Determined

What really causes you to do what you do? In Determined, Robert Sapolsky argues that your choices are not authored by a freestanding inner homunculus but arise from layers of prior causes—biology, development, culture, and context—stacked like turtles all the way down. He contends that once you follow those turtles honestly, the classic notion of free will that grounds moral desert evaporates, and with it the foundations of retributive blame and praise.

You discover how seconds-old sensory cues, minutes-old hormone surges, years-long neural development, fetal exposures, genes, and centuries of cultural evolution shape intent. You then learn why late-breaking neuroscience about readiness potentials (Libet, Haynes, Fried) can’t carry the free-will debate by itself. Finally, you confront the big temptations—chaos, emergence, quantum indeterminacy—and see why unpredictability or micro-randomness doesn’t restore responsible agency, even as the science still leaves room for optimism about change.

The core claim: seamless causation

Sapolsky’s central metaphor is disarming: every behavior rests on prior turtles—determinants that reach back seconds, years, and evolutionary epochs. Swap the genes, uteruses, childhoods, and cultures of a commencement speaker and a groundskeeper, and you likely swap life trajectories. That thought experiment, not Laplace’s demon, is the kind of determinism at stake here—practical, cumulative, and relentlessly biological and social.

He piles on examples to anchor the idea. A tamping rod through Phineas Gage’s frontal cortex rewrote his personality. A judge’s hunger systematically shifts parole decisions across a day. Disgusting smells bias moral judgments via the insula. These are not metaphors; they’re experimentally replicated effects with neural correlates. When you look closely, what felt like uncaused willing turns into context-sensitive neural machinery doing what circumstances have prepared it to do.

Not about prediction, but about control

Determinism here doesn’t mean omniscient prediction. Chaos theory shows deterministic systems can be effectively unpredictable because tiny initial differences blow up over time (Lorenz’s butterfly effect; cellular automata like Rule 22/90). Emergent complexity means simple local rules can yield surprising global patterns (ants, bees, slime molds solving mazes; Tero’s slime-mold rail networks). Unpredictability complicates forecasting, but it doesn’t conjure metaphysical freedom. The parts still follow lawful causes.

Quantum indeterminacy, meanwhile, is a dead end for agency. Even if micro-events are ontically random, decoherence in warm, wet brains (per Max Tegmark’s critiques of Penrose–Hameroff) prevents sustained quantum control. And randomness isn’t authorship—if a quantum coin flip tips your decision, that’s not the kind of control that grounds responsibility.

Why the last seconds mislead

Much debate fixates on the final second before action. Libet’s readiness potentials precede reported intent by ~300 ms; fMRI classifiers predict simple choices seconds ahead at ~60% accuracy (Haynes); single-neuron work pushes to ~80% (Fried). Sapolsky agrees these are provocative but insists they’re the last three minutes of a long movie. These tasks involve trivial button presses, not life-shaping choices, and the data are noisy and context-bound.

Even the cherished “free won’t” veto recruits the same deterministically built frontal circuits (pre-SMA, right inferior frontal gyrus). Inhibitory control is a brain process like any other, molded by your development, hormones, and stress. To ask where intent came from, you must zoom out to minutes, years, and lifetimes of prior shaping.

What this means for praise and blame

If behavior is determined, moral desert loses its footing. You still protect society—incapacitate dangerous people, deter harm, rehabilitate where possible—but you drop retribution as payback for metaphysical guilt. Praise and gratitude become tools to encourage prosocial behavior, not badges of cosmic merit. This shift mirrors historical moves from demonology to medicine in epilepsy and schizophrenia: we learned to replace blame with understanding and safeguards.

Key Idea

“When you behave in a particular way … it is because of the determinism that came just before, which was caused by the determinism just before that, and before that, all the way down.”

Roadmap for the rest of the book

You’ll trace intent across timescales—from instant sensory primes and hormone pulses to adolescent frontal-cortex remodeling and the epigenetics of childhood adversity. You’ll examine why willpower and “grit” are properties of the prefrontal cortex under metabolic and social constraints, not freestanding virtues. You’ll see why chaos, emergence, and quantum strangeness don’t rescue responsibility, even as they enrich how you think about brains near criticality.

Then you’ll learn how real change works mechanistically—through conserved plasticity cascades (cAMP → PKA → MAPK → CREB) from sea slugs to humans—and how the same conditioning machinery can be hijacked for political fear-mongering and later unlearned. Finally, you’ll survey evidence on religion, free-will belief, and morality; reimagine punishment via quarantine and restorative approaches; and translate determinism into a humane social program focused on prevention, rehabilitation, and structural justice. The upshot is sobering but hopeful: you lose metaphysical blame, not meaningful progress.

