The Beauty of Settled Science

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The Beauty Of Settled Science - by Scott Alexander

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The Beauty Of Settled Science<br>...

Scott Alexander<br>Aug 04, 2026

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Commenters convinced me I made a subtle mis-step in my framing of Psychology Research Is Mostly Fine.<br>My framing emphasized that social priming studies had failed to replicate, but that many other subfields of psychology hadn’t. This naturally led commenters to point to failed replications in other subfields. Although none of these were as bad as social priming, few or none were entirely problem-free.<br>Instead of emphasizing the difference between social priming and other subfields, I should have emphasized the difference between settled science and novel research.<br>Here are some of my favorite psychology findings:<br>The brain is sculpted by reinforcement learning, and a key driver of this learning is a prediction-error-based algorithm located in the nucleus accumbens and implemented through dopamine.

Psychedelic drugs exert their effects through 5-HT2A receptors, pointing to a role for these receptors in some sort of construct like the balance between priors and new evidence.

Certain cognitive functions are localized to certain brain areas (for example, impulse control to the frontal lobes; linguistic structure to Broca’s area, linguistic meaning to Wernicke’s area. But injure one of these areas, or render a certain function useless (eg a blind person having no more use for their visual cortex), and these mappings can gradually shift - suggesting that neurons are general-purpose compute whose specialization is a contingent fact about convenience and efficiency rather than a necessity.

Most personality traits and general capabilities are about 50% genetic and 50% random, with little role for family environment or childhood history, with a few notable exceptions like partisan preference. Recent research complicates this story, but the further you go from this basic picture, the gnarlier the chains of indirect causation you require.

Neurons fire together in “brain waves”, whose exact frequency corresponds with the character of consciousness; These divide neurons into natural subpopulations and linked graphs. The gamma rhythm corresponds surprisingly well to items in conscious awareness.

GABA receptors seem to be involved in something like relaxation. By hitting different GABA receptors in different ways, you can modulate the exact type of relaxation you produce. Hitting GABA-A directly is too powerful and can cause dangerous levels of sedation, but allosteric modulation of GABA is an incredibly fruitful strategy that underlies drugs from benzos to barbituates to alcohol. If you know your GABA-A subunits, you can target specific subtypes of relaxation; for example, Ambien hits GABA-A1 and induces sleep.

Memory divides somewhat fuzzily into bins of immediate-sensory, short-term, and long-term, with separate retrieval and storage functions, and separate systems for declarative vs. procedural learning. These can be harmed selectively, usually by hippocampal injury, so that some patients can remember their life stories but not form new long-term memories, or learn new skills like bike-riding but not new facts. The exact substrate of memory is unclear but seems to involve new synaptic connections between neurons in at least some way.

The ability of modern psychology and psychiatry to treat mental illness is real but limited. SSRIs work for half or slightly fewer than half of patients; antipsychotics work with extreme side effects; benzodiazpines work but produce addiction and tolerance in many (not all) people. Most supplements are stuck in Poor Quality Study Replication Crisis Hell, but melatonin and l-theanine stand out as especially promising. Psychotherapy works with moderate effect size, but (with a few exceptions) seems to be more about the relationship with the provider than the details of the therapy itself. Mental hospitalization can sometimes defuse immediate crises but work less well than mental hospitals would like, with some studies showing overall negative effects.

Schizophrenia is mostly genetic, but risk also increases with prenatal infection (especially rubella) and obstetric complications; there is suggestive evidence for roles of social stress and drug use (with psychedelics and marijuana making things worse, and nicotine if anything making things better). Bipolar and schizophrenia are so closely linked on a pathophysiological level that it seems like they might be the same disease; on the clinical level, they do seem to follow two separate courses/prognoses but can sometimes surprise clinicians by eg someone who seemed condemned to permanent schizophrenia unexpectedly recovering.

The brain’s native reinforcement learning algorithms cash out in the phenomena of classical and operant conditioning; different reinforcement schedules reinforce at different levels, which can be exploited by bad actors to make especially...

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