HoldsUp

David Eagleman

Stanford University

David Eagleman is a neuroscientist, author, and professor at Stanford University. His published research examines sensory substitution, haptic devices for sensory boosting, time perception, synesthesia, and mechanisms of REM sleep. He has also investigated mobile neurocognitive screening tools for detecting cognitive impairment and concussions, as well as assessing recidivism risk in correctional settings.

32 claims checked on air: 3 context 1 overstated 27 supported 1 unverified

What they said on air

3 citing their own research

0:03:33supportedmoderateScience & Tools of Learning & Memory | Dr. David Eagleman

The human brain contains approximately 86 billion neurons, each forming an average of 10,000 connections with neighboring neurons.

"You've got 86 billion neurons. And really, the way to think about it, these are like little creatures that are all crawling around and moving around. Each one is, you know, on average contacting 10,000 of its neighbors" (said at 0:03:33)

The estimate of approximately 86 billion neurons in the human brain is well-established by quantitative isotropic fractionator studies (Azevedo et al., 2009; Herculano-Houzel, 2012). Quantitative stereological estimates of synaptic density in the human neocortex find approximately 0.15 quadrillion (1.5 x 10^14) synapses across ~19-20 billion cortical neurons, averaging roughly 7,000 to 10,000 synaptic connections per neuron.

0:06:36supportedmoderateScience & Tools of Learning & Memory | Dr. David Eagleman

Humans have roughly four times as much cerebral cortex as our nearest evolutionary relatives in the animal kingdom.

"We have four times as much cortex as our nearest neighbors in the animal kingdom." (said at 0:06:36)

Comparative neuroanatomical studies demonstrate that the human cerebral cortex is roughly 3 to 4 times larger in volume, surface area, and neuronal count compared to our closest living relatives, chimpanzees (Pan troglodytes) and bonobos. While the chimpanzee brain weighs approximately 350–400 grams, the human brain averages about 1,300–1,400 grams, accompanied by marked increases in cortical gyrification and prefrontal white matter volume.

0:06:43supportedhighScience & Tools of Learning & Memory | Dr. David Eagleman

The human cerebral cortex is roughly 3 millimeters thick and composed of a canonical six-layered circuitry across different functional regions.

"the cortex is just the outer 3 millimeters of the brain. It's that wrinkly bit. And that's the magic stuff because it turns out cortex is a one-trick pony. The reason the cortex looks the same everywhere is because it is the same. It's got the same circuitry. It's got six little layers." (said at 0:06:43)

The human cerebral cortex (specifically the neocortex, which constitutes the vast majority of the cortex) is well established in neuroanatomy as having an average thickness of approximately 2 to 4 mm (roughly 3 mm, varying regionally) and is characterized by a canonical six-layered laminar organization and microcircuitry across cortical areas.

0:07:31supportedvery lowScience & Tools of Learning & Memory | Dr. David Eagleman

In a 2000 study by Mriganka Sur, rerouting visual projections to the auditory cortex in developing ferrets caused the auditory cortex to become visually responsive.

"So you may know this study in 2000 by Mriganka Sur at MIT where he in a ferret took the visual information, the optic nerve, and he plugged it into the auditory cortex and then what would have been the auditory cortex became visually responsive and it started caring about vision." (said at 0:07:31)

Mriganka Sur's laboratory published classic papers in 2000 (such as von Melchner et al. and Sharma et al. in Nature) demonstrating that neonatal redirection of retinal projections into the auditory pathway of ferrets induced visual responsiveness, orientation tuning modules, and visual perceptual processing in the primary auditory cortex. Because the supporting evidence consists of experimental animal neurophysiology studies, GRADE certainty is very low.

0:09:13supportedmoderateScience & Tools of Learning & Memory | Dr. David Eagleman

In people born blind, the visual cortex is repurposed for tactile sensation, auditory processing, and memory, resulting in heightened tactile and auditory discrimination.

"people who are born blind, what we call the visual cortex at the back of the head here, that gets taken over. It's no longer visual. It becomes devoted to hearing, to touch, to memory, things like this. And you can demonstrate that people who are born blind are better at hearing and touch and so on. They can discriminate things much more finely." (said at 0:09:13)

Extensive neuroimaging, systematic reviews, and behavioral studies confirm cross-modal neuroplasticity in congenitally blind individuals. Deprived visual (occipital) cortex is recruited for non-visual sensory inputs, including tactile processing (e.g., Braille reading), auditory localization and processing, language, and working memory tasks, which is associated with compensatory enhancements in tactile and auditory discrimination.

