Daniel Poneman

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Daniel Poneman

Daniel Poneman

@DanielPoneman

Founder, Servant, Teacher, Student, Friend, Agent, @WEAVE 🧶

Chicago, IL Katılım Temmuz 2009
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Daniel Poneman
Daniel Poneman@DanielPoneman·
I started in this business 18 years ago, at age 14. I didn’t make enough money to support myself until I was 24. I never did it for the money. I did it because I love this game with every fiber of my being. 🧵 1/6
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Joe Tipton
Joe Tipton@JoeTipton·
Xavier forward Filip Borovicanin has re-committed to the Musketeers for the 2026-27 season despite having the option to enter the transfer portal, his agent @DanielPoneman of WEAVE, told @On3. The 6-9 senior averaged 10.8 points, 7.4 rebounds, and 4.2 assists per game last season. He was among the 15 athletes granted an additional year of eligibility in Ohio through a recent injunction. on3.com/college/xavier…
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Tommy Reamon Jr.
Tommy Reamon Jr.@tommyreamon·
To all my high school coaches… If you’ve spent years busting your butt building a program, and then a private school offers you 2 or 3 times the salary… Did they “steal” you? Or did they simply offer a better opportunity? Funny how it’s called “stealing” when it’s a player, but “career advancement” when it’s a coach.
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farbood
farbood@farbood·
Hope you get better my brother. Here to help however I can. The AI in A-LIST is the most advanced health AI Agent in the world. Please put it to use to help you. Personally I can’t live without it and it’s solved several people’s gut issues and more.
Bryan Johnson@bryan_johnson

