https://www.spreaker.com/podcast/bizarre-medical-history--7195845
Join us for a fascinating exploration into the forgotten corners of medical history, from ancient remedies to the origins of modern surgery, revealing the incredible journeys and sometimes misguided attempts to heal. We delve into the lives of pioneering doctors, the patients who endured their treatments, and the fascinating evolution of healthcare. Discover the surprising origins of common medical terms and the groundbreaking (and sometimes terrifying) discoveries that shaped our understanding of the human body.

New episodes arrive every single day, Monday through Sunday, bright and early at 4:00 AM, offering a daily dose of medical oddities and historical insights. Each episode provides a meticulously researched narrative, perfect for your morning commute or daily routine.

This podcast is for anyone curious about the human body, the history of science, or simply enjoys a well-told story about humanity's quest for health. If you're intrigued by historical medicine, medical curiosities, and the strange path to modern healthcare, this is your ultimate destination.

Subscribe now to Bizarre Medical History and unlock the secrets of the past.]]>enTrue CrimeCopyright OBOMEDIA ENTERTAINMENThttps://d3wo5wojvuv7l.cloudfront.net/t_rss_itunes_square_1400/images.spreaker.com/original/e0677721a198bdd21f1ae73afd963f1c.jpghttps://www.spreaker.com/podcast/bizarre-medical-history--7195845Tue, 21 Jul 2026 23:42:14 +0000OBOMEDIA ENTERTAINMENTOBOMEDIA ENTERTAINMENTcreators@obomedia.comEver wondered about the strange cures, bizarre medical practices, and shocking experiments from history? Bizarre Medical History uncovers the most unbelievable and often disturbing chapters in the annals of medicine. Join us for a fascinating...
Join us for a fascinating exploration into the forgotten corners of medical history, from ancient remedies to the origins of modern surgery, revealing the incredible journeys and sometimes misguided attempts to heal. We delve into the lives of pioneering doctors, the patients who endured their treatments, and the fascinating evolution of healthcare. Discover the surprising origins of common medical terms and the groundbreaking (and sometimes terrifying) discoveries that shaped our understanding of the human body.

New episodes arrive every single day, Monday through Sunday, bright and early at 4:00 AM, offering a daily dose of medical oddities and historical insights. Each episode provides a meticulously researched narrative, perfect for your morning commute or daily routine.

This podcast is for anyone curious about the human body, the history of science, or simply enjoys a well-told story about humanity's quest for health. If you're intrigued by historical medicine, medical curiosities, and the strange path to modern healthcare, this is your ultimate destination.

Subscribe now to Bizarre Medical History and unlock the secrets of the past.]]>falseepisodichttps://www.spreaker.com/episode/the-drug-that-looked-real-simufilam-s-pixel-proofed-promise--73090293
Hope and doubt collided over a pattern of repeating pixels in a lab image, triggering retractions, sixteen million dollars in federal funding, and trials that enrolled hundreds of Alzheimer's patients - but what did those repeating pixels really mean for the people who took the drug? Which part of simufilam’s story was science, and which was something else?

In this episode, we trace the sequence of events that connected lab images, biomarker shifts, and clinical trials: how FLNA-based theory led to PTI-125 (renamed simufilam), why key experiments all came from a single research group, and how May 2020 biomarker failures were later reported as improvements - but by the same laboratory. What does that chain of evidence reveal about the drug and the trials?

Person: Hoau-Yan Wang
Company: Cassava Sciences
Drug: PTI-125 / simufilam
Funding: $16,000,000 federal
Date of confirmation: November 25, 2024

- Two scientific papers were retracted because the background pixels in western blot images looked too similar.
- Simufilam produced no clinical benefit and the program was discontinued as confirmed by Cassava Sciences on November 25, 2024.
- Sixteen million dollars in federal funding supported early clinical trials beginning after NIH funding in 2018.
- Biomarker results in May 2020 reported failure, then were reported as improved by September 2020, with the later results originating from the same laboratory.
- All key papers linking FLNA dysregulation and simufilam’s mechanism traced back to Hoau-Yan Wang's lab with no independent replication.

To listen to this podcast ad-free and access premium episodes, try our subscription with a 14-day free trial at obomedia.com.

© 2026 OBOMEDIA. All rights reserved.
This episode and its content (audio, text, and related materials) are the exclusive property of OBOMEDIA and are protected by applicable copyright laws. Reproduction, distribution, editing, or commercial use, in whole or in part, without prior written permission from OBOMEDIA is prohibited. For permissions, licensing, and business inquiries: business@obomedia.com.]]>https://api.spreaker.com/episode/73090293Tue, 21 Jul 2026 17:27:44 +0000OBOMEDIA ENTERTAINMENTThe Drug That Looked Real: Simufilam's Pixel-Proofed Promise Hope and doubt collided over a pattern of repeating pixels in a lab image, triggering retractions, sixteen million dollars in federal funding, and trials that enrolled hundreds of...
Hope and doubt collided over a pattern of repeating pixels in a lab image, triggering retractions, sixteen million dollars in federal funding, and trials that enrolled hundreds of Alzheimer's patients - but what did those repeating pixels really mean for the people who took the drug? Which part of simufilam’s story was science, and which was something else?

In this episode, we trace the sequence of events that connected lab images, biomarker shifts, and clinical trials: how FLNA-based theory led to PTI-125 (renamed simufilam), why key experiments all came from a single research group, and how May 2020 biomarker failures were later reported as improvements - but by the same laboratory. What does that chain of evidence reveal about the drug and the trials?

Person: Hoau-Yan Wang
Company: Cassava Sciences
Drug: PTI-125 / simufilam
Funding: $16,000,000 federal
Date of confirmation: November 25, 2024

- Two scientific papers were retracted because the background pixels in western blot images looked too similar.
- Simufilam produced no clinical benefit and the program was discontinued as confirmed by Cassava Sciences on November 25, 2024.
- Sixteen million dollars in federal funding supported early clinical trials beginning after NIH funding in 2018.
- Biomarker results in May 2020 reported failure, then were reported as improved by September 2020, with the later results originating from the same laboratory.
- All key papers linking FLNA dysregulation and simufilam’s mechanism traced back to Hoau-Yan Wang's lab with no independent replication.

To listen to this podcast ad-free and access premium episodes, try our subscription with a 14-day free trial at obomedia.com.

© 2026 OBOMEDIA. All rights reserved.
This episode and its content (audio, text, and related materials) are the exclusive property of OBOMEDIA and are protected by applicable copyright laws. Reproduction, distribution, editing, or commercial use, in whole or in part, without prior written permission from OBOMEDIA is prohibited. For permissions, licensing, and business inquiries: business@obomedia.com.]]>1420falsefullhttps://www.spreaker.com/episode/lab-printout-with-repeated-pixels-became-the-thread--73090292
The discovery that two western blot images were pixel-for-pixel identical - not similar, identical - triggered an unraveling that touched $16,000,000 in federal grants and sent hundreds of Alzheimer's patients into clinical trials. How could a microscopic flaw in image backgrounds help propel a drug to human trials, and what exactly remains unknown about the science behind it?

In this episode, we tell the sequence of events that followed that matched background pixels: the history of the academic collaboration, the drug candidate simufilam, the federal funding and clinical trials, and the unresolved questions left by conflicting expert opinions. How did a single laboratory's findings become the foundation for a treatment that showed no biomarker benefit in a phase IIb study?

Person: Hoau-Yan Wang
Person: Lindsay Burns
Company: Pain Therapeutics (later Cassava Sciences)
Compound: PTI-125 (simufilam)
Finding: phase IIb biomarker results failed two months after first patient dosing in March 2020

- The identical western blot pixels were detected in images that were supposed to represent different experiments on different days.
- $16,000,000 in federal grants were implicated as unraveling after the image discovery.
- Hundreds of Alzheimer's patients were enrolled in clinical trials of simufilam following the published research.
- All evidence supporting the filamin A - amyloid beta 42 mechanism came from Wang's laboratory at CUNY, with no independent replication reported.
- The phase IIb biomarker study reported results that did not show the expected biological improvement two months after dosing began in March 2020.

To listen to this podcast ad-free and access premium episodes, try our subscription with a 14-day free trial at obomedia.com.

© 2026 OBOMEDIA. All rights reserved.
This episode and its content (audio, text, and related materials) are the exclusive property of OBOMEDIA and are protected by applicable copyright laws. Reproduction, distribution, editing, or commercial use, in whole or in part, without prior written permission from OBOMEDIA is prohibited. For permissions, licensing, and business inquiries: business@obomedia.com.]]>https://api.spreaker.com/episode/73090292Tue, 21 Jul 2026 17:27:41 +0000OBOMEDIA ENTERTAINMENTlab printout with repeated pixels became the thread The discovery that two western blot images were pixel-for-pixel identical - not similar, identical - triggered an unraveling that touched $16,000,000 in federal grants and sent hundreds of...
The discovery that two western blot images were pixel-for-pixel identical - not similar, identical - triggered an unraveling that touched $16,000,000 in federal grants and sent hundreds of Alzheimer's patients into clinical trials. How could a microscopic flaw in image backgrounds help propel a drug to human trials, and what exactly remains unknown about the science behind it?

In this episode, we tell the sequence of events that followed that matched background pixels: the history of the academic collaboration, the drug candidate simufilam, the federal funding and clinical trials, and the unresolved questions left by conflicting expert opinions. How did a single laboratory's findings become the foundation for a treatment that showed no biomarker benefit in a phase IIb study?

Person: Hoau-Yan Wang
Person: Lindsay Burns
Company: Pain Therapeutics (later Cassava Sciences)
Compound: PTI-125 (simufilam)
Finding: phase IIb biomarker results failed two months after first patient dosing in March 2020

- The identical western blot pixels were detected in images that were supposed to represent different experiments on different days.
- $16,000,000 in federal grants were implicated as unraveling after the image discovery.
- Hundreds of Alzheimer's patients were enrolled in clinical trials of simufilam following the published research.
- All evidence supporting the filamin A - amyloid beta 42 mechanism came from Wang's laboratory at CUNY, with no independent replication reported.
- The phase IIb biomarker study reported results that did not show the expected biological improvement two months after dosing began in March 2020.

To listen to this podcast ad-free and access premium episodes, try our subscription with a 14-day free trial at obomedia.com.

© 2026 OBOMEDIA. All rights reserved.
This episode and its content (audio, text, and related materials) are the exclusive property of OBOMEDIA and are protected by applicable copyright laws. Reproduction, distribution, editing, or commercial use, in whole or in part, without prior written permission from OBOMEDIA is prohibited. For permissions, licensing, and business inquiries: business@obomedia.com.]]>1279falsefullhttps://www.spreaker.com/episode/the-quipazine-puzzle-tiny-dose-giant-psychedelic-question--73090290
A single bracketed word - "[sic]" - appeared next to a reported dose of 0.5 mg, implying someone claimed a mescaline-like effect from less than a grain of salt. Quipazine has been studied since 1966, produced LSD-like substitution in animals, and provoked projectile vomiting in primates; so what exactly does it do in the human brain?

In this episode, we trace quipazine’s scientific trail from 1966 through rodent and primate studies, the shifting labels from antidepressant to psychedelic candidate, and the locked doctoral thesis that may hold part of the answer - can one molecule explain both psychedelic and emetic effects at similar doses?

Person: researchers (unnamed) who reported 0.5 mg dose marked "[sic]"
Date: 1966 (first appearance in literature)
Event: 1977 animal studies documenting psychedelic-like behaviors
Topic: serotonin 2-A receptor activation (head-twitch response, ketanserin blockade)
Status: doctoral thesis under embargo until 2030

- Reported dose printed next to the notation "[sic]": 0.5 mg
- First appearance of quipazine in scientific literature: 1966
- By 1971 quipazine described as an antidepressant-like agent
- 1977 animal studies showed head-twitch response indicative of serotonin 2-A activation
- Primate studies produced LSD-like behaviors plus projectile vomiting, linking psychedelic and emetic effects

To listen to this podcast ad-free and access premium episodes, try our subscription with a 14-day free trial at obomedia.com.

© 2026 OBOMEDIA. All rights reserved.
This episode and its content (audio, text, and related materials) are the exclusive property of OBOMEDIA and are protected by applicable copyright laws. Reproduction, distribution, editing, or commercial use, in whole or in part, without prior written permission from OBOMEDIA is prohibited. For permissions, licensing, and business inquiries: business@obomedia.com.]]>https://api.spreaker.com/episode/73090290Tue, 21 Jul 2026 17:27:38 +0000OBOMEDIA ENTERTAINMENTThe Quipazine Puzzle: Tiny Dose, Giant Psychedelic Question A single bracketed word - "[sic]" - appeared next to a reported dose of 0.5 mg, implying someone claimed a mescaline-like effect from less than a grain of salt. Quipazine has been studied...
A single bracketed word - "[sic]" - appeared next to a reported dose of 0.5 mg, implying someone claimed a mescaline-like effect from less than a grain of salt. Quipazine has been studied since 1966, produced LSD-like substitution in animals, and provoked projectile vomiting in primates; so what exactly does it do in the human brain?

In this episode, we trace quipazine’s scientific trail from 1966 through rodent and primate studies, the shifting labels from antidepressant to psychedelic candidate, and the locked doctoral thesis that may hold part of the answer - can one molecule explain both psychedelic and emetic effects at similar doses?

Person: researchers (unnamed) who reported 0.5 mg dose marked "[sic]"
Date: 1966 (first appearance in literature)
Event: 1977 animal studies documenting psychedelic-like behaviors
Topic: serotonin 2-A receptor activation (head-twitch response, ketanserin blockade)
Status: doctoral thesis under embargo until 2030

- Reported dose printed next to the notation "[sic]": 0.5 mg
- First appearance of quipazine in scientific literature: 1966
- By 1971 quipazine described as an antidepressant-like agent
- 1977 animal studies showed head-twitch response indicative of serotonin 2-A activation
- Primate studies produced LSD-like behaviors plus projectile vomiting, linking psychedelic and emetic effects

To listen to this podcast ad-free and access premium episodes, try our subscription with a 14-day free trial at obomedia.com.

© 2026 OBOMEDIA. All rights reserved.
This episode and its content (audio, text, and related materials) are the exclusive property of OBOMEDIA and are protected by applicable copyright laws. Reproduction, distribution, editing, or commercial use, in whole or in part, without prior written permission from OBOMEDIA is prohibited. For permissions, licensing, and business inquiries: business@obomedia.com.]]>1904falsefullhttps://www.spreaker.com/episode/the-0-5-mg-mystery-why-quipazine-s-psychedelic-secret-remains-locked--73090289
A single notation - "0.5 mg [sic]" - sits in a published paper as a tiny flag of doubt that has gone unexplained for sixty years, attached to a compound tested in humans, animals, and written about by a meticulous twentieth-century chemist; can a drug that reliably causes nausea also hide a psychedelic action at 5-HT2A? What keeps this answer sealed until 2030?

In this episode, we trace the scientific record of quipazine from its chemical synthesis and antidepressant hopes in the 1960s and 1970s through human dosing trials that stopped at 25 mg for gastrointestinal reasons, and the contrasting animal evidence that produced robust head-twitch responses linked to 5-HT2A - how did these two paths diverge and what remains locked away in an unread thesis?

Person: one author noted "0.5 mg [sic]" beside a reported figure
Date: first described in scientific literature in 1966
Date: by 1971 characterized as an antidepressant-like agent
Dose: 25 mg given orally in human subjects produced nausea and GI symptoms
Response: head-twitch response observed in mice, rats, and monkeys and blocked by ketanserin

- The transcript states there are exactly three human data points for quipazine.
- Quipazine's formal chemical name is one-(two-quinolinyl)piperazine and was shortened to two-QP in the lab.
- At 25 mg orally, human subjects reported nausea, flatulence, gastrointestinal discomfort, and diarrhea with no psychedelic effects.
- Animal studies by 1977 documented a head-twitch response in rodents linked to 5-HT2A activation.
- A doctoral thesis containing key data on the question cannot be read until 2030.

To listen to this podcast ad-free and access premium episodes, try our subscription with a 14-day free trial at obomedia.com.

© 2026 OBOMEDIA. All rights reserved.
This episode and its content (audio, text, and related materials) are the exclusive property of OBOMEDIA and are protected by applicable copyright laws. Reproduction, distribution, editing, or commercial use, in whole or in part, without prior written permission from OBOMEDIA is prohibited. For permissions, licensing, and business inquiries: business@obomedia.com.]]>https://api.spreaker.com/episode/73090289Tue, 21 Jul 2026 17:27:34 +0000OBOMEDIA ENTERTAINMENTThe 0.5 mg Mystery: Why Quipazine's Psychedelic Secret Remains Locked A single notation - "0.5 mg [sic]" - sits in a published paper as a tiny flag of doubt that has gone unexplained for sixty years, attached to a compound tested in humans,...
A single notation - "0.5 mg [sic]" - sits in a published paper as a tiny flag of doubt that has gone unexplained for sixty years, attached to a compound tested in humans, animals, and written about by a meticulous twentieth-century chemist; can a drug that reliably causes nausea also hide a psychedelic action at 5-HT2A? What keeps this answer sealed until 2030?

In this episode, we trace the scientific record of quipazine from its chemical synthesis and antidepressant hopes in the 1960s and 1970s through human dosing trials that stopped at 25 mg for gastrointestinal reasons, and the contrasting animal evidence that produced robust head-twitch responses linked to 5-HT2A - how did these two paths diverge and what remains locked away in an unread thesis?

Person: one author noted "0.5 mg [sic]" beside a reported figure
Date: first described in scientific literature in 1966
Date: by 1971 characterized as an antidepressant-like agent
Dose: 25 mg given orally in human subjects produced nausea and GI symptoms
Response: head-twitch response observed in mice, rats, and monkeys and blocked by ketanserin

- The transcript states there are exactly three human data points for quipazine.
- Quipazine's formal chemical name is one-(two-quinolinyl)piperazine and was shortened to two-QP in the lab.
- At 25 mg orally, human subjects reported nausea, flatulence, gastrointestinal discomfort, and diarrhea with no psychedelic effects.
- Animal studies by 1977 documented a head-twitch response in rodents linked to 5-HT2A activation.
- A doctoral thesis containing key data on the question cannot be read until 2030.

To listen to this podcast ad-free and access premium episodes, try our subscription with a 14-day free trial at obomedia.com.

© 2026 OBOMEDIA. All rights reserved.
This episode and its content (audio, text, and related materials) are the exclusive property of OBOMEDIA and are protected by applicable copyright laws. Reproduction, distribution, editing, or commercial use, in whole or in part, without prior written permission from OBOMEDIA is prohibited. For permissions, licensing, and business inquiries: business@obomedia.com.]]>1865falsefullhttps://www.spreaker.com/episode/the-sic-mark-at-0-5-mg-why-quipazine-haunted-science--73090286
A single bracketed "sic" beside the dose 0.5 mg has haunted nearly six decades of literature on quipazine, a compound that behaves like a psychedelic in animals yet produced only severe gastrointestinal effects in humans-what really happened at that dose and why did editors leave the doubt standing? This episode follows the molecule from its 1966 entry into the literature to the conflicting animal and human records and asks whether the unresolved 0.5 mg notation obscures a missing human response.

In this episode, we trace quipazine's path through receptor studies, animal behaviors, primate reports and a human trial to lay out the precise mismatch between preclinical signals and clinical outcomes, and we return to the unresolved 0.5 mg entry to ask whether the literature ever answered its own question.

Person: quipazine
Date: 1966 (entry into literature)
Receptor: 5-HT3 and 5-HT2A/2B/2C
Event: 1977 animal studies documenting head-twitch response
Dose: 25 mg (first human trial, oral)

- Quipazine entered the scientific literature no later than 1966.
- By 1971 researchers labeled it "antidepressant-like" but it was never developed as an antidepressant.
- In 1977 animal studies showed a consistent head-twitch response blocked by ketanserin, indicating 5-HT2A activation.
- Drug discrimination studies found quipazine fully substituted for LSD and DOM, and animals trained on quipazine generalized to LSD, mescaline, and psilocybin.
- A human oral trial at 25 mg produced only nausea, flatulence, gastrointestinal discomfort and diarrhea, with no LSD-like visual or perceptual effects.