0:09:36supportedmoderateScience & Tools of Learning & Memory | Dr. David Eagleman

In people who become deaf, the auditory cortex is reorganized for visual processing tasks, including enhanced lip-reading ability.

"Same with people who go deaf, that the auditory cortex, all that real estate—nothing lies fallow in the brain—all that gets taken over for different tasks and they can do things like see your accent. Just by lip reading, they can tell where in the country you're from and so on." (said at 0:09:36)

Extensive neuroimaging and electrophysiological research confirms that auditory deprivation leads to cross-modal plasticity, whereby regions of the auditory cortex (such as the superior temporal cortex) are recruited for visual tasks, including visual language processing and speechreading (lip-reading). Studies demonstrate that visual speech stimuli activate auditory cortical regions in deaf individuals and that this cross-modal activity correlates with visual speechreading proficiency.

0:17:40supportedmoderateScience & Tools of Learning & Memory | Dr. David Eagleman

Children raised bilingually or trilingually tend to have a smaller single-language vocabulary size in each language compared to monolingual peers.

"when children grow up, let's say, trilingually or even bilingually, they end up having a lower vocabulary in both languages than if they grow up monolingually." (said at 0:17:40)

A well-established finding in developmental linguistics is that bilingual and multilingual children generally have smaller single-language receptive and expressive vocabularies in each individual language compared to monolingual peers of the same age. This reflects divided language input across multiple languages. When their vocabularies are assessed across both or all languages combined (total or conceptual vocabulary), multilingual children typically match or exceed the vocabulary size of monolinguals.

0:28:49supportedhighScience & Tools of Learning & Memory | Dr. David Eagleman

In the Religious Orders Study in Chicago, autopsy evaluations showed that some elderly participants had extensive Alzheimer's disease pathology despite displaying no clinical cognitive deficits while alive.

"There's been this this study going on for decades now called the the what is it? Religious Orders Study uh up in Chicago area where there's a whole bunch of nuns and priests that agreed to donate their brains when they passed away. And then when they donate their brains, the researchers uh you know examine them, do autopsies on them. What the researchers found is that some fraction of these nuns had Alzheimer's disease, but nobody knew it when they were alive. Nobody saw any cognitive deficits." (said at 0:28:49)

The Religious Orders Study (often evaluated in conjunction with the Rush Memory and Aging Project) has repeatedly demonstrated that postmortem neuropathologic assessments reveal substantial Alzheimer's disease pathology (including amyloid-beta plaques and neurofibrillary tangles) in a notable proportion of elderly participants who exhibited no cognitive impairment or clinical dementia during life. This landmark finding is central to research on cognitive reserve, preclinical Alzheimer's disease, and clinicopathologic discordance.

0:33:13supportedhighScience & Tools of Learning & Memory | Dr. David Eagleman

Classic psychedelics primarily act via serotonergic receptors.

"So many of the interesting studies on psychedelics are using psychedelics that are GUEST1: kind of like serotonin. I mean they act on different receptors, but they're very serotonergic." (said at 0:33:13)

Classic psychedelics (such as LSD, psilocybin, DMT, and mescaline) primarily mediate their perceptual and psychoactive effects through agonist or partial agonist activity at serotonergic receptors, most notably the serotonin 5-HT2A receptor subtype.

0:34:03unverifiedvery lowScience & Tools of Learning & Memory | Dr. David Eagleman

In infants, acetylcholine is released broadly across the brain during prediction errors, whereas in adults, acetylcholine release becomes localized to specific cortical sites undergoing plasticity.

