvement in our treatment. The current definition basically centers around a quarter of the patients whose PFS is less than 2 to 3 years. And those would require some more involved therapeutic management. So that was a starting point of defining patients and the features. As we developed this consensus amongst ourselves - and it's titled as “International Myeloma Society, International Myeloma Working Group Consensus Recommendation” - this IMS-IMWG type of recommendation we have done for many years, improvising in various areas of myeloma care. Now, here, we looked at the data that was existing all across the globe, utilizing newer treatment and trying to identify that with these four-drug regimens, with transplant and some of the immunotherapy, which group of patients do not do as well. And this is where this current algorithm comes up. So before I answer your question straight, “How do we use it?” I might like to just suggest, “What are those features that we have identified?” There are four features which constitute high-risk disease in the newer definition. Those with deletion 17p with 20% clonality and/or TP53 mutation. Number two, patients with one of the translocations - t(4;14), t(14;16), or t(14;20) - co-occurring with 1q amplification or deletion 1p32. And that's a change. Previously, just the translocation was considered high-risk. Now we need a co-occurrence for it to be called high-risk. The third group is patients having biallelic deletion 1p32 or monoallelic deletion 1p32 along with 1q amplification. And finally, patients with high beta-2 microglobulin, more than or equal to 5.5 mg/dL, with normal creatinine less than 1.2 mg/dL. And the question, “How do we use this?” There are multiple areas where we incorporate high-risk features in our treatment algorithm. One of the first areas is where we would consider the induction regimen. If a patient has a high-risk disease, we would definitely consider a four-drug regimen rather than a three-drug regimen, although we are beginning to incorporate four-drug for all groups. That's one important thing. Number two, those are the patients where we do consider consolidation with transplant or maybe in the new world, considering some of the immunotherapeutic consolidation more early or more aggressively. Number three, these are the patients who get a little bit more maintenance therapy. So normally, lenalidomide might end up being our standard maintenance regimen. In patients who have high-risk disease, we incorporate either addition of daratumumab or the anti-CD38 targeting antibody and/or addition of proteasome inhibitor, either bortezomib or carfilzomib. So you would have multi-drug maintenance therapy in these patients. And in high-risk patients, we follow them with maintenance longer periods of time. One very critically important point to keep in mind is that to get the better outcome in high-risk disease, we must try to get them into MRD negativity because there is clear data that patients who do achieve MRD negativity, despite having high-risk disease, have a much superior outcome. They become near to standard-risk disease. And so, in high-risk patients, I would try to do whatever various options I have to try and get them into MRD-negative status. And when these patients relapse, we do not wait for the classic progression criteria to be met before we intervene. We would propose and suggest that we intervene earlier before the disease really blasts off. And so there are a number of areas in our setting where this high-risk definition will help us intervene appropriately and also with appropriate aggressiveness to achieve better outcome, to make this similar to standard-risk disease. Michael Hughes: Thank you, Dr. Munshi. And thoughts on how to really integrate this not only into academic centers but also lower-resource settings? Dr. Nikhil Munshi: So that's a very important question, Michael. And when we were developing this consensus, we were very cognizant of that fact. So wherever available, I think we are recommending that over a period of next 2, 3, 5 years, we should begin to switch over to sequencing-based methods because two components of this definition, one is TP53 mutation, which we cannot do without sequencing, and also reliably detecting deletion 1p requires sequencing-based method. So in the low-resource countries - and there are many in this world, and also even in our own country, patients may not be able to afford it - the older method with FISH or similar such technology, which is more affordable, is also acceptable for current time. They may miss a very small number of patients, maybe 2% to 3%, where these finer changes are not picked up, but a majority of this would be captured by them. So the current practice might still be applicable with some limitation in those patient populations, and that's what we would recommend. What is happening, fortunately, is that actually sequencing-based method is becoming cheaper. And in many centers, it is cheaper to do the sequencing rather than to do the FISH analysis. And so my hope is that even in low-resource centers, sequencing might be more economical in the end. It's, I think, the access to technology, which is a little bit limited currently, but it's hopefully becoming available soon. Michael Hughes: Thank you, Dr. Munshi. And staying for a minute and looking at the multiple myeloma subsets which might be missed by this really still very broad-ranging high-risk definition, at least by prior risk stratification systems, right, there is this group of patients who have standard-risk cytogenetics by R-ISS or R2-ISS, but they have primary refractory disease or they relapse early. We call these, as you are well aware, functionally high-risk disease. What proportion of previously FHR, functionally high-risk, myeloma patients do you expect to be captured by this novel definition? Dr. Nikhil Munshi: So I think the newer definition - and we can look at it both ways, but the newer definition should capture most of the functionally high-risk definition. To put it differently, Michael, there are patients who we know are, as you mentioned, functionally high-risk. Those are the patients who might have plasma cell leukemia, those who might have extramedullary disease, those who might not respond to our four-drug induction. If you don't respond to the four-drug induction, almost by definition, they are high-risk. However, a majority of them have one of the abnormalities that we are describing here. There would be a very small proportion which may not have. And if they do not have, we know one of the important components of this definition here is also that the genome, we know, keeps on evolving. So there may be a very small clone with the high-risk feature which was not obvious in the beginning. Following treatments or following relapse, that clone predominates, and now the patient's disease becomes high-risk.  So the definition would incorporate or would capture these functional high-risk patients, but as you said, in countries where resources are not available, using this functional high-risk would also be helpful and advantageous. Sometimes LDH ends up being a high-risk. In our studies, LDH has not come out to be high-risk anymore because the features we are describing captures most of those patients, but those alternatives, older, can still be considered if other newer techniques are not available. Michael Hughes: Got you. And in terms of these older definitions, yes, that incorporate tumor burden, these empirical observations about how myeloma presents, do you foresee any additional tumor burden indicators being added to future definitions of high-risk disease? Or do you instead see this particular definition as a major waypoint on the journey towards a fully biologically grounded definition of high-risk disease? Dr. Nikhil Munshi: I think your second part is what is going to happen. I think the tumor burden-related definition is being now replaced by the biological or genomic-based definition. And I think at some point, it will be quite fully replaced. One component not here, and it is because one thing, we don't have enough data; number two, we don't know how it will pan out, is also the influence of the microenvironment on the risk definition. For example, the immune system, the immune function, etc. But not enough data exists to suggest how it would change the current definition. So in future, would a definition be totally genomic or it could be more integrative? And my personal guess is that it would be more integrative and that some immune features might come into the picture, especially now that we are using immune-based therapy as a very important component of treatment - CAR T-cells, bispecific, and antibody-based treatments. What role the immune system plays in either supporting tumor or what role suppression of the anti-tumor immunity plays? They all will be important how patient outcomes end up being, and which in turn could translate into how patient's risk stratification might happen. So I think the older tumor burden-related definitions probably will become things of the past. What we have currently proposed and consensus developed is the new path forward, and over time, some microenvironmental influences, if defined and found to be important, may get some more incorporation if it compares favorably with the genomic features. Michael Hughes: Thank you, Dr. Munshi for that enlightening response.  To conclude the podcast, I'd like to look to the future and to the immediate future, what are the next steps for high-risk disease definition between now and discussing an integrated genomic-microenvironment-based definition? Will we see attempts to refine? Will we see a multi-level system, things like this? Dr. Nikhil Munshi: Yeah, so I think the current definition will be here to stay for the next 10 years or so. I think this has been developed using a large amount of data, so we do believe that this will remain fine. It has been validated now within the last six months by a few of the other studies. So there won't be a quick change. But we will try to, all of us will try to innovate. And as you very rightly bring up, the areas of research would include looking at the expression or transcriptomic component. Does that matter? And we do believe a small number of patients will have transcriptomic changes, not looked at the DNA changes, and may play a role. There are newer components, so long non-coding RNA, for example, is going to be an important component to look at, how it impacts the disease outcome, etc. There are also some of the proteomic-related changes which may become important in our studies. And then as we discussed, microenvironment and immunological changes. So these are the future areas of ongoing research where we all should collect data, and then in the next 5 to 10 years, we'll have another group meeting to see has anything changed or any of the features have become more important.  Most of the time, some of the older features are lost because they are not as critically high-risk, and the newer features come in. And so the historical background for just one second, there was a time when chromosome 13 was considered a high-risk disease. We now don't even mention it because it's not high-risk. The newer treatments have improved the outcome. t(4;14) used to be a high-risk disease. Now by itself today, in this definition by itself is not; it needs to be with something else. And so I think this is a great sign of progress. As we improve the treatment and outcomes, some of the features will become less important, new features will come up, and we'll need to keep on evolving with time and with technology and make it better for patients. Michael Hughes: Thank you so much, Dr. Munshi, for your wisdom, for your sagacity, for your historical perspective as well.  Thank you for listening to JCO Article Insights. Please come back for more interviews and article summaries. And be sure to leave us a rating and review so others can find our show. For more podcasts and episodes from ASCO, please visit asco.org/podcasts. The purpose of this podcast is to educate and to inform. This is not a substitute for professional medical care and is not intended for use in the diagnosis or treatment of individual conditions.  Guests on this podcast express their own opinions, experience, and conclusions. Guest statements on the podcast do not express the opinions of ASCO. The mention of any product, service, organization, activity, or therapy should not be construed as an ASCO endorsement.  