To listen to this podcast ad-free and access premium episodes, try our subscription with a 14-day free trial at obomedia.com.

© 2026 OBOMEDIA. All rights reserved.
This episode and its content (audio, text, and related materials) are the exclusive property of OBOMEDIA and are protected by applicable copyright laws. Reproduction, distribution, editing, or commercial use, in whole or in part, without prior written permission from OBOMEDIA is prohibited. For permissions, licensing, and business inquiries: business@obomedia.com.]]>https://api.spreaker.com/episode/73090286Tue, 21 Jul 2026 17:27:30 +0000OBOMEDIA ENTERTAINMENTThe Sic Mark at 0.5 mg: Why Quipazine Haunted Science A single bracketed "sic" beside the dose 0.5 mg has haunted nearly six decades of literature on quipazine, a compound that behaves like a psychedelic in animals yet produced only severe...
A single bracketed "sic" beside the dose 0.5 mg has haunted nearly six decades of literature on quipazine, a compound that behaves like a psychedelic in animals yet produced only severe gastrointestinal effects in humans-what really happened at that dose and why did editors leave the doubt standing? This episode follows the molecule from its 1966 entry into the literature to the conflicting animal and human records and asks whether the unresolved 0.5 mg notation obscures a missing human response.

In this episode, we trace quipazine's path through receptor studies, animal behaviors, primate reports and a human trial to lay out the precise mismatch between preclinical signals and clinical outcomes, and we return to the unresolved 0.5 mg entry to ask whether the literature ever answered its own question.

Person: quipazine
Date: 1966 (entry into literature)
Receptor: 5-HT3 and 5-HT2A/2B/2C
Event: 1977 animal studies documenting head-twitch response
Dose: 25 mg (first human trial, oral)

- Quipazine entered the scientific literature no later than 1966.
- By 1971 researchers labeled it "antidepressant-like" but it was never developed as an antidepressant.
- In 1977 animal studies showed a consistent head-twitch response blocked by ketanserin, indicating 5-HT2A activation.
- Drug discrimination studies found quipazine fully substituted for LSD and DOM, and animals trained on quipazine generalized to LSD, mescaline, and psilocybin.
- A human oral trial at 25 mg produced only nausea, flatulence, gastrointestinal discomfort and diarrhea, with no LSD-like visual or perceptual effects.

To listen to this podcast ad-free and access premium episodes, try our subscription with a 14-day free trial at obomedia.com.

© 2026 OBOMEDIA. All rights reserved.
This episode and its content (audio, text, and related materials) are the exclusive property of OBOMEDIA and are protected by applicable copyright laws. Reproduction, distribution, editing, or commercial use, in whole or in part, without prior written permission from OBOMEDIA is prohibited. For permissions, licensing, and business inquiries: business@obomedia.com.]]>1528falsefullhttps://www.spreaker.com/episode/the-single-secret-human-trip-that-animal-tests-couldn-t-predict--73090285
A single anonymous human report in 2007 claims a full psychedelic experience from a compound never approved for human use, yet every controlled human trial since produced only severe nausea and gastrointestinal distress. How did decades of animal data-head-twitches in mice, LSD-like responses in monkeys-fail to predict that human outcome?

In this episode, we present the history of quipazine from its first reports in 1966 through behavioral pharmacology in the 1970s and the halted human dosing that followed, and we ask why animal models missed a crucial human effect: could a structural limitation in common laboratory species explain the disconnect?

Person: anonymous human reporter (2007)
Period: 1966-2007 (literature and single human report)
Event: animal head-twitch response documented (1977)
Dose: 25 mg oral human trial produced intolerable nausea
Status: doctoral thesis on quipazine sealed until 2030

- Quipazine first appeared in the literature in 1966 as one-(2-quinolinyl)piperazine (2-QP).
- In 1977 quipazine reliably produced the head-twitch response in mice and rats, a marker of 5-HT2A activation.
- Rodent drug discrimination tests showed quipazine generalized to LSD, DOM, mescaline, and psilocybin.
- Primate studies showed LSD-like behavioral disruption but also projectile vomiting in monkeys.
- A human oral dose of 25 mg produced severe nausea, flatulence, gastrointestinal discomfort, and diarrhea with no reported psychedelic effects.

To listen to this podcast ad-free and access premium episodes, try our subscription with a 14-day free trial at obomedia.com.

© 2026 OBOMEDIA. All rights reserved.
This episode and its content (audio, text, and related materials) are the exclusive property of OBOMEDIA and are protected by applicable copyright laws. Reproduction, distribution, editing, or commercial use, in whole or in part, without prior written permission from OBOMEDIA is prohibited. For permissions, licensing, and business inquiries: business@obomedia.com.]]>https://api.spreaker.com/episode/73090285Tue, 21 Jul 2026 17:27:26 +0000OBOMEDIA ENTERTAINMENTThe Single Secret Human Trip That Animal Tests Couldn't Predict A single anonymous human report in 2007 claims a full psychedelic experience from a compound never approved for human use, yet every controlled human trial since produced only severe...
A single anonymous human report in 2007 claims a full psychedelic experience from a compound never approved for human use, yet every controlled human trial since produced only severe nausea and gastrointestinal distress. How did decades of animal data-head-twitches in mice, LSD-like responses in monkeys-fail to predict that human outcome?

In this episode, we present the history of quipazine from its first reports in 1966 through behavioral pharmacology in the 1970s and the halted human dosing that followed, and we ask why animal models missed a crucial human effect: could a structural limitation in common laboratory species explain the disconnect?

Person: anonymous human reporter (2007)
Period: 1966-2007 (literature and single human report)
Event: animal head-twitch response documented (1977)
Dose: 25 mg oral human trial produced intolerable nausea
Status: doctoral thesis on quipazine sealed until 2030

- Quipazine first appeared in the literature in 1966 as one-(2-quinolinyl)piperazine (2-QP).
- In 1977 quipazine reliably produced the head-twitch response in mice and rats, a marker of 5-HT2A activation.
- Rodent drug discrimination tests showed quipazine generalized to LSD, DOM, mescaline, and psilocybin.
- Primate studies showed LSD-like behavioral disruption but also projectile vomiting in monkeys.
- A human oral dose of 25 mg produced severe nausea, flatulence, gastrointestinal discomfort, and diarrhea with no reported psychedelic effects.

To listen to this podcast ad-free and access premium episodes, try our subscription with a 14-day free trial at obomedia.com.

© 2026 OBOMEDIA. All rights reserved.
This episode and its content (audio, text, and related materials) are the exclusive property of OBOMEDIA and are protected by applicable copyright laws. Reproduction, distribution, editing, or commercial use, in whole or in part, without prior written permission from OBOMEDIA is prohibited. For permissions, licensing, and business inquiries: business@obomedia.com.]]>1663falsefullhttps://www.spreaker.com/episode/the-molecule-that-vomited-its-way-out-of-human-psychedelia--73090284
A single physiological reflex stood between decades of animal evidence and human confirmation: a molecule that triggered both psychedelic-linked behavior and uncontrollable vomiting. Quipazine activated the same serotonin receptor tied to psychedelic head-twitches in mice and LSD-like effects in monkeys - so why did human trials report sickness instead of altered consciousness?

In this episode, we tell the sequence of experiments, publications and unanswered gaps that surround quipazine, and we follow the thread from 1977 mouse studies to 2011 archival notes and a 2025 doctoral thesis that remains embargoed; what did the vomiting hide about quipazine's effects?

Person: Alexander Shulgin
Person: Yilun Yang
Date: 1977
Date: 2011
Event: human trials administering 25 mg of quipazine

- 1977: researchers first documented the head-twitch response in mice linked to psychedelic drug action.
- Quipazine fully substituted for LSD, mescaline and psilocybin in animal drug discrimination studies.
- In primate studies quipazine produced LSD-like agitation and disrupted behavior alongside projectile vomiting.
- 2011: Alexander Shulgin published a brief account of a 2007 experiment in The Shulgin Index with no subject name or institutional affiliation.
- 2025: a doctoral thesis by Yilun Yang on quipazine and its analogs was completed and will remain unavailable until 2030.

To listen to this podcast ad-free and access premium episodes, try our subscription with a 14-day free trial at obomedia.com.

© 2026 OBOMEDIA. All rights reserved.
This episode and its content (audio, text, and related materials) are the exclusive property of OBOMEDIA and are protected by applicable copyright laws. Reproduction, distribution, editing, or commercial use, in whole or in part, without prior written permission from OBOMEDIA is prohibited. For permissions, licensing, and business inquiries: business@obomedia.com.]]>https://api.spreaker.com/episode/73090284Tue, 21 Jul 2026 17:27:23 +0000OBOMEDIA ENTERTAINMENTThe Molecule That Vomited Its Way Out of Human Psychedelia A single physiological reflex stood between decades of animal evidence and human confirmation: a molecule that triggered both psychedelic-linked behavior and uncontrollable vomiting....
A single physiological reflex stood between decades of animal evidence and human confirmation: a molecule that triggered both psychedelic-linked behavior and uncontrollable vomiting. Quipazine activated the same serotonin receptor tied to psychedelic head-twitches in mice and LSD-like effects in monkeys - so why did human trials report sickness instead of altered consciousness?

In this episode, we tell the sequence of experiments, publications and unanswered gaps that surround quipazine, and we follow the thread from 1977 mouse studies to 2011 archival notes and a 2025 doctoral thesis that remains embargoed; what did the vomiting hide about quipazine's effects?

Person: Alexander Shulgin
Person: Yilun Yang
Date: 1977
Date: 2011
Event: human trials administering 25 mg of quipazine

- 1977: researchers first documented the head-twitch response in mice linked to psychedelic drug action.
- Quipazine fully substituted for LSD, mescaline and psilocybin in animal drug discrimination studies.
- In primate studies quipazine produced LSD-like agitation and disrupted behavior alongside projectile vomiting.
- 2011: Alexander Shulgin published a brief account of a 2007 experiment in The Shulgin Index with no subject name or institutional affiliation.
- 2025: a doctoral thesis by Yilun Yang on quipazine and its analogs was completed and will remain unavailable until 2030.

To listen to this podcast ad-free and access premium episodes, try our subscription with a 14-day free trial at obomedia.com.

© 2026 OBOMEDIA. All rights reserved.
This episode and its content (audio, text, and related materials) are the exclusive property of OBOMEDIA and are protected by applicable copyright laws. Reproduction, distribution, editing, or commercial use, in whole or in part, without prior written permission from OBOMEDIA is prohibited. For permissions, licensing, and business inquiries: business@obomedia.com.]]>1809falsefullhttps://www.spreaker.com/episode/the-psychedelic-that-vomited-its-way-out-of-science--73090283
A single three-character annotation - "0.5 mg (sic)" - sits in a scientific paper and betrays sixty years of pharmacology: a compound with consistent animal evidence for psychedelic action that never produced psychedelic effects in humans because it makes people violently ill. How did quipazine become a standard reference drug in animal studies yet remain effectively undtestable in people?

In this episode, we trace quipazine’s origin, its unexpected behavioral effects in rodents and primates, and the pharmacological barrier that stopped human research - and we ask whether a simple receptor blocker could have changed the course of study.

Person: Jerrold C. Winter
Period: 1966-1994 (key developments noted)
Compound: quipazine (one-(two-quinolinyl)piperazine; two-QP)
Trial Dose: 25 mg (human oral trial reported nausea and gastrointestinal effects)
Intervention Proposed: ondansetron (1994 hypothesis to block 5-HT3)

- Quipazine was first described in 1966 and by 1971 was characterized as an antidepressant-like agent.
- By 1977 mice, rats, and monkeys showed consistent head-twitch responses and monkeys displayed LSD-like behavior with projectile vomiting.
- Quipazine’s dominant action at practical oral doses is potent 5-HT3 receptor agonism, which causes nausea and vomiting rather than altered consciousness.
- A 25 mg human oral trial produced nausea, flatulence, gastrointestinal discomfort, and diarrhea with no LSD-like subjective effects observed.
- In 1994 Jerrold C. Winter proposed using ondansetron, a 5-HT3 antagonist, to block emesis and reveal quipazine’s potential 5-HT2A-mediated psychedelic effects, but no controlled human trial followed.

To listen to this podcast ad-free and access premium episodes, try our subscription with a 14-day free trial at obomedia.com.

© 2026 OBOMEDIA. All rights reserved.
This episode and its content (audio, text, and related materials) are the exclusive property of OBOMEDIA and are protected by applicable copyright laws. Reproduction, distribution, editing, or commercial use, in whole or in part, without prior written permission from OBOMEDIA is prohibited. For permissions, licensing, and business inquiries: business@obomedia.com.]]>https://api.spreaker.com/episode/73090283Tue, 21 Jul 2026 17:27:19 +0000OBOMEDIA ENTERTAINMENTThe Psychedelic That Vomited Its Way Out of Science A single three-character annotation - "0.5 mg (sic)" - sits in a scientific paper and betrays sixty years of pharmacology: a compound with consistent animal evidence for psychedelic action that...
A single three-character annotation - "0.5 mg (sic)" - sits in a scientific paper and betrays sixty years of pharmacology: a compound with consistent animal evidence for psychedelic action that never produced psychedelic effects in humans because it makes people violently ill. How did quipazine become a standard reference drug in animal studies yet remain effectively undtestable in people?

In this episode, we trace quipazine’s origin, its unexpected behavioral effects in rodents and primates, and the pharmacological barrier that stopped human research - and we ask whether a simple receptor blocker could have changed the course of study.

Person: Jerrold C. Winter
Period: 1966-1994 (key developments noted)
Compound: quipazine (one-(two-quinolinyl)piperazine; two-QP)
Trial Dose: 25 mg (human oral trial reported nausea and gastrointestinal effects)
Intervention Proposed: ondansetron (1994 hypothesis to block 5-HT3)

- Quipazine was first described in 1966 and by 1971 was characterized as an antidepressant-like agent.
- By 1977 mice, rats, and monkeys showed consistent head-twitch responses and monkeys displayed LSD-like behavior with projectile vomiting.
- Quipazine’s dominant action at practical oral doses is potent 5-HT3 receptor agonism, which causes nausea and vomiting rather than altered consciousness.
- A 25 mg human oral trial produced nausea, flatulence, gastrointestinal discomfort, and diarrhea with no LSD-like subjective effects observed.
- In 1994 Jerrold C. Winter proposed using ondansetron, a 5-HT3 antagonist, to block emesis and reveal quipazine’s potential 5-HT2A-mediated psychedelic effects, but no controlled human trial followed.

To listen to this podcast ad-free and access premium episodes, try our subscription with a 14-day free trial at obomedia.com.

© 2026 OBOMEDIA. All rights reserved.
This episode and its content (audio, text, and related materials) are the exclusive property of OBOMEDIA and are protected by applicable copyright laws. Reproduction, distribution, editing, or commercial use, in whole or in part, without prior written permission from OBOMEDIA is prohibited. For permissions, licensing, and business inquiries: business@obomedia.com.]]>1795falsefullhttps://www.spreaker.com/episode/the-drug-that-made-champions-and-secretly-gave-them-cancer--73090281
Fear and fascination collide: a drug that turned muscles into fat-burning engines and boosted endurance was also linked to widespread cancer in animal tests, yet it resurfaced on the black market for $1,000 per ten grams-how did it reach elite athletes despite an internal pharmaceutical shutdown? What happened in the six-year gap between GlaxoSmithKline’s 2007 discontinuation and WADA’s 2013 cancer warning that allowed GW501516 to spread through sport?

In this episode, we trace the compound’s path from a genetics lab to the podium and the grey market, charting the scientific breakthroughs, the unpublished cancer data, and the cases that reveal who paid the price for performance. How did a selective PPARδ agonist celebrated in Cell become a hidden public health threat?

Person: Ronald M. Evans
Date: 1992
Date: 2007
Event: Vuelta Ciclista a Costa Rica positive tests
Price: $1,000 per ten grams

- GW501516 had a binding affinity around one nanomolar and more than 1,000-fold selectivity over related receptors.
- GlaxoSmithKline discontinued development in 2007 after animal studies showed cancer at 3 mg/kg/day in mice and rats across multiple organs.
- A 2001 Phase One human trial and a 2001 PNAS paper were published; a Cell paper in 2007 reported extreme endurance gains in mice.
- By 2009 WADA had banned GW501516 before any athlete had been publicly caught using it.
- In December 2012 four Costa Rican cyclists tested positive for GW501516; three received two-year bans and one received a twelve-year ban.

To listen to this podcast ad-free and access premium episodes, try our subscription with a 14-day free trial at obomedia.com.

© 2026 OBOMEDIA. All rights reserved.
This episode and its content (audio, text, and related materials) are the exclusive property of OBOMEDIA and are protected by applicable copyright laws. Reproduction, distribution, editing, or commercial use, in whole or in part, without prior written permission from OBOMEDIA is prohibited. For permissions, licensing, and business inquiries: business@obomedia.com.]]>https://api.spreaker.com/episode/73090281Tue, 21 Jul 2026 17:27:15 +0000OBOMEDIA ENTERTAINMENTThe Drug That Made Champions - and Secretly Gave Them Cancer Fear and fascination collide: a drug that turned muscles into fat-burning engines and boosted endurance was also linked to widespread cancer in animal tests, yet it resurfaced on the...
Fear and fascination collide: a drug that turned muscles into fat-burning engines and boosted endurance was also linked to widespread cancer in animal tests, yet it resurfaced on the black market for $1,000 per ten grams-how did it reach elite athletes despite an internal pharmaceutical shutdown? What happened in the six-year gap between GlaxoSmithKline’s 2007 discontinuation and WADA’s 2013 cancer warning that allowed GW501516 to spread through sport?

In this episode, we trace the compound’s path from a genetics lab to the podium and the grey market, charting the scientific breakthroughs, the unpublished cancer data, and the cases that reveal who paid the price for performance. How did a selective PPARδ agonist celebrated in Cell become a hidden public health threat?

Person: Ronald M. Evans
Date: 1992
Date: 2007
Event: Vuelta Ciclista a Costa Rica positive tests
Price: $1,000 per ten grams

- GW501516 had a binding affinity around one nanomolar and more than 1,000-fold selectivity over related receptors.
- GlaxoSmithKline discontinued development in 2007 after animal studies showed cancer at 3 mg/kg/day in mice and rats across multiple organs.
- A 2001 Phase One human trial and a 2001 PNAS paper were published; a Cell paper in 2007 reported extreme endurance gains in mice.
- By 2009 WADA had banned GW501516 before any athlete had been publicly caught using it.
- In December 2012 four Costa Rican cyclists tested positive for GW501516; three received two-year bans and one received a twelve-year ban.

To listen to this podcast ad-free and access premium episodes, try our subscription with a 14-day free trial at obomedia.com.

© 2026 OBOMEDIA. All rights reserved.
This episode and its content (audio, text, and related materials) are the exclusive property of OBOMEDIA and are protected by applicable copyright laws. Reproduction, distribution, editing, or commercial use, in whole or in part, without prior written permission from OBOMEDIA is prohibited. For permissions, licensing, and business inquiries: business@obomedia.com.]]>1702falsefullhttps://www.spreaker.com/episode/the-sleeping-pill-that-vanished-the-molecule-no-pharma-could-explain--73090280
A legal drug derived from a poisonous mushroom promised deeper, more restorative sleep without morning sedation - yet it never reached a pharmacy shelf. Gaboxadol traced from Amanita muscaria to a synthetic analog with potency 30-100 times its parent, produced Phase Three hopes and then disappeared; what in the clinical record made companies walk away?

In this episode, we tell the sequence of events from discovery to late-stage trials, showing how a compound moved from forest lore to lab patent to multinational development and then to abandonment, and we ask whether the decision to stop was science, business, or something else.