"When you are a baby, you've got acetylcholine going everywhere whenever you're trying to figure out the world. Whenever something's not matching a prediction and you've got acetylcholine going everywhere that says, 'Hey, I got to figure out what just happened and how to link this with what I did,' and so on. As you get older, it's more like, you know, a pointillist artist who just dabs things here or there. You get acetylcholine release very locally in very in small places and that's where you make changes." (said at 0:34:03)

No published studies directly comparing the spatial topography of prediction-error-evoked acetylcholine release across the whole brain between infants and adults were located. While acetylcholine is established to modulate cortical plasticity and signal unexpected uncertainty or prediction errors in various animal models, the specific developmental shift from broad/diffuse whole-brain release in human infants to highly localized release in adults remains unverified in the indexed literature.

0:35:10supportedhighScience & Tools of Learning & Memory | Dr. David Eagleman

Dopamine-increasing medications used in Parkinson's disease alter risk aversion and can cause compulsive gambling as a side effect.

"with Parkinson's, people get have less dopamine and so the medications are to crank up the dopamine. What that led to, you may know this fascinating story, this probably 25 years ago now, where you know, observant clinicians noted that people on these Parkinson's medications were becoming hypercompulsive gamblers... when you crank up the dopamine that changes your risk aversion such that people are taking So now it's a it's a contraindication that's listed on the bottle." (said at 0:35:10)

There is extensive clinical, registry, and neurobiological evidence demonstrating that dopaminergic medications used in Parkinson's disease—particularly dopamine receptor agonists (especially those targeting D2/D3 receptors)—alter decision-making and impulse control, leading to impulse control disorders such as pathological (compulsive) gambling, compulsive buying, hypersexuality, and binge eating.

0:36:10supportedmoderateScience & Tools of Learning & Memory | Dr. David Eagleman

Primary visual cortex locks down early in development and shows very limited plasticity in adulthood compared to downstream visual areas that retain lifelong plasticity.

"your primary visual cortex at the back of the head, that locks down early. You really can't do much to change that. And um you know there were studies by Logothetis' lab years ago where they looked at changes to let's say the retina in an adult monkey and they expected to see changes in the visual cortex of the monkey and they didn't see any changes at all, and that surprised them given all the plasticity literature. But it's because the visual cortex locks down. In contrast, these downstream areas from the visual cortex that care about things like recognizing faces or new brands of fast food restaurants or whatever it is, those stay plastic your whole life" (said at 0:36:10)

The claim accurately reflects the classical neurobiological principle that primary visual cortex (V1) undergoes a defined critical period early in postnatal development, after which large-scale structural reorganization and ocular dominance plasticity become markedly restricted compared to higher-order, downstream visual areas that exhibit lifelong functional and synaptic plasticity. While adult V1 is not entirely inert—retaining localized forms of homeostatic plasticity, perceptual learning, and short-term adaptation—its capacity for large-scale topographic reorganization is constrained.

0:41:30overstatedmoderateScience & Tools of Learning & Memory | Dr. David Eagleman

Human prefrontal cortex is proportionally much larger than that of any other animal species, including closely related primates.

"we also have this capacity to look into the future and think about who we want to be. And that is essentially subserved by our prefrontal cortex, which as we mentioned earlier is something that is a, you know, the size of it is unique to humans. All of our closest cousins in the animal kingdom don't have a prefrontal cortex that's a fraction of what we have." (said at 0:41:30)

Comparative neuroanatomical studies show that while the prefrontal cortex is proportionally expanded in humans compared to non-ape primates, this non-allometric prefrontal expansion is shared with closely related great apes. Evidence indicates that prefrontal enlargement originated at the root of the great ape clade (approximately 15–19 million years ago) rather than being uniquely or disproportionately enlarged in humans relative to other hominoids.

0:51:45supportedmoderateScience & Tools of Learning & Memory | Dr. David Eagleman

Mental imagery exists on a neurological spectrum ranging from a total lack of visual imagery (aphantasia) to extremely vivid, movie-like visual imagery (hyperphantasia).

"one of the things I've studied is, um, aphantasia all the way to hyperphantasia. That means when, you know, if I ask you to visualize an ant crawling on a tablecloth towards a jar of purple jelly, some people see it like a movie in their head. That's called hyperphantasia. Some people have no picture at all in their head. That's called aphantasia. And everyone is somewhere in between on the spectrum." (said at 0:51:45)

Visual imagery vividness varies continuously across the population, anchored at the extremes by aphantasia (the absence of conscious visual imagery) and hyperphantasia (imagery vivid enough to rival actual perception). Neuroimaging and behavioral studies demonstrate corresponding neural signatures, including differences in functional connectivity between prefrontal/frontoparietal networks and the visual cortex across this spectrum.