When a climber wins one stage at the Tour de France, that's usually that. Job done, get to Paris. But not Thymen Arensman. What a ride from INEOS' Dutchman on the final mountain stage at this year's Tour. Chapeau, Sir. And Pogi? Well, he did what he needed to do. Barring disaster, that's number four for the remarkable Slovenian. Luke and Tom recapped all the action - and got to the bottom of the Yates Snr mystery. He's not happy with G! We'll be back on Sunday with a VERY special pod from Paris. Don't forget, we have a brilliant offer from our friends at Rouleur for July. Use code WATTS at rouleur.cc/subscribe to get 10% any of their subscription offers and enjoy their unparalleled daily Tour de France coverage. Want to try NordVPN? Head to ⁠⁠⁠http://nordvpn.com/gtcc⁠⁠⁠ for a special sign up deal. Watts Occurring is brought to you by Continental Tyres Learn more about your ad choices. Visit podcastchoices.com/adchoices

Welcome to It Was What It Was, the football history podcast. In this episode, co-hosts Rob Draper and Jonathan Wilson bring their second and final part of their series on the Death Match, one of the most mythologized football games of all time. Occurring in Nazi-occupied Kyiv, Ukraine, this match between Start, a team formed mostly of former Dinamo Kiev players, and Flakelf, a Luftwaffe team, has become a symbol of resistance. The hosts discuss the brutal context of the occupation, the complex legacies of the players, and the role football played in these extraordinary historical circumstances. Jonathan Wilson critically examines how much of the narrative is based on verifiable facts and how much may have been post-war Soviet propaganda. This episode provides a nuanced understanding of how football intersected with geopolitics, resistance, and national identity during one of history's darkest periods.00:00 Introduction to the Death Match Series01:27 Historical Context: Nazi Occupation and Football02:26 The Rise of Team Start03:07 Early Matches and Growing Tensions04:21 Embarrassing Defeats for Axis Teams05:28 Public Perception and Propaganda06:29 The Turning Point: German Concerns14:13 The First Clash with Flakelf18:05 Setting the Stage for the Death Match26:06 The Referee's Influence and Game Dynamics27:10 Halftime Tensions and Orders to Lose28:39 Second Half and Controversial Moments32:35 Post-Match Arrests and Interrogations35:50 Life in the Prison Camp43:10 Escape and Kyiv's Liberation44:33 Legacy and Mythology of the Death Match Hosted on Acast. See acast.com/privacy for more information.

Introducing... Watts Occurring Femmes! Yes, that's right, Manon Lloyd and Emma Finucane have joined the Watts Occurring family. They'll be bringing you weekly episodes from inside the world of women's cycling, welcoming guests, eating Welsh cakes, and we'll also be tracking Emma's journey to the LA Olympics. This could be the best idea Luke and G have ever had. Luke joined the girls for part one of their first episode, before they delved into the Tour de France Femmes. Enjoy. Watts Occurring Femmes is brought to you by Rouvy, and hosted by Pinarello. Want a free month on ROUVY, on us? Use code FEMMES when you sign up and explore everything ROUVY has to offer. ROUVY connects indoor and outdoor by bringing the real routes from around the world to your home and ROUVY's new Route Creator tool allows users to film, upload and ride their favourite loops on ROUVY. Sign up here. Want to check out your local Pinarello retailer? Visit pinarello.com/global/en/store-locator to find your local store today. Oh, and a huge thank you to Arlo & Jacob for Emma and Manon's snazzy armchairs. The girls will be back next week. Learn more about your ad choices. Visit podcastchoices.com/adchoices

G's ridden his final ever Tour de France queen stage - and now he's got just three days left to go. He hopped on the massage table (once he'd warmed up) to tell Tom all about his day on the fearsome Col de la Loze and his desire to be handed chocolate bars on the mountain tomorrow. If you're out there, Watts Occurring listeners, you know what to do. The whole Watts team is excited to see G in Paris on Sunday, but Tom and Luke will be back tomorrow night with one final pod before then. Don't forget, we have a brilliant offer from our friends at Rouleur for July. Use code WATTS at rouleur.cc/subscribe to get 10% any of their subscription offers and enjoy their unparalleled daily Tour de France coverage. Want to try NordVPN? Head to ⁠⁠https://nordvpn.com/gtcc⁠⁠ for a special sign up deal. Watts Occurring is brought to you by Continental Tyres Learn more about your ad choices. Visit podcastchoices.com/adchoices

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That's that then. G's final ever (competitive) time up Mont Ventoux. And the stage really did not disappoint. We saw the breakaway duke it out for the win, Pog and Jonas come within a whisker of catching them, and just generally some excellent Ventoux fireworks. One of the stages of the race so far. Five days to go. Each and every one is going to be a belter. We'll be back soon. Don't forget, we have a brilliant offer from our friends at Rouleur for July. Use code WATTS at rouleur.cc/subscribe to get 10% any of their subscription offers and enjoy their unparalleled daily Tour de France coverage. Want to try NordVPN? Head to ⁠https://nordvpn.com/gtcc⁠ for a special sign up deal. Watts Occurring is brought to you by Continental Tyres Learn more about your ad choices. Visit podcastchoices.com/adchoices

