Chris Williamson · 2026-05-25 · Andrew Huberman, Chris Williamson (host), Tom Segura, Matt McCusker
Andrew Huberman, Matt McCusker & Tom Segura - Mostly Wise #1
64 claims checked against research: 5 contradicted 1 contradicted online 9 overstated 6 needing context 36 supported 1 corroborated online 6 unverified
5 Contradicted by research
Tadalafil was developed first as a prostate health drug before it was found to treat erectile dysfunction at higher doses.
"So, tadalafil, which is the generic name for Cialis, was developed first as a prostate health drug. And then people took more of it and realized that at higher dosages it can be effective for erectile dysfunction." (said at 0:00:05)
The speaker's claim inverts the actual development and regulatory history of tadalafil. Tadalafil was originally developed as a phosphodiesterase type 5 (PDE5) inhibitor for the treatment of erectile dysfunction (and later pulmonary arterial hypertension). It was approved by regulatory bodies (such as the US FDA in 2003) for erectile dysfunction at on-demand doses of 5–20 mg. Its application for benign prostatic hyperplasia (BPH) and lower urinary tract symptoms (LUTS) was investigated and approved years later (FDA approval in 2011) as a daily low-dose regimen (5 mg), after urinary improvements were observed in clinical trials and post-marketing use for erectile dysfunction.
- contradicts: Selective targeting phosphodiesterase-5 (PDE5): clinical progress, design strategies, and … (Journal of enzyme inhibition and medicinal chemistry 2026)
"To date, a few inhibitors targeting PDE5, exemplified by sildenafil, tadalafil, and vardenafil, have been approved for the treatment of several diseases including pulmonary arterial hypertension and erectile dysfunction." (abstract, passage verified)
pubmedfull study (doi) - context: Pharmacologic and clinical considerations of phosphodiesterase type 5 inhibitors and β-adr… (Expert opinion on drug metabolism & toxicology 2026)
"While many medication classes exist for treatment of LUTS secondary to BPH, their increasing prevalence in a growing and aging population begs the need for novel therapeutic avenues." (abstract, background, passage verified)
pubmedfull study (doi)
Narcissists do not tend to commit suicide.
"Also he was a narcissist. Everyone agrees on that. Like, they don't tend to kill themselves." (said at 1:03:18)
Psychiatric literature contradicts the claim that narcissists do not tend to die by suicide or make suicide attempts. Clinical and systematic reviews indicate that narcissistic personality disorder and narcissistic traits are well-documented risk factors for suicidal behavior. Suicide risk is recognized as a significant clinical concern, particularly following severe narcissistic injury (e.g., public shame or perceived failure). While grandiose narcissism can be protective against chronic suicidal ideation in some contexts, it is associated with highly lethal, well-planned suicide attempts and severe self-harm, while vulnerable narcissism is linked to frequent suicidal ideation and self-harm.
As dopamine levels rise, testosterone levels increase in both men and women.
"And as dopamine goes up, testosterone goes up in women and men, okay?" (said at 1:35:32)
There is no general physiological principle stating that rising dopamine increases testosterone levels in healthy men and women. In randomized, placebo-controlled human trials evaluating the endocrine effects of dopaminergic stimulation (such as dopamine reuptake inhibition via methylphenidate or dopamine/norepinephrine release via d-amphetamine and lisdexamfetamine), acute elevations in dopaminergic activity failed to alter circulating testosterone levels in healthy men and women. Dopamine agonists only increase testosterone in specific clinical pathologies—such as hyperprolactinemia or prolactin-secreting pituitary adenomas—where dopamine restores testosterone indirectly by relieving prolactin-mediated suppression of the hypothalamic-pituitary-gonadal axis, rather than by directly driving testosterone production.
Growth hormone secretagogues such as tesamorelin and sermorelin increase slow-wave deep sleep but reduce REM sleep.
"So if you take something to increase the amount of slow wave deep sleep that you get. Let's say and I'm not recommending this cuz these growth hormone secretagogues so increase growth hormone, but things like tesamorelin um sermorelin, you'll get a bigger growth hormone surge and you'll get more deep sleep, but you'll get less REM." (said at 1:38:23)
The claim that growth hormone secretagogues such as sermorelin or tesamorelin increase slow-wave deep sleep while suppressing REM sleep is contradicted by randomized clinical trials in humans. In healthy men, administration of growth hormone-releasing hormone (GHRH)—of which sermorelin is a synthetic peptide fragment—increases both slow-wave sleep (deep sleep) and rapid eye movement (REM) sleep, rather than decreasing REM sleep. In young women, GHRH administration was found to decrease both REM sleep and stage 4 slow-wave sleep. No evidence supports a selective effect where GHRH secretagogues expand deep sleep while reducing REM sleep.
- contradicts: Sleep and endocrine changes after intranasal administration of growth hormone-releasing ho… (Psychoneuroendocrinology 1999) · cited 81x in the literature
"Moreover, results indicated that after intranasal administration GHRH increased rapid-eye-movement (REM) sleep and slow wave sleep (SWS), with this influence concentrating on the second half of sleep time." (abstract, results, passage verified)
pubmedfull study (doi) - contradicts: Sleep-promoting effects of growth hormone-releasing hormone in normal men. (The American journal of physiology 1993) · cited 146x in the literature
"In the absence of sleep deprivation, injection of GHRH in early sleep did not modify SW sleep but increased REM sleep." (abstract, results, passage verified)
pubmedfull study (doi) - contradicts: Greater efficacy of episodic than continuous growth hormone-releasing hormone (GHRH) admin… (The Journal of clinical endocrinology and metabolism 1996) · cited 72x in the literature
"Compared with a placebo condition, episodic administration of GHRH enhanced SWS (P < 0.01) and rapid eye movement (REM) sleep (P < 0.05) and diminished time spent in wakefulness and sleep stage 1 (P < 0.05)." (abstract, results, passage verified)
pubmedfull study (doi)
In the original Stanford marshmallow experiment, no child was able to wait the full 15 minutes to receive the second marshmallow without eating the first.
"turns out the way the experiment was done is every kid got a marshmallow in front of them. A timer was set for 15 minutes. Every kid ate the marshmallow. Nobody talks about this. No kid waited for the second marshmallow." (said at 2:26:58)
The claim that every child ate the treat and no child waited the full time in the original Stanford marshmallow / delay of gratification studies is contradicted by the published experimental record. In Walter Mischel and colleagues' original experiments conducted at Stanford University's Bing Nursery School in the late 1960s and early 1970s, many children successfully waited the full duration (typically 15 minutes) without eating the initial treat. Decades of subsequent longitudinal research traced these exact participants, categorizing them into 'high delayers' (those who waited the full duration) and 'low delayers' (those who rang the bell or ate the treat before the time elapsed) to assess later cognitive, behavioral, and neural outcomes.
Unverified means no publication matching the claim was located; it does not prove the claim false. Spotted an error? See the corrections policy - disputes from the people quoted are prioritized.