Sapolsky answers the question “Where did that intent come from?” by widening your lens. Intent is a biological history rendered in the present—a product of what you sensed a moment ago, the hormone bath you’re swimming in today, the adolescence that sculpted your prefrontal cortex, the womb you developed in, the genes you carry, and the culture your ancestors built. When you zoom across timescales, the idea of a will detached from causes starts to look like a mirage.

Seconds to minutes: the immediate context

Right now, subtle cues are tugging on your judgments. A disgusting odor can make you moralize more harshly via the insula. Attractive faces engage orbitofrontal cortex and bias you toward leniency—the beauty-as-goodness effect. Even hunger shifts decisions: the famous parole study shows approval rates decline as a judge gets further from a meal. These effects, replicated across labs, demonstrate how fast-changing sensory and physiological states nudge your “choices.”

You don’t experience a “smell making your ethics stricter,” but your circuitry does. Your brain integrates the last few seconds of sensory context into valuation systems before you even name what’s happening. The upshot: intent is always marinated in the immediate now.

Minutes to days: hormones in motion

Hormones tune your circuits in real time. Testosterone tilts you toward risk-taking and dominance (it amplifies preexisting motives rather than creating them from scratch). Cortisol during stress downshifts the prefrontal cortex and upshifts the amygdala, making impulsive, habitual responses more likely. Oxytocin raises trust—especially toward in-groups—but can sharpen out-group suspicion (Dutch subjects became more punitive toward Germans when dosed). These aren’t moral properties; they’re modulators of neural probabilities.

Across a week of stress or a day of hormonal ebb and flow, the same person inhabits different decision landscapes. A policy takeaway follows: support sleep, nutrition, and stress reduction if you want better PFC-mediated restraint in schools, courts, and workplaces.

Years back: development and adolescence

Your frontal cortex is late to the party. During adolescence, massive synaptic pruning and myelination shape executive functions—planning, impulse control, delayed gratification. Social experiences, trauma, and enrichment during these years wire up circuitry you will carry for decades. Childhood adversity doesn’t just sting; it writes on gene regulation (via epigenetic marks), shifting stress reactivity and impulse control.

This is why two teenagers with different early lives can bring very different PFC toolkits into adulthood. It’s also why “try harder” pep talks can be cruel—if your adolescent PFC matured under chronic stress, your baseline for executive control is simply different.

Fetal life, genes, and culture

Go back further. Fetal hormone exposure biases later traits; maternal stress, alcohol, and nutrition alter neurodevelopmental trajectories. Genes set parameters for neurotransmitters and receptors, nudging vulnerability or resilience. And culture—centuries of rice versus wheat agriculture, pastoralist honor norms—shapes parenting, cooperation, and conflict expectations that feed into development.

Consider ACEs (Adverse Childhood Experiences): each added adversity robustly raises the odds of antisocial outcomes and poor health later. The mechanism is not mystical; it is stress biology and plasticity doing what they do, shaped by early conditions. “Couldn’t you have chosen differently?” becomes the wrong question. The capacity to form a different intent was itself the product of earlier conditions you did not choose.

A practical reframing for you

Instead of moralizing in the moment, ask across scales: What just primed this decision? What hormones are at work? What adolescent experiences shaped this person’s PFC? What fetal and genetic factors shifted stress circuits? And what culture tutored their expectations? You’ll still hold people accountable in a forward-looking way (to protect others and encourage change). But you’ll stop pretending that desert rests on uncaused choice rather than on stacked, interacting histories.

(Note: This multi-scale lens echoes thinkers from Tinbergen’s four questions to contemporary developmental psychobiology; Sapolsky’s gift is integrating them into the ethics of everyday judgment.)

Modern culture idolizes grit—as if willpower were a moral muscle independent of biology. Sapolsky flips that script. What you call grit mostly reflects how well your prefrontal cortex (PFC) can regulate impulses, weigh long-term payoffs, and dampen emotional storms. That circuitry is an organ, not a halo, and it depends on genes, hormones, development, sleep, hunger, and stress.