Person: Povl Krogsgaard-Larsen
Date: 1977
Location: Denmark
Company: Lundbeck
Development code: MK-0928

- The active natural compound is muscimol from Amanita muscaria.
- Gaboxadol was synthesized in 1977 and patented in 1978, patent granted in 1981 with Lundbeck as assignee.
- Gaboxadol’s potency was estimated at 30 to 100 times greater than muscimol.
- In 1997 a human clinical sleep study showed 5-20 mg doses reduced sleep onset, increased slow wave activity, preserved REM, and produced no next-morning sedation.
- In Phase Three development with Merck (MK-0928), three-month trials showed initial improvement that faded by month three, and misuse-liability testing at higher doses produced concerning dose-response data.

To listen to this podcast ad-free and access premium episodes, try our subscription with a 14-day free trial at obomedia.com.

© 2026 OBOMEDIA. All rights reserved.
This episode and its content (audio, text, and related materials) are the exclusive property of OBOMEDIA and are protected by applicable copyright laws. Reproduction, distribution, editing, or commercial use, in whole or in part, without prior written permission from OBOMEDIA is prohibited. For permissions, licensing, and business inquiries: business@obomedia.com.]]>https://api.spreaker.com/episode/73090280Tue, 21 Jul 2026 17:27:12 +0000OBOMEDIA ENTERTAINMENTThe Sleeping Pill That Vanished: The Molecule No Pharma Could Explain A legal drug derived from a poisonous mushroom promised deeper, more restorative sleep without morning sedation - yet it never reached a pharmacy shelf. Gaboxadol traced from...
A legal drug derived from a poisonous mushroom promised deeper, more restorative sleep without morning sedation - yet it never reached a pharmacy shelf. Gaboxadol traced from Amanita muscaria to a synthetic analog with potency 30-100 times its parent, produced Phase Three hopes and then disappeared; what in the clinical record made companies walk away?

In this episode, we tell the sequence of events from discovery to late-stage trials, showing how a compound moved from forest lore to lab patent to multinational development and then to abandonment, and we ask whether the decision to stop was science, business, or something else.

Person: Povl Krogsgaard-Larsen
Date: 1977
Location: Denmark
Company: Lundbeck
Development code: MK-0928

- The active natural compound is muscimol from Amanita muscaria.
- Gaboxadol was synthesized in 1977 and patented in 1978, patent granted in 1981 with Lundbeck as assignee.
- Gaboxadol’s potency was estimated at 30 to 100 times greater than muscimol.
- In 1997 a human clinical sleep study showed 5-20 mg doses reduced sleep onset, increased slow wave activity, preserved REM, and produced no next-morning sedation.
- In Phase Three development with Merck (MK-0928), three-month trials showed initial improvement that faded by month three, and misuse-liability testing at higher doses produced concerning dose-response data.

To listen to this podcast ad-free and access premium episodes, try our subscription with a 14-day free trial at obomedia.com.

© 2026 OBOMEDIA. All rights reserved.
This episode and its content (audio, text, and related materials) are the exclusive property of OBOMEDIA and are protected by applicable copyright laws. Reproduction, distribution, editing, or commercial use, in whole or in part, without prior written permission from OBOMEDIA is prohibited. For permissions, licensing, and business inquiries: business@obomedia.com.]]>1655falsefullhttps://www.spreaker.com/episode/the-sleep-drug-that-came-from-a-poisonous-mushroom-and-vanished--73090279
A single molecule traced from a poisonous mushroom to a patent in 1981 promised a new kind of sleep drug with a novel target on GABA-A receptors, yet it never reached patients-why did a compound that decreased lethality by over 14-fold and increased affinity for the extrasynaptic delta-subunit disappear? What happened to gaboxadol between Danish labs, hundreds of trials, and abandoned pediatric studies?

In this episode, you will hear the story of gaboxadol from its discovery through decades of clinical trials, the companies and researchers involved, and the surprising clinical signals that alternately excited and stalled its development. We follow the chemistry from muscimol to THIP and track the key findings that kept reopening-and then closing-the molecule's pathways to market.

Person: Povl Krogsgaard-Larsen
Date: 1977 (origin of idea), 1978 (patent filed), 1981 (patent granted)
Author: H. Lundbeck A/S (patent assignee)
Topic: Gaboxadol (THIP), a direct GABA-A orthosteric agonist
Period: Trials spanning 1980s through 2021

- LD50 in mice for muscimol: 22 mg/kg
- LD50 in mice for gaboxadol: >320 mg/kg
- Gaboxadol had roughly 10x greater affinity for the extrasynaptic delta-subunit than existing drugs
- Patent filed in 1978 and granted in 1981 with Lundbeck as assignee
- Clinical programs tested gaboxadol for pain, anxiety, schizophrenia, epilepsy and sleep across hundreds of human trials

To listen to this podcast ad-free and access premium episodes, try our subscription with a 14-day free trial at obomedia.com.

© 2026 OBOMEDIA. All rights reserved.
This episode and its content (audio, text, and related materials) are the exclusive property of OBOMEDIA and are protected by applicable copyright laws. Reproduction, distribution, editing, or commercial use, in whole or in part, without prior written permission from OBOMEDIA is prohibited. For permissions, licensing, and business inquiries: business@obomedia.com.]]>https://api.spreaker.com/episode/73090279Tue, 21 Jul 2026 17:27:08 +0000OBOMEDIA ENTERTAINMENTThe Sleep Drug That Came From a Poisonous Mushroom-and Vanished A single molecule traced from a poisonous mushroom to a patent in 1981 promised a new kind of sleep drug with a novel target on GABA-A receptors, yet it never reached patients-why did...
A single molecule traced from a poisonous mushroom to a patent in 1981 promised a new kind of sleep drug with a novel target on GABA-A receptors, yet it never reached patients-why did a compound that decreased lethality by over 14-fold and increased affinity for the extrasynaptic delta-subunit disappear? What happened to gaboxadol between Danish labs, hundreds of trials, and abandoned pediatric studies?

In this episode, you will hear the story of gaboxadol from its discovery through decades of clinical trials, the companies and researchers involved, and the surprising clinical signals that alternately excited and stalled its development. We follow the chemistry from muscimol to THIP and track the key findings that kept reopening-and then closing-the molecule's pathways to market.

Person: Povl Krogsgaard-Larsen
Date: 1977 (origin of idea), 1978 (patent filed), 1981 (patent granted)
Author: H. Lundbeck A/S (patent assignee)
Topic: Gaboxadol (THIP), a direct GABA-A orthosteric agonist
Period: Trials spanning 1980s through 2021

- LD50 in mice for muscimol: 22 mg/kg
- LD50 in mice for gaboxadol: >320 mg/kg
- Gaboxadol had roughly 10x greater affinity for the extrasynaptic delta-subunit than existing drugs
- Patent filed in 1978 and granted in 1981 with Lundbeck as assignee
- Clinical programs tested gaboxadol for pain, anxiety, schizophrenia, epilepsy and sleep across hundreds of human trials

To listen to this podcast ad-free and access premium episodes, try our subscription with a 14-day free trial at obomedia.com.

© 2026 OBOMEDIA. All rights reserved.
This episode and its content (audio, text, and related materials) are the exclusive property of OBOMEDIA and are protected by applicable copyright laws. Reproduction, distribution, editing, or commercial use, in whole or in part, without prior written permission from OBOMEDIA is prohibited. For permissions, licensing, and business inquiries: business@obomedia.com.]]>1806falsefullhttps://www.spreaker.com/episode/the-urine-hormone-that-fooled-medicine-for-decades--73090277
Estrone, a hormone crystallized from pregnant women's urine in 1929, became a worldwide prescribed injection within months despite binding estrogen receptors at only about 4% the affinity of estradiol. How could a weak molecule produce dramatic restoration of tissue and symptoms - and why did its true mechanism remain hidden for decades?

In this episode, we tell how researchers moved from lab flasks to pharmacy ampoules in under two years, what clinicians observed in ovariectomized women after injection, and the unresolved question that kept medicine misled: if estrone was so weak at receptors, what was actually driving the clinical effects?

Person: Bernhard Zondek and Selmar Aschheim
Date: 1927-1929
Event: Isolation and commercialization of crystalline estrone
Product: Amniotin (Squibb), Progynon (Schering), Theelin (Parke-Davis)
Topic: Estrogen replacement after ovariectomy

- In 1927 Zondek and Aschheim discovered large quantities of estrogen in pregnant women's urine.
- Pure crystalline estrone was isolated by multiple teams in 1929 and characterized that same year.
- Three pharmaceutical companies launched estrone oil-solution ampoules for intramuscular injection in 1929.
- Clinical records from the early 1930s show restored breast, endometrial, and vaginal tissue and relief of hot flashes after estrone injections.
- Estrone binds estrogen receptors with about 4% of the affinity of estradiol, a discrepancy unexplained at the time.

To listen to this podcast ad-free and access premium episodes, try our subscription with a 14-day free trial at obomedia.com.

© 2026 OBOMEDIA. All rights reserved.
This episode and its content (audio, text, and related materials) are the exclusive property of OBOMEDIA and are protected by applicable copyright laws. Reproduction, distribution, editing, or commercial use, in whole or in part, without prior written permission from OBOMEDIA is prohibited. For permissions, licensing, and business inquiries: business@obomedia.com.]]>https://api.spreaker.com/episode/73090277Tue, 21 Jul 2026 17:27:04 +0000OBOMEDIA ENTERTAINMENTThe Urine Hormone That Fooled Medicine for Decades Estrone, a hormone crystallized from pregnant women's urine in 1929, became a worldwide prescribed injection within months despite binding estrogen receptors at only about 4% the affinity of...
Estrone, a hormone crystallized from pregnant women's urine in 1929, became a worldwide prescribed injection within months despite binding estrogen receptors at only about 4% the affinity of estradiol. How could a weak molecule produce dramatic restoration of tissue and symptoms - and why did its true mechanism remain hidden for decades?

In this episode, we tell how researchers moved from lab flasks to pharmacy ampoules in under two years, what clinicians observed in ovariectomized women after injection, and the unresolved question that kept medicine misled: if estrone was so weak at receptors, what was actually driving the clinical effects?

Person: Bernhard Zondek and Selmar Aschheim
Date: 1927-1929
Event: Isolation and commercialization of crystalline estrone
Product: Amniotin (Squibb), Progynon (Schering), Theelin (Parke-Davis)
Topic: Estrogen replacement after ovariectomy

- In 1927 Zondek and Aschheim discovered large quantities of estrogen in pregnant women's urine.
- Pure crystalline estrone was isolated by multiple teams in 1929 and characterized that same year.
- Three pharmaceutical companies launched estrone oil-solution ampoules for intramuscular injection in 1929.
- Clinical records from the early 1930s show restored breast, endometrial, and vaginal tissue and relief of hot flashes after estrone injections.
- Estrone binds estrogen receptors with about 4% of the affinity of estradiol, a discrepancy unexplained at the time.

To listen to this podcast ad-free and access premium episodes, try our subscription with a 14-day free trial at obomedia.com.

© 2026 OBOMEDIA. All rights reserved.
This episode and its content (audio, text, and related materials) are the exclusive property of OBOMEDIA and are protected by applicable copyright laws. Reproduction, distribution, editing, or commercial use, in whole or in part, without prior written permission from OBOMEDIA is prohibited. For permissions, licensing, and business inquiries: business@obomedia.com.]]>1603falsefullhttps://www.spreaker.com/episode/the-urine-cure-how-pregnant-vials-became-the-first-hormone-drug--73090276
A vial of urine from a pregnant woman became the world’s first commercial hormone medicine in 1929, and that drug worked well enough to restore menstruation, reverse atrophy, and stop hot flashes - but the active molecule was later measured at only about 4% the potency of the body’s main estrogen. How did a supposedly weak compound produce such clear clinical reversals, and what did that mismatch mean for patients and pharmaceuticals?

In this episode, we tell the episode’s story from laboratory observation to commercial product, following the scientists, surgeries, and medicines involved, and we ask how a treatment could function widely for decades when its biochemical explanation was wrong. What gap between chemistry and clinical effect went unrecognized for nearly a century?

Person: Selmar Aschheim
Person: Bernhard Zondek
Date: 1929
Event: Commercial release of Amniotin, Progynon, Theelin
Topic: Estrone isolated from pregnant urine

- 1929: a researcher in Berlin injected urine from a pregnant woman into a patient with no hormone production and observed symptom reversal.
- 1929: three commercial preparations reached the market the same year - Amniotin, Progynon, and Theelin.
- Approximately 4%: estrone’s measured estrogenic activity relative to estradiol.
- Surgical context: women who had undergone ovariectomy experienced abrupt hormonal deprivation and rapid onset of menopause-like symptoms.
- Clinical effects documented: return of menstruation, breast tissue response, and cessation of hot flashes after estrone administration.

To listen to this podcast ad-free and access premium episodes, try our subscription with a 14-day free trial at obomedia.com.

© 2026 OBOMEDIA. All rights reserved.
This episode and its content (audio, text, and related materials) are the exclusive property of OBOMEDIA and are protected by applicable copyright laws. Reproduction, distribution, editing, or commercial use, in whole or in part, without prior written permission from OBOMEDIA is prohibited. For permissions, licensing, and business inquiries: business@obomedia.com.]]>https://api.spreaker.com/episode/73090276Tue, 21 Jul 2026 17:27:01 +0000OBOMEDIA ENTERTAINMENTThe Urine Cure: How Pregnant Vials Became the First Hormone Drug A vial of urine from a pregnant woman became the world’s first commercial hormone medicine in 1929, and that drug worked well enough to restore menstruation, reverse atrophy, and stop...
A vial of urine from a pregnant woman became the world’s first commercial hormone medicine in 1929, and that drug worked well enough to restore menstruation, reverse atrophy, and stop hot flashes - but the active molecule was later measured at only about 4% the potency of the body’s main estrogen. How did a supposedly weak compound produce such clear clinical reversals, and what did that mismatch mean for patients and pharmaceuticals?

In this episode, we tell the episode’s story from laboratory observation to commercial product, following the scientists, surgeries, and medicines involved, and we ask how a treatment could function widely for decades when its biochemical explanation was wrong. What gap between chemistry and clinical effect went unrecognized for nearly a century?

Person: Selmar Aschheim
Person: Bernhard Zondek
Date: 1929
Event: Commercial release of Amniotin, Progynon, Theelin
Topic: Estrone isolated from pregnant urine

- 1929: a researcher in Berlin injected urine from a pregnant woman into a patient with no hormone production and observed symptom reversal.
- 1929: three commercial preparations reached the market the same year - Amniotin, Progynon, and Theelin.
- Approximately 4%: estrone’s measured estrogenic activity relative to estradiol.
- Surgical context: women who had undergone ovariectomy experienced abrupt hormonal deprivation and rapid onset of menopause-like symptoms.
- Clinical effects documented: return of menstruation, breast tissue response, and cessation of hot flashes after estrone administration.

To listen to this podcast ad-free and access premium episodes, try our subscription with a 14-day free trial at obomedia.com.

© 2026 OBOMEDIA. All rights reserved.
This episode and its content (audio, text, and related materials) are the exclusive property of OBOMEDIA and are protected by applicable copyright laws. Reproduction, distribution, editing, or commercial use, in whole or in part, without prior written permission from OBOMEDIA is prohibited. For permissions, licensing, and business inquiries: business@obomedia.com.]]>1520falsefullhttps://www.spreaker.com/episode/the-drug-that-never-left-how-one-injection-outlived-its-patients--73090275
A single intramuscular oil injection of one hundred milligrams could result in estradiol levels averaging 598 pg/mL at trough - roughly 17 times the normal male upper limit - and yet this compound was used for decades across Europe and Japan. How did a molecule designed to solve adherence become a lingering source of harm, and why did screened low-risk patients still suffer widespread cardiovascular complications?

In this episode, we narrate the clinical history and biochemical design of estradiol undecylate, outline its adoption in multiple countries and indications, and follow the Mainz Trial that revealed unexpected cardiovascular risk. What happened when a drug built to last simply would not leave?

Compound: estradiol undecylate
Inventor: Karl Junkmann
First clinical use: 1956
Patent filed: 1958, granted 1961
Mainz Trial enrollment: 191 men (subgroup of 42 men ages 51-84, mean age 68)

- A single 100 mg intramuscular dose was intended as a monthly injection but produced mean trough estradiol of 598 pg/mL.
- The normal male upper limit for estradiol cited in the records is 35 pg/mL.
- Estradiol undecylate was used clinically in France, Germany, the United Kingdom, Monaco, the Netherlands, Switzerland, and Japan.
- In one clinical trial run on medically screened cardiovascular low-risk men, 76% suffered cardiovascular complications.
- The Mainz Trial randomized 191 men with prostate cancer to 100 mg/month estradiol undecylate versus 300 mg/week cyproterone acetate, excluding patients with pre-existing cardiovascular disease.

To listen to this podcast ad-free and access premium episodes, try our subscription with a 14-day free trial at obomedia.com.

© 2026 OBOMEDIA. All rights reserved.
This episode and its content (audio, text, and related materials) are the exclusive property of OBOMEDIA and are protected by applicable copyright laws. Reproduction, distribution, editing, or commercial use, in whole or in part, without prior written permission from OBOMEDIA is prohibited. For permissions, licensing, and business inquiries: business@obomedia.com.]]>https://api.spreaker.com/episode/73090275Tue, 21 Jul 2026 17:26:57 +0000OBOMEDIA ENTERTAINMENTThe Drug That Never Left: How One Injection Outlived Its Patients A single intramuscular oil injection of one hundred milligrams could result in estradiol levels averaging 598 pg/mL at trough - roughly 17 times the normal male upper limit - and yet...
A single intramuscular oil injection of one hundred milligrams could result in estradiol levels averaging 598 pg/mL at trough - roughly 17 times the normal male upper limit - and yet this compound was used for decades across Europe and Japan. How did a molecule designed to solve adherence become a lingering source of harm, and why did screened low-risk patients still suffer widespread cardiovascular complications?

In this episode, we narrate the clinical history and biochemical design of estradiol undecylate, outline its adoption in multiple countries and indications, and follow the Mainz Trial that revealed unexpected cardiovascular risk. What happened when a drug built to last simply would not leave?

Compound: estradiol undecylate
Inventor: Karl Junkmann
First clinical use: 1956
Patent filed: 1958, granted 1961
Mainz Trial enrollment: 191 men (subgroup of 42 men ages 51-84, mean age 68)

- A single 100 mg intramuscular dose was intended as a monthly injection but produced mean trough estradiol of 598 pg/mL.
- The normal male upper limit for estradiol cited in the records is 35 pg/mL.
- Estradiol undecylate was used clinically in France, Germany, the United Kingdom, Monaco, the Netherlands, Switzerland, and Japan.
- In one clinical trial run on medically screened cardiovascular low-risk men, 76% suffered cardiovascular complications.
- The Mainz Trial randomized 191 men with prostate cancer to 100 mg/month estradiol undecylate versus 300 mg/week cyproterone acetate, excluding patients with pre-existing cardiovascular disease.

To listen to this podcast ad-free and access premium episodes, try our subscription with a 14-day free trial at obomedia.com.

© 2026 OBOMEDIA. All rights reserved.
This episode and its content (audio, text, and related materials) are the exclusive property of OBOMEDIA and are protected by applicable copyright laws. Reproduction, distribution, editing, or commercial use, in whole or in part, without prior written permission from OBOMEDIA is prohibited. For permissions, licensing, and business inquiries: business@obomedia.com.]]>1805falsefullhttps://www.spreaker.com/episode/the-vanishing-vial-did-3-000-frogs-ever-yield-epibatidine--73090273
A single vial held less than one milligram of residue after nearly 3,000 frogs and eighteen years of work - a sample claimed to contain a compound 2,900 times more potent than morphine and active on nicotinic receptors, not opioids. If that residue was real, it promised pain relief without addiction; if it was not, the entire story of epibatidine unravels - so what did that vial actually contain?

In this episode, we trace the field collections, lab delays, and the surprising pharmacology tied to that tiny sample, and ask whether the compound isolated from Epipedobates tricolor was a genuine breakthrough or an analytical artifact. How did one less-than-milligram vial become the fulcrum of an eighteen-year scientific mystery?