1:00:15supportedmoderateScience & Tools of Learning & Memory | Dr. David Eagleman

A human child develops hyperconnected neuronal synapses during the first two years of life, which are subsequently pruned back based on environmental experience.

"What happens is over the first two years, those neurons connect more and more and more and more. And what you end up getting is this hyperconnection by the time you're two years old. And from there, it's just a matter of pruning an overgrown garden. And that's all that's happening. And the way the pruning happens is based on what you're experiencing in the world." (said at 1:00:15)

Extensive postmortem electron microscopy and neurodevelopmental research demonstrates that humans undergo a burst of exuberant synaptogenesis during infancy and early childhood, with synaptic densities peaking well above adult levels (in the prefrontal cortex peaking around 1 to 2 years of age). These overproduced synapses are subsequently pruned back through childhood and adolescence in an activity- and experience-dependent manner.

1:03:17supportedmoderateScience & Tools of Learning & Memory | Dr. David Eagleman

Time perception relies on multiple distinct neural mechanisms for different timescales rather than a single dedicated brain region.

"one of the things that is so striking about time perception is that you don't have a single part of the brain that deals with that. You actually have different mechanisms that deal with thinking about long eras of time and seconds and subseconds." (said at 1:03:17)

Extensive neuroscientific evidence and neuroimaging meta-analyses demonstrate that temporal processing does not rely on a single, centralized clock region. Instead, time perception is mediated by distributed, multi-component neural networks and intrinsic population dynamics (such as striatal, cerebellar, cortical, and insular circuits) that differ depending on the timescale (e.g., sub-second vs. supra-second durations), task modality, and context.

1:09:32supportedmoderatetheir own paperScience & Tools of Learning & Memory | Dr. David Eagleman

Visual temporal resolution (flicker fusion frequency) does not increase during life-threatening situations, demonstrating that time is not visually processed in slow motion.

"The results are very clear: people do not see any faster in a life-threatening situation. And yet when we ask people retrospectively with a stopwatch to judge how long their fall was versus watching someone else do the fall, their own fall felt much longer to them." (said at 1:09:32)

The claim directly reflects the findings of the 2007 study by Stetson, Fiesta, and Eagleman (PMID 18074019). Researchers tested participants experiencing a 31-meter free fall using a perceptual chronometer measuring visual temporal resolution (flickering stimuli alternating near the threshold of perceptual fusion). While participants experienced subjective duration dilation (estimating their falls to last 36% longer), their visual temporal resolution did not increase during the event, indicating that perceived slow motion is not driven by higher visual sampling speed/temporal resolution during the frightening event, but rather is a retrospective memory effect.

1:09:52supportedlowtheir own paperScience & Tools of Learning & Memory | Dr. David Eagleman

In life-threatening situations, the amygdala mediates a secondary memory encoding pathway that creates denser memories, causing retrospective estimation of time to feel longer.

"when you're in a life-threatening situation, you recruit not just your hippocampus for laying down memory, but a a secondary memory track mediated by the amygdala. You've got this emergency control center, and you're writing down memories in this other secondary track. When you read that back out, you say, "What just happened? What just happened?" You've got all this density of memory that you don't normally have because you've written down every detail." (said at 1:09:52)

Experimental research demonstrates that the subjective experience of time slowing down during a life-threatening or frightening event is driven by retrospective memory recollection rather than an increase in real-time perceptual temporal resolution. In a classic behavioral experiment testing individuals during a 31-meter free fall (Stetson et al., 2007), participants retrospectively estimated the duration of their fall to be 36% longer than control estimates, while objective visual temporal resolution remained unchanged. The researchers proposed that high-arousal threat triggers richer, denser memory encoding (theoretically mediated by the amygdala), causing the recalled event to feel subjectively prolonged in retrospect.

1:15:15needs contextmoderateScience & Tools of Learning & Memory | Dr. David Eagleman

In 1969, Paul Bach-y-Rita published a landmark paper in Nature demonstrating tactile-to-visual sensory substitution in blind participants using a 40x40 solenoid grid on the back.