What the PFC does when it works

The dorsolateral PFC supports planning and working memory; the ventromedial PFC integrates value and emotion. Together they implement rules like “no dessert now so I feel better later.” Damaging them famously changes people—Phineas Gage’s tamping-rod injury transformed a diligent foreman into a disinhibited wanderer. You see, in living color, that “character” is a neural configuration with a metabolic budget.

Now add neuroeconomics: the PFC must compete with reward circuits for scarce resources. Under fatigue or stress, PFC signaling falters, and habitual, impulsive systems dominate. You didn’t suddenly become immoral; your executive network ran out of fuel.

Biological limits on willpower

PFC function is exquisitely state-dependent. Poor sleep, low glucose, acute stress, and hormonal shifts degrade its control. Look at the parole-judges study: favorable rulings plummet as time since the last meal increases, then rebound after breaks. That’s not cosmic unfairness; it’s biology changing thresholds in real time.

Hormones matter too. Cortisol during stress biases you toward fast, habitual responses; testosterone can amplify dominance motives and risk tolerance; oxytocin’s same-camp warmth can harden out-group boundaries. The story isn’t “good” or “bad” people; it is PFC machinery trying to do cost–benefit control in a moving internal weather system.

Why grit doesn’t vindicate desert

Ask where a person’s strong PFC came from. Safe neighborhoods, enriched language environments, secure attachment, good schools, low early-life stress, sleep and nutrition—these build executive function. Chronic poverty, trauma, and discrimination impair it (think ACEs and their epigenetic fingerprints). You do not choose the scaffolding that tunes your control systems, so “I succeeded because I had grit” easily slides into “I won the neurodevelopmental lottery.”

This doesn’t mean you never commend effort. It means you use praise instrumentally—to encourage patterns that help people and protect others—without pretending it ratifies metaphysical merit. Likewise, when someone fails self-control under stress, you respond pragmatically: adjust environments, support sleep and nutrition, add coaching and therapy, and reserve coercion for safety, not moral payback.

Implications for schools, clinics, and courts

If grit lives in the PFC, then policy should invest where PFC function grows. Schools that bake in predictable routines, movement, nutritious meals, and mindfulness give kids a fairer shot at executive control. Clinicians can frame relapse in addiction as lapses in a stressed control system, not as proof of moral rot, and then target sleep, stress, and social triggers. Courts can schedule high-stakes decisions when judges are rested and fed (practical nudges beat pieties).

(Note: This reframing echoes Angela Duckworth’s “grit” work but relocates its engine in biology; Sapolsky’s point is not to dump grit but to unmask its mechanistic roots so we stop confusing lucked-into circuitry with desert.)

The free-will debate often camps in the final seconds before action. Sapolsky walks you through the famous studies and shows why they matter—and why they can’t settle the question of agency. The last-second view is like watching only the final three minutes of a movie and claiming you grasp the plot.

What Libet and successors found

Benjamin Libet discovered that a readiness potential in motor areas (SMA/pre-SMA) ramps up about 300 milliseconds before people report deciding to move. Later, John-Dylan Haynes used fMRI pattern classifiers to predict left/right button presses seconds in advance at modest accuracy (~60%). Itzhak Fried’s single-neuron recordings in epilepsy patients pushed predictions higher (~80%) a second or two before awareness. These data suggest conscious intention often trails upstream neural events.

Critics fairly note the tasks are trivial and the timing of “awareness” is fuzzy. Readiness potentials could reflect motor preparation rather than decisions, and the brain’s predictions are probabilistic, not fate carved in stone. Still, the pattern is hard to square with a sovereign conscious decider issuing first causes in real time.

“Free won’t” and frontal brakes

Libet emphasized a potential veto: perhaps you can consciously stop an action already in motion. Neuroscience maps that inhibition to frontal circuits (pre-SMA, right inferior frontal gyrus) that implement stopping. But those inhibitory capacities are themselves shaped by development, hormones, fatigue, and training. Your “free won’t” is a causal process with a history, not a magic override somehow floating above biology.

You can strengthen these brakes with practice and environment (sleep, stress reduction), which is good news for behavior change. The philosophical point remains: better brakes do not become metaphysical authorship; they are still parts in the same deterministic engine.

Noise is real—and regulated

Neurons and synapses are noisy. Bernard Katz showed synapses release neurotransmitter in discrete quanta and sometimes “spontaneously.” Presynaptic calcium dynamics and molecular machinery (e.g., separable spontaneous vs. evoked release pathways) set release probabilities, and neuromodulators, stress hormones, alcohol, and endocannabinoids alter those odds. Sapolsky calls this “determined indeterminacy”: there’s stochasticity, but biology corrals it.