Person: John Daly
Location: Ecuador (western slopes of the Andes)
Species: Epipedobates tricolor
Quantity collected: approximately 3,000 specimens (1974-1979)
Residue remaining: less than one milligram

- 3,000 specimens of Epipedobates tricolor were collected between 1974 and 1979.
- The remaining lab sample from those collections measured less than one milligram.
- Reported analgesic potency required 2.5 micrograms per kilogram in rodents for complete analgesia.
- Morphine required 10 milligrams for the same effect in the comparison cited.
- The compound was reported to act on nicotinic acetylcholine receptors rather than opioid receptors.

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© 2026 OBOMEDIA. All rights reserved.
This episode and its content (audio, text, and related materials) are the exclusive property of OBOMEDIA and are protected by applicable copyright laws. Reproduction, distribution, editing, or commercial use, in whole or in part, without prior written permission from OBOMEDIA is prohibited. For permissions, licensing, and business inquiries: business@obomedia.com.]]>https://api.spreaker.com/episode/73090273Tue, 21 Jul 2026 17:26:53 +0000OBOMEDIA ENTERTAINMENTThe Vanishing Vial: Did 3,000 Frogs Ever Yield Epibatidine? A single vial held less than one milligram of residue after nearly 3,000 frogs and eighteen years of work - a sample claimed to contain a compound 2,900 times more potent than morphine and...
A single vial held less than one milligram of residue after nearly 3,000 frogs and eighteen years of work - a sample claimed to contain a compound 2,900 times more potent than morphine and active on nicotinic receptors, not opioids. If that residue was real, it promised pain relief without addiction; if it was not, the entire story of epibatidine unravels - so what did that vial actually contain?

In this episode, we trace the field collections, lab delays, and the surprising pharmacology tied to that tiny sample, and ask whether the compound isolated from Epipedobates tricolor was a genuine breakthrough or an analytical artifact. How did one less-than-milligram vial become the fulcrum of an eighteen-year scientific mystery?

Person: John Daly
Location: Ecuador (western slopes of the Andes)
Species: Epipedobates tricolor
Quantity collected: approximately 3,000 specimens (1974-1979)
Residue remaining: less than one milligram

- 3,000 specimens of Epipedobates tricolor were collected between 1974 and 1979.
- The remaining lab sample from those collections measured less than one milligram.
- Reported analgesic potency required 2.5 micrograms per kilogram in rodents for complete analgesia.
- Morphine required 10 milligrams for the same effect in the comparison cited.
- The compound was reported to act on nicotinic acetylcholine receptors rather than opioid receptors.

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© 2026 OBOMEDIA. All rights reserved.
This episode and its content (audio, text, and related materials) are the exclusive property of OBOMEDIA and are protected by applicable copyright laws. Reproduction, distribution, editing, or commercial use, in whole or in part, without prior written permission from OBOMEDIA is prohibited. For permissions, licensing, and business inquiries: business@obomedia.com.]]>1643falsefullhttps://www.spreaker.com/episode/the-molecule-that-should-have-ended-opioids-but-vanished--73090269
A tiny frog in Ecuador carried a molecule in 1974 that proved up to 2,900 times more potent than morphine and acted on alpha-4 beta-2 nicotinic receptors - yet less than one milligram was ever recovered. How did a compound with zero opioid activity and a binding affinity of 0.05 nM disappear between field trips, and did the frog ever make it at all?

In this episode, you will hear the story of John W. Daly and Charles Myers’ fieldwork, the laboratory findings about epibatidine’s potency and receptor activity, and the baffling gap between discovery and follow-up samples. What caused a previously record-setting analgesic to vanish from the same population two years later?

Person: John W. Daly
Person: Charles Myers
Species: Epipedobates anthonyi
Period: 1974-1979 (field collection) and 17-year storage gap
Potency comparison: up to 2,900:1 morphine (at 2.5 µg/kg vs ~10 mg/kg)

- Daly and Myers collected approximately 3,000 frog skins between 1974 and 1979.
- Total combined extract yielded less than one milligram of epibatidine.
- Early assays placed epibatidine’s analgesic dose at 2.5 micrograms per kilogram.
- Epibatidine bound alpha-4 beta-2 nicotinic receptors with an affinity of 0.05 nanomolars.
- A 1976 return to the original site produced zero detectable epibatidine in the same species.

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© 2026 OBOMEDIA. All rights reserved.
This episode and its content (audio, text, and related materials) are the exclusive property of OBOMEDIA and are protected by applicable copyright laws. Reproduction, distribution, editing, or commercial use, in whole or in part, without prior written permission from OBOMEDIA is prohibited. For permissions, licensing, and business inquiries: business@obomedia.com.]]>https://api.spreaker.com/episode/73090269Tue, 21 Jul 2026 17:26:50 +0000OBOMEDIA ENTERTAINMENTThe Molecule That Should Have Ended Opioids - But Vanished A tiny frog in Ecuador carried a molecule in 1974 that proved up to 2,900 times more potent than morphine and acted on alpha-4 beta-2 nicotinic receptors - yet less than one milligram was...
A tiny frog in Ecuador carried a molecule in 1974 that proved up to 2,900 times more potent than morphine and acted on alpha-4 beta-2 nicotinic receptors - yet less than one milligram was ever recovered. How did a compound with zero opioid activity and a binding affinity of 0.05 nM disappear between field trips, and did the frog ever make it at all?

In this episode, you will hear the story of John W. Daly and Charles Myers’ fieldwork, the laboratory findings about epibatidine’s potency and receptor activity, and the baffling gap between discovery and follow-up samples. What caused a previously record-setting analgesic to vanish from the same population two years later?

Person: John W. Daly
Person: Charles Myers
Species: Epipedobates anthonyi
Period: 1974-1979 (field collection) and 17-year storage gap
Potency comparison: up to 2,900:1 morphine (at 2.5 µg/kg vs ~10 mg/kg)

- Daly and Myers collected approximately 3,000 frog skins between 1974 and 1979.
- Total combined extract yielded less than one milligram of epibatidine.
- Early assays placed epibatidine’s analgesic dose at 2.5 micrograms per kilogram.
- Epibatidine bound alpha-4 beta-2 nicotinic receptors with an affinity of 0.05 nanomolars.
- A 1976 return to the original site produced zero detectable epibatidine in the same species.

To listen to this podcast ad-free and access premium episodes, try our subscription with a 14-day free trial at obomedia.com.

© 2026 OBOMEDIA. All rights reserved.
This episode and its content (audio, text, and related materials) are the exclusive property of OBOMEDIA and are protected by applicable copyright laws. Reproduction, distribution, editing, or commercial use, in whole or in part, without prior written permission from OBOMEDIA is prohibited. For permissions, licensing, and business inquiries: business@obomedia.com.]]>1652falsefullhttps://www.spreaker.com/episode/the-needle-size-molecule-that-rewrote-pain-then-vanished--73090268
A grain smaller than a sewing needle held a compound up to 2,900 times more potent than morphine, yet the frogs that yielded it never produced it again - where did it come from and why did it disappear? Discover the vanished molecule that forced scientists to rethink pain pathways and chemical ecology.

In this episode, we trace the decades-long arc from a single sub-milligram extract gathered in Ecuador to high-resolution spectrometry in 1991 that revealed a chlorinated alkaloid binding nicotinic acetylcholine receptors instead of opioid receptors. How could one tiny sample rewrite analgesic science and leave such unsolved questions about origin and stability?

Person: John W. Daly
Species: Epipedobates anthonyi
Date (first collection): 1974-1979
Analysis date: 1991
Status: Species protected by IUCN since 1984

- Total number of frogs collected: roughly 3,000
- Total extractable material from all frogs: less than 1 milligram
- Reported rodent analgesic potency: 2.5 micrograms/kg equaled 10 mg/kg morphine
- Estimated potency compared to morphine by weight: up to 2,900 times (conservative estimate 200×)
- Year Daly published his paper noting local absence of traditional use: 2000

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© 2026 OBOMEDIA. All rights reserved.
This episode and its content (audio, text, and related materials) are the exclusive property of OBOMEDIA and are protected by applicable copyright laws. Reproduction, distribution, editing, or commercial use, in whole or in part, without prior written permission from OBOMEDIA is prohibited. For permissions, licensing, and business inquiries: business@obomedia.com.]]>https://api.spreaker.com/episode/73090268Tue, 21 Jul 2026 17:26:46 +0000OBOMEDIA ENTERTAINMENTThe Needle-Size Molecule That Rewrote Pain - Then Vanished A grain smaller than a sewing needle held a compound up to 2,900 times more potent than morphine, yet the frogs that yielded it never produced it again - where did it come from and why did...
A grain smaller than a sewing needle held a compound up to 2,900 times more potent than morphine, yet the frogs that yielded it never produced it again - where did it come from and why did it disappear? Discover the vanished molecule that forced scientists to rethink pain pathways and chemical ecology.

In this episode, we trace the decades-long arc from a single sub-milligram extract gathered in Ecuador to high-resolution spectrometry in 1991 that revealed a chlorinated alkaloid binding nicotinic acetylcholine receptors instead of opioid receptors. How could one tiny sample rewrite analgesic science and leave such unsolved questions about origin and stability?

Person: John W. Daly
Species: Epipedobates anthonyi
Date (first collection): 1974-1979
Analysis date: 1991
Status: Species protected by IUCN since 1984

- Total number of frogs collected: roughly 3,000
- Total extractable material from all frogs: less than 1 milligram
- Reported rodent analgesic potency: 2.5 micrograms/kg equaled 10 mg/kg morphine
- Estimated potency compared to morphine by weight: up to 2,900 times (conservative estimate 200×)
- Year Daly published his paper noting local absence of traditional use: 2000

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© 2026 OBOMEDIA. All rights reserved.
This episode and its content (audio, text, and related materials) are the exclusive property of OBOMEDIA and are protected by applicable copyright laws. Reproduction, distribution, editing, or commercial use, in whole or in part, without prior written permission from OBOMEDIA is prohibited. For permissions, licensing, and business inquiries: business@obomedia.com.]]>1711falsefullhttps://www.spreaker.com/episode/the-molecule-that-vanished-doet-s-strange-split-second-fate--73090267
A single extra carbon atom turned DOM into DOET - and turned clinical promise into an unresolved mystery that would outpace the science around it. A compound patented by Dow in 1966, tested twice by colleagues with opposite results, and shelved before its final trial report was published - what exactly happened in between?

In this episode, we trace the sequence from Shulgin’s bench at Dow Chemical to the clinical program at Johns Hopkins and the quiet disappearance of a molecule called DOET, asking whether DOET was a mood elevator, a dangerous outlier, or simply a casualty of events outside the lab.

Person: Alexander Shulgin
Date: 1966
Location: Dow Chemical, California
Event: Patent filed for 4-ethyl-2,5-dimethoxyamphetamine (DOET)
Period: 1960s

- DOET differs from DOM by one structural change: a methyl group replaced with an ethyl group (one extra carbon).
- Shulgin reported onset between 1 and 1.5 hours, peak at 3-4 hours, and a 5-6 hour duration at lower doses.
- Patent for DOET was filed by Shulgin and Dow Chemical in 1966 under the name Hecate/DOET.
- One month after Shulgin’s self-test, a colleague at comparable dose experienced intense lethargy and prolonged depression.
- Solomon Snyder began controlled human trials for DOET at Johns Hopkins in 1968 with funding from Dow Chemical.

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© 2026 OBOMEDIA. All rights reserved.
This episode and its content (audio, text, and related materials) are the exclusive property of OBOMEDIA and are protected by applicable copyright laws. Reproduction, distribution, editing, or commercial use, in whole or in part, without prior written permission from OBOMEDIA is prohibited. For permissions, licensing, and business inquiries: business@obomedia.com.]]>https://api.spreaker.com/episode/73090267Tue, 21 Jul 2026 17:26:42 +0000OBOMEDIA ENTERTAINMENTThe Molecule That Vanished: DOET's Strange Split‑Second Fate A single extra carbon atom turned DOM into DOET - and turned clinical promise into an unresolved mystery that would outpace the science around it. A compound patented by Dow in 1966,...
A single extra carbon atom turned DOM into DOET - and turned clinical promise into an unresolved mystery that would outpace the science around it. A compound patented by Dow in 1966, tested twice by colleagues with opposite results, and shelved before its final trial report was published - what exactly happened in between?

In this episode, we trace the sequence from Shulgin’s bench at Dow Chemical to the clinical program at Johns Hopkins and the quiet disappearance of a molecule called DOET, asking whether DOET was a mood elevator, a dangerous outlier, or simply a casualty of events outside the lab.

Person: Alexander Shulgin
Date: 1966
Location: Dow Chemical, California
Event: Patent filed for 4-ethyl-2,5-dimethoxyamphetamine (DOET)
Period: 1960s

- DOET differs from DOM by one structural change: a methyl group replaced with an ethyl group (one extra carbon).
- Shulgin reported onset between 1 and 1.5 hours, peak at 3-4 hours, and a 5-6 hour duration at lower doses.
- Patent for DOET was filed by Shulgin and Dow Chemical in 1966 under the name Hecate/DOET.
- One month after Shulgin’s self-test, a colleague at comparable dose experienced intense lethargy and prolonged depression.
- Solomon Snyder began controlled human trials for DOET at Johns Hopkins in 1968 with funding from Dow Chemical.

To listen to this podcast ad-free and access premium episodes, try our subscription with a 14-day free trial at obomedia.com.

© 2026 OBOMEDIA. All rights reserved.
This episode and its content (audio, text, and related materials) are the exclusive property of OBOMEDIA and are protected by applicable copyright laws. Reproduction, distribution, editing, or commercial use, in whole or in part, without prior written permission from OBOMEDIA is prohibited. For permissions, licensing, and business inquiries: business@obomedia.com.]]>1833falsefullhttps://www.spreaker.com/episode/the-medicine-that-worked-buried-by-san-francisco-s-stp-panic--73090266
A Johns Hopkins neuroscientist ran controlled clinical trials for six years on a compound that produced no hallucinations, no cognitive impairment, and measurable mood elevation - yet the program was killed by a street drug crisis in San Francisco. The drug passed every test, the patent sat unused since 1966, and three peer‑reviewed papers survive; so how did a medicine that may have worked get buried under the wreckage of something it had nothing to do with?

In this episode, we trace the clinical record, corporate filings, and street history to show what the trials recorded, what Dow Chemical patented, and how a separate outbreak of high‑dose tablets in San Francisco changed the law and the science. What actually happened between laboratory notes, a 1966 patent, and the STP panic that ended the program?

Person: Alexander Shulgin
Person: Solomon Snyder
Event: STP distribution in San Francisco summer 1967
Date: 1966 (patent filed), 1968 (trials began)
Publication: Three peer‑reviewed papers

- The compound DOET was patented by Dow Chemical in 1966 and never developed into a pharmaceutical product.
- Controlled clinical trials on DOET began at Johns Hopkins in 1968 under neuroscientist Solomon Snyder.
- Three peer‑reviewed papers on the compound remain in the scientific literature authored by Snyder.
- Alexander Shulgin synthesized DOM in 1963 and created DOET by replacing a methyl group with an ethyl group.
- Owsley Stanley distributed high‑dose DOM tablets called STP in San Francisco in summer 1967, producing extended trips lasting 12-16 hours and hospitalizations.

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© 2026 OBOMEDIA. All rights reserved.
This episode and its content (audio, text, and related materials) are the exclusive property of OBOMEDIA and are protected by applicable copyright laws. Reproduction, distribution, editing, or commercial use, in whole or in part, without prior written permission from OBOMEDIA is prohibited. For permissions, licensing, and business inquiries: business@obomedia.com.]]>https://api.spreaker.com/episode/73090266Tue, 21 Jul 2026 17:26:38 +0000OBOMEDIA ENTERTAINMENTThe Medicine That Worked - Buried by San Francisco's STP Panic A Johns Hopkins neuroscientist ran controlled clinical trials for six years on a compound that produced no hallucinations, no cognitive impairment, and measurable mood elevation - yet...
A Johns Hopkins neuroscientist ran controlled clinical trials for six years on a compound that produced no hallucinations, no cognitive impairment, and measurable mood elevation - yet the program was killed by a street drug crisis in San Francisco. The drug passed every test, the patent sat unused since 1966, and three peer‑reviewed papers survive; so how did a medicine that may have worked get buried under the wreckage of something it had nothing to do with?

In this episode, we trace the clinical record, corporate filings, and street history to show what the trials recorded, what Dow Chemical patented, and how a separate outbreak of high‑dose tablets in San Francisco changed the law and the science. What actually happened between laboratory notes, a 1966 patent, and the STP panic that ended the program?

Person: Alexander Shulgin
Person: Solomon Snyder
Event: STP distribution in San Francisco summer 1967
Date: 1966 (patent filed), 1968 (trials began)
Publication: Three peer‑reviewed papers

- The compound DOET was patented by Dow Chemical in 1966 and never developed into a pharmaceutical product.
- Controlled clinical trials on DOET began at Johns Hopkins in 1968 under neuroscientist Solomon Snyder.
- Three peer‑reviewed papers on the compound remain in the scientific literature authored by Snyder.
- Alexander Shulgin synthesized DOM in 1963 and created DOET by replacing a methyl group with an ethyl group.
- Owsley Stanley distributed high‑dose DOM tablets called STP in San Francisco in summer 1967, producing extended trips lasting 12-16 hours and hospitalizations.

To listen to this podcast ad-free and access premium episodes, try our subscription with a 14-day free trial at obomedia.com.

© 2026 OBOMEDIA. All rights reserved.
This episode and its content (audio, text, and related materials) are the exclusive property of OBOMEDIA and are protected by applicable copyright laws. Reproduction, distribution, editing, or commercial use, in whole or in part, without prior written permission from OBOMEDIA is prohibited. For permissions, licensing, and business inquiries: business@obomedia.com.]]>1757falsefullhttps://www.spreaker.com/episode/hecate-the-lost-mood-drug-banned-before-it-was-proven--73090262
A forgotten psychiatric compound promised quiet, sustained mood elevation without hallucinations, yet it was placed on Schedule I before clinical results were published-how did a potentially safer mood drug become buried by a crisis it didn’t cause? Discover the strange link between a Dow patent, a Summer of Love emergency, and a scientist who kept testing after industry walked away.

In this episode, we trace the timeline from the 1966 Dow patent through the 1967 San Francisco crisis to the clinical trials that followed, describing who developed the molecule, what the early human data showed, and why the research program collapsed-was the drug outlawed because of science or because of circumstance?

Person: Alexander Shulgin
Person: Owsley Stanley
Person: Solomon Snyder
Date: 1966 (patent filed)
Event: San Francisco crisis, 1967

- Dow Chemical filed the DOET patent in 1966 describing a compound intended to elevate mood without producing hallucinations.
- California made LSD illegal in 1966, shifting underground chemists into criminal status and prompting changes in the drug market.
- Owsley Stanley distributed DOM as STP in 1967, with high-dose tablets that produced effects lasting three to four days and led to emergency room cases.
- Dow terminated the DOET clinical program in 1967; the patent was published in 1970 after the program had ended.
- Solomon Snyder conducted a DOET trial in 1968 administering 1.5 mg orally, with onset at 1-1.5 hours, peak at 3-4 hours, duration 5-6 hours, and reports of mild euphoria and heightened self-awareness without hallucinations.

To listen to this podcast ad-free and access premium episodes, try our subscription with a 14-day free trial at obomedia.com.

© 2026 OBOMEDIA. All rights reserved.
This episode and its content (audio, text, and related materials) are the exclusive property of OBOMEDIA and are protected by applicable copyright laws. Reproduction, distribution, editing, or commercial use, in whole or in part, without prior written permission from OBOMEDIA is prohibited. For permissions, licensing, and business inquiries: business@obomedia.com.]]>https://api.spreaker.com/episode/73090262Tue, 21 Jul 2026 17:26:35 +0000OBOMEDIA ENTERTAINMENTHecate: The Lost Mood Drug Banned Before It Was Proven A forgotten psychiatric compound promised quiet, sustained mood elevation without hallucinations, yet it was placed on Schedule I before clinical results were published-how did a potentially...
A forgotten psychiatric compound promised quiet, sustained mood elevation without hallucinations, yet it was placed on Schedule I before clinical results were published-how did a potentially safer mood drug become buried by a crisis it didn’t cause? Discover the strange link between a Dow patent, a Summer of Love emergency, and a scientist who kept testing after industry walked away.