My guest is Dr. Chris McCurdy, PhD, FAAPS, professor of medicinal chemistry at the University of Florida and a world expert on the pharmacology of kratom and other plant-derived medicinal compounds. We discuss kratom's wide-ranging effects, including its use for boosting energy, enhancing mood, managing pain and as a potential opioid substitute, while also explaining its critical safety concerns and addictive potential, especially for kratom-derived/isolate products. We also discuss plant-based compounds more generally for their potential benefits and risks. Dr. McCurdy offers a balanced perspective on kratom and other plant-based and naturally occurring medicinal compounds, highlighting and contrasting their promise for human health with potential serious risks. Read the episode show notes at hubermanlab.com. Thank you to our sponsors AG1: https://drinkag1.com/huberman David Protein: https://davidprotein.com/huberman Eight Sleep: https://eightsleep.com/huberman ROKA: https://roka.com/huberman Function: https://functionhealth.com/huberman Timestamps 00:00:00 Chris McCurdy 00:02:51 Kratom (Mitragyna speciosa), Origin, Effects, Low vs High Doses 00:07:19 Sponsors: David Protein & Eight Sleep 00:10:07 Kratom, Traditional Use vs Commercial Kratom Products, Absorption 00:17:00 Kratom Products, Serving Size, Kids; Semi-Synthetics; Tool: Understand Kratom Product Labels 00:23:16 Kratom Products & Various Desired Effects; Physical Dependence 00:32:53 Different Kratom Usage Patterns, Opioid Dependence 00:36:59 Alkaloid Compounds, Nitrogen, Nicotine; Animals & Self-Experimentation 00:47:47 Sponsors: AG1 & ROKA 00:51:05 Medicine Development, Disconnection from Nature, Product Concentrations 00:59:00 Alkaloids & Natural Products, Opium Poppy, Coca Leaf, Tool: Kratom Leaf vs Extracts (Kratom-Derived/Kratom Isolates) 01:09:06 Is It Safe for Kids to Consume Kratom Products? 01:12:19 Kratom, Energy, Mood & Pain Management, Dose; Caffeine 01:16:56 Respiratory Depression & Kratom Products 01:20:16 Sponsor: Function 01:22:04 Kratom Leaf vs Derivatives, FDA Regulations, Usage Guidelines 01:26:59 Kratom, Alcohol Consumption, Respiratory Failure? 01:29:09 Kratom Alkaloids, Mood & Stimulant Effects, Multiple Pathways for Pain Relief 01:38:17 Plant Alkaloids & Chemical Defense, Kratom & Antifungal Alkaloids; Geckos 01:44:35 White, Red & Brown Vein Kratom, Leaf Processing; Terpenes 01:51:08 Kratom as an Anti-Depressant?; Discontinuing Kratom Use, Opioid Use 01:58:03 Kratom, Drug Interactions & Seizure, Opioids 02:01:51 Cacao Beans, Chocolate 02:09:34 Coca-Cola, Coca Plant & Cocaine, History of Soft Drinks 02:19:49 Career Journey, Pharmacy, Chemistry & Education, Lobelia 02:28:44 Nicotine; Natural Products & Career Journey, Salvia divinorum, Kratom 02:40:22 Zero-Cost Support, YouTube, Spotify & Apple Follow & Reviews, Sponsors, YouTube Feedback, Protocols Book, Social Media, Neural Network Newsletter Disclaimer & Disclosures Learn more about your ad choices. Visit megaphone.fm/adchoices

It's rest day number two at the Tour and there's a big weekend of racing to reflect upon - and a huge final week coming right up. Luke and Tom recapped all the action, cast their eye over the teams who'll be hoping for a change of fortunes, and plenty more besides. We'll be back with G tomorrow night, fresh from conquering Mont Ventoux for the final time. Don't forget, we have a brilliant offer from our friends at Rouleur for July. Use code WATTS at rouleur.cc/subscribe to get 10% any of their subscription offers and enjoy their unparalleled daily Tour de France coverage. Watts Occurring is brought to you by Continental Tyres Learn more about your ad choices. Visit podcastchoices.com/adchoices

Lee Gayle is an entheogenic researcher and educator passionate about the science and sacred use of psychoactive plants, animals, and fungi. She's the creator of the Psychedelic Society's course on Naturally Occurring Psychotropics, where she shares accessible, research-based knowledge on mind-altering medicines and their ritual use. Her work blends deep curiosity, cultural respect, and a grounded approach to self-love and transformation.The next NATURALLY OCCURRING PSYCHOTROPICS course begins 16th September 2025.In this 9 week online course:- Gain essential knowledge for facilitators, space-holders and any curious mind caleld to the psychedelic path- Deepen your foundational understanding, depth and integrity in this exciting and expanding fieldThe course includes weekly modules that unlock as you progress, with written content, reading materials, and self-assessment tests to help you engage with the material. We also meet live every Wednesday from 6–8pm (SA time) on Zoom for interactive webinars where we explore the week's topic in more depth and open the space for questions and discussion.Topics we cover include: • The chemistry, history, and cultural use of psychoactive plants, fungi, and animals • Indigenous knowledge systems and ceremonial use • Pharmacology, safety, and harm reduction • Addiction, integration, and ethical considerations • Case studies, legal context, and emerging researchTo receive your certificate, you'll need to complete all the modules and pass the final exam. The certificate reflects 120 hours of training and is recognised within psychedelic education and harm reduction circles, especially through the Psychedelic Society of South Africa.Register for this incredible course by visiting www.psychedelicsociety.co.za

In 2007, a baby faced Geraint Thomas rolled out on the streets of London to start his first-ever Tour de France time trial. Today, he rode his last. This one happened to be up a brutal Pyrenean mountain under the blazing French summer sun, so we'll forgive G for not going full gas. Up front, Tadej Pogacar and Jonas Vingegaard battled it out once again. And, well, you can probably guess what happened. G's teammate Connor Swift joined him to chat all about it. Nice one Swifty. Don't forget, we have a brilliant offer from our friends at Rouleur for July. Use code WATTS at rouleur.cc/subscribe to get 10% any of their subscription offers and enjoy their unparalleled daily Tour de France coverage. Watts Occurring is brought to you by Continental Tyres Learn more about your ad choices. Visit podcastchoices.com/adchoices

It was nearly 8pm and G messaged the famous Watts Occurring WhatsApp group. 'Boys I'm not really in the mood. I'm nailed.' But we knew an hour on the massage table chatting to Luke was exactly what he needed - and by the end of tonight's pod, he'd come round. And what a day it was at the Tour. A huge break, GC gaps aplenty and - of course - an absolute clinic from Pog. We are witnessing greatness. Incredibly though... he didn't win our Continental Tyres Chapeau of the Day. You'll have to listen to find out who claimed the crown today. And we also have a brilliant offer from our friends at Rouleur for July. Use code WATTS at rouleur.cc/subscribe to get 10% any of their subscription offers and enjoy their unparalleled daily Tour de France coverage. Watts Occurring is brought to you by Continental Tyres Learn more about your ad choices. Visit podcastchoices.com/adchoices

Bastille Day in France and the Tour usually serves up a route that will cause some drama. Well, today didn't disappoint. A nail-biting wait for young Ben Healy to see if he could nab yellow off Pogacar, a typically classy stage win from the Giro d'Italia winner, and plenty of typical Tour drama aplenty. What a race it is. The new yellow jersey won our Continental Tyres Chapeau of the Day and Tom and Luke also awarded yesterday's to a rider who achieved a life dream. Pretty special stuff. And we also have a brilliant offer from our friends at Rouleur for July. Use code WATTS at rouleur.cc/subscribe to get 10% any of their subscription offers and enjoy their unparalleled daily Tour de France coverage. Watts Occurring is brought to you by Continental Tyres Learn more about your ad choices. Visit podcastchoices.com/adchoices