This matters for free will because “random” isn’t “responsible.” If a spontaneous vesicle release helps tip a motor neuron and a finger twitches, that doesn’t bestow authorship any more than a noisy microphone makes a singer sovereign. The system uses noise adaptively, especially in development and plasticity, but it remains embedded in causes.

Why the origin story is upstream

Sapolsky’s clincher is conceptual: even if all last-second signals were preconscious, you’d still need to ask where the underlying preferences and thresholds came from. Those live in the “minutes to lifetimes” you inherited and experienced. The way your amygdala weights threats today may have been tuned by adolescent stress, fetal exposures, and culture. That’s where intent comes from, not from a ghost in the synapses three hundred milliseconds before you act.

(Note: Philosophers call Sapolsky’s stance “hard incompatibilism.” Compatibilists try to rescue responsibility without contra-causal freedom; Sapolsky thinks the science plus the desert concept won’t fit. Either way, both sides can agree the last-second view is too narrow.)

When people hunt for free-will loopholes, they often point to chaos, emergent complexity, or quantum mechanics. Sapolsky tours each and shows why they change how you think about prediction and structure, but not about responsible authorship. The key error to avoid is confusing unpredictability or micro-chance with control.

Chaos: deterministic and wild

Edward Lorenz’s weather models launched chaos theory: small rounding differences ballooned into divergent forecasts—the butterfly effect. Cellular automata, such as Wolfram’s Rules 22 and 90, show how simple update rules produce mesmerizing complexity. Strange attractors pull systems into fractal orbits that never exactly repeat. The punchline: deterministic rules can be effectively unpredictable. That limits your forecasting power but doesn’t mint free will. The system’s future still depends on its prior states by law-like rules.

For behavior, this means even if you can’t predict a person’s path well, it can still be fully caused. Epistemic limits (your ignorance) don’t create ontological gaps (uncaused choices).

Emergence: from local rules to global order

Emergence shows how many simple agents, following local rules, yield sophisticated patterns. Ant colonies recruit via pheromones; bees “waggle” to share nectar locations; slime molds (Nakagaki, Tero) trace efficient networks that inspired human transport designs. In development, branching morphogenesis and L-systems produce fractal lungs and vasculature; Turing’s reaction–diffusion can paint zebra stripes. Neurons wire under constraints favoring wiring economy and small-world topology, with hub-like structures enabling integration.

These top-down patterns are astonishing and useful (engineers copy them in ant-colony optimization and decentralized robotics), but they don’t float free of parts. No emergent “captain” sits above ant rules; the colony remains the sum of interacting causes.

Critical brains: balance, not magic

Brains often look poised near criticality—balanced between order and chaos—with pink (1/f) noise signatures across scales. Tilt toward too much synchrony and you get seizures (white-noise-leaning patterns); tilt toward fragmentation and you approach the brown-noise disconnection of neurodegeneration. Organoids even show early oscillatory signatures suggestive of such balance. The lesson is architectural: cognition thrives in scale-free, small-world networks—but the physics of that balance doesn’t grant contra-causal freedom.

Quantum: weird, fragile, and not agency

Quantum phenomena—superposition, entanglement, tunneling—are real (double-slit experiments, satellite entanglement). But brains are decoherence factories; sustained quantum computation in microtubules (Penrose–Hameroff) faces steep physical objections (Tegmark’s timescale arguments). Even if micro-indeterminacy influenced a neuron, that would add randomness, not authorship. Philosophers and neuroscientists (e.g., Shadlen & Roskies) converge on this: you need stable policies to harness noise, and noise is not control.

Put plainly: chaos complicates prediction, emergence builds wonders from parts, and quantum injects chance—but none supplies the missing ingredient of metaphysical responsibility. You still return to the turtles: biology and environment, all the way down.

If your behavior is determined, can you change? Yes—because the same causal machinery that built your habits can rebuild them. Sapolsky anchors this in Eric Kandel’s Nobel-winning work on sea slugs (Aplysia) and traces the molecular cascades that convert experience into lasting synaptic change. From gill-withdrawal reflexes to human therapy, the gears are conserved and mechanistic.

Aplysia’s staircase of change

Touch a siphon, the gill withdraws. Pair touches with tail shocks, and withdrawal strengthens and lasts longer. Kandel dissected the circuit and the biochemistry: serotonin release elevates cAMP, activates PKA, and boosts transmitter release (short term). With more pairings, MAPK and CREB turn on early genes to stabilize changes (intermediate). With extensive training, a cascade (including C/EBP) activates late genes and grows new synaptic branches (long term). The more steps you climb, the longer the behavior persists.