Bad news #1: I have an autoimmune disease. My stomach is eating itself. Bad news #2: 2–5% of people have this, too. Likely more, because it hides. Good news: I'm going to try and solve it. Will share all. As a kid, I ate sugar cereal, drank sugary soda, and gobbled down fast food. I had a few healthy years in my early 20s but then became a young father of three and began building a business. Juggling that stress and grind, I let my health slip and gained 40 lbs. Within a few years I’d fallen into a deep, chronic depression. Somewhere in that timeline, my body began developing an autoimmune process affecting my thyroid and then my stomach lining. It’s called Autoimmune Gastritis (AIG). My hypothyroidism got diagnosed when I was 21 years old with a routine blood draw. That enabled me to begin proactive management, supplementing levothyroxine and Armour Thyroid. They are the hormones my body should be producing on its own but wasn’t. By taking these pills daily, my body was able to operate as though my thyroid was functioning properly. What I didn’t know was that something else was going on inside my body: my stomach had begun attacking itself. But there was no routine test to find out and I didn’t have any symptoms. I just discovered it in May. I'm unsure how long I've had it. AIG causes irreversible damage: nutritional deficiency, anemia, and over a long horizon, elevated cancer risk. When AIG is discovered today, standard medical care concedes defeat, stating that nothing can be done except managing the condition, no matter how awful or lethal the effects. Looking back over the past few years, I can now see the early signals we were picking up in measurement but hadn’t connected the dots. For 11 years, I’ve had low ferritin, without anemia. We continually tried to raise my iron levels with food and supplementation but nothing would work. We chased the obvious solutions first. A plant-based diet means all my iron is the hard-to-absorb, non-heme kind. Hard training, sauna, and hyperbaric oxygen all raise the body's demand for iron. But none of them explained the core failure: despite me taking iron orally, trialing every formulation, and using every timing trick, none of the iron would stick. What I didn’t fully appreciate until recently is how many stones my previous providers had left unturned. The low ferritin kept getting explained away but not fixed. I overhauled my medical team earlier this year. It was the rebuild to lay the groundwork for Immortals Care, our $1M a year protocol. With greater capacity, we revisited everything. On the surface, my low ferritin was easy to dismiss by most standards of care. My hemoglobin and hematocrit were normal. Ferritin measures stored iron, while hemoglobin measures circulating iron, and because the body drains its reserves first to keep hemoglobin normal, you can be fully iron deficient with a perfectly normal hemoglobin and hematocrit. This is why my low ferritin kept getting dismissed: the numbers that define anemia looked fine, so no one asked why my iron reserves wouldn't refill. My team pressed on that question. They first turned to a colonoscopy. I was 48 years old and overdue. It was good health hygiene to have while also serving a specific purpose of searching for a hidden source of blood loss such as a polyp or even cancer in my bowels. Either one of those would be an explanation of why the iron kept disappearing. At the same time, they began connecting the dots. Iron absorption depends on stomach acid, so one theory was that my stomach acid was disrupted. They also knew that thyroid and stomach autoimmunity often travel together, so often that the pairing has a name: thyrogastric syndrome. Put against my 27+ year history of autoimmune thyroid disease, the pieces pointed to a single hypothesis: my own immune system was attacking my stomach. To our surprise, my colonoscopy came back clean. A perfectly healthy colon, better than 95% of colonoscopies of men, according to the gastroenterologist. That ruled out the first concern and worst possible outcome: slow continuous bleeding from colon cancer, or pre-cancerous polyp. My team had exercised great foresight though, anticipating this possible outcome. In addition to a colonoscopy, they’d ordered an upper endoscopy to be performed at the same time. The combined procedure is a bi-directional endoscopy. Probes would look at my entire intestinal tract, up from below and down the throat. Additionally, we had several blood biomarkers measured ahead of the procedure to try and pick up on any signals that would give the gastroenterologist guidance for what to look for while doing visual inspections. Fifteen minutes before the procedure, my blood results returned, finding elevated levels of anti-parietal-cells-antibodies (APCA). They came back at roughly five times the upper limit of normal (103, against a ceiling of 20 Units/mL). It was a positive result confirming the suspicion of AIG being the culprit behind my low ferritin, the other type of gastritis, driven by a bacterial infection, was already ruled out, as we knew I am negative to H. pylori. Even before this finding, my team had ordered five biopsies to be taken from three regions of my stomach. The biopsies were the critical piece. Had they not been ordered, the bi-directional endoscopy would have been completed and AIG remained undiagnosed as there were no visual signatures of the condition in my intestines. Two days later, the results of biopsies came in, showing clear signs of early autoimmune gastritis: early atrophy confined to the acid-producing lining, with the rest of the stomach still spared. My team had anticipated this, methodically tracing every line of evidence. We now had a formal diagnosis. I have autoimmune gastritis AIG. My stomach is eating itself. So this was never one problem. It was three, linked to one another: the iron deficiency, the autoimmune gastritis driving it, and the autoimmune thyroid disease alongside it. Iron and thyroid feed each other both ways, low iron impairs the conversion of thyroid hormone into its active form, and an under active thyroid impairs how the body uses iron. Each made the other harder to fix. Autoimmune gastritis affects an estimated 2–5% of people, and likely more, because it hides and is challenging to diagnose. It's usually silent for years, surfacing only once the stomach has atrophied enough to do real damage: iron deficiency first, then B12 deficiency, then anemia from both, and over a long horizon, raised stomach-cancer risk. In one study of people with precancerous gastric lesions, roughly 18% carried the autoimmune antibodies, and only about 1% had ever been diagnosed. And the earliest clue, low ferritin, is the one standard medicine waves through. Low iron stores get normalized and rarely investigated at all when anemia hasn't shown up yet. That blind spot is what hid mine for a decade. The good news: the iron deficiency is now corrected. I received a 1,000 mg Monoferric iron infusion. This was chosen for two reasons after considering multiple formulations. First, it can safely deliver a full dose of iron in a single infusion (1,000 mg), while older options like Venofer require several separate appointments to reach the same total. Second, certain other IV iron formulations can cause a drop in blood phosphate levels, an important mineral for bones and energy. Monoferric is much less likely to do this, which matters given how closely we track long-term metabolic and bone health parameters. As mentioned earlier, current medical standards treat AIG as something to be managed, not resolved. It's worth noting that many of you give me a hard time, inviting me to "live life" and engage in self-destructive behaviors like a "normal person". I'm cool with the playful ribbing. Also, had I not taken care of my health during the past five years, my situation could potentially be very serious. You too may have a lurking health issue that is undiagnosed and could increase in severity from unhealthy life choices, without your knowing. The absence of symptoms is not the presence of health. A gentle nudge that minding your health, no matter your situation in life, is good decision making. My team and I are going to try and solve my AIG. This is how we’re approaching it: First, routine monitoring keeps the disease in view: ferritin and iron, B12, the pepsinogen I/II ratio, gastrin, and chromogranin A. Gastrin is the dial to watch. If it climbs, the disease is advancing, and the risk of gastric neuroendocrine tumors climbs with it. Second, we’re doing advanced characterization of the disease. We’ll do a repeat biopsy to read the immune infiltrate, deep cytokine profiling, and T-cell subset analysis, to see which pathways are actually firing. That testing drives the intervention plan, including the experimental approaches we intend to develop. + If gastrin and chromogranin rise: damp the gastrin drive (netazepide) and tighten endoscopic surveillance. If the profile is Th1 / interferon-driven: target JAK/STAT. + If it's Th17 / IL-17-driven: target IL-17 and STAT3. + If regulatory T cells are failing: rebuild them (low-dose IL-2, induced Tregs). + If it's antibody- and B-cell-driven and antigen-specific: engineered cell therapy (CAAR-T). Which organizes into four tiers, from available today to frontier: Tier 1, now: protect and support; zinc-L-carnosine, and acid replacement (betaine HCl with pepsin) under physician supervision. This is specific to my case and not something to self-prescribe, especially given the cancer-surveillance considerations above. Tier 2, target the signaling , JAK/STAT, GSK-3, IL-17, and damp the gastrin drive (netazepide). Tier 3, reset the cells, induced regulatory T cells (iTregs). Tier 4, frontier: engineered T-cell therapy (CAR-T / CAAR-T), custom AI-designed antibodies, or synthetic proteins, that can specifically seek out inactivate or destroy the rogue immune cells attacking my stomach lining. To be clear: there's no approved cure for autoimmune gastritis today. Medicine treats it as something to manage, not solve. Tiers 2 through 4 are investigational preclinical evidence at best, and in several cases therapies that still have to be built. If you're working on autoimmune gastritis, antigen-specific tolerance, regulatory T cells, or CAAR-T for organ-specific autoimmunity, please reach out. Modern medicine has normalized too many conditions that erode our health, function, and comfort, shrinking the goal to monitoring and management while a cure is rarely even attempted. Most of these verdicts were handed down decades ago, in an era that predates nearly all of our current tech and science, and they have gone largely unchallenged. We want to change that. In the age of AI, multiomics, and custom-built DNA, proteins, and cells, no condition should be presumed incurable simply because no one has yet tried to cure it with today's stack. I’ll end on a personal note. We fill our days mostly on things that are trivial next to what we ultimately care about. We know, deep down, however, that in the noise of it all, health is easily forgotten until it’s the only thing that matters. We spend a fraction of our lives truly sober to the preciousness of life. We feel it when someone we love dies, when a child is born, when we come close to death ourselves, or when a diagnosis marks our limit. In those moments, we are sobered, and the rarity of it all becomes self evident. Imagine the existence we’d build together if that clarity didn’t fade. I wish all of you the very best. Care for yourself, care for others, care for the planet and care for our animal friends. Care for life as it’s the most precious gift there is.