Welcome or welcome back to Authentically ADHD, the podcast where we embrace the chaos and magic of the ADHD brain. Im carmen and today we're diving into a topic that's as complex as my filing system (which is to say, very): ADHD and its common co-occurring mood and learning disorders. Fasten your seatbelts (and if you're like me, try not to get distracted by the shiny window view) – we're talking anxiety, depression, OCD, dyslexia, dyscalculia, and bipolar disorder, all hanging out with ADHD.Why cover this? Because ADHD rarely rides solo. In fact, research compiled by Dr. Russell Barkley finds that over 80% of children and adults with ADHD have at least one other psychiatric disorder, and more than half have two or more coexisting conditions. Two-thirds of folks with ADHD have at least one coexisting condition, and often the classic ADHD symptoms (you know, fidgeting, daydreaming, “Did I leave the stove on?” moments) can overshadow those other disorders. It's like ADHD is the friend who talks so loud at the party that you don't notice the quieter buddies (like anxiety or dyslexia) tagging along in the background.But we're going to notice them today. With a blend of humor, sass, and solid neuroscience (yes, we can be funny and scientific – ask me how I know!), we'll explore how each of these conditions shows up alongside ADHD. We'll talk about how they can be misdiagnosed or missed entirely, and—most importantly—we'll dish out strategies to tell them apart and tackle both. Knowledge is power and self-awareness is the key, especially when it comes to untangling ADHD's web of quirks and comrades in chaos. So, let's get into it!ADHD and Anxiety: Double Trouble in OverdriveLet's start with anxiety, ADHD's frequent (and frantic) companion. Ever had your brain ping-pong between “I can't focus on this work” and “I'm so worried I'll mess it up”? That's ADHD and anxiety playing tango in your head. It's a double whammy: ADHD makes it hard to concentrate, and anxiety cranks up the worry about consequences. As one study notes, about 2 in 5 children with ADHD have significant problems with anxiety, and over half of adults with ADHD do as well. In other words, if you have ADHD and feel like a nervous wreck half the time, you're not alone – you're in very good (and jittery) company.ADHD and anxiety can look a lot alike on the surface. Both can make you restless, unfocused, and irritable. I mean, is it ADHD distractibility or am I just too busy worrying about everything to pay attention? (Hint: it can be both.) Especially for women, ADHD is often overlooked and mislabeled as anxiety. Picture a girl who can't concentrate in class: if she's constantly daydreaming and fidgety, one teacher calls it ADHD. Another sees a quiet, overwhelmed student and calls it anxiety. Same behavior, different labels. Women in particular have had their ADHD misdiagnosed as anxiety or mood issues for years, partly because anxious females tend to internalize symptoms (less hyperactive, more “worrier”), and that masks the ADHD beneath.So how do we tell ADHD and anxiety apart? One clue is where the distraction comes from. ADHD is like having 100 TV channels in your brain and someone else is holding the remote – your attention just flips on its own. Anxiety, on the other hand, is like one channel stuck on a horror movie; you can't focus on other things because a worry (or ten) is running on repeat. An adult with ADHD might forget a work deadline because, well, ADHD. An adult with anxiety might miss the deadline because they were paralyzed worrying about being perfect. Both end up missing the deadline (relatable – ask me how I know), but for different reasons.Neuroscience is starting to unravel this knot. There's evidence of a genetic link between ADHD and anxiety – the two often run in the family together. In brain studies, both conditions involve irregularities in the prefrontal cortex (the brain's command center for focus and planning) and the limbic system (emotion center). Essentially, if your brain were a car, ADHD means the brakes (inhibition) are a bit loose, and anxiety means the alarm system is hyper-sensitive. Combine loose brakes with a blaring alarm and you get… well, us. Fun times, right?Here's an interesting tidbit: Females with ADHD are more likely to report anxiety than males. Some experts think this is partly due to underdiagnosed ADHD – many girls grew up being told they were just “worrywarts” when in fact ADHD was lurking underneath, making everyday life more overwhelming and thus feeding anxiety. As Dr. Thomas Brown (a top ADHD expert) points out, emotional regulation difficulties (like chronic stress or worry) are characteristic of ADHD, even though they're not in the official DSM checklist. Our ADHD brains can amplify emotions – so a normal worry for someone else becomes a five-alarm fire for us.Now, action time: How do we manage this dynamic duo? The first step is getting the right diagnosis. A clinician should untangle whether symptoms like trouble concentrating are from anxiety, ADHD, or both. They might ask: Have you always had concentration issues (pointing to ADHD), or did they start when your anxiety kicked into high gear? Also, consider context – ADHD symptoms occur in most settings (school, work, home), while pure anxiety might spike in specific situations (say, social anxiety in crowds, or panic attacks only under stress).Treatment has to tackle both. Therapy – especially Cognitive Behavioral Therapy (CBT) – is a rockstar here. CBT can teach you skills to manage worry (hello, deep breathing and logical rebuttals to “what if” thoughts) and also help with ADHD organization hacks (like breaking tasks down, creating routines). Many find that medication is needed for one or both conditions. Stimulant meds (like methylphenidate or amphetamines) treat ADHD, but in someone with severe anxiety, a stimulant alone can sometimes ramp up the jitters. In fact, children (and adults) with ADHD + anxiety often don't respond as well to ADHD meds unless the anxiety is also addressed. Doctors might add an SSRI or other anti-anxiety medication to the mix, or choose a non-stimulant ADHD med if stimulants prove too anxiety-provoking.Let me share a quick personal strategy (with a dash of humor): I have ADHD and anxiety, so my brain is basically an internet browser with 50 tabs open – and 10 of them are frozen on a spinning “wheel of doom” (those are the anxieties). One practical tip that helps me distinguish the two is to write down my racing thoughts. If I see worries like “I'll probably get fired for sending that email typo” dominating the page, I know anxiety is flaring. If the page is blank because I got distracted after one sentence... well, hello ADHD! This silly little exercise helps me decide: do I need to do some calming techniques, or do I need to buckle down and use an ADHD strategy like the Pomodoro method? Try it out: Knowledge is power, and self-awareness is the key.Quick Tips – ADHD vs Anxiety: When in doubt, ask what's driving the chaos.* Content of Thoughts: Racing mind full of specific worries (anxiety) vs. racing mind full of everything except what you want to focus on (ADHD).* Physical Symptoms: Anxiety often brings friends like sweaty palms, racing heart, and tummy trouble. ADHD's restlessness isn't usually accompanied by fear, just boredom or impulsivity.* Treatment Approaches: For co-occurring cases, consider therapy and possibly a combo of medications. Experts often treat the most impairing symptom first – if panic attacks keep you homebound, address that alongside ADHD. Conversely, untreated ADHD can actually fuel anxiety (ever notice how missing deadlines and forgetfulness make you more anxious? Ask me how I know!). A balanced plan might be, say, stimulant medication + talk therapy for anxiety, or an SSRI combined with ADHD coaching. Work closely with a professional to fine-tune this.Alright, take a breath (seriously, if you've been holding it – breathing is good!). We've tackled anxiety; now let's talk about the dark cloud that can sometimes follow ADHD: depression.ADHD and Depression: When the Chaos Brings a CloudADHD is often associated with being energetic, spontaneous, even optimistic (“Sure, I can start a new project at 2 AM!”). So why do so many of us also struggle with depression? The reality is, living with unmanaged ADHD can be tough. Imagine years of what Dr. Russell Barkley calls “developmental delay” in executive function – always feeling one step behind in managing life, despite trying so hard. It's no surprise that about 1 in 5 kids with ADHD also has a diagnosable depression, and studies show anywhere from 8% to 55% of adults with ADHD have experienced a depressive disorder in their lifetime. (Yes, that range is huge – it depends how you define “depression” – but even on the low end it's a lot.) Dr. Barkley himself notes that roughly 25% of people with ADHD will develop significant depression by adulthood. In short, ADHD can come with a case of the blues (not the fun rhythm-and-blues kind, unfortunately).So what does ADHD + depression look like? Picture this: You've got a pile of unfinished projects, bills, laundry – the ADHD “trail of crumbs.” Initially, you shrug it off or maybe crack a joke (“organizational skills, who's she?”). But over time, the failures and frustrations can chip away at your self-esteem. You start feeling helpless or hopeless: “Why bother trying if I'm just going to screw it up or forget again?” That right there is the voice of depression sneaking in. ADHD's impulsivity might also lead to regrettable decisions or conflicts that you later brood over, another pathway to depressed mood.In fact, the Attention Deficit Disorder Association points out that ADHD's impact on our lives – trouble with self-esteem, work or school difficulties, and strained relationships – can contribute to depression. It's like a one-two punch: ADHD creates problems; those problems make you sad or defeated, which then makes it even harder to deal with ADHD. Fun cycle, huh?Now, depression itself can mask as ADHD in some cases, especially in adults. Poor concentration, low motivation, fatigue, social withdrawal – these can appear in major depression and look a lot like ADHD symptoms. If an adult walks into a doctor's office saying “I can't focus and I'm procrastinating a ton,” a cursory eval might yield an ADHD diagnosis. But if that focus problem started only after they, say, lost a loved one or fell into a deep funk, and they also feel worthless or have big sleep/appetite changes, depression may be the primary culprit. On the flip side, a person with lifelong ADHD might be misdiagnosed as just depressed, because they seem down or overwhelmed. As always, timeline is key: ADHD usually starts early (childhood), whereas depression often has a more defined onset. Also, ask: Is the inability to focus present even when life's going okay? If yes, ADHD is likely in the mix. If the focus issues wax and wane with mood, depression might be the driver.There's also a nuance: ADHD mood issues vs. clinical depression. People with ADHD can have intense emotions and feel demoralized after a bad day, but often these feelings can lift if something positive happens (say, an exciting new interest appears – suddenly we have energy!). Clinical depression is more persistent – even good news might not cheer you up much. As Dr. Thomas Brown emphasizes, ADHD includes difficulty regulating emotion; an ADHD-er might feel sudden anger or sadness that's intense but then dissipates . By contrast, depression is a consistent low mood or loss of pleasure in things over weeks or months. Knowing this difference can be huge in sorting out what's going on.Now, how do we deal with this combo? The good news: many treatments for depression also help ADHD and vice versa. Therapy is a prime example. Cognitive Behavioral Therapy and related approaches can address negative thought patterns (“I'm just a failure”) and also help with practical skills for ADHD (like scheduling, or as I call it, tricking my brain into doing stuff on time). There are even specialized therapies for adults with ADHD that blend mood and attention strategies. On the medication front, sometimes a single med can pull double duty. One interesting option is bupropion (Wellbutrin) – an antidepressant that affects dopamine and norepinephrine, which can improve both depression and ADHD symptoms in some people. There's also evidence that stimulant medications plus an antidepressant can be a powerful combo: stimulants to improve concentration and energy, antidepressant to lift mood. Psychiatrists will tailor this to the individual – for instance, if someone is severely depressed (can't get out of bed), treating depression first may be priority. If the depression seems secondary to ADHD struggles, improving the ADHD could automatically boost mood. Often, it's a balancing act of treating both concurrently – maybe starting an antidepressant and an ADHD med around the same time, or ensuring therapy covers both bases.Let's not forget lifestyle: exercise, sleep, nutrition – these affect both ADHD and mood. Regular exercise, for example, can increase BDNF (a brain growth factor) and neurotransmitters that help both attention and mood. Personally, I found that when I (finally) started a simple exercise routine, my mood swings evened out a bit and my brain felt a tad less foggy. (Of course, starting that routine required overcoming my ADHD inertia – ask me how I know that took a few tries... or twenty.)Quick Tips – ADHD vs Depression:* Check Your Joy Meter: With ADHD alone, you can still feel happy/excited when something engaging happens (ADHD folks light up for interesting tasks!). With depression, even things you normally love barely register. If your favorite hobbies no longer spark any joy, that's a red flag for depression.* All in Your Head? ADHD negative thoughts sound like “Ugh, I forgot again, I need a better system.” Depression thoughts sound like “I forgot again because I'm useless and nothing will ever change.” Listen to that self-talk; depression is a sneaky bully.* Professional Help: A thorough evaluation can include psychological tests or questionnaires to measure attention and mood separately. For treatment, consider a combined approach: therapy (like CBT or coaching) plus meds as needed. According to research, a mix of stimulant medication and therapy (especially CBT) can help treat both conditions. And remember, addressing one can often relieve the other: improve your ADHD coping skills, and you might start seeing hope instead of disappointment (boosting mood); treat your depression, and suddenly you have the energy to tackle that ADHD to-do list.Before we move on, one more important note: if you ever have thoughts of self-harm or suicide, please reach out to a professional immediately. Depression is serious, and when compounded with ADHD impulsivity, it can be dangerous. There is help, and you're not alone – so many of us have been in that dark place, and it can get better with the right support. Knowledge is power and self-awareness is the key, yes, but sometimes you also need a good therapist, maybe a support group, and possibly medication to truly turn things around. There's no shame in that game.Alright, deep breath. It's getting a bit heavy in here, so let's pivot to something different: a condition that seems like the opposite of ADHD in some ways, yet can co-occur – OCD. And don't worry, we'll crank the sass back up a notch.ADHD and OCD: The Odd Couple of AttentionWhen you think of Obsessive-Compulsive Disorder (OCD), you might picture someone extremely organized, checking the stove 10 times, everything neat and controlled. When you think ADHD… well, “organized” isn't the first word that comes to mind, right?