In this episode, we trace the timeline from the 1966 Dow patent through the 1967 San Francisco crisis to the clinical trials that followed, describing who developed the molecule, what the early human data showed, and why the research program collapsed-was the drug outlawed because of science or because of circumstance?

Person: Alexander Shulgin
Person: Owsley Stanley
Person: Solomon Snyder
Date: 1966 (patent filed)
Event: San Francisco crisis, 1967

- Dow Chemical filed the DOET patent in 1966 describing a compound intended to elevate mood without producing hallucinations.
- California made LSD illegal in 1966, shifting underground chemists into criminal status and prompting changes in the drug market.
- Owsley Stanley distributed DOM as STP in 1967, with high-dose tablets that produced effects lasting three to four days and led to emergency room cases.
- Dow terminated the DOET clinical program in 1967; the patent was published in 1970 after the program had ended.
- Solomon Snyder conducted a DOET trial in 1968 administering 1.5 mg orally, with onset at 1-1.5 hours, peak at 3-4 hours, duration 5-6 hours, and reports of mild euphoria and heightened self-awareness without hallucinations.

To listen to this podcast ad-free and access premium episodes, try our subscription with a 14-day free trial at obomedia.com.

© 2026 OBOMEDIA. All rights reserved.
This episode and its content (audio, text, and related materials) are the exclusive property of OBOMEDIA and are protected by applicable copyright laws. Reproduction, distribution, editing, or commercial use, in whole or in part, without prior written permission from OBOMEDIA is prohibited. For permissions, licensing, and business inquiries: business@obomedia.com.]]>1688falsefullhttps://www.spreaker.com/episode/the-drug-that-didn-t-trip-why-ariadne-s-trial-vanished-in-1974--73090258
Alerting clarity without hallucinations: Ariadne, code BL-3912, produced measurable antidepressant, antimanic and Parkinsonian benefits across a wide dose range - and yet its phase three human trial data were never published. Why did Bristol Laboratories halt public release despite completed multi-clinic trials and no safety crisis?

In this episode, we follow the path from Alexander Shulgin’s 1968 synthesis to Bristol Laboratories’ decision to have every board member ingest the drug before approving human testing, and we track the unpublished phase three program around 1974. What can the sealed trial results tell us about a molecule that woke subjects without tripping them into hallucination?

Person: Alexander Shulgin
Date: 1968 (synthesis), 1974 (board dosing and phase three start)
Company: Bristol Laboratories
Compound: Ariadne (internal code BL-3912, active enantiomer BL-3912A; proposed brand Dimoxamine)
Status: Phase three completed; results unpublished

- Bristol board members each swallowed Ariadne themselves before authorizing human trials in 1974.
- At 25-50 mg BL-3912A produced alertness and measurable well-being, placing it in antidepressant range.
- At 50-100 mg the compound produced effects relevant to manic depression in psychotic individuals.
- At 100 mg daily Ariadne reversed motor deficits in animal Parkinson’s models at rates comparable to levodopa.
- At 300 mg (ten times minimum active dose) no subject reported hallucinations.

To listen to this podcast ad-free and access premium episodes, try our subscription with a 14-day free trial at obomedia.com.

© 2026 OBOMEDIA. All rights reserved.
This episode and its content (audio, text, and related materials) are the exclusive property of OBOMEDIA and are protected by applicable copyright laws. Reproduction, distribution, editing, or commercial use, in whole or in part, without prior written permission from OBOMEDIA is prohibited. For permissions, licensing, and business inquiries: business@obomedia.com.]]>https://api.spreaker.com/episode/73090258Tue, 21 Jul 2026 17:26:31 +0000OBOMEDIA ENTERTAINMENTThe Drug That Didn't Trip: Why Ariadne's Trial Vanished in 1974 Alerting clarity without hallucinations: Ariadne, code BL-3912, produced measurable antidepressant, antimanic and Parkinsonian benefits across a wide dose range - and yet its phase...
Alerting clarity without hallucinations: Ariadne, code BL-3912, produced measurable antidepressant, antimanic and Parkinsonian benefits across a wide dose range - and yet its phase three human trial data were never published. Why did Bristol Laboratories halt public release despite completed multi-clinic trials and no safety crisis?

In this episode, we follow the path from Alexander Shulgin’s 1968 synthesis to Bristol Laboratories’ decision to have every board member ingest the drug before approving human testing, and we track the unpublished phase three program around 1974. What can the sealed trial results tell us about a molecule that woke subjects without tripping them into hallucination?

Person: Alexander Shulgin
Date: 1968 (synthesis), 1974 (board dosing and phase three start)
Company: Bristol Laboratories
Compound: Ariadne (internal code BL-3912, active enantiomer BL-3912A; proposed brand Dimoxamine)
Status: Phase three completed; results unpublished

- Bristol board members each swallowed Ariadne themselves before authorizing human trials in 1974.
- At 25-50 mg BL-3912A produced alertness and measurable well-being, placing it in antidepressant range.
- At 50-100 mg the compound produced effects relevant to manic depression in psychotic individuals.
- At 100 mg daily Ariadne reversed motor deficits in animal Parkinson’s models at rates comparable to levodopa.
- At 300 mg (ten times minimum active dose) no subject reported hallucinations.

To listen to this podcast ad-free and access premium episodes, try our subscription with a 14-day free trial at obomedia.com.

© 2026 OBOMEDIA. All rights reserved.
This episode and its content (audio, text, and related materials) are the exclusive property of OBOMEDIA and are protected by applicable copyright laws. Reproduction, distribution, editing, or commercial use, in whole or in part, without prior written permission from OBOMEDIA is prohibited. For permissions, licensing, and business inquiries: business@obomedia.com.]]>1531falsefullhttps://www.spreaker.com/episode/the-girl-who-broke-hormones-how-a-seizure-drug-revealed-cancer-therapy--73090257
A child in 1963 collapsed not from a seizure but from adrenal failure after taking aminoglutethimide, an anticonvulsant not designed to touch steroid production - a reaction that later redirected cancer pharmacology. How did a single adverse event with a pediatric epilepsy drug lead to an entirely new therapeutic pathway?

In this episode, we tell the story of that drug's unexpected effect and its aftermath. You will hear how aminoglutethimide, approved for petit mal epilepsy, produced widespread toxicity, was withdrawn in 1966, and yet planted the seed for drugs treating hormone-sensitive cancers - but how exactly did that accidental discovery survive near-erasure?

Person: unnamed girl patient
Date: 1963 (collapse); 1960 (approval); 1966 (withdrawal)
Drug: aminoglutethimide (brand name Elipten)
Condition: adrenal insufficiency consistent with Addison's disease
Adverse effect rates: 45-85% experienced at least one adverse effect

- Aminoglutethimide was approved in 1960 for petit mal epilepsy and prescribed as an oral anticonvulsant.
- The 1963 patient developed life-threatening adrenal failure while taking the drug, resembling Addison's disease.
- Across observations, 45-85% of patients experienced at least one adverse effect from aminoglutethimide.
- Lethargy occurred in 31-70% of cases; skin rash and low blood pressure in roughly 15% of patients.
- Approximately 10% of patients experienced severe toxicity, including circulatory instability and adrenal failure, leading to the drug's market withdrawal in 1966.

To listen to this podcast ad-free and access premium episodes, try our subscription with a 14-day free trial at obomedia.com.

© 2026 OBOMEDIA. All rights reserved.
This episode and its content (audio, text, and related materials) are the exclusive property of OBOMEDIA and are protected by applicable copyright laws. Reproduction, distribution, editing, or commercial use, in whole or in part, without prior written permission from OBOMEDIA is prohibited. For permissions, licensing, and business inquiries: business@obomedia.com.]]>https://api.spreaker.com/episode/73090257Tue, 21 Jul 2026 17:26:27 +0000OBOMEDIA ENTERTAINMENTThe Girl Who Broke Hormones: How a Seizure Drug Revealed Cancer Therapy A child in 1963 collapsed not from a seizure but from adrenal failure after taking aminoglutethimide, an anticonvulsant not designed to touch steroid production - a reaction...
A child in 1963 collapsed not from a seizure but from adrenal failure after taking aminoglutethimide, an anticonvulsant not designed to touch steroid production - a reaction that later redirected cancer pharmacology. How did a single adverse event with a pediatric epilepsy drug lead to an entirely new therapeutic pathway?

In this episode, we tell the story of that drug's unexpected effect and its aftermath. You will hear how aminoglutethimide, approved for petit mal epilepsy, produced widespread toxicity, was withdrawn in 1966, and yet planted the seed for drugs treating hormone-sensitive cancers - but how exactly did that accidental discovery survive near-erasure?

Person: unnamed girl patient
Date: 1963 (collapse); 1960 (approval); 1966 (withdrawal)
Drug: aminoglutethimide (brand name Elipten)
Condition: adrenal insufficiency consistent with Addison's disease
Adverse effect rates: 45-85% experienced at least one adverse effect

- Aminoglutethimide was approved in 1960 for petit mal epilepsy and prescribed as an oral anticonvulsant.
- The 1963 patient developed life-threatening adrenal failure while taking the drug, resembling Addison's disease.
- Across observations, 45-85% of patients experienced at least one adverse effect from aminoglutethimide.
- Lethargy occurred in 31-70% of cases; skin rash and low blood pressure in roughly 15% of patients.
- Approximately 10% of patients experienced severe toxicity, including circulatory instability and adrenal failure, leading to the drug's market withdrawal in 1966.

To listen to this podcast ad-free and access premium episodes, try our subscription with a 14-day free trial at obomedia.com.

© 2026 OBOMEDIA. All rights reserved.
This episode and its content (audio, text, and related materials) are the exclusive property of OBOMEDIA and are protected by applicable copyright laws. Reproduction, distribution, editing, or commercial use, in whole or in part, without prior written permission from OBOMEDIA is prohibited. For permissions, licensing, and business inquiries: business@obomedia.com.]]>1585falsefullhttps://www.spreaker.com/episode/the-truth-about-expired-drugs-military-tests-that-changed-nothing--73090255
Nearly 90% of over 100 tested drugs remained effective up to fifteen years past their printed expiration dates, yet the findings were kept from hospitals, state health departments, and foreign governments-so why did nothing change for the public? What did the military do differently after learning that most expiration dates are conservative estimates?

In this episode, we lay out the Shelf Life Extension Program and the FDA tests it funded for the Department of Defense, describing what the study covered and how its conclusions contradicted common assumptions about expiration dates. How did a formal, fifteen-year-spanning body of research lead to a practice that saved the military money while remaining largely invisible to everyone else?

Person: Joel Davis
Organization: Food and Drug Administration
Program: Shelf Life Extension Program
Scope: more than 100 drugs tested
Result: roughly 90% effective up to 15 years past expiration

- The Department of Defense commissioned the FDA to test military stockpiles beginning in the mid-1980s.
- The FDA tested more than 100 prescription and over-the-counter drugs under proper storage conditions.
- Roughly 90% of those drugs were found safe and effective up to 15 years past their official expiration dates.
- Ciprofloxacin was found effective nine years past its official shelf life under proper storage conditions.
- The Shelf Life Extension Program continues to operate, allowing the military to extend usable life of tested stockpiles.

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© 2026 OBOMEDIA. All rights reserved.
This episode and its content (audio, text, and related materials) are the exclusive property of OBOMEDIA and are protected by applicable copyright laws. Reproduction, distribution, editing, or commercial use, in whole or in part, without prior written permission from OBOMEDIA is prohibited. For permissions, licensing, and business inquiries: business@obomedia.com.]]>https://api.spreaker.com/episode/73090255Tue, 21 Jul 2026 17:26:23 +0000OBOMEDIA ENTERTAINMENTThe Truth About "Expired" Drugs: Military Tests That Changed Nothing Nearly 90% of over 100 tested drugs remained effective up to fifteen years past their printed expiration dates, yet the findings were kept from hospitals, state health...
Nearly 90% of over 100 tested drugs remained effective up to fifteen years past their printed expiration dates, yet the findings were kept from hospitals, state health departments, and foreign governments-so why did nothing change for the public? What did the military do differently after learning that most expiration dates are conservative estimates?

In this episode, we lay out the Shelf Life Extension Program and the FDA tests it funded for the Department of Defense, describing what the study covered and how its conclusions contradicted common assumptions about expiration dates. How did a formal, fifteen-year-spanning body of research lead to a practice that saved the military money while remaining largely invisible to everyone else?

Person: Joel Davis
Organization: Food and Drug Administration
Program: Shelf Life Extension Program
Scope: more than 100 drugs tested
Result: roughly 90% effective up to 15 years past expiration

- The Department of Defense commissioned the FDA to test military stockpiles beginning in the mid-1980s.
- The FDA tested more than 100 prescription and over-the-counter drugs under proper storage conditions.
- Roughly 90% of those drugs were found safe and effective up to 15 years past their official expiration dates.
- Ciprofloxacin was found effective nine years past its official shelf life under proper storage conditions.
- The Shelf Life Extension Program continues to operate, allowing the military to extend usable life of tested stockpiles.

To listen to this podcast ad-free and access premium episodes, try our subscription with a 14-day free trial at obomedia.com.

© 2026 OBOMEDIA. All rights reserved.
This episode and its content (audio, text, and related materials) are the exclusive property of OBOMEDIA and are protected by applicable copyright laws. Reproduction, distribution, editing, or commercial use, in whole or in part, without prior written permission from OBOMEDIA is prohibited. For permissions, licensing, and business inquiries: business@obomedia.com.]]>1605falsefullhttps://www.spreaker.com/episode/the-iron-lung-doctor-who-built-the-world-s-drug-alert-system--73090254
Fear of hidden harm: a paralyzed Cambridge graduate who spent two years in an iron lung went on to create a worldwide drug-surveillance system after thalidomide, and a 2020 document alleges he destroyed case material during a government review-what really happened and why did he still feel his work was unfinished?

In this episode, we trace William Inman's life from polio in his early twenties to his role in government and industry, showing how his experiences shaped the yellow card system and the unresolved allegation that clouds parts of his legacy. How did a single yellow form become an international model, and what questions remain about the records he kept?

Person: William Howard Wallace Inman
Date of birth: 1 August 1929
Date of death: 20 October 2005
Event: Creation of the yellow card adverse drug reporting system
Period: 1950s-2000s

- Spent two years inside an iron lung after contracting polio at age 22
- Graduated as the first clinical medical graduate from the University of Cambridge in 1956
- Delivered approximately 50 babies from an adapted wheelchair while working at Addenbrooke's Hospital
- Worked five years as a medical adviser at ICI Pharmaceutical Division before joining the Department of Health
- A 2020 document alleged he destroyed case material during a government review, though he was never formally accused

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© 2026 OBOMEDIA. All rights reserved.
This episode and its content (audio, text, and related materials) are the exclusive property of OBOMEDIA and are protected by applicable copyright laws. Reproduction, distribution, editing, or commercial use, in whole or in part, without prior written permission from OBOMEDIA is prohibited. For permissions, licensing, and business inquiries: business@obomedia.com.]]>https://api.spreaker.com/episode/73090254Tue, 21 Jul 2026 17:26:20 +0000OBOMEDIA ENTERTAINMENTThe Iron Lung Doctor Who Built the World's Drug-Alert System Fear of hidden harm: a paralyzed Cambridge graduate who spent two years in an iron lung went on to create a worldwide drug-surveillance system after thalidomide, and a 2020 document...
Fear of hidden harm: a paralyzed Cambridge graduate who spent two years in an iron lung went on to create a worldwide drug-surveillance system after thalidomide, and a 2020 document alleges he destroyed case material during a government review-what really happened and why did he still feel his work was unfinished?

In this episode, we trace William Inman's life from polio in his early twenties to his role in government and industry, showing how his experiences shaped the yellow card system and the unresolved allegation that clouds parts of his legacy. How did a single yellow form become an international model, and what questions remain about the records he kept?

Person: William Howard Wallace Inman
Date of birth: 1 August 1929
Date of death: 20 October 2005
Event: Creation of the yellow card adverse drug reporting system
Period: 1950s-2000s

- Spent two years inside an iron lung after contracting polio at age 22
- Graduated as the first clinical medical graduate from the University of Cambridge in 1956
- Delivered approximately 50 babies from an adapted wheelchair while working at Addenbrooke's Hospital
- Worked five years as a medical adviser at ICI Pharmaceutical Division before joining the Department of Health
- A 2020 document alleged he destroyed case material during a government review, though he was never formally accused

To listen to this podcast ad-free and access premium episodes, try our subscription with a 14-day free trial at obomedia.com.

© 2026 OBOMEDIA. All rights reserved.
This episode and its content (audio, text, and related materials) are the exclusive property of OBOMEDIA and are protected by applicable copyright laws. Reproduction, distribution, editing, or commercial use, in whole or in part, without prior written permission from OBOMEDIA is prohibited. For permissions, licensing, and business inquiries: business@obomedia.com.]]>1720falsefullhttps://www.spreaker.com/episode/when-medicine-hurts-your-unborn-children-the-des-generation-reveal--73090253
A chilling gap between warning and withdrawal let harmful medicines persist for decades - Mrs. Winslow's Soothing Syrup was labeled "Baby Killers" in 1911 yet still sold in 1930 - and one drug, DES, carried damage into the next generation. How did a medication given to protect pregnancies end up increasing cancer and infertility risks two generations later?

In this episode, we trace the timeline and systems that allowed dangerous products to stay on shelves, outline who was affected by DES, and ask how regulatory processes and mislabeling shaped the outcomes for millions. Can a recall ever fully undo harm passed on before birth?

Person: American Medical Association
Event: "Baby Killers" article published
Date: 1911
Drug: diethylstilbestrol (DES)
Estimate: 5-10 million people exposed before 1971 recall

- Mrs. Winslow's Soothing Syrup was called "Baby Killers" in a medical journal in 1911 yet remained on sale in the UK in 1930.
- DES was given to women during pregnancy and an estimated 5-10 million people were exposed before its 1971 recall.
- Daughters exposed in utero to DES were more than twice as likely to develop breast cancer.
- DES-exposed daughters had a 2.4 times higher risk of infertility compared with the general population.
- In 2015, 42% of pharmaceutical recalls were due to misbranding, and 45 new drugs received approval that year.

To listen to this podcast ad-free and access premium episodes, try our subscription with a 14-day free trial at obomedia.com.

© 2026 OBOMEDIA. All rights reserved.
This episode and its content (audio, text, and related materials) are the exclusive property of OBOMEDIA and are protected by applicable copyright laws. Reproduction, distribution, editing, or commercial use, in whole or in part, without prior written permission from OBOMEDIA is prohibited. For permissions, licensing, and business inquiries: business@obomedia.com.]]>https://api.spreaker.com/episode/73090253Tue, 21 Jul 2026 17:26:16 +0000OBOMEDIA ENTERTAINMENTWhen Medicine Hurts Your Unborn Children: The DES Generation Reveal A chilling gap between warning and withdrawal let harmful medicines persist for decades - Mrs. Winslow's Soothing Syrup was labeled "Baby Killers" in 1911 yet still sold in 1930 -...
A chilling gap between warning and withdrawal let harmful medicines persist for decades - Mrs. Winslow's Soothing Syrup was labeled "Baby Killers" in 1911 yet still sold in 1930 - and one drug, DES, carried damage into the next generation. How did a medication given to protect pregnancies end up increasing cancer and infertility risks two generations later?

In this episode, we trace the timeline and systems that allowed dangerous products to stay on shelves, outline who was affected by DES, and ask how regulatory processes and mislabeling shaped the outcomes for millions. Can a recall ever fully undo harm passed on before birth?