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Daniel Marks
Daniel Marks@dgm591·
When you go to @NBASummerLeague , you often have under 5 minutes to make an impression on someone. Learn how to refine your elevator pitch and maximize your opportunity to land a job during tonight’s “Summer League Crash Course”. Code BISON for 10% off. getinthegame101.com/shop/p/nba-dra…
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Darren Heitner
Darren Heitner@heitner·
As the week begins and I put the final touches on a few new NCAA eligibility lawsuits, it strikes me how backward the waiver process is altogether. The NCAA has a process that allows exceptions to its rules that are intended to benefit athletes, but those athletes can’t even seek the relief on their own. It has to be a compliance office that files the waiver request. Why is a compliance officer the gatekeeper to an individual athlete’s relief? The whole system is ridiculous.
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Chas. Wolfe
Chas. Wolfe@highmajorscoop·
For those Evaluating Prospects in a LIVE Setting: Compliments of Dave Telep
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Daniel Poneman
Daniel Poneman@DanielPoneman·
“We’ve all seen many of the criticisms of NIL. People say ‘you’re giving these young guys all this money, they’re going to blow it. They don’t know what to do with it. They’re just going to waste it.’ We want to be the ones who buck that trend. We want to be the ones where they say, ‘no, you can’t say that about WEAVE guys… we don’t blow our money. We save our money. We invest our money. We make our money work for us.” @WEAVE
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Scott Schneider
Scott Schneider@EdLawDude·
Maybe the deeper problem is treating “college athletics” as one undifferentiated mass. The SEC, Big Ten, Big 12, Ivy League, Patriot League, SWAC, D-III, mid-majors, commuter schools, regional publics, and small privates are not operating the same enterprise. They should not all be forced into the same model. Some schools can and will compete in the professionalized, high-revenue version of college sports. Others should be able to build a different model around participation, education, campus life, Olympic sports, regional identity, and athlete development. The obsession with one national solution for “500,000 athletes” is part of what keeps making the problem worse.
BlindPass@pass_blind