An hour into today's Tour stage and news filtered out: Geraint Thomas is in the breakaway. Hold the phone. In the end, it wasn't to be for the break - Nils Politt, 'the Flying Dentist', set the pace in the bunch and they were caught the first time up the famous Mur de Bretagne. G enjoyed himself though, and joined Luke on the pod to chat all about it. The boys will be back on Monday. Don't forget the incredible competition from our friends at Continental Tyres. Visit www.continental-tyres.co.uk/watts-occurring before it closes this Sunday to enter and you could join us in Paris for the final weekend of the Tour. It's a once in a lifetime trip. What have you got to lose? And we also have a brilliant offer from our friends at Rouleur for July. Use code WATTS at rouleur.cc/subscribe to get 10% any of their subscription offers and enjoy their unparalleled daily Tour de France coverage. Watts Occurring is brought to you by Continental Tyres Learn more about your ad choices. Visit podcastchoices.com/adchoices

G's back on the pod tonight and he settled in for a long old catch up with Luke after today's 33km time trial in Caen. They chatted the TT, G's form, INEOS' plans, Remco's ride... and plenty more besides. Quintessential Watts Occurring, this. Enjoy. Don't forget the incredible competition from our friends at Continental Tyres. Visit www.continental-tyres.co.uk/watts-occurring before it closes this Sunday to enter and you could join us in Paris for the final weekend of the Tour. It's a once in a lifetime trip. What have you got to lose? And we also have a brilliant offer from our friends at Rouleur for July. Use code WATTS at rouleur.cc/subscribe to get 10% any of their subscription offers and enjoy their unparalleled daily Tour de France coverage. Watts Occurring is brought to you by Continental Tyres Learn more about your ad choices. Visit podcastchoices.com/adchoices

That was a wild finale and another relentless day at the Tour. Will this year's race ever quieten down? Luke and Tom hopped on the pod to analyse a fascinating day which turned into a full on GC battle... plus the incredible MVDP. G will be back tomorrow for a TT recap. Don't forget the incredible competition from our friends at Continental Tyres. Visit www.continental-tyres.co.uk/watts-occurring before it closes this Sunday to enter and you could join us in Paris for the final weekend of the Tour. It's a once in a lifetime trip. What have you got to lose? And we also have a brilliant offer from our friends at Rouleur for July. Use code WATTS at rouleur.cc/subscribe to get 10% any of their subscription offers and enjoy their unparalleled daily Tour de France coverage. Watts Occurring is brought to you by Continental Tyres Learn more about your ad choices. Visit podcastchoices.com/adchoices