Person: American Medical Association
Event: "Baby Killers" article published
Date: 1911
Drug: diethylstilbestrol (DES)
Estimate: 5-10 million people exposed before 1971 recall

- Mrs. Winslow's Soothing Syrup was called "Baby Killers" in a medical journal in 1911 yet remained on sale in the UK in 1930.
- DES was given to women during pregnancy and an estimated 5-10 million people were exposed before its 1971 recall.
- Daughters exposed in utero to DES were more than twice as likely to develop breast cancer.
- DES-exposed daughters had a 2.4 times higher risk of infertility compared with the general population.
- In 2015, 42% of pharmaceutical recalls were due to misbranding, and 45 new drugs received approval that year.

To listen to this podcast ad-free and access premium episodes, try our subscription with a 14-day free trial at obomedia.com.

© 2026 OBOMEDIA. All rights reserved.
This episode and its content (audio, text, and related materials) are the exclusive property of OBOMEDIA and are protected by applicable copyright laws. Reproduction, distribution, editing, or commercial use, in whole or in part, without prior written permission from OBOMEDIA is prohibited. For permissions, licensing, and business inquiries: business@obomedia.com.]]>1397falsefullhttps://www.spreaker.com/episode/the-man-lying-at-the-bottom-of-the-stairs-could-not-move-his-legs--73090252
He was told he would never walk again, yet he taught himself to walk in the dark at night - and later built a company that resolved $15 billion in consumer debt and employed 3,900 people. How did a one-time carnival worker and slaughterhouse employee turn five cents on the dollar into a Harvard Business School case and draw the ire of the Department of Justice?

In this episode, we tell the story of William R. Bartmann from his origins in Dubuque through the staircase that changed his life, his rise in debt collection using a novel repayment strategy, and the federal prosecution that failed on every count. What is the detail at the center of this case that reframes everything and makes the staircase the whole argument?

Person: William R. Bartmann
Location: Dubuque, Iowa
Date of birth: 1948
Event: Resolved $15 billion in consumer debt
Status: Federal jury rejected prosecution on every count

- Bartmann left school at age 14 and later earned a GED, college degrees, and a law degree.
- A fall down a staircase left him unable to move his legs until he retrained himself to walk in private.
- In 1986 he built a debt-buying company in Tulsa that eventually employed more than 3,900 people.
- His company’s approach bought charged-off accounts at five cents on the dollar and offered reasonable repayment options.
- The United States Department of Justice convened three grand juries and prosecuted him, but a federal jury rejected every count.

To listen to this podcast ad-free and access premium episodes, try our subscription with a 14-day free trial at obomedia.com.

© 2026 OBOMEDIA. All rights reserved.
This episode and its content (audio, text, and related materials) are the exclusive property of OBOMEDIA and are protected by applicable copyright laws. Reproduction, distribution, editing, or commercial use, in whole or in part, without prior written permission from OBOMEDIA is prohibited. For permissions, licensing, and business inquiries: business@obomedia.com.]]>https://api.spreaker.com/episode/73090252Tue, 21 Jul 2026 17:26:13 +0000OBOMEDIA ENTERTAINMENTThe man lying at the bottom of the stairs could not move his legs He was told he would never walk again, yet he taught himself to walk in the dark at night - and later built a company that resolved $15 billion in consumer debt and employed 3,900...
He was told he would never walk again, yet he taught himself to walk in the dark at night - and later built a company that resolved $15 billion in consumer debt and employed 3,900 people. How did a one-time carnival worker and slaughterhouse employee turn five cents on the dollar into a Harvard Business School case and draw the ire of the Department of Justice?

In this episode, we tell the story of William R. Bartmann from his origins in Dubuque through the staircase that changed his life, his rise in debt collection using a novel repayment strategy, and the federal prosecution that failed on every count. What is the detail at the center of this case that reframes everything and makes the staircase the whole argument?

Person: William R. Bartmann
Location: Dubuque, Iowa
Date of birth: 1948
Event: Resolved $15 billion in consumer debt
Status: Federal jury rejected prosecution on every count

- Bartmann left school at age 14 and later earned a GED, college degrees, and a law degree.
- A fall down a staircase left him unable to move his legs until he retrained himself to walk in private.
- In 1986 he built a debt-buying company in Tulsa that eventually employed more than 3,900 people.
- His company’s approach bought charged-off accounts at five cents on the dollar and offered reasonable repayment options.
- The United States Department of Justice convened three grand juries and prosecuted him, but a federal jury rejected every count.

To listen to this podcast ad-free and access premium episodes, try our subscription with a 14-day free trial at obomedia.com.

© 2026 OBOMEDIA. All rights reserved.
This episode and its content (audio, text, and related materials) are the exclusive property of OBOMEDIA and are protected by applicable copyright laws. Reproduction, distribution, editing, or commercial use, in whole or in part, without prior written permission from OBOMEDIA is prohibited. For permissions, licensing, and business inquiries: business@obomedia.com.]]>1455falsefullhttps://www.spreaker.com/episode/the-schoolteacher-who-saved-a-nation-then-lost-it-all--73090251
A tiny country with fewer than ten thousand people was kept standing by a schoolteacher-turned-prime minister who borrowed 1.5 million Swiss francs and secured a personal donation of 1,000,000 from the prince after the Alpine Rhine flood of 25 September 1927 - yet within a year roughly 4,000,000 francs were quietly removed from the National Bank by four men from his own party. How did the man who built Liechtenstein's emergency savings bank and anchored its currency lose everything he had fought to protect?

In this episode, we tell the story of Gustav Schädler’s rise from village teacher to Prime Minister and the sequence of events from the 1927 flood to the political crisis that ended his leadership. We cover his early life, key financial decisions during crisis, and the constitutional vacuum that left the nation without a procedure to remove a sitting prime minister - so what ultimately became of Schädler’s authority?

Person: Gustav Schädler
Date: 25 September 1927
Event: Alpine Rhine flood
Amount borrowed: 1,500,000 Swiss francs
Amount emptied: approximately 4,000,000 francs

- Schädler was born 18 November 1883 in Triesenberg and trained as a teacher at Bad Saulgau.
- He studied linguistics and history in Zurich from 1906 to 1912 and taught in Vaduz from 1914 to 1922.
- On 16 December 1918 he married Olga Real (born 29 July 1889); they had two children.
- As Prime Minister from 6 June 1922, he secured the first Swiss loan and the 1924 customs union adopting the Swiss franc.
- After the 1927 flood he borrowed 1,500,000 Swiss francs and obtained a 1,000,000 personal donation from the prince to build a state savings bank.

To listen to this podcast ad-free and access premium episodes, try our subscription with a 14-day free trial at obomedia.com.

© 2026 OBOMEDIA. All rights reserved.
This episode and its content (audio, text, and related materials) are the exclusive property of OBOMEDIA and are protected by applicable copyright laws. Reproduction, distribution, editing, or commercial use, in whole or in part, without prior written permission from OBOMEDIA is prohibited. For permissions, licensing, and business inquiries: business@obomedia.com.]]>https://api.spreaker.com/episode/73090251Tue, 21 Jul 2026 17:26:10 +0000OBOMEDIA ENTERTAINMENTThe Schoolteacher Who Saved a Nation - Then Lost It All A tiny country with fewer than ten thousand people was kept standing by a schoolteacher-turned-prime minister who borrowed 1.5 million Swiss francs and secured a personal donation of 1,000,000...
A tiny country with fewer than ten thousand people was kept standing by a schoolteacher-turned-prime minister who borrowed 1.5 million Swiss francs and secured a personal donation of 1,000,000 from the prince after the Alpine Rhine flood of 25 September 1927 - yet within a year roughly 4,000,000 francs were quietly removed from the National Bank by four men from his own party. How did the man who built Liechtenstein's emergency savings bank and anchored its currency lose everything he had fought to protect?

In this episode, we tell the story of Gustav Schädler’s rise from village teacher to Prime Minister and the sequence of events from the 1927 flood to the political crisis that ended his leadership. We cover his early life, key financial decisions during crisis, and the constitutional vacuum that left the nation without a procedure to remove a sitting prime minister - so what ultimately became of Schädler’s authority?

Person: Gustav Schädler
Date: 25 September 1927
Event: Alpine Rhine flood
Amount borrowed: 1,500,000 Swiss francs
Amount emptied: approximately 4,000,000 francs

- Schädler was born 18 November 1883 in Triesenberg and trained as a teacher at Bad Saulgau.
- He studied linguistics and history in Zurich from 1906 to 1912 and taught in Vaduz from 1914 to 1922.
- On 16 December 1918 he married Olga Real (born 29 July 1889); they had two children.
- As Prime Minister from 6 June 1922, he secured the first Swiss loan and the 1924 customs union adopting the Swiss franc.
- After the 1927 flood he borrowed 1,500,000 Swiss francs and obtained a 1,000,000 personal donation from the prince to build a state savings bank.

To listen to this podcast ad-free and access premium episodes, try our subscription with a 14-day free trial at obomedia.com.

© 2026 OBOMEDIA. All rights reserved.
This episode and its content (audio, text, and related materials) are the exclusive property of OBOMEDIA and are protected by applicable copyright laws. Reproduction, distribution, editing, or commercial use, in whole or in part, without prior written permission from OBOMEDIA is prohibited. For permissions, licensing, and business inquiries: business@obomedia.com.]]>1719falsefullhttps://www.spreaker.com/episode/the-unburied-president-why-edgar-lungu-s-coffin-never-came-home--73090249
Grief turned into a political standoff: former Zambian president Edgar Chagwa Lungu died on June 5, 2025, in Pretoria and his body was never returned home, while his explicit instruction barred sitting president Hakainde Hichilema from approaching the coffin - so why did a death spark an unburied dispute that outlasted the man? What did that written ban reveal about Lungu’s final power and the fractures in Zambian politics?

In this episode, we trace Lungu’s life from his birth in Ndola to his legal career, rise through the Patriotic Front, and contested presidency, and we follow the chain of events after his death that left his remains abroad and a nation divided - what did his documented final wish change about political rituals and power?

Person: Edgar Chagwa Lungu
Date of death: June 5, 2025
Location of death: Pretoria, South Africa
Instruction: Hakainde Hichilema forbidden from approaching remains
Birth date and place: November 11, 1956; Ndola Central Hospital

- Lungu left a documented instruction forbidding sitting president Hakainde Hichilema from being permitted near his remains.
- He died on June 5, 2025, on a surgical table in Pretoria, South Africa.
- Zambia declared seven days of mourning after his death.
- Lungu was born on November 11, 1956, in Ndola Central Hospital in then Northern Rhodesia.
- He won the January 20, 2015 presidential by-election by 27,757 votes out of more than 1.6 million cast (1.66% margin) with 32.36% nationwide participation.

To listen to this podcast ad-free and access premium episodes, try our subscription with a 14-day free trial at obomedia.com.

© 2026 OBOMEDIA. All rights reserved.
This episode and its content (audio, text, and related materials) are the exclusive property of OBOMEDIA and are protected by applicable copyright laws. Reproduction, distribution, editing, or commercial use, in whole or in part, without prior written permission from OBOMEDIA is prohibited. For permissions, licensing, and business inquiries: business@obomedia.com.]]>https://api.spreaker.com/episode/73090249Tue, 21 Jul 2026 17:26:06 +0000OBOMEDIA ENTERTAINMENTThe Unburied President: Why Edgar Lungu's Coffin Never Came Home Grief turned into a political standoff: former Zambian president Edgar Chagwa Lungu died on June 5, 2025, in Pretoria and his body was never returned home, while his explicit...
Grief turned into a political standoff: former Zambian president Edgar Chagwa Lungu died on June 5, 2025, in Pretoria and his body was never returned home, while his explicit instruction barred sitting president Hakainde Hichilema from approaching the coffin - so why did a death spark an unburied dispute that outlasted the man? What did that written ban reveal about Lungu’s final power and the fractures in Zambian politics?

In this episode, we trace Lungu’s life from his birth in Ndola to his legal career, rise through the Patriotic Front, and contested presidency, and we follow the chain of events after his death that left his remains abroad and a nation divided - what did his documented final wish change about political rituals and power?

Person: Edgar Chagwa Lungu
Date of death: June 5, 2025
Location of death: Pretoria, South Africa
Instruction: Hakainde Hichilema forbidden from approaching remains
Birth date and place: November 11, 1956; Ndola Central Hospital

- Lungu left a documented instruction forbidding sitting president Hakainde Hichilema from being permitted near his remains.
- He died on June 5, 2025, on a surgical table in Pretoria, South Africa.
- Zambia declared seven days of mourning after his death.
- Lungu was born on November 11, 1956, in Ndola Central Hospital in then Northern Rhodesia.
- He won the January 20, 2015 presidential by-election by 27,757 votes out of more than 1.6 million cast (1.66% margin) with 32.36% nationwide participation.

To listen to this podcast ad-free and access premium episodes, try our subscription with a 14-day free trial at obomedia.com.

© 2026 OBOMEDIA. All rights reserved.
This episode and its content (audio, text, and related materials) are the exclusive property of OBOMEDIA and are protected by applicable copyright laws. Reproduction, distribution, editing, or commercial use, in whole or in part, without prior written permission from OBOMEDIA is prohibited. For permissions, licensing, and business inquiries: business@obomedia.com.]]>1461falsefullhttps://www.spreaker.com/episode/a-30-km-h-crash-that-should-have-been-survived-the-airbag-was-the-weapon--73090246
A forty-two-year-old pregnant woman died in a collision at just thirty kilometers per hour when a metal fragment from her own dashboard severed her neck; the device meant to save her life detonated instead. How did a company that started making parachute cord end up filling hundreds of millions of cars with explosive inflators, and why were regulators and automakers still driving those cars years after engineers flagged the danger?

In this episode, we trace the path from a 1933 parachute-cord manufacturer to a global airbag supplier and the decisions in the 1990s that swapped stability for cost savings, the pattern of concealment across decades, and the lawsuit in Miami that began to pull the thread. What unfolded after three injury complaints triggered a regulatory file, and how did recalls grow from millions to the largest in U.S. history?

Person: Takezo Takada
Period: 1933-2014 (company history and crisis timeline)
Topic: Takata airbag inflator defect and concealment
Event: 2014 Honda City fatality in Malaysia
Status: Thirty-five confirmed deaths worldwide as of September 2024

- The crash speed was thirty kilometers per hour, described as barely faster than a bicycle.
- By 2014 Takata supplied roughly twenty percent of the global airbag market with manufacturing on four continents.
- Takata switched propellants in the 1990s to ammonium nitrate because it was cheaper and easier to manufacture.
- Ammonium nitrate degrades with repeated temperature and humidity cycling, causing inflators to detonate and send metal fragments outward.
- In April-May 2013 six manufacturers recalled 3.6 million cars tied to the Monclova Plant in Coahuila.

To listen to this podcast ad-free and access premium episodes, try our subscription with a 14-day free trial at obomedia.com.

© 2026 OBOMEDIA. All rights reserved.
This episode and its content (audio, text, and related materials) are the exclusive property of OBOMEDIA and are protected by applicable copyright laws. Reproduction, distribution, editing, or commercial use, in whole or in part, without prior written permission from OBOMEDIA is prohibited. For permissions, licensing, and business inquiries: business@obomedia.com.]]>https://api.spreaker.com/episode/73090246Tue, 21 Jul 2026 17:26:03 +0000OBOMEDIA ENTERTAINMENTA 30-km/h crash that should have been survived - the airbag was the weapon A forty-two-year-old pregnant woman died in a collision at just thirty kilometers per hour when a metal fragment from her own dashboard severed her neck; the device meant to...
A forty-two-year-old pregnant woman died in a collision at just thirty kilometers per hour when a metal fragment from her own dashboard severed her neck; the device meant to save her life detonated instead. How did a company that started making parachute cord end up filling hundreds of millions of cars with explosive inflators, and why were regulators and automakers still driving those cars years after engineers flagged the danger?

In this episode, we trace the path from a 1933 parachute-cord manufacturer to a global airbag supplier and the decisions in the 1990s that swapped stability for cost savings, the pattern of concealment across decades, and the lawsuit in Miami that began to pull the thread. What unfolded after three injury complaints triggered a regulatory file, and how did recalls grow from millions to the largest in U.S. history?

Person: Takezo Takada
Period: 1933-2014 (company history and crisis timeline)
Topic: Takata airbag inflator defect and concealment
Event: 2014 Honda City fatality in Malaysia
Status: Thirty-five confirmed deaths worldwide as of September 2024

- The crash speed was thirty kilometers per hour, described as barely faster than a bicycle.
- By 2014 Takata supplied roughly twenty percent of the global airbag market with manufacturing on four continents.
- Takata switched propellants in the 1990s to ammonium nitrate because it was cheaper and easier to manufacture.
- Ammonium nitrate degrades with repeated temperature and humidity cycling, causing inflators to detonate and send metal fragments outward.
- In April-May 2013 six manufacturers recalled 3.6 million cars tied to the Monclova Plant in Coahuila.

To listen to this podcast ad-free and access premium episodes, try our subscription with a 14-day free trial at obomedia.com.

© 2026 OBOMEDIA. All rights reserved.
This episode and its content (audio, text, and related materials) are the exclusive property of OBOMEDIA and are protected by applicable copyright laws. Reproduction, distribution, editing, or commercial use, in whole or in part, without prior written permission from OBOMEDIA is prohibited. For permissions, licensing, and business inquiries: business@obomedia.com.]]>1433falsefullhttps://www.spreaker.com/episode/how-a-fishing-town-s-babies-were-poisoned-by-invisible-industrial-mercury--73090245
Fear and disbelief swept a fishing town where cats convulsed, birds fell from the sky, and fishing yields plunged 91% - but why were infants who never ate fish also stricken? In Minamata, a factory’s unseen methylmercury turned bay sediment into an ore deposit at 2 kilograms per ton, and the answer to who was poisoned would take years to surface; what hidden pathway reached those children?

In this episode, we tell what happened in Minamata between 1956 and 1959: the arrival of patients with numbness, vision narrowing, convulsions and death, the town’s dependence on the Chisso Corporation, the discovery of extreme mercury contamination in bay sediment, and the company’s response that moved wastewater into the Minamata River - could that decision explain the spreading illness?

Person: Chisso Corporation
Location: Minamata, Kyūshū, Japan
Date: May 1, 1956 (first documented patient), November 4, 1956 (research finding), February 1959 (sediment measurement), September 1958 (wastewater rerouting)
Event: Discovery of methylmercury poisoning transmitted through fish and shellfish

- Fishing yields fell by 91% from earlier levels in the early 1950s.
- By October 1956, 40 people were identified with the disease and 14 were dead (case fatality rate 35%).
- Sediment sampling at the mouth of the wastewater canal measured 2 kilograms of mercury per ton of sediment in February 1959.
- Chisso began producing acetaldehyde in 1932 using mercury as a catalyst, which led to methylmercury discharge into Hyakken Harbour.
- In September 1958 Chisso rerouted its wastewater discharge from the bay to the Minamata River.

To listen to this podcast ad-free and access premium episodes, try our subscription with a 14-day free trial at obomedia.com.

© 2026 OBOMEDIA. All rights reserved.
This episode and its content (audio, text, and related materials) are the exclusive property of OBOMEDIA and are protected by applicable copyright laws. Reproduction, distribution, editing, or commercial use, in whole or in part, without prior written permission from OBOMEDIA is prohibited. For permissions, licensing, and business inquiries: business@obomedia.com.]]>https://api.spreaker.com/episode/73090245Tue, 21 Jul 2026 17:26:00 +0000OBOMEDIA ENTERTAINMENTHow a Fishing Town's Babies Were Poisoned by Invisible Industrial Mercury Fear and disbelief swept a fishing town where cats convulsed, birds fell from the sky, and fishing yields plunged 91% - but why were infants who never ate fish also stricken?...
Fear and disbelief swept a fishing town where cats convulsed, birds fell from the sky, and fishing yields plunged 91% - but why were infants who never ate fish also stricken? In Minamata, a factory’s unseen methylmercury turned bay sediment into an ore deposit at 2 kilograms per ton, and the answer to who was poisoned would take years to surface; what hidden pathway reached those children?