@EdLawDude It’s the arms race prisoners dilemma we flame You have to agree that when $150 isn’t enough to maintain college athletics, you don’t blame the schools dragging the bottom

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Darren Heitner
Darren Heitner@heitner·
Three of Sports Law's most respected scholars, @MarcEdelman, @McCannSportsLaw, and John Holden, disagree with Cody Campbell's position that collective bargaining is not an option for college athletes. They demonstrate that employee status for at least some college athletes is all but inevitable under existing FLSA and NLRA frameworks, as confirmed by decisions in cases like Johnson v. NCAA and the Dartmouth basketball unionization effort. Instead of producing chaos, they say the path of collective bargaining will deliver stability because it can create a system all stakeholders can accept, facilitate reasonable dispute resolution, and preempt most antitrust litigation through established labor exemptions. Legislation is not the "only choice." But maybe Campbell knows more than leading Sports Law scholars.
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Amanda Christovich@achristovichh

Cody Campbell on collective bargaining: "That escape hatch does not exist. Legislation is our only choice."

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Darren Heitner
Darren Heitner@heitner·
Pre-2019: NCAA policy was that college athletes aren't like everyone else. They shouldn't be able to earn any money from their fame. 2019-2021: States enact laws to level the playing field and supersede the NCAA blanket prohibitions on the commercial exploitation of their #NIL. July 1, 2021: NCAA removes its blanket NIL prohibition, but intends to prohibit pay-for-play, inducements, and payments from schools to players. Includes a requirement that NIL agreements include quid pro quo. 2021-2026: Various lawsuits eliminate the NCAA's "guardrails," and the House settlement allows schools to pay players directly. June 18, 2026: Lawmakers consider legislation in the Protect College Sports Act that would eliminate many of the rights college athletes and their advocates have fought to receive through state governments and the judiciary. Let me be clear. If the federal government strips athletes of their rights, there will be litigation. I will not stop fighting to protect athletes against those who seek to impoverish them.
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Mit Winter
Mit Winter@WinterSportsLaw·
Anyone supporting the bill in its current form is completely selling out athletes, by creating a federally mandated cap on their compensation that goes beyond even the House settlement’s limits. This is a perfect example of why athletes need to be at the negotiating table.
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Ross Dellenger@RossDellenger

In an ambiguous section of the Protect College Sports Act, NIL deals with “associated entities” may count against the rev-share cap. While closing a loophole, this may limit athlete pay by “hundreds of millions” of dollars, stakeholders tell @YahooSports bit.ly/3QlnAKV

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Undiscovered World 48
Undiscovered World 48@undiscoverd48·
One month since the inaugural Undiscovered World 48 took over the National Basketball Arena in Ireland! 🇮🇪🏀 48 players from 22 countries 25 U.S. college coaches 1000+ streaming worldwide 🇮🇪🇱🇻🇸🇪🇭🇺🇧🇷🇫🇷🇷🇸🇺🇸🇩🇰🇽🇰🇬🇧 🇩🇪🇬🇷🇨🇭🇪🇸🇦🇹🇬🇪🏴󠁧󠁢󠁳󠁣󠁴󠁿🇵🇱🇱🇹🇸🇮🇧🇬 Where should we go next year?
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Undiscovered World 48
Undiscovered World 48@undiscoverd48·
🌎🧶🏀 BIG NEWS 🌎🧶🏀 Congratulations to World 48 attendee Colin Schroeder on his commitment to Fresno State! Colin earned this opportunity with an outstanding performance at Undiscovered World 48 in Ireland.
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Undiscovered World 48
Undiscovered World 48@undiscoverd48·
🌎🧶🏀 BIG NEWS 🌎🧶🏀 Congratulations to World 48 attendee Tristen Kuska on his commitment to the University at Buffalo! Tristen earned this opportunity with an outstanding performance at Undiscovered World 48 in Ireland.
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Daniel Poneman
Daniel Poneman@DanielPoneman·
My only NBA finals analysis is that I knew Jalen Brunson fairly well when he was in high school, and now run into him like once every 12 to 18 months at NBA events, and he is still consistently kind, humble, thoughtful and friendly. Ego has not visibly grown since he was 16. Real deal human being in public and private. Happy to see someone so deserving having so much success.
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Jeff Goodman
Jeff Goodman@GoodmanHoops·
Juwan Ekanga, a 6-6 combo guard from France, has committed to Gonzaga, @weave told @thefieldof68. The 18-year-old will play for Mark Few and the Zags this season. Considered by some as one of the most talented young players coming out of France.
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