Ben Swift should have been in France right now, battling the weather and the best riders in the world on a brutal stage two at the Tour. But, alas, a shoulder fracture and subsequent illness ruled 'Swifty' out of INEOS' Tour selection, so Luke called him up to get his expert thoughts on the pod. Today's late climbs lived up to the hype - and while the favourites battled it out up front, we were delighted to see G hanging tough behind. Two days in and the Tour is already flying. Don't forget the incredible competition from our friends at Continental Tyres. Visit www.continental-tyres.co.uk/watts-occurring to enter and you could join us in Paris for the final weekend of the Tour. It's a once in a lifetime trip. What have you got to lose? And we also have a brilliant offer from our friends at Rouleur for July. Use code WATTS at rouleur.cc/subscribe to get 10% any of their subscription offers and enjoy their unparalleled daily Tour de France coverage. Watts Occurring is brought to you by Continental Tyres Learn more about your ad choices. Visit podcastchoices.com/adchoices

Watts Occurring is now on YOUTUBE! Click HERE to watch G podding from his Tour de France massage table. The Tour de France always starts with a bang. You never want to miss the first stage... and this year was no different. G made it through unscathed and joined Tom on the massage table to tell you all about it. See you tomorrow with Luke and special guest Ben Swift. Don't forget the incredible competition from our friends at Continental Tyres. Visit www.continental-tyres.co.uk/watts-occurring, enter, and you could join us in Paris for the final weekend of the Tour. It's a once in a lifetime trip. What have you got to lose? And we also have a brilliant offer from our friends at Rouleur for July. Use code WATTS at rouleur.cc/subscribe to get 10% any of their subscription offers and enjoy their unparalleled daily Tour de France coverage. Watts Occurring is brought to you by Continental Tyres Learn more about your ad choices. Visit podcastchoices.com/adchoices

Yes, it's that time again. The Tour de France is here - and G is ready for his final one. He joined Luke fresh from arriving in Lille to chat through the INEOS lineup, Pog vs Jonas, the sprint battle, his own ambitions... and lots more. You know the drill. You'll also be able to watch this episode on our brand new shiny YouTube channel! Just search 'Geraint Thomas Cycling Club' on YouTube and hit that subscribe button. Please. We've also got another incredible competition for you to enter from our friends at Continental Tyres. Visit www.continental-tyres.co.uk/watts-occurring to enter - and have the chance of joining us in Paris for the final weekend of the Tour. It's a once in a lifetime trip. What have you got to lose? And we also have a brilliant offer from our friends at Rouleur for July. Use code WATTS at rouleur.cc/subscribe to get 10% any of their subscription offers and enjoy their unparalleled daily Tour de France coverage. Right, that's all for now. See you this weekend when the fireworks begin. Watts Occurring is brought to you by Continental Tyres Learn more about your ad choices. Visit podcastchoices.com/adchoices

Last week we previewed the Tour de Suisse with an excited G - but this week we had to ask him about an innocuous crash that saw him have to head home from Switzerland early. Has it wrecked his Tour prep? Is he recovered? He answers both of those questions in this week's pod and looks back at the winner in Suisse, the impressive Joao Almeida. And next week? Well, you can expect a Tour de France preview from us - and then the greatest cycling show in the world starts just a few days later... We'll see you then. Watts Occurring is brought to you by Continental Tyres. Learn more about your ad choices. Visit podcastchoices.com/adchoices

The influenza pandemic of 1918-20 infected about one-third of the world's population at the time, killing at least 50 million people. Occurring during the First World War, what became known as the Spanish Flu spread rapidly as soldiers moved across continents. It overwhelmed hospitals, led to mass graves, and disrupted societies worldwide. But what made the disease so deadly? Was it really Spanish? And what lessons had been learned by the time Covid-19 emerged, a century later? This is a Short History Of The Spanish Flu. A Noiser Production. Written by Nicola Rayner. With thanks to Mark Honigsbaum, a medical historian, and author of The Pandemic Century: One Hundred Years of Panic, Hysteria, and Hubris.  Get every episode of Short History Of a week early with Noiser+. You'll also get ad-free listening, bonus material, and early access to shows across the Noiser network. Click the Noiser+ banner to get started. Or, if you're on Spotify or Android, go to noiser.com/subscriptions. Learn more about your ad choices. Visit podcastchoices.com/adchoices

Want to win a VIP trip to the Tour's Grand Depart AND the chance to ride on the cobblestones of Paris-Roubaix? Of course you do. Continental Tyres are running an incredible competition to do just that right now. Enter here: https://www.continental-tyres.co.uk/wattsoccurring/ Right, now you've entered that, let's get on with the show - and G's got an update after two days at the Tour de Suisse, where he's putting the finishing touches to his Tour de France prep. We're excited to see him rip it up in the mountains this week... fingers crossed. And, of course, we've got another Pog show to dissect. What a display he put on at the Dauphine. Can Vingegaard close the gap before the Tour? Hmm... See you next week. Learn more about your ad choices. Visit podcastchoices.com/adchoices

Joyce discusses the anti-semitism and attacks against Jewish people in America. See Privacy Policy at https://art19.com/privacy and California Privacy Notice at https://art19.com/privacy#do-not-sell-my-info.

Attorney Tony Buzbee has revealed that several of Sean "Diddy" Combs' celebrity friends have been quietly settling with victims to avoid being publicly named in the ongoing legal scandal. Buzbee, who represents over 120 accusers, noted that demand letters were sent to these individuals, giving them an opportunity to settle their involvement privately before formal lawsuits are filed. The settlements allegedly relate to their attendance and knowledge of illegal activities at Diddy's infamous parties, which have been the center of accusations involving sexual assault and coercion.Buzbee has emphasized that anyone who participated in or allowed these activities to occur without intervention could face legal consequences. He hinted that more lawsuits will be filed, with the potential to implicate additional high-profile figures in the entertainment industry. Buzbee's strategy includes meticulously vetting each claim and sending demand letters to ensure the legal process is thorough. This approach signals that the legal battle surrounding Diddy and his associates may expand, drawing further scrutiny to those who were complicit..(commercial at 10:53)to contact me:bobbycapucci@protonmail.comsource:Diddy's celebrity accomplices have quietly paid-off victims to avoid being named publicly, lawyer claims | Daily Mail OnlineBecome a supporter of this podcast: https://www.spreaker.com/podcast/the-epstein-chronicles--5003294/support.

The guys discuss how there are technical issues at the iHeart Studios and Producer Aaron's only logic is Blame Ukraine.

What's the odds? Geraint Thomas is stinking hot up a mountain, but he's still got time to catch up with Luke Rowe for a proper debrief into this year's dramatic Giro d'Italia.  Learn more about your ad choices. Visit podcastchoices.com/adchoices