In this episode, we tell what happened in Minamata between 1956 and 1959: the arrival of patients with numbness, vision narrowing, convulsions and death, the town’s dependence on the Chisso Corporation, the discovery of extreme mercury contamination in bay sediment, and the company’s response that moved wastewater into the Minamata River - could that decision explain the spreading illness?

Person: Chisso Corporation
Location: Minamata, Kyūshū, Japan
Date: May 1, 1956 (first documented patient), November 4, 1956 (research finding), February 1959 (sediment measurement), September 1958 (wastewater rerouting)
Event: Discovery of methylmercury poisoning transmitted through fish and shellfish

- Fishing yields fell by 91% from earlier levels in the early 1950s.
- By October 1956, 40 people were identified with the disease and 14 were dead (case fatality rate 35%).
- Sediment sampling at the mouth of the wastewater canal measured 2 kilograms of mercury per ton of sediment in February 1959.
- Chisso began producing acetaldehyde in 1932 using mercury as a catalyst, which led to methylmercury discharge into Hyakken Harbour.
- In September 1958 Chisso rerouted its wastewater discharge from the bay to the Minamata River.

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© 2026 OBOMEDIA. All rights reserved.
This episode and its content (audio, text, and related materials) are the exclusive property of OBOMEDIA and are protected by applicable copyright laws. Reproduction, distribution, editing, or commercial use, in whole or in part, without prior written permission from OBOMEDIA is prohibited. For permissions, licensing, and business inquiries: business@obomedia.com.]]>1738falsefullhttps://www.spreaker.com/episode/the-luggage-sized-blast-that-shattered-al-ahli-s-silence--73090242
Hospitals are supposed to be sanctuaries; on October 17, 2023 a crater no larger than a carry-on suitcase appeared in Al-Ahli Arab Hospital’s courtyard and, according to the Gaza Health Organization, 471 people were killed-so how can such a small blast produce such a devastating death toll?

In this episode, we lay out the documented record: timelines, competing forensic claims, and the gaps where evidence ends. What each investigation found, where they contradict, and the single unresolved question-what actually detonated in that hospital courtyard-frames the narrative.

Person: Al-Ahli Arab Hospital staff and displaced civilians
Date: October 17, 2023
Location: Gaza City
Event: Courtyard explosion/crater roughly 1.0 m by 0.75 m and 0.3-0.4 m deep
Reported Death Toll: 471 (Gaza Health Organization), figures disputed

- Time of main strike recorded on Al Jazeera livestream: 18:59:55 local time
- Number of people inside hospital at time: roughly 600 patients and staff
- Number of displaced civilians sheltering in courtyard/parking lot: approximately 1,000
- Size of crater as measured by French intelligence: about 1 meter long, 75 centimeters wide, 30-40 centimeters deep
- Number of attacks on Gaza health facilities recorded by WHO from Oct 7-17: 51 attacks, with 15 healthcare workers killed and 27 injured

To listen to this podcast ad-free and access premium episodes, try our subscription with a 14-day free trial at obomedia.com.

© 2026 OBOMEDIA. All rights reserved.
This episode and its content (audio, text, and related materials) are the exclusive property of OBOMEDIA and are protected by applicable copyright laws. Reproduction, distribution, editing, or commercial use, in whole or in part, without prior written permission from OBOMEDIA is prohibited. For permissions, licensing, and business inquiries: business@obomedia.com.]]>https://api.spreaker.com/episode/73090242Tue, 21 Jul 2026 17:25:55 +0000OBOMEDIA ENTERTAINMENTThe Luggage-Sized Blast That Shattered Al-Ahli's Silence Hospitals are supposed to be sanctuaries; on October 17, 2023 a crater no larger than a carry-on suitcase appeared in Al-Ahli Arab Hospital’s courtyard and, according to the Gaza Health...
Hospitals are supposed to be sanctuaries; on October 17, 2023 a crater no larger than a carry-on suitcase appeared in Al-Ahli Arab Hospital’s courtyard and, according to the Gaza Health Organization, 471 people were killed-so how can such a small blast produce such a devastating death toll?

In this episode, we lay out the documented record: timelines, competing forensic claims, and the gaps where evidence ends. What each investigation found, where they contradict, and the single unresolved question-what actually detonated in that hospital courtyard-frames the narrative.

Person: Al-Ahli Arab Hospital staff and displaced civilians
Date: October 17, 2023
Location: Gaza City
Event: Courtyard explosion/crater roughly 1.0 m by 0.75 m and 0.3-0.4 m deep
Reported Death Toll: 471 (Gaza Health Organization), figures disputed

- Time of main strike recorded on Al Jazeera livestream: 18:59:55 local time
- Number of people inside hospital at time: roughly 600 patients and staff
- Number of displaced civilians sheltering in courtyard/parking lot: approximately 1,000
- Size of crater as measured by French intelligence: about 1 meter long, 75 centimeters wide, 30-40 centimeters deep
- Number of attacks on Gaza health facilities recorded by WHO from Oct 7-17: 51 attacks, with 15 healthcare workers killed and 27 injured

To listen to this podcast ad-free and access premium episodes, try our subscription with a 14-day free trial at obomedia.com.

© 2026 OBOMEDIA. All rights reserved.
This episode and its content (audio, text, and related materials) are the exclusive property of OBOMEDIA and are protected by applicable copyright laws. Reproduction, distribution, editing, or commercial use, in whole or in part, without prior written permission from OBOMEDIA is prohibited. For permissions, licensing, and business inquiries: business@obomedia.com.]]>1743falsefullhttps://www.spreaker.com/episode/the-hidden-crystals-that-turned-pet-food-into-poison--73090239
Fear and outrage: visible crystalline particles in wheat gluten shipped from China made their way into canned pet food on shelves across North America, Europe, and South Africa, and by the time anyone looked closely animals were already dying - why did the FDA receive roughly 8,500 reports of pet deaths but officially confirm only 14, and what deadly chemistry hid inside a bowl of gravy?

In this episode, we lay out the timeline and evidence from the spring of 2007, tracing how wheat gluten used as a thickener and protein source traveled from China to a Menu Foods factory in Ontario, was mixed into canned gravy products under roughly one hundred brand names, and was linked to sudden renal failure in household pets - could a chemical present at 6.6% explain the mass outbreak?

Person: Menu Foods
Event: Pet food recall in 2007
Date: March 16, 2007 (recall announced)
Location: Ontario factory, products on shelves in North America, Europe, and South Africa
Reports: FDA received roughly 8,500 reports of pet deaths; FDA officially confirmed 14

- Visible crystalline particles were present in a shipment of wheat gluten used for pet food gravy.
- The contaminated gluten contained a chemical measured at 6.6% in initial findings.
- Menu Foods manufactured wet pet food under approximately 100 brand names at its Streetsville, Ontario facility.
- The recall announced on March 16, 2007 pulled more than 5,300 products from shelves.
- A New York State lab reported finding aminopterin, but Cornell University and the FDA could not replicate that result.

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© 2026 OBOMEDIA. All rights reserved.
This episode and its content (audio, text, and related materials) are the exclusive property of OBOMEDIA and are protected by applicable copyright laws. Reproduction, distribution, editing, or commercial use, in whole or in part, without prior written permission from OBOMEDIA is prohibited. For permissions, licensing, and business inquiries: business@obomedia.com.]]>https://api.spreaker.com/episode/73090239Tue, 21 Jul 2026 17:25:50 +0000OBOMEDIA ENTERTAINMENTThe Hidden Crystals That Turned Pet Food Into Poison Fear and outrage: visible crystalline particles in wheat gluten shipped from China made their way into canned pet food on shelves across North America, Europe, and South Africa, and by the time...
Fear and outrage: visible crystalline particles in wheat gluten shipped from China made their way into canned pet food on shelves across North America, Europe, and South Africa, and by the time anyone looked closely animals were already dying - why did the FDA receive roughly 8,500 reports of pet deaths but officially confirm only 14, and what deadly chemistry hid inside a bowl of gravy?

In this episode, we lay out the timeline and evidence from the spring of 2007, tracing how wheat gluten used as a thickener and protein source traveled from China to a Menu Foods factory in Ontario, was mixed into canned gravy products under roughly one hundred brand names, and was linked to sudden renal failure in household pets - could a chemical present at 6.6% explain the mass outbreak?

Person: Menu Foods
Event: Pet food recall in 2007
Date: March 16, 2007 (recall announced)
Location: Ontario factory, products on shelves in North America, Europe, and South Africa
Reports: FDA received roughly 8,500 reports of pet deaths; FDA officially confirmed 14

- Visible crystalline particles were present in a shipment of wheat gluten used for pet food gravy.
- The contaminated gluten contained a chemical measured at 6.6% in initial findings.
- Menu Foods manufactured wet pet food under approximately 100 brand names at its Streetsville, Ontario facility.
- The recall announced on March 16, 2007 pulled more than 5,300 products from shelves.
- A New York State lab reported finding aminopterin, but Cornell University and the FDA could not replicate that result.

To listen to this podcast ad-free and access premium episodes, try our subscription with a 14-day free trial at obomedia.com.

© 2026 OBOMEDIA. All rights reserved.
This episode and its content (audio, text, and related materials) are the exclusive property of OBOMEDIA and are protected by applicable copyright laws. Reproduction, distribution, editing, or commercial use, in whole or in part, without prior written permission from OBOMEDIA is prohibited. For permissions, licensing, and business inquiries: business@obomedia.com.]]>1782falsefullhttps://www.spreaker.com/episode/the-grey-dust-that-killed-a-town-armley-s-asbestos-secret-revealed--73090237
Gray, invisible fibres settled on windowsills and children made snowballs from factory dust; decades later whole streets paid with their lives. Three hundred streets and a thousand homes lay downwind of blue asbestos, and when a court finally found for victims in 1995, the fifty people awarded compensation had all died - how did a company and a council keep this secret for so long?

In this episode, we lay out the timeline of exposure, corporate records, council surveys and legal outcomes to show what was known, when it was known, and what was done with that knowledge; could the contamination under Armley have been prevented or properly disclosed?

Person: R. D. Lunt
Company: Turner and Newall Ltd.
Factory: Midland Works (originally J. W. Roberts Ltd)
Period: 1855-1959 (factory operation and closure)
Event: Court ruling in 1995 awarding compensation to fifty people

- The Midland Works began manufacturing asbestos insulation mattresses in 1906 and processed blue asbestos, the most lethal variety.
- The factory’s peak workforce reached around 250 people who lived in streets immediately surrounding the site.
- Up to 50 years of latency existed between inhalation of asbestos fibres and diagnosis of mesothelioma.
- In 1978 Leeds City Council found “hundreds of tonnes of blue asbestos waste” mixed into the soil beneath the factory floor.
- Turner and Newall agreed to pay £15,000 for the factory clean-up in 1978 while excluding surrounding residential houses from the arrangement.

To listen to this podcast ad-free and access premium episodes, try our subscription with a 14-day free trial at obomedia.com.

© 2026 OBOMEDIA. All rights reserved.
This episode and its content (audio, text, and related materials) are the exclusive property of OBOMEDIA and are protected by applicable copyright laws. Reproduction, distribution, editing, or commercial use, in whole or in part, without prior written permission from OBOMEDIA is prohibited. For permissions, licensing, and business inquiries: business@obomedia.com.]]>https://api.spreaker.com/episode/73090237Tue, 21 Jul 2026 17:25:46 +0000OBOMEDIA ENTERTAINMENTThe Grey Dust That Killed a Town: Armley's Asbestos Secret Revealed Gray, invisible fibres settled on windowsills and children made snowballs from factory dust; decades later whole streets paid with their lives. Three hundred streets and a thousand...
Gray, invisible fibres settled on windowsills and children made snowballs from factory dust; decades later whole streets paid with their lives. Three hundred streets and a thousand homes lay downwind of blue asbestos, and when a court finally found for victims in 1995, the fifty people awarded compensation had all died - how did a company and a council keep this secret for so long?

In this episode, we lay out the timeline of exposure, corporate records, council surveys and legal outcomes to show what was known, when it was known, and what was done with that knowledge; could the contamination under Armley have been prevented or properly disclosed?

Person: R. D. Lunt
Company: Turner and Newall Ltd.
Factory: Midland Works (originally J. W. Roberts Ltd)
Period: 1855-1959 (factory operation and closure)
Event: Court ruling in 1995 awarding compensation to fifty people

- The Midland Works began manufacturing asbestos insulation mattresses in 1906 and processed blue asbestos, the most lethal variety.
- The factory’s peak workforce reached around 250 people who lived in streets immediately surrounding the site.
- Up to 50 years of latency existed between inhalation of asbestos fibres and diagnosis of mesothelioma.
- In 1978 Leeds City Council found “hundreds of tonnes of blue asbestos waste” mixed into the soil beneath the factory floor.
- Turner and Newall agreed to pay £15,000 for the factory clean-up in 1978 while excluding surrounding residential houses from the arrangement.

To listen to this podcast ad-free and access premium episodes, try our subscription with a 14-day free trial at obomedia.com.

© 2026 OBOMEDIA. All rights reserved.
This episode and its content (audio, text, and related materials) are the exclusive property of OBOMEDIA and are protected by applicable copyright laws. Reproduction, distribution, editing, or commercial use, in whole or in part, without prior written permission from OBOMEDIA is prohibited. For permissions, licensing, and business inquiries: business@obomedia.com.]]>1543falsefullhttps://www.spreaker.com/episode/the-doctor-who-turned-medicine-into-murder-karl-brandt-s-wake--73090235
The image of Karl Brandt speaking as the hood came down and the trapdoor opened captures a cold fusion of clinical expertise and engineered killing; he was Hitler's personal physician who specialized in head and spinal injuries and authorized the first infant killing that led to a program of medicalized murder. How did a trained surgeon, steeped in ideas that placed the “health of the social organism” above individuals, turn clinical knowledge into state-directed killing?

In this episode, we tell the story of Karl Brandt's rise from surgeon to Hitler's escort physician and the decisions that led from a single case to a systematized program of killing, and we ask the central question that emerged at Nuremberg: at what point does a physician become something else entirely?

Person: Karl Brandt
Date of birth: 8 January 1904
Event: Execution by hanging at Landsberg Prison on 2 June 1948
Case: Gerhard Kretschmar killed on 25 July 1939
Profession: Surgeon specializing in head and spinal injuries

- Brandt was hanged at Landsberg Prison on 2 June 1948 at age 44.
- He joined the Nazi Party in January 1932 at age 28 and joined the SS on 29 July 1934.
- Brandt examined and authorized the killing of five-month-old Gerhard Kretschmar on 25 July 1939.
- He completed his surgical training by 1928 with a specialty in injuries to the head and vertebral column.
- Brandt married Anni Rehborn on 17 March 1934 and their son Karl Brandt was born on 4 October 1935.

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© 2026 OBOMEDIA. All rights reserved.
This episode and its content (audio, text, and related materials) are the exclusive property of OBOMEDIA and are protected by applicable copyright laws. Reproduction, distribution, editing, or commercial use, in whole or in part, without prior written permission from OBOMEDIA is prohibited. For permissions, licensing, and business inquiries: business@obomedia.com.]]>https://api.spreaker.com/episode/73090235Tue, 21 Jul 2026 17:25:43 +0000OBOMEDIA ENTERTAINMENTThe Doctor Who Turned Medicine into Murder: Karl Brandt's Wake The image of Karl Brandt speaking as the hood came down and the trapdoor opened captures a cold fusion of clinical expertise and engineered killing; he was Hitler's personal physician...
The image of Karl Brandt speaking as the hood came down and the trapdoor opened captures a cold fusion of clinical expertise and engineered killing; he was Hitler's personal physician who specialized in head and spinal injuries and authorized the first infant killing that led to a program of medicalized murder. How did a trained surgeon, steeped in ideas that placed the “health of the social organism” above individuals, turn clinical knowledge into state-directed killing?

In this episode, we tell the story of Karl Brandt's rise from surgeon to Hitler's escort physician and the decisions that led from a single case to a systematized program of killing, and we ask the central question that emerged at Nuremberg: at what point does a physician become something else entirely?

Person: Karl Brandt
Date of birth: 8 January 1904
Event: Execution by hanging at Landsberg Prison on 2 June 1948
Case: Gerhard Kretschmar killed on 25 July 1939
Profession: Surgeon specializing in head and spinal injuries

- Brandt was hanged at Landsberg Prison on 2 June 1948 at age 44.
- He joined the Nazi Party in January 1932 at age 28 and joined the SS on 29 July 1934.
- Brandt examined and authorized the killing of five-month-old Gerhard Kretschmar on 25 July 1939.
- He completed his surgical training by 1928 with a specialty in injuries to the head and vertebral column.
- Brandt married Anni Rehborn on 17 March 1934 and their son Karl Brandt was born on 4 October 1935.

To listen to this podcast ad-free and access premium episodes, try our subscription with a 14-day free trial at obomedia.com.

© 2026 OBOMEDIA. All rights reserved.
This episode and its content (audio, text, and related materials) are the exclusive property of OBOMEDIA and are protected by applicable copyright laws. Reproduction, distribution, editing, or commercial use, in whole or in part, without prior written permission from OBOMEDIA is prohibited. For permissions, licensing, and business inquiries: business@obomedia.com.]]>1785falsefullhttps://www.spreaker.com/episode/the-judge-s-handwritten-plea-that-began-britain-s-blood-scandal--73090234
Fear that the state failed its most vulnerable: 962 haemophiliacs and their families were infected with HIV through NHS-prescribed clotting factor, and a High Court judge resorted to a handwritten plea because "the law had run out of instruments." What was in the 600 sealed files that the government refused to hand over, and why did a judge ask both sides to settle with no legal power to compel it?

In this episode, we follow the timeline from contaminated clotting factor in the late 1970s through the litigation that peaked in 1990, outlining who sued whom and what was at stake for families and children - and asking how much the state knew and when. Can a handwritten note from Mr Justice Ognall tell us where accountability begins?

Person: Mr Justice Ognall
Date: June 26, 1990
Case: 1,217 plaintiffs listed in litigation
Event: 600 files withheld covering 1972-1986
Status: 163 plaintiffs diagnosed with AIDS, 107 dead by November 1989

- 962 haemophiliacs and their families contracted HIV from NHS-prescribed clotting factor.
- Clotting factor was pooled from thousands of donors and used by the NHS from the late 1970s.
- By November 1989, 163 plaintiffs had developed AIDS and 107 were dead.
- The initial deadline to join proceedings was Feb 2, 1990, later extended to add 200 haemophiliac children.
- The government held 600 files covering 1972-1986 that were not handed over to plaintiffs.

To listen to this podcast ad-free and access premium episodes, try our subscription with a 14-day free trial at obomedia.com.

© 2026 OBOMEDIA. All rights reserved.
This episode and its content (audio, text, and related materials) are the exclusive property of OBOMEDIA and are protected by applicable copyright laws. Reproduction, distribution, editing, or commercial use, in whole or in part, without prior written permission from OBOMEDIA is prohibited. For permissions, licensing, and business inquiries: business@obomedia.com.]]>https://api.spreaker.com/episode/73090234Tue, 21 Jul 2026 17:25:39 +0000OBOMEDIA ENTERTAINMENTThe Judge's Handwritten Plea That Began Britain's Blood Scandal Fear that the state failed its most vulnerable: 962 haemophiliacs and their families were infected with HIV through NHS-prescribed clotting factor, and a High Court judge resorted to a...
Fear that the state failed its most vulnerable: 962 haemophiliacs and their families were infected with HIV through NHS-prescribed clotting factor, and a High Court judge resorted to a handwritten plea because "the law had run out of instruments." What was in the 600 sealed files that the government refused to hand over, and why did a judge ask both sides to settle with no legal power to compel it?

In this episode, we follow the timeline from contaminated clotting factor in the late 1970s through the litigation that peaked in 1990, outlining who sued whom and what was at stake for families and children - and asking how much the state knew and when. Can a handwritten note from Mr Justice Ognall tell us where accountability begins?