"The first major paper was in 1969 in Nature. A guy named Paul Bach-y-Rita took blind people and he put them in a dental chair and he had this thing that would poke them in the back. A grid of 40x40 little solenoids that would poke you in the back, and he set up a video camera." (said at 1:15:15)

Paul Bach-y-Rita and colleagues published the landmark paper 'Vision substitution by tactile image projection' in Nature in 1969 (PMID: 5818337), demonstrating tactile-to-visual sensory substitution in blind subjects via a grid of stimulators on the skin of the back. However, the original apparatus used a 20x20 matrix (400 vibrating solenoids/stimulators), rather than a 40x40 grid.

1:33:20supportedmoderateScience & Tools of Learning & Memory | Dr. David Eagleman

The BrainPort sensory substitution device transmits camera-captured visual patterns to an electrotactile grid on the tongue, allowing blind users to recognize objects and navigate obstacle courses.

"So with the BrainPort, the way this works is you're wearing this little camera on your head on glasses, and you've got this uh little electrical grid on your tongue. And so whatever the camera is seeing, you feel that on your tongue... And blind people can get so good at this, they can do things like, you know, throw a ball into a basket or navigate a complex obstacle course." (said at 1:33:20)

The BrainPort vision device captures images via a digital camera and translates visual patterns into electrotactile stimulation delivered to the user's tongue via an electrode array. Clinical studies and reviews demonstrate that with training, blind users can utilize the device to localize and recognize simple objects, read short words, and navigate obstacle courses.

1:38:36supportedmoderateScience & Tools of Learning & Memory | Dr. David Eagleman

Sighted humans can learn to echolocate using sound reflections to navigate spatial environments.

"It also turns out that seeing people can echolocate if it is relevant to them. You know, if you really want to put the effort into it, you can learn how to do it." (said at 1:38:36)

Evidence from controlled training studies confirms that sighted human adults can readily learn click-based echolocation to perceive spatial features and navigate environments. After structured training programs (such as 10-week, 20-session protocols), sighted participants show substantial improvements in practical and virtual spatial navigation and room-size discrimination, accompanied by functional neuroplastic changes in auditory and visual cortices.

1:42:56supportedmoderateScience & Tools of Learning & Memory | Dr. David Eagleman

Tightly blindfolding sighted adults for 60 to 90 minutes induces measurable cross-modal activation in the visual cortex in response to auditory and tactile stimuli.

"By about 2013, some of our colleagues at Harvard did this experiment where they put people on the scanner and they blindfolded them tightly and they were looking at what was going on in the brain, you know, with touch and with sounds. And it turns out that if you're blindfolded after about an hour, you start seeing a little bit of activity in the visual cortex when you are touched or when you hear something... within 60 to 90 minutes, you start seeing little blips of activity." (said at 1:42:56)

Neuroimaging and neurophysiological studies demonstrate that short-term visual deprivation (via blindfolding for minutes to hours) in normally sighted adults rapidly unmasks existing cross-modal connections, leading to measurable activation and excitability changes within the primary visual cortex in response to non-visual (tactile and auditory) stimulation.

1:46:11supportedmoderateScience & Tools of Learning & Memory | Dr. David Eagleman

Human infants spend approximately 50% of their total sleep time in REM sleep.

"Infants spend 50% of their time in REM sleep. As you get older and your brain becomes less plastic, you have a drop-off in REM sleep." (said at 1:46:11)

Standard developmental sleep physiology establishes that full-term human neonates and young infants spend approximately 50% of their total sleep time in active (REM) sleep. This proportion is highest around birth and gradually declines over infancy and early childhood toward the adult level of roughly 20–25%. Longitudinal polysomnographic and ontogeny studies confirm this high initial proportion of REM/active sleep and its subsequent developmental decrease.

1:46:22supportedmoderateScience & Tools of Learning & Memory | Dr. David Eagleman

Mammals born immature (altricial) exhibit significantly more REM sleep than precocial species that are born mobile and mature.