“GEMINI MOON PHASES & Jupiter in Cancer” presented by Talk Cosmos Kaleidoscope Visions.The Gemini New Moon and 1st quarter lead up to Jupiter's new year cycle in Cancer. Occurring a few days before the Sagittarius Full Moon, the social planets Jupiter and Saturn push us towards making actions to define cultural perspectives,” said Sue Minahan, founder, and host of the weekly show. “What makes up our personal foundation and security philosophically is an ongoing story for the year Jupiter is in Cancer. Understanding the lunar cycle impacts one's foundation, emotions, and emotional story.”The moon's our personal planet regulating the past coming into the present. Weekly the moon systematic monthly cycle transitions from the New Moon to first quarter, Full Moon, and third quarter moon phases. Daily transiting 12-13 degrees, the moon moves through a Zodiac sign in two & a half days. Join Sue Rose Minahan of Kailua-Kona, Hawai'i with Kaleidoscope Visions panel members, Amanda Pierce, and John Chinworth of Seattle. Bios below and on Talk Cosmos website for Season 8. Subscribe on Talk Cosmos website. Follow on YouTube @TalkCosmos. Weekly on YouTube, Facebook, Radio and Podcasts.JOHN CHINWORTH: Consultant, Conference Lecturer, Writer/Poet. Diploma from the International Academy of Astrology (IAA) in 2021. More than two decades of experience. https://www.skypathastro.com/ email: ... at NORWAC, and SFAS | Obsessed with mythology & branded the Greco-Roman pantheon into his psyche | Past board member of WSAA |Teaches and mentors developmentally disabled and resource students for many years | Pens poems and does road trips around Washington. https://www.skypathastro.comAMANDA PIERCE: blends her eclectic style of astrology and energy magic around a soul-centered approach to life and healing. With a B.A. in Psychology, Astrology and Energy Work Consultation | Meditation | Writing & Editing. Empowerment-based Meditation: teaching in-person 4-week series classes. Amandamoonastrology@gmail.com Past WSAA Board Member | UAC 2018 Volunteer Coordinator.SUE ‘ROSE' MINAHAN: Evolutionary Astrologer Consultant, studying Vibrational Astrology. Speaker, Writer. Dwarf Planet Astrology graduate and tutor; Kepler Astrology Toastmaster Charter Member; Associate of Fine Arts Music Degree, & a Certificate of Fine Arts in Jazz. Artist & musician. Mythology enthusiast. Founder of Talk Cosmos delivering weekly insightful conversations to awaken heart and soul-growth consciousness. 2025 Season 8. https://www.talkcosmos.com/#TalkCosmosKaleidoscopeVisions #SueMinahan #JohnChinworth #AmandaPierce #astrologyYouTubeconversations #MajorLunarPhases #marsinleo #astrologypodcastweather #TalkCosmos #SkyPathAstro #TalkCosmosYouTubeChannel #KKNW1150AM #ScorpioFullMoon #gemininewmoon #firstquarterMoon #QuarterMoon #radiopodcast #youtubeconversationpodcasts #mercury #jupiterincancer #saturninaries #neptuneinaires #astroweather #cosmosTalk Cosmos is your opportunity to ponder realms of what Carl Jung called the collective unconsciousness that's shared through time to the present…all through the lens of Sue's lifetime of peering into astrology.“Thankfully, I discovered Evolutionary astrology. Its perspective points directly to our unique personal spiritual soul growth…driven by our aligned intentions. Its promising purpose of soul growth ignited an entirely alive Zodiac. Captured, I felt compelled to study the deep significance of astrological application,” said Sue.Sue is your guide to focusing the Cosmos kaleidoscope. In the words of Einstein, “Energy's never destroyed, energy only changes.”Discover the energy that is Talk Cosmos, every Sunday from 1 p.m. to 2 p.m. right here on Alternative Talk 1150!Contact https://talkcosmos.com for weekly schedule, blog, and information.See Privacy Policy at https://art19.com/privacy and California Privacy Notice at https://art19.com/privacy#do-not-sell-my-info.

Luke, G and De Pluski all hop on in typically chaotic fashion to digest the 20th stage of the Giro. And everyone is baffled! There's huge praise for Wout Van Aert, G's mind is blown by UAE tactics and our Chapeau of the Day goes to a Brit. Join us here back on Tuesday for a FULL Giro debrief, when hopefully we'll have some answers. See you then. Learn more about your ad choices. Visit podcastchoices.com/adchoices

It's a GC battle for the ages! With three stages to go, the maglia rosa is still up for grabs. Luke and G unpack a busy stage 18 including Ayuso being stung by a bee, and discuss all the contenders for the podium. G's backing Carapaz, Luke has a soft spot for Derek Gee, but could Briton Simon Yates sneak it? We'll see you back here after the final stage for our big Giro debrief! Learn more about your ad choices. Visit podcastchoices.com/adchoices

A huge day in the GC at the Giro and Geraint and Laurens De Pluski are debriefing it all from training camp in Tenerife. After some big name exits and cracks on stage 16, who's left standing? Is Derek Gee still De Pluski's man? Is Simon Yates smelling blood? There's also Continental chapeau of the day for Astana after a first and second finish, and we get the low-down on G's birthday celebrations including a suspect cheesecake. Learn more about your ad choices. Visit podcastchoices.com/adchoices

It's G's birthday eve and he's spending it in the best way possible... podding with Luke! There's a lesson on pronunciation from a fan in the Czech Republic to start, followed by a fierce debate over the aero helmet. But are you for or against? And following an unexpected day on stage 14, is Del Toro now a serious contender for GC? Or is it still Roglic's to lose as we go into the final week? Learn more about your ad choices. Visit podcastchoices.com/adchoices

Who are G and Luke backing as we head into the business end of the Giro? Will Tom Pidcock win a stage? And why is Luke wearing Christmas pyjamas in May? Plus Luke offers G the chance to rip up his pre-Giro predictions. Will he take it? Learn more about your ad choices. Visit podcastchoices.com/adchoices

G's back on top of Mount Teide and reunited with Luke on the pod as they review an eventful weekend at the Giro. Who got their tactics wrong on stage 9? Is Isaac del Toro a serious threat for GC and should Tom Pidcock ride GC to Rome? Plus after 9 days of racing we pick our Chapeau of the Week and the boys preview Tuesday's TT. Is it Josh Tarling's to lose? Learn more about your ad choices. Visit podcastchoices.com/adchoices

Watts ambassador De Pluski is in the hot seat today with Tom Fordyce to look back on the last few days of Giro action including the longest stage of the race. Stage 6 had it all towards the end - a big crash, retirements and a gutsy sprint finish. Plus someone collected a hat-trick of wins on stage 5. G and Luke will be back on Monday to review the opening week and preview the second TT. And, check out our social channels to see our Continental Tyres Chapeau of the Day every day of the race. See you then. Learn more about your ad choices. Visit podcastchoices.com/adchoices

After facing the unimaginable heartbreak of losing a child, Stephanie Marquesano transformed her grief into a powerful mission to advocate for individuals battling co-occurring disorders. Her son Harris's struggle with mental health and substance use inspired the creation of The Harris Project, an initiative focused on holistic care. Stephanie's journey from personal tragedy to activism underscores the critical need for integrated approaches to mental health and addiction treatment, offering hope and insight to families and professionals dealing with similar challenges. Throughout our conversation, we explore the intricate link between mental health issues and substance misuse, uncovering the root causes like genetics and trauma. Highlighting the societal shift required to address these challenges, we draw attention to the disparity in care and perception compared to other illnesses. By advocating for early intervention and education, we aim to inspire communities to challenge the stigma surrounding these issues, ultimately leading to better outcomes for youth and adults alike. In this episode, you will hear: Stephanie Marquesano's journey from personal tragedy to founding The Harris Project The importance of integrated mental health and addiction care for co-occurring disorders Harris's story: early anxiety, substance misuse, and systemic failures in treatment Advocating for early intervention and education to combat stigma and improve outcomes Collaborative efforts like the "You Don't Know the Half of It" PSA to reshape public perception The role of media and partnerships in changing narratives around mental health and addiction Follow and Review: We'd love for you to follow us if you haven't yet. Click that purple '+' in the top right corner of your Apple Podcasts app. We'd love it even more if you could drop a review or 5-star rating over on Apple Podcasts. Simply select “Ratings and Reviews” and “Write a Review” then a quick line with your favorite part of the episode. It only takes a second and it helps spread the word about the podcast. Supporting Resources: NovusMindfulLife.com Episode Credits If you like this podcast and are thinking of creating your own, consider talking to my producer, Emerald City Productions. They helped me grow and produce the podcast you are listening to right now. Find out more at https://emeraldcitypro.com Let them know we sent you. Learn more about your ad choices. Visit megaphone.fm/adchoicesSee Privacy Policy at https://art19.com/privacy and California Privacy Notice at https://art19.com/privacy#do-not-sell-my-info.