Person: Mr Justice Ognall
Date: June 26, 1990
Case: 1,217 plaintiffs listed in litigation
Event: 600 files withheld covering 1972-1986
Status: 163 plaintiffs diagnosed with AIDS, 107 dead by November 1989

- 962 haemophiliacs and their families contracted HIV from NHS-prescribed clotting factor.
- Clotting factor was pooled from thousands of donors and used by the NHS from the late 1970s.
- By November 1989, 163 plaintiffs had developed AIDS and 107 were dead.
- The initial deadline to join proceedings was Feb 2, 1990, later extended to add 200 haemophiliac children.
- The government held 600 files covering 1972-1986 that were not handed over to plaintiffs.

To listen to this podcast ad-free and access premium episodes, try our subscription with a 14-day free trial at obomedia.com.

© 2026 OBOMEDIA. All rights reserved.
This episode and its content (audio, text, and related materials) are the exclusive property of OBOMEDIA and are protected by applicable copyright laws. Reproduction, distribution, editing, or commercial use, in whole or in part, without prior written permission from OBOMEDIA is prohibited. For permissions, licensing, and business inquiries: business@obomedia.com.]]>1384falsefullhttps://www.spreaker.com/episode/the-factory-that-shouldn-t-have-died-al-shifa-s-missing-evidence--73090232
Half of Sudan’s medicines vanished in a single night: thirteen cruise missiles crossed the Red Sea on August 20, 1998 and destroyed the al-Shifa pharmaceutical factory that supplied more than 50% of the country’s pharmaceutical output. Yet the United States never allowed an on-site inspection, and the sole soil sample tying the site to VX precursor EMPTA came from a single Egyptian asset-so who really decided the factory’s fate?

In this episode, we trace the timeline from the soil sample and internal intelligence memos to the White House Small Group decision made twelve days after the East Africa embassy bombings, asking whether the strike was based on solid evidence or political urgency. Was al-Shifa targeted despite dissenting analysis, or was critical intelligence simply missing?

Person: Salah Idris
Date: August 20, 1998
Location: Khartoum, Sudan
Event: Operation Infinite Reach
Topic: EMPTA soil sample

- 13 cruise missiles struck the al-Shifa factory at 7:30 PM on August 20, 1998.
- The factory supplied more than 50% of Sudan’s pharmaceutical output and employed 300 workers.
- An Egyptian asset collected one soil sample in December 1997 that tested positive for EMPTA at 2.5 times trace levels.
- The factory held a United States Oil-for-Food contract worth $199,000 and had an assessed value of $30 million.
- A State Department Bureau of Intelligence and Research memo dated August 6, 1998 and a CIA report dated July 24, 1998 opposed the attack on al-Shifa.

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© 2026 OBOMEDIA. All rights reserved.
This episode and its content (audio, text, and related materials) are the exclusive property of OBOMEDIA and are protected by applicable copyright laws. Reproduction, distribution, editing, or commercial use, in whole or in part, without prior written permission from OBOMEDIA is prohibited. For permissions, licensing, and business inquiries: business@obomedia.com.]]>https://api.spreaker.com/episode/73090232Tue, 21 Jul 2026 17:25:36 +0000OBOMEDIA ENTERTAINMENTThe Factory That Shouldn't Have Died: Al-Shifa's Missing Evidence Half of Sudan’s medicines vanished in a single night: thirteen cruise missiles crossed the Red Sea on August 20, 1998 and destroyed the al-Shifa pharmaceutical factory that supplied...
Half of Sudan’s medicines vanished in a single night: thirteen cruise missiles crossed the Red Sea on August 20, 1998 and destroyed the al-Shifa pharmaceutical factory that supplied more than 50% of the country’s pharmaceutical output. Yet the United States never allowed an on-site inspection, and the sole soil sample tying the site to VX precursor EMPTA came from a single Egyptian asset-so who really decided the factory’s fate?

In this episode, we trace the timeline from the soil sample and internal intelligence memos to the White House Small Group decision made twelve days after the East Africa embassy bombings, asking whether the strike was based on solid evidence or political urgency. Was al-Shifa targeted despite dissenting analysis, or was critical intelligence simply missing?

Person: Salah Idris
Date: August 20, 1998
Location: Khartoum, Sudan
Event: Operation Infinite Reach
Topic: EMPTA soil sample

- 13 cruise missiles struck the al-Shifa factory at 7:30 PM on August 20, 1998.
- The factory supplied more than 50% of Sudan’s pharmaceutical output and employed 300 workers.
- An Egyptian asset collected one soil sample in December 1997 that tested positive for EMPTA at 2.5 times trace levels.
- The factory held a United States Oil-for-Food contract worth $199,000 and had an assessed value of $30 million.
- A State Department Bureau of Intelligence and Research memo dated August 6, 1998 and a CIA report dated July 24, 1998 opposed the attack on al-Shifa.

To listen to this podcast ad-free and access premium episodes, try our subscription with a 14-day free trial at obomedia.com.

© 2026 OBOMEDIA. All rights reserved.
This episode and its content (audio, text, and related materials) are the exclusive property of OBOMEDIA and are protected by applicable copyright laws. Reproduction, distribution, editing, or commercial use, in whole or in part, without prior written permission from OBOMEDIA is prohibited. For permissions, licensing, and business inquiries: business@obomedia.com.]]>1903falsefullhttps://www.spreaker.com/episode/when-diagnosis-becomes-a-prison-the-soviet-crime-of-sluggish-schizophrenia--73090231
Fear that a medical label can erase a life: Soviet psychiatry used a diagnosis called "sluggish schizophrenia" to confine dissenters, believers, and critics without trial. How did a diagnostic category with no hallucinations or conventional psychosis come to replace courts and prisons?

In this episode, we lay out the evidence brought to light by an American psychiatric delegation in February 1989 and earlier whistleblowers, showing how clinical records and human testimony diverged - and ask what it means when medicine is turned into a tool of repression.

Person: Vladimir Bukovsky
Person: Natalya Gorbanevskaya
Person: Pyotr Grigorenko
Event: American psychiatric delegation visit
Date: February 1989

- The American delegation arrived with a list of 48 names of people allegedly involuntarily committed to Soviet psychiatric hospitals.
- Roughly half of the 48 people were discharged in the two months between the list's submission and the Americans' arrival (about 24 people).
- Of the patients still in hospital, 15 were examined by the American team; one had an active schizophrenia diagnosis but showed no evidence of mental disorder.
- Twelve of the discharged individuals agreed to be examined; Americans found 9 of those 12 showed no evidence of current or past mental illness.
- The World Psychiatric Association formally condemned Soviet practices in 1977, and the Soviet psychiatric society withdrew from the WPA in 1983 before the vote.

To listen to this podcast ad-free and access premium episodes, try our subscription with a 14-day free trial at obomedia.com.

© 2026 OBOMEDIA. All rights reserved.
This episode and its content (audio, text, and related materials) are the exclusive property of OBOMEDIA and are protected by applicable copyright laws. Reproduction, distribution, editing, or commercial use, in whole or in part, without prior written permission from OBOMEDIA is prohibited. For permissions, licensing, and business inquiries: business@obomedia.com.]]>https://api.spreaker.com/episode/73090231Tue, 21 Jul 2026 17:25:31 +0000OBOMEDIA ENTERTAINMENTWhen Diagnosis Becomes a Prison: The Soviet Crime of Sluggish Schizophrenia Fear that a medical label can erase a life: Soviet psychiatry used a diagnosis called "sluggish schizophrenia" to confine dissenters, believers, and critics without trial....
Fear that a medical label can erase a life: Soviet psychiatry used a diagnosis called "sluggish schizophrenia" to confine dissenters, believers, and critics without trial. How did a diagnostic category with no hallucinations or conventional psychosis come to replace courts and prisons?

In this episode, we lay out the evidence brought to light by an American psychiatric delegation in February 1989 and earlier whistleblowers, showing how clinical records and human testimony diverged - and ask what it means when medicine is turned into a tool of repression.

Person: Vladimir Bukovsky
Person: Natalya Gorbanevskaya
Person: Pyotr Grigorenko
Event: American psychiatric delegation visit
Date: February 1989

- The American delegation arrived with a list of 48 names of people allegedly involuntarily committed to Soviet psychiatric hospitals.
- Roughly half of the 48 people were discharged in the two months between the list's submission and the Americans' arrival (about 24 people).
- Of the patients still in hospital, 15 were examined by the American team; one had an active schizophrenia diagnosis but showed no evidence of mental disorder.
- Twelve of the discharged individuals agreed to be examined; Americans found 9 of those 12 showed no evidence of current or past mental illness.
- The World Psychiatric Association formally condemned Soviet practices in 1977, and the Soviet psychiatric society withdrew from the WPA in 1983 before the vote.

To listen to this podcast ad-free and access premium episodes, try our subscription with a 14-day free trial at obomedia.com.

© 2026 OBOMEDIA. All rights reserved.
This episode and its content (audio, text, and related materials) are the exclusive property of OBOMEDIA and are protected by applicable copyright laws. Reproduction, distribution, editing, or commercial use, in whole or in part, without prior written permission from OBOMEDIA is prohibited. For permissions, licensing, and business inquiries: business@obomedia.com.]]>1897falsefullhttps://www.spreaker.com/episode/how-a-nail-riddled-dentist-escaped-asylum-and-haunted-small-town-medicine--73090229
A man drives down the highway with nails embedded in his skull, laughing and pulling a nail free to use as a toothpick - an image that opens and closes The Dentist 2. Why did a production made in five weeks, with one weekend of pre-production and a $700,000 budget, produce a film that earned a Sitges nomination while scoring zero percent on Rotten Tomatoes?

In this episode, we tell how a sequel was assembled from withheld scripts, Southern California stand-ins for a Missouri town, and a cast and crew who improvised their way through cramped schedules and practical effects. How did these choices shape a film built around a dentist who escaped a maximum-security psychiatric facility and assumed a new identity in a place called Paradise?

Person: Corbin Bernsen
Director: Brian Yuzna
Producer: Pierre David
Budget: $700,000
Principal photography: February 23, 1998 - March 1998

- The director had one weekend of pre-production and was not permitted to read the finished script before shooting began.
- Principal photography ran roughly five weeks, starting on February 23, 1998.
- The film premiered on HBO on December 11, 1998.
- Rotten Tomatoes scored the film at 0% from five critics with an average rating of 3.7/10.
- The production used locations in Southern California to portray Paradise, Missouri, including South Myrtle Avenue in Monrovia and the El Royale Motel on Rossmore Avenue.

To listen to this podcast ad-free and access premium episodes, try our subscription with a 14-day free trial at obomedia.com.

© 2026 OBOMEDIA. All rights reserved.
This episode and its content (audio, text, and related materials) are the exclusive property of OBOMEDIA and are protected by applicable copyright laws. Reproduction, distribution, editing, or commercial use, in whole or in part, without prior written permission from OBOMEDIA is prohibited. For permissions, licensing, and business inquiries: business@obomedia.com.]]>https://api.spreaker.com/episode/73090229Tue, 21 Jul 2026 17:25:27 +0000OBOMEDIA ENTERTAINMENTHow a Nail‑Riddled Dentist Escaped Asylum and Haunted Small‑Town Medicine A man drives down the highway with nails embedded in his skull, laughing and pulling a nail free to use as a toothpick - an image that opens and closes The Dentist 2. Why did...
A man drives down the highway with nails embedded in his skull, laughing and pulling a nail free to use as a toothpick - an image that opens and closes The Dentist 2. Why did a production made in five weeks, with one weekend of pre-production and a $700,000 budget, produce a film that earned a Sitges nomination while scoring zero percent on Rotten Tomatoes?

In this episode, we tell how a sequel was assembled from withheld scripts, Southern California stand-ins for a Missouri town, and a cast and crew who improvised their way through cramped schedules and practical effects. How did these choices shape a film built around a dentist who escaped a maximum-security psychiatric facility and assumed a new identity in a place called Paradise?

Person: Corbin Bernsen
Director: Brian Yuzna
Producer: Pierre David
Budget: $700,000
Principal photography: February 23, 1998 - March 1998

- The director had one weekend of pre-production and was not permitted to read the finished script before shooting began.
- Principal photography ran roughly five weeks, starting on February 23, 1998.
- The film premiered on HBO on December 11, 1998.
- Rotten Tomatoes scored the film at 0% from five critics with an average rating of 3.7/10.
- The production used locations in Southern California to portray Paradise, Missouri, including South Myrtle Avenue in Monrovia and the El Royale Motel on Rossmore Avenue.

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© 2026 OBOMEDIA. All rights reserved.
This episode and its content (audio, text, and related materials) are the exclusive property of OBOMEDIA and are protected by applicable copyright laws. Reproduction, distribution, editing, or commercial use, in whole or in part, without prior written permission from OBOMEDIA is prohibited. For permissions, licensing, and business inquiries: business@obomedia.com.]]>1462falsefullhttps://www.spreaker.com/episode/bound-and-breathless-how-restraints-killed-kelly-savage--73090228
A loved, 27-year-old dual citizen was strapped at five points to a hospital bed without having harmed anyone, then ten days later his heart stopped - what did paperwork, a holiday week and a nine percent statistic have to do with his death?

In this episode, we lay out the sequence of events, hospital records and family context from admission to aftermath, and ask how contradictory notes and a system already using restraints on thousands could end in a preventable death.

Person: Kelly Robert Savage
Date: April 30, 2017 (admission); ten days later (death)
Location: Yamato Hospital, Kanagawa Prefecture, Japan
Age: 27
Previous hospitalization: five weeks in 2012 for a psychotic episode

- Kelly Savage was placed in five-point restraints on admission: both wrists, both ankles and a waist belt.
- He had not harmed anyone or himself prior to being restrained on April 30, 2017.
- Kelly stopped taking psychiatric medication by April 2017 and developed a manic-psychotic state.
- Medical records from the same week contained contradictory entries describing him as both "calm" and at ongoing "risk."
- No criminal charges, independent investigation, or hospital acknowledgement of irregularity followed his death.

To listen to this podcast ad-free and access premium episodes, try our subscription with a 14-day free trial at obomedia.com.

© 2026 OBOMEDIA. All rights reserved.
This episode and its content (audio, text, and related materials) are the exclusive property of OBOMEDIA and are protected by applicable copyright laws. Reproduction, distribution, editing, or commercial use, in whole or in part, without prior written permission from OBOMEDIA is prohibited. For permissions, licensing, and business inquiries: business@obomedia.com.]]>https://api.spreaker.com/episode/73090228Tue, 21 Jul 2026 17:25:24 +0000OBOMEDIA ENTERTAINMENTBound and Breathless: How Restraints Killed Kelly Savage A loved, 27-year-old dual citizen was strapped at five points to a hospital bed without having harmed anyone, then ten days later his heart stopped - what did paperwork, a holiday week and a...
A loved, 27-year-old dual citizen was strapped at five points to a hospital bed without having harmed anyone, then ten days later his heart stopped - what did paperwork, a holiday week and a nine percent statistic have to do with his death?

In this episode, we lay out the sequence of events, hospital records and family context from admission to aftermath, and ask how contradictory notes and a system already using restraints on thousands could end in a preventable death.

Person: Kelly Robert Savage
Date: April 30, 2017 (admission); ten days later (death)
Location: Yamato Hospital, Kanagawa Prefecture, Japan
Age: 27
Previous hospitalization: five weeks in 2012 for a psychotic episode

- Kelly Savage was placed in five-point restraints on admission: both wrists, both ankles and a waist belt.
- He had not harmed anyone or himself prior to being restrained on April 30, 2017.
- Kelly stopped taking psychiatric medication by April 2017 and developed a manic-psychotic state.
- Medical records from the same week contained contradictory entries describing him as both "calm" and at ongoing "risk."
- No criminal charges, independent investigation, or hospital acknowledgement of irregularity followed his death.

To listen to this podcast ad-free and access premium episodes, try our subscription with a 14-day free trial at obomedia.com.

© 2026 OBOMEDIA. All rights reserved.
This episode and its content (audio, text, and related materials) are the exclusive property of OBOMEDIA and are protected by applicable copyright laws. Reproduction, distribution, editing, or commercial use, in whole or in part, without prior written permission from OBOMEDIA is prohibited. For permissions, licensing, and business inquiries: business@obomedia.com.]]>1775falsefullhttps://www.spreaker.com/episode/the-bodies-we-built-medicine-on-theft-silence-and-reckoning--73090227
Grief and outrage are threaded through medical history: a biopsy taken without consent became the HeLa cell line that powered vaccines and gene research, yet Henrietta Lacks’s family waited seventy-two years for formal acknowledgment-how did institutions normalize taking and displaying bodies as if they were data rather than people?

In this episode, we trace three linked stories across centuries to show how bodies were converted into specimens, artifacts, and cell lines without consent, and we ask how a pattern that began with public displays in nineteenth-century Europe led to modern laboratories still using tissues taken in secrecy.

Person: Henrietta Lacks
Date: 1951
Location: Johns Hopkins Hospital, Baltimore
Person: Sarah Baartman
Date: 1815
Person: James Marion Sims
Date: 1840s

- Henrietta Lacks arrived at Johns Hopkins in 1951 with vaginal bleeding and a malignant cervical tumor.
- Dr. George Gey labeled Lacks’s cells “immortal” after they survived and replicated outside the body, creating the HeLa cell line.
- HeLa cells were used in research on polio vaccine development, chemotherapy, gene mapping, cloning, and in vitro fertilization.
- Sarah Baartman was exhibited in London and Paris for five years and died in 1815; her brain, genitalia, and skeleton were preserved and displayed for over a century.
- James Marion Sims practiced in the American South in the 1840s and developed a technique for vesicovaginal fistula repair that is still taught in medical schools.

To listen to this podcast ad-free and access premium episodes, try our subscription with a 14-day free trial at obomedia.com.

© 2026 OBOMEDIA. All rights reserved.
This episode and its content (audio, text, and related materials) are the exclusive property of OBOMEDIA and are protected by applicable copyright laws. Reproduction, distribution, editing, or commercial use, in whole or in part, without prior written permission from OBOMEDIA is prohibited. For permissions, licensing, and business inquiries: business@obomedia.com.]]>https://api.spreaker.com/episode/73090227Tue, 21 Jul 2026 17:25:19 +0000OBOMEDIA ENTERTAINMENTThe Bodies We Built Medicine On: Theft, Silence, and Reckoning Grief and outrage are threaded through medical history: a biopsy taken without consent became the HeLa cell line that powered vaccines and gene research, yet Henrietta Lacks’s family...
Grief and outrage are threaded through medical history: a biopsy taken without consent became the HeLa cell line that powered vaccines and gene research, yet Henrietta Lacks’s family waited seventy-two years for formal acknowledgment-how did institutions normalize taking and displaying bodies as if they were data rather than people?

In this episode, we trace three linked stories across centuries to show how bodies were converted into specimens, artifacts, and cell lines without consent, and we ask how a pattern that began with public displays in nineteenth-century Europe led to modern laboratories still using tissues taken in secrecy.

Person: Henrietta Lacks
Date: 1951
Location: Johns Hopkins Hospital, Baltimore
Person: Sarah Baartman
Date: 1815
Person: James Marion Sims
Date: 1840s

- Henrietta Lacks arrived at Johns Hopkins in 1951 with vaginal bleeding and a malignant cervical tumor.
- Dr. George Gey labeled Lacks’s cells “immortal” after they survived and replicated outside the body, creating the HeLa cell line.
- HeLa cells were used in research on polio vaccine development, chemotherapy, gene mapping, cloning, and in vitro fertilization.
- Sarah Baartman was exhibited in London and Paris for five years and died in 1815; her brain, genitalia, and skeleton were preserved and displayed for over a century.
- James Marion Sims practiced in the American South in the 1840s and developed a technique for vesicovaginal fistula repair that is still taught in medical schools.

To listen to this podcast ad-free and access premium episodes, try our subscription with a 14-day free trial at obomedia.com.

© 2026 OBOMEDIA. All rights reserved.
This episode and its content (audio, text, and related materials) are the exclusive property of OBOMEDIA and are protected by applicable copyright laws. Reproduction, distribution, editing, or commercial use, in whole or in part, without prior written permission from OBOMEDIA is prohibited. For permissions, licensing, and business inquiries: business@obomedia.com.]]>1551falsefull