"when you look across animal species of all types, you find that the animals that are born with extended infancies and need to figure out how to do stuff in the world, they all have much more REM sleep, like eight times more REM sleep than animals that are born essentially mature, like cows and giraffes and zebras" (said at 1:46:22)

Comparative developmental sleep research demonstrates that altricial mammals (born immature and dependent, such as rats, cats, and humans) spend significantly larger proportions of early life in rapid eye movement (REM) or paradoxical sleep (PS), which declines sharply with maturation. In contrast, precocial species (born mature and mobile, such as guinea pigs and ungulates) are born with low, adult-like amounts of REM sleep. However, broad phylogenetic comparative studies note that interspecific differences in adult sleep durations are also heavily shaped by ecological constraints, predation risk, and recording conditions.

1:47:43supportedlowScience & Tools of Learning & Memory | Dr. David Eagleman

People who are blind experience dreams centered on non-visual modalities such as auditory and tactile sensations rather than visual imagery.

"By the way, people who are blind still have dreams, but their dreams are not visual. They have a dream like, "Oh, I was, you know, feeling my way around the living room... But it's sound, it's touch, it's things like that." (said at 1:47:43)

Empirical studies comparing dream content across congenitally blind, late blind, and sighted individuals confirm that blindness substantially reduces visual dream imagery and increases reliance on non-visual sensory modalities, particularly auditory, tactile (haptic), gustatory, and olfactory impressions. In individuals with congenital blindness, dreams are predominantly constructed from these non-visual modalities.

1:51:12supportedmoderateScience & Tools of Learning & Memory | Dr. David Eagleman

Longitudinal research by Elizabeth Phelps found that flashbulb memories of traumatic events (9/11) degrade and distort over time at the same rate as everyday autobiographical memories.

"So our colleague Elizabeth Phelps did this experiment right after 9/11 in 2001 shortly after the event happened. She went and interviewed lots of people in downtown and Midtown New York about what they saw on September 11th, and she was smart enough to interview them also about what they remembered from September 10th... She then found them three months later. She followed up a year later. She ended up doing that 10 years later as well. What they found is that the traumatic memories of 9/11, even though those are amygdala memories, they drifted just as much as the memories of, you know, what they ate for lunch on September 10th." (said at 1:51:12)

Longitudinal research led by Elizabeth Phelps, William Hirst, and colleagues tracked thousands of participants' recollections of the September 11 terrorist attacks over years (at 1 week, 11 months, 35 months, and up to 10 years). They demonstrated that flashbulb memories for the traumatic event were subject to forgetting, distortion, and inconsistency over time—stabilizing in content after the first year rather than remaining indelible—while participants retained high subjective confidence in their accuracy.

1:56:22supportedhighScience & Tools of Learning & Memory | Dr. David Eagleman

False autobiographical memories can be implanted in individuals through suggestive interviewing techniques, such as the 'lost in the mall' paradigm by Elizabeth Loftus.

"So Elizabeth Loftus at Irvine ran these studies years ago where what she's doing in these cases is she says to someone, "Hey, I talked to your parents." She actually did talk to the person and she says, "I found out a story from when you were younger about the time you got lost in the mall and you were found by this woman in a red hat..." And it turns out she can make these stories completely up, and people will come to believe these." (said at 1:56:22)

Extensive experimental literature, including Elizabeth Loftus's seminal 'lost in the mall' paradigm and subsequent replications and mega-analyses, demonstrates that suggestive interview procedures, familial misinformation, and guided imagination can implant rich false autobiographical memories for non-experienced childhood events in a significant proportion of individuals.

2:01:25supportedmoderateScience & Tools of Learning & Memory | Dr. David Eagleman

Viewing pain inflicted on an outgroup member elicits significantly lower neural activation in the brain's pain matrix compared to viewing pain inflicted on an ingroup member.

"What happens is you have this empathic response, specifically this network of areas that we summarize as the pain matrix comes online... Now, what we do is we put a one-word label on each hand: Christian, Jewish, Muslim, Scientologist, Hindu, atheist... Turns out the answer, depressingly, is that your brain cares much less. So the size of the empathic response, if it's your in-group, is enhanced from what it was, and if it's any one of your outgroups, it's diminished." (said at 2:01:25)

Multiple functional neuroimaging (fMRI) studies demonstrate that observing physical pain inflicted on outgroup members (such as racial or rival social group outgroups) elicits significantly reduced activation in core pain matrix regions—most notably the anterior cingulate cortex (ACC) and anterior insula—compared to observing pain inflicted on ingroup members.