After facing the unimaginable heartbreak of losing a child, Stephanie Marquesano transformed her grief into a powerful mission to advocate for individuals battling co-occurring disorders. Her son Harris's struggle with mental health and substance use inspired the creation of The Harris Project, an initiative focused on holistic care. Stephanie's journey from personal tragedy to activism underscores the critical need for integrated approaches to mental health and addiction treatment, offering hope and insight to families and professionals dealing with similar challenges. Throughout our conversation, we explore the intricate link between mental health issues and substance misuse, uncovering the root causes like genetics and trauma. Highlighting the societal shift required to address these challenges, we draw attention to the disparity in care and perception compared to other illnesses. By advocating for early intervention and education, we aim to inspire communities to challenge the stigma surrounding these issues, ultimately leading to better outcomes for youth and adults alike. In this episode, you will hear: Stephanie Marquesano's journey from personal tragedy to founding The Harris Project The importance of integrated mental health and addiction care for co-occurring disorders Harris's story: early anxiety, substance misuse, and systemic failures in treatment Advocating for early intervention and education to combat stigma and improve outcomes Collaborative efforts like the "You Don't Know the Half of It" PSA to reshape public perception The role of media and partnerships in changing narratives around mental health and addiction Follow and Review: We'd love for you to follow us if you haven't yet. Click that purple '+' in the top right corner of your Apple Podcasts app. We'd love it even more if you could drop a review or 5-star rating over on Apple Podcasts. Simply select “Ratings and Reviews” and “Write a Review” then a quick line with your favorite part of the episode. It only takes a second and it helps spread the word about the podcast. Supporting Resources: NovusMindfulLife.com Episode Credits If you like this podcast and are thinking of creating your own, consider talking to my producer, Emerald City Productions. They helped me grow and produce the podcast you are listening to right now. Find out more at https://emeraldcitypro.com Let them know we sent you. Learn more about your ad choices. Visit megaphone.fm/adchoices

G's back on the pod to reflect on the first three days of Giro action - and it's fair to say Albania kicked up a storm for its first-ever Grand Tour Grande Partenza. Again, there's no spoilers here... but it's fair to say Mads Pedersen had an excellent few days, while Primoz Roglic cemented his reputation as the favourite for the maglia rosa. G also got on the phone to young star and teammate Josh Tarling, to ask him all about his huge TT win on day two. He joined G for the final 10 minutes of today's pod to go through the action and give the inside line on the INEOS camp. Our stage three Continental Tyres Chapeau of the Day is a leadout man who's already made a big impact on the race and, as the race now hits Italy, we'll be picking our Chapeau of the Day after every single stage. Check out our social channels to see our picks. G and Tom will be back later in the week as the race heads for the high mountains for the first time. See you then. Learn more about your ad choices. Visit podcastchoices.com/adchoices

The Giro d'Italia is officially underway in Albania - and the opening two days have already lived up to the hype. A crazy stage one saw a reduced bunch do battle for the stage win, today's TT was won by a second, we've seen two maglia rosa wearers , GC hopes extinguished... Ahhh you can't beat Grand Tour racing. No spoilers here, but tune in and let Tom and Luke talk you through the action from the first two days. G will be back Monday to recap stage three - and pick our Continental Tyres Chapeau of the Day. See you then. Learn more about your ad choices. Visit podcastchoices.com/adchoices

It's Affordable Housing Month on the Beyond the Resume Podcast!Today, on this installment of our Webinar Series, leaders from across the affordable housing sector explore how to elevate resident voices and build authentic community engagement into every facet of development and operations. From co-governance and workforce housing preservation to fund development strategies that align with equity goals—this is a must-watch for housing professionals, organizers, and mission-driven investors.Learn how naturally occurring affordable housing (NOAH) can serve as a resilient, resident-centered solution to the housing crisis—and how organizations are shifting from transactional models to long-term, community-powered partnerships.LinksYouTube: https://youtu.be/Rqx3HimLnGgSpotify: https://spoti.fi/35ZJGLTApple Podcasts: https://apple.co/3I3nkG9Web: https://www.jacksonlucas.com/podcast/webinar-noah

G's home from Romandie and has got a hefty debrief for Luke from the comings and goings in Switzerland. It was another solid week for G on his course to the Tour in July. Next up? Tenerife for his birthday. Ahh, lovely. Luke's been busy recording his new book - no wonder his voice sounds a bit croaky - and the boys throw their hats into the ring with some bold Giro predictions. Who do you think will make up the podium? Let us know by emailing gtcc@crowdnetwork.co.uk. See you next week, when the racing for the pink jersey will be well underway - and keep an eye on our social channels from stage one on Friday, where we'll be naming our Chapeau of the Day, sponsored by Continental Tyres. Learn more about your ad choices. Visit podcastchoices.com/adchoices

Today's episode title says it all. We've got Sam 'Skippy' Watson winning the Romandie prologue 24 hours after being told to get a flight; a rundown on INEOS' kitchen sink-esque Liege-Bastogne-Liege tactics; and Pogi unsettling G by having a quiet convo with him at 420 watts. That's plenty to be going on with, but don't worry. There's lots more than that too. A classic Watts Occurring if ever we've heard one. See you next week. Learn more about your ad choices. Visit podcastchoices.com/adchoices

We've got a treat for you all this week: Ambassador De Pluski's back on the pod. He joined Luke, who was fresh home from the Amstel Gold Race, where... well, where he got lost. Long story. In one of the most dramatic Classics of the season, Pog didn't win. Remco didn't win. But Matthias Skjelmose did. Chapeau, Sir. Next up for both Luke (in the car) and De Pluski (on the bike) is Liege-Bastogne-Liege this Sunday. Will it be Pogi vs Remco again? Or will De Pluski pull off a wild long-range attack of his own? Who knows. Maybe if he fuels with the Luke Rowe sandwich, he'll be fine. (You'll have to listen for that one to make sense.) G will be back next week. See you then. Want to try NordVPN? Head to https://nordvpn.com/gtcc for a special sign up deal. We're also hosting a retirement party for G at the Millenium Centre in Cardiff on Sunday 16th November! Tickets are available here: https://www.livenation.co.uk/geraint-thomas-tickets-adp1206752 Learn more about your ad choices. Visit podcastchoices.com/adchoices

We're back baby. That's right, Luke and G are reunited for the first official Watts Occurring of 2025. The season starts now. And, of course, there is a lot to catch up on - first and foremost, Sunday's Roubaix. And it was a cracker. Mathieu van der Poel won his third on the bounce (how nuts is that?) and Tadej Pogacar showed the world that one day he could well add it to his palmares. Luke's day was equally eventful and he told G all about his first Paris-Roubaix as a Sport Director. Attention now switches to the Ardennes - and G's eyeing up a final ride at Liege-Bastogne-Liege. What do you reckon: should he do it? Let us know by emailing gtcc@crowdnetwork.co.uk. We'll be back next week with a bumper pod. Want to try NordVPN? Head to https://nordvpn.com/gtcc for a special sign up deal. We're also hosting a retirement party for G at the Millenium Centre in Cardiff on Sunday 16th November! Tickets are available here: https://www.livenation.co.uk/geraint-thomas-tickets-adp1206752 Learn more about your ad choices. Visit podcastchoices.com/adchoices

President Trump holds a cabinet meeting where we are seeing transformational change occurring for America Learn more about your ad choices. Visit megaphone.fm/adchoices

Send us a textToday, we cover the only major schism in Russian Orthodox history, known as the Raskol. Occurring in the mid-17th century, the reforms of Patriarch Nikon, led to the schism that would pit one side, the central church, against those known as the Old Believers, millions who exist to this day.Support the show