This same trio—short, intermediate, long-term plasticity—operates in mammalian learning, such as eyeblink conditioning. Evolution reused the parts; experience leaves a physical trace in your nervous system without consulting a metaphysical chooser.

Conditioning and the politics of fear

Your amygdala is a coincidence detector. When a neutral cue (a word, image, out-group) is paired with an aversive outcome (crime stories, violent videos), amygdala synapses strengthen through those same cAMP/PKA/CREB cascades. Rhetoric that pairs “Mexicans” with “rapists” exploits this circuitry. Over time, the category itself evokes fear and disgust. That conditioned response depends on your internal state (fatigue, intoxication), hormones (testosterone peaks), history (early trauma), genes (stress-reactivity variants)—the whole determinist stack.

The hopeful part: conditioning is reversible. Extinction training, counterexamples, different primes (reminders of shared identities), oxytocin, SSRIs, and structural changes that reduce stress can weaken toxic associations. Plasticity cuts both ways.

From mechanism to intervention

Seeing plasticity as biochemical opens doors. Therapies time exposures and reconsolidation windows to rewrite memories. Schools structure repetition and sleep to stabilize learning. Public-health interventions (reducing childhood adversity) shift entire probabilistic futures by altering stress biology early. Even when early adversity impairs later eyeblink conditioning in rats, enriched environments can partially rescue performance—a reminder that biology is a moving target, not a sentence.

For you, the implication is practical: if you want to change, design environments and routines that repeatedly trigger the right cascades. Don’t wait for willpower; build contexts that the PFC can win within. Reward small steps often; sleep on new skills; reduce stressors that tilt you back to habit. Determinism doesn’t kill change—it specifies the levers.

(Note: Kandel’s Aplysia is not a metaphorical cousin but a molecular one; the same CREB family you read about in slugs shows up in your cortex after therapy homework.)

Won’t society run amok if people stop believing in God or free will? Sapolsky separates intuition from evidence. The best data suggest that briefly weakening free-will belief nudges beliefs a bit but doesn’t reliably corrupt behavior, and that religious versus secular prosociality depends heavily on in-group identity and institutions rather than metaphysical creed alone.

What experiments actually show

Early lab studies found that priming determinism increased cheating or aggression in some tasks, with neural correlates like reduced error-monitoring. But a large 2022 meta-analysis of 145 experiments reported small shifts in belief and no consistent behavioral degradation. Replications are mixed, publication bias is real, and effects concentrate in people whose beliefs are malleable. Lifelong skeptics and steadfast believers tend to behave similarly on moral tasks.

The best single predictor across studies is moral identity: how central being a “moral person” is to you. Make morality part of identity, and behavior follows—regardless of metaphysical stance.

Religion, prosociality, and in-groups

Religious people often report more charity, but behavioral measures (blood donation, tipping, honor-system payments) shrink or erase differences. Prosocial boosts from religious primes usually target in-group recipients. Secular primes (“civic,” “duty”) produce similar boosts for nonreligious people. The mechanism is identity salience, not necessarily theology.

Meanwhile, anti-atheist prejudice can be strong enough to shape behavior against atheists (e.g., the “Atheist Shoes” mailing anecdote). The point is not “atheists are better,” but “moral behavior is more about norms and networks than about metaphysical labels.”

Societies without metaphysical props

If godlessness or free-will skepticism doomed morality, Scandinavia would be dystopian. It isn’t. Highly secular nations show low violence, high trust, and robust welfare systems (correlation is not causation, but the pattern punctures doomsday claims). What sustains cooperation are institutions, shared identities, and safeguards—moral scaffolding that doesn’t require desert rhetoric.

For policy, this means you nurture prosocial behavior by strengthening communities, civic rituals, and fair institutions; by reducing stressors that erode PFC control; and by appealing to identities that include out-groups. The metaphysics can remain a live debate without holding society hostage.

(Note: Ara Norenzayan’s work on “moralizing gods” explains why belief once stabilized large-scale cooperation; Sapolsky’s point is that other scalable mechanisms—states, norms, surveillance, education—can now do much of that work.)

If no one deserves blame in the metaphysical sense, how should you respond to harm? Sapolsky surveys why humans love punishing, how punishment sustains cooperation, and what a forward-looking, humane system could look like. The hardest obstacle isn’t logic; it’s that punishment feels good.