2:05:34supportedmoderateScience & Tools of Learning & Memory | Dr. David Eagleman

Observing harm or misfortune befalling an unfair or disliked individual can activate the brain's reward circuitry rather than empathic pain networks.

"there's a whole lot of experiments from my lab and other labs that shows that sometimes when something happens to someone that we don't like, the reward system actually comes on. Tania Singer had a Nature paper on this showing that you actually show reward system activation when something happens" (said at 2:05:34)

Neuroimaging studies directly support this claim. A landmark fMRI study by Singer et al. (2006) showed that while observing a fair player receive pain activated pain- and empathy-related networks (fronto-insular and anterior cingulate cortices), observing an unfair player receive pain resulted in reduced empathic response and increased activation in reward-related areas (particularly in male participants, correlated with a desire for revenge). Furthermore, Takahashi et al. (2009) demonstrated that misfortune befalling envied or disliked targets triggers schadenfreude alongside ventral striatal reward activation.

2:08:39needs contextlowScience & Tools of Learning & Memory | Dr. David Eagleman

Capuchin monkeys display inequity aversion, exhibiting frustration and refusing to participate when observing another monkey receive a higher-value reward for the same task.

"there are experiments on capuchin monkeys where the monkey does something and then gets a piece of banana, and then the other monkey does something in the neighboring cage and gets a piece of banana. And so they're doing this, but then the other monkey doing it gets a grape, which is a big treat for the monkey. And the first monkey goes nuts and is shaking the bars, he's so angry that the other monkey got a better reward." (said at 2:08:39)

The speaker accurately describes the findings of the classic 2003 study by Brosnan and de Waal, in which brown capuchin monkeys (Cebus apella) refused to perform a token-exchange task or rejected cucumber slices after witnessing a conspecific receive higher-value grapes for the same task. However, the interpretation that this represents genuine 'inequity aversion' (a social sense of fairness) rather than simple individual frustration or food expectation violations has been heavily contested. A comprehensive 2024 meta-analysis synthesizing primary data across 23 studies and 18 species (including capuchins) found no consistent evidence for inequity aversion in accept/reject paradigms.

2:09:39supportedlowScience & Tools of Learning & Memory | Dr. David Eagleman

Dehumanizing social groups decreases activation in prefrontal cortex networks typically associated with social cognition and empathy.

"you simply dehumanize the other group by calling them an animal, or like a virus, you know, a pestilence, rats... anything that's not human that turns off these networks that we have in the prefrontal lobe that care about other humans and how to interact with other humans. Our colleague Lasana Harris has studied this stuff." (said at 2:09:39)

The claim is supported by foundational neuroimaging research by Harris and Fiske (2006). In an fMRI experiment, viewing members of social groups typically elicited activation in the medial prefrontal cortex (mPFC), an area essential for social cognition and mentalizing. However, viewing extreme out-groups that elicit disgust and dehumanization (such as homeless individuals and drug addicts) failed to significantly activate the mPFC, mirroring responses typically seen for non-human objects. Evidence is graded as low certainty due to the small sample size (n=10-12) typical of early task-based fMRI studies.

2:16:50needs contextmoderatetheir own paperScience & Tools of Learning & Memory | Dr. David Eagleman

Arbitrarily designating an outgroup as an ally rapidly increases an individual's empathic neural response when observing members of that group experiencing physical pain.

"What we now do is we say the year is 2029 and these three religions have teamed up against these three religions. And now you see the different hands get stabbed. But the ones who I just told you in one sentence are your allies now, you care more about them just because I arbitrarily told you that they're your allies." (said at 2:16:50)

Neuroimaging studies using minimal group paradigms and group allegiance manipulations demonstrate that empathic neural responses to observing others in physical pain can be modulated by arbitrary group assignments and newly defined group affiliations (e.g., classifying arbitrarily formed ingroups vs. outgroups based on neural responses in pain-related networks). However, the evidence is nuanced: while arbitrary coalition and group cues can rapidly modulate neural responses in certain subcortical and visual processing regions or classifier predictions, some studies show that minimal group designations do not always override more entrenched, automatic biases (such as racial ingroup empathy biases) in core affective pain regions like the anterior cingulate and anterior insula.

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