Why we punish—and enjoy it

Evolutionary game theory shows punishment stabilizes cooperation (Axelrod; Boyd, Gintis & Bowles). Neuroimaging reveals that retribution activates reward circuits (nucleus accumbens), and even children and chimps will pay to watch bad actors punished (Tania Singer’s work on Schadenfreude). Many people cling to belief in free will partly to justify that gratifying payback. Knowing this helps you see why reform is emotionally uphill.

Historically, the spectacle of punishment—Damiens publicly quartered in 1757; Bundy-era crowds—served communal catharsis more than rational prevention. Modern justice has pulled back from spectacle, but retributive rhetoric remains our default grammar.

The quarantine model

Derk Pereboom’s quarantine model reframes dangerous individuals as public-health risks: you can constrain them to protect others, but only minimally and always with rehabilitation and prevention in mind. Four principles guide it: some people pose genuine future risk; that risk isn’t necessarily their fault; society may constrain to protect; constraints must be least-infringing and paired with root-cause interventions.

This is not soft-on-crime sentimentalism. It is a pivot from past-tense blame to future-tense safety. Norway’s response to Anders Breivik—strict but humane imprisonment, a refusal of vengeful theater—shows a society choosing principles over spectacle.

Real-world gray zones

Hard cases remain. Consider drivers with uncontrolled seizures who kill after ignoring medical advice (Dorothy Bruns). We can acknowledge disease while still imposing constraints and accountability instruments (license suspensions, mandatory treatment) for public safety. The rhetoric shifts from “you deserve pain” to “we must reduce risk, repair harm, and fix systems that bred this danger.”

Restorative justice and truth commissions (e.g., South Africa) demonstrate that non-retributive practices can promote healing and reduce recidivism, even if they sometimes lean on responsibility talk as social technology. Reform requires building institutions and also doing cultural work to cool the warm glow of revenge.

(Note: Philosophers Gregg Caruso and Pereboom provide detailed policy blueprints; Sapolsky’s contribution is knitting those to neuroscience and human appetite for punishment.)

Accepting determinism can sting. It undercuts pride in “deserving” success and threatens narratives of redemption through sheer will. Sapolsky doesn’t sugarcoat that psychological cost, yet he argues that determinism unlocks a more honest, compassionate politics—especially when biology and circumstance predetermine outcomes long before anyone “chooses.”

Hard truths about control

Studies suggest depressed people sometimes estimate control more accurately than the nondepressed, which hints that comforting illusions can buoy morale. Compatibilists often retool “free will” to preserve meaning. Sapolsky’s reply: we can build meaning in forward-looking ways without metaphysical desert—through relationships, projects, and institutions that harness known levers of change.

Concrete cases drive the point home. Discovering leptin mutations reframed some severe obesity as biology, relieving cruel self-blame. ACEs research quantifies how stacked adversities (each increment boosts antisocial risks by sizable margins) shape adult outcomes. You don’t fix these with sermons about willpower; you change upstream conditions.

John Henryism and structural stress

Sherman James’s “John Henryism” shows that exhorting heroic effort in the face of structural barriers can be literally pathogenic—raising blood pressure and heart-disease risk among people battling racism and poverty. Determinism here is a demand for justice: stop prescribing grit where the system bleeds people dry, and start redesigning the system.

A determinist ethic therefore invests in prenatal care, reduces childhood adversity, equalizes schooling, feeds kids, lowers neighborhood stressors, and funds rehabilitation. You measure success by less harm and more flourishing, not by how much righteous pain you can inflict.

A humane program you can live with

Meaning survives as a verb, not a verdict. You still celebrate achievements to reinforce what helps; you still mourn harms and protect the vulnerable. You stop asking “who truly deserves blame or praise?” and start asking “what works, what heals, what prevents?” That moral shift is already how we treat epilepsy and schizophrenia compared with centuries past. Extending it to addiction, violence, and inequality is the next step.

In daily life, determinism can make you slower to condemn and quicker to help. In policy, it can move budgets from cages to clinics, from punishment to prevention. You risk losing a pleasing myth; you stand to gain a society that understands itself well enough to change.

(Note: Sapolsky’s stance rhymes with public-health models of behavior; if you’ve read Michelle Alexander or Bryan Stevenson on criminal justice, you’ll recognize the throughline: diagnosis before blame, and repair over